CHAPTER 4 Cardiac Ultrasound

Summary

Physical and technical principles of echocardiography

Specific cardiovascular structures

Key echocardiographic features of frequent diseases and clinical scenarios

Personal perspective

Additional online material

Further reading

References

Summary

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Cardiac ultrasound, or echocardiography, is by far the most extensively used imaging modality for the diagnosis of cardiovascular disease. Two- and three-dimensional real-time echocardiography provide comprehensive cardiac morphology at very high spatial (with good images, <1mm) and temporal (>100 frames/s) resolution. Moreover, Doppler and speckle tracking techniques are able to measure the local velocity of blood flow and of the myocardium throughout the heart, thus allowing blood flow analysis in valvular lesions (stenosis or regurgitation) and shunt lesions, as well as analysis of motion and deformation of the myocardium, enabling detection of functional abnormalities, e.g. in the presence of ischaemia or cardiomyopathy. Echocardiography is non-invasive and devoid of ionizing radiation; the hardware is mobile and ideal for bedside use. For special purposes, ultrasound imaging can also be performed semi-invasively via the oesophagus or invasively via the vessels. Further refinements include its application during stress, in particular to elicit an ischaemic myocardial response, and with right and left heart contrast. Because of its ubiquitous availability, lack of untoward biologic effects, relatively low cost, and unparalleled diagnostic power, it is the first-line imaging approach in cardiology and indicated in practically all cardiovascular diseases.

Physical and technical principles of echocardiography

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Sound is an audible pressure wave which transmits pressure energy through media such as air or water. As a wave, it can be characterized by the parameters wavelength λ (in length units, e.g. mm or μm), frequency f (in 1/s, or Hz), and velocity of propagation c (in m/s; Fig. 4.1); these parameters have the relation:

Sound waves with frequencies above the audible range (>20,000Hz) are denominated ultrasound. The velocity of sound in water is 1540m/s, much faster than in air, and this velocity is assumed when ultrasound travels in biologic tissue. Diagnostic ultrasound utilizes frequencies typically in the range of 2–7MHz (1MHz = 10⁶Hz), with corresponding wavelengths of 0.8–0.2mm; intravascular ultrasound catheters use frequencies up to 40MHz ( Table 4.1). The energy of a sound wave is characterized as ultrasound intensity per unit area (in W/cm²) where the area is positioned orthogonal to the propagation direction of the sound wave. Diagnostic ultrasound machines are set to operate at sound intensities which are considered biologically safe. Since intensity is not easy to measure in tissue, a surrogate parameter of ultrasound intensity is mandatorily displayed on echo machines, the ‘Mechanical Index’. This is the dimensionless ratio of peak rarefactional pressure (in megapascal, MPa) divided by the square root of the carrier frequency (in MHz), which should not exceed the value of 2 for diagnostic purposes.

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Figure 4.1 Schematic representation of a sound wave. Top image: zones of compression (high pressure) and of rarefaction (low pressure) alternate; the distance between two pressure peaks is one wavelength (λ). Lower image: the course of pressure (on the y-axis) over distance (on the x-axis) can be represented as a sine wave. A similar wave would represent pressure over time at a fixed location; the time interval of two pressure peaks would be 1/f with f for frequency. Modified with permission from Weyman AE. Principles and Practice of Echocardiography, 2nd edn., 1994. Philadelphia, PA: Lea & Febiger.

Table 4.1 Typical diagnostic ultrasound frequencies

Audible sound: <20kHz (1kHz = 103Hz)

Transthoracic echocardiography: 2–3MHz (1MHz = 106Hz)

Transoesophageal echocardiography: 5–7MHz

Intravascular ultrasound: 40MHz

Acoustic microscopy: 100–1000MHz

When ultrasound is transmitted through tissue, several interactions take place:

• ♦ Pressure energy is dissipated (mainly into heat), and the intensity of ultrasound decreases with progressive distance from the ultrasound source; this process is called attenuation and increases with ultrasound frequency. Thus, lower frequencies suffer less attenuation per travelled distance unit and are more suitable to image deep structures than higher frequencies.
  
• ♦ When ultrasound strikes the interface between media of different acoustic properties, several interactions are possible ( Fig. 4.2): if the media are acoustically very different, like air and water (technically, this difference is quantified as ‘acoustic impedance’), reflection occurs, meaning that the ultrasound is not transmitted further but sent back from the interface at an angle depending on the angle of incidence. Reflection can be total or partial. If the interface (the ‘reflector’) is small, i.e. of a size comparable with the wavelength of the sound, a process called scattering occurs, where instead of unidirectional reflection ultrasound is redirected into many directions (‘scattered’). In the body, all of these sound–tissue interactions can occur, with a multitude of tissue reflectors creating complex wave interactions which form the basis for the ‘echo texture’ or ‘speckle pattern’ of a tissue.
  
• ♦ Passage of ultrasound through tissue creates a subtle distortion of the waveform which can be understood as the addition of ‘harmonic frequencies’ (double, thrice, etc., the original transmitted frequency) to the original ‘fundamental’ frequency. These ‘harmonics’, while weak in intensity, can be extracted from the reflected ultrasound signal and are used in ultrasound imaging to improve signal-to-noise ratio, since they are less prone to near-field artefacts and other factors detrimental to image quality.
  
• ♦ When a sound wave is reflected by a moving reflector, the reflected wave undergoes a shift in frequency which is proportional to the reflector’s velocity relative to the ultrasound source. This effect, named after the Austrian physicist Christian Doppler, allows measurement of the velocity of moving blood or tissue in the heart by analyzing the frequency shift Δf of reflected ultrasound. The relation involved, the ‘Doppler equation’, is
  
  
  where f is the carrier frequency emitted by the transducer, c the velocity of sound propagation in tissue, and v the velocity of the moving reflector (towards or away from the transducer).
  
• The velocity v of the moving reflector relative to the sound source (in practice, the transducer) can therefore be calculated from the frequency shift and the known velocity of sound in tissue. However, the calculated velocity depends on the angle in which the velocity vector is oriented compared to the ultrasound beam ( Fig. 4.3). Since only the velocity towards or away from the transducer is calculated correctly from the Doppler equation, velocities not aligned with the ultrasound beam will be measured falsely too low. The measured velocity vDOPP differs from the true velocity vTRUE by
  
  
  where α is the angle between true velocity vector and ultrasound beam direction. Importantly, Doppler measurement of velocities works for both the very weak, but comparatively fast-moving reflections from blood (typical normal velocities <1.5m/s) and the strong, comparatively slow-moving reflections from heart tissue, especially the myocardium (typical normal velocities <15cm/s; Fig. 4.4). Blood flow Doppler and tissue Doppler signals can be selectively recorded and displayed by appropriate use of electronic filters and thresholds.
  
• 
  
  
• ♦ Measurements of blood flow velocity are crucial in the assessment of valvular disease, allowing detection and (semi-)quantitation of valvular stenosis, stroke volume, regurgitation, shunts, and others. Tissue velocities, on the other hand, contain information on myocardial function which can be further refined by analyzing regional deformation. Recently, measurement of velocities in tissue by a different technique has become available, so-called ‘speckle tracking’, where tissue texture (‘speckle’) patterns are tracked from two-dimensional frame to two-dimensional frame, yielding the translation of a given set of reflectors from one frame to the next, thus also allowing calculation of motion and velocity ( Fig. 4.4). This technique, while still in its infancy, is angle-independent and may in the future be extended to blood velocity measurements.
  

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Figure 4.2 Reflexion, refraction, and scattering of sound. All of these processes take place when ultrasound interacts with tissue. (A) If a sound wave hits a large interface where acoustic impedances suddenly changes (a reflector), sound is partially reflected in a direction which depends on the angle of incidence. The amount of reflected energy increases with increasing difference in acoustic impedances of the two media forming the interface. Another part of the sound wave energy proceeds into the second medium, but the direction of propagation is changed. This is called refraction. (B) If the reflector size is in the range of the sound wave’s wavelength or the interface is ‘rough’ (left), sound is redirected in all directions, a process called scattering. Note that some sound energy is cast back in the direction of the original source of the sound wave. Reproduced with permission from Flachskampf FA. Kursbuch Echokardiographie, 4th edn., 2008. Stuttgart: Thieme.

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Figure 4.3 Angle dependency of Doppler interrogation of flow velocity. If the interrogating ultrasound beam and the direction of blood flow are at an angle α, the velocity calculated from the Doppler shift vDOPP only represents the magnitude of the partial vector parallel to the ultrasound beam. Thus, non-coaxial velocities are underestimated. Adapted with permission from Flachskampf FA. Kursbuch Echokardiographie, 4th edn., 2008. Stuttgart: Thieme.

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Figure 4.4 Principle of speckle tracking: features of the image are detected and tracked frame by frame. From the measured displacement of the features and the known frame rate, amplitude and direction within the image plane can be calculated, and from these velocity and deformation parameters of the myocardium can be derived.

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Figure 4.5 Principle of depth measurement by pulsed ultrasound. In this schematic example, the pulse P, a short ultrasound wave train generated by a short burst of activity of the transducer, is reflected by the wall of the container at the far right and returns to the transducer after a measurable time interval T. Since sound propagation velocity c is known, this allows calculation of the distance of the reflector as c × T/2. Modified with permission from Weyman AE. Principles and Practice of Echocardiography, 2nd edn., 1994. Philadelphia, PA: Lea & Febiger.

In echo machines, focused ultrasound is emitted from a transducer, an instrument containing an array of piezoelectric elements (‘crystals’), which transform electromagnetic waves into ultrasound waves and vice versa. The ultrasound transducer both generates and receives ultrasound waves. Echocardiography uses ultrasound pulses, meaning that ultrasound emission occurs during a very short period, followed by a period in which the transducer is ‘listening’ to returning, reflected ultrasound. Since the speed of sound is known, the amount of time that it takes for an ultrasound pulse to strike a reflector in the tissue and to return to the transducer defines the distance of this reflector from the transducer ( Fig. 4.5). This principle allows the construction of images. One piezoelectric element or crystal can only generate a one-dimensional representation of reflectors along the direction of the emitted ultrasound wave. This is the principle of the oldest form of echocardiography, the M-mode (M for motion, if displayed over time), which nowadays is still often used for linear measurements ( Fig. 4.6). The typical two-dimensional echocardiographic image today is generated by a multitude of near-simultaneously firing crystals, a ‘two-dimensional array’ of typically 64–96 elements. This allows steering the resulting ultrasound beam electronically so that an image sector is created successively, which provides an accurate tomographic image of the scanned structure, i.e. the heart ( Figs. 4.7–4.9). The electromagnetic waveforms generated by the piezoelectric elements of the transducer in response to the received ultrasound echoes are called the radiofrequency signal; these waveforms are digitally processed in several steps (envelope detection, compression, scan conversion) to finally generate digital images in the DICOM (Digital Images and Communication in Medicine) format, which is adhered to by all manufacturers (for more detail see [1, 2]). All of this happens fast enough to allow creation of real-time tomographic images of the heart at frame rates >100/s, a temporal resolution unmatched by any other cardiac imaging modality.

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Figure 4.6 Schematic diagram showing the creation of the M-mode echocardiogram. A long-axis cross-section of the heart from base to apex with cardiac structures is shown. The single sound beam produced by the transducer (T) on the chest wall (CW) is aimed so that it traverses from anterior to posterior: right ventricular free wall (RVFW), right ventricle (RV), interventricular septum (IVS), left ventricular cavity (LV), anterior and posterior mitral valve leaflets (aML and pML) and the posterior wall (LVPW). The echoes originating from the structure boundaries can be represented in three types of oscilloscope display: A-mode, B-mode and M-mode. Ao, aorta; LA, left atrium; aAo and pAo, anterior and posterior aortic wall; ppm, posteromedial papillary muscle.

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Figure 4.7 (A) M-mode registration of a normal subject showing the structures discussed in Fig. 4.6. The anterior mitral valve leaflet moves anteriorly and the posterior leaflet posteriorly with less excursion but a similar pattern. The recording speed is 50mm/s. The calibration scale of depth is in centimetres from top to bottom and time in seconds from left to right. (B) Two-dimensional reference image shows the cursor indicating the direction of the sampling sound beam in the short-axis view through the base of the aorta and aortic valve. The aorta (Ao) is seen as two parallel structures moving in an anterior direction in systole. The aortic valve cusps (c) are open in systole and are seen as a single echo when closed in diastole, with the same motion as the aortic walls. The left atrium (LA) is posterior to the aorta. Arrows 1 and 2 indicate the landmarks for diameter measurements. (C) M-mode registration of the left ventricle (LV) at the tips of the mitral valve leaflets showing inward motion of the interventricular septum (IVS) and posterior wall (PW) in systole. The cursor in the two-dimensional image shows the direction of the sampling sound beam. The arrows indicate landmarks for diameter measurements of the right ventricle (RV) (3), left ventricular end-diastolic diameter (4), left ventricular end-systolic diameter (5), interventricular septal thickness (6), and posterior wall thickness (7). (Courtesy of J. Roelandt and R. Erbel).

Currently in early clinical use are transthoracic and transoesophageal transducers generating three-dimensional images from two-dimensional piezoelectric element arrays (‘matrix arrays’ of several thousand single elements), which capture a whole three-dimensional, pyramidal data set (also called ‘volume data set’) in real time. This data set can be sliced and cropped off-line at will, similar to data sets from other tomographic techniques such as magnetic resonance or computed tomography ( Fig. 4.10; 4.1).

Besides morphologic imaging, echocardiography provides data on motion of cardiac structures and derived parameters. Doppler echocardiography of blood flow velocity is of paramount importance in echocardiography for functional information, especially in valvular heart disease, shunt lesions, and for the assessment of left ventricular filling. At the core of Doppler measurements is the calculation of motion velocity of a reflector from the Doppler shift of the reflected signal; this calculation is performed by a Fourier type analysis called the fast Fourier transform, which is applied to the returning Doppler shifted ultrasound data (for more detail see [1]). The Doppler shift typically is within the audible range and can be displayed as sound by the echo machine. Note that all Doppler measurements are angle dependent such that only the velocity component parallel to the ultrasound beam is correctly measured, while velocities oblique or orthogonal to the ultrasound beam are reduced by cosine α. For measuring and displaying blood flow velocity, three Doppler modalities are used ( Fig. 4.11):

• ♦ Pulsed-wave (PW) Doppler, which allows local interrogation of a flow field by placing a sample volume into a blood filled space, e.g. the left ventricular outflow tract. Blood flow velocities are displayed over time in a so-called spectral display with velocity on the y-axis and time (parallel to an ECG signal) on the x-axis. The integral of this curve is the velocity-time integral (unit cm). PW Doppler is limited in the maximal velocity (towards or away from the transducer) which it can unambiguously display, typically in the range of 1–2m/s; this velocity is termed the Nyquist velocity or limit. Above this velocity a measurement ambiguity termed ‘aliasing’ occurs, which precludes unequivocally measuring higher velocities.
  
• ♦ Continuous-wave (CW) Doppler, which allows interrogation of blood flow velocities of all magnitudes. However, it does not allow identification of the location where they occur along the ultrasound beam. CW and PW Doppler thus are complementary, the former allowing identification of very high velocities without spatial resolution, the latter limited in velocity resolution but providing good spatial resolution.
  
• ♦ Colour Doppler mapping. This is a form of parametric imaging where flow velocities are coded by colours and the colour map overlaid on two- or three-dimensional images. Conventionally, red colour codes flow velocities towards the transducer and blue colour velocities away from the transducer. The velocities coded in colours are derived from multiple PW-like Doppler interrogations by a simplified analysis technique called autocorrelation.
  

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Figure 4.8 The concept of electronic beam steering. (A) Seven elements of a phased-array transducer firing simultaneously. A short distance from the transducer the individual wavelets from each of the elements merge to produce a compound wavefront, which creates a sound beam in the direction perpendicular to the transducer face. (B) The elements are now fired in sequence but are all used to create a single sound beam. When the individual wavelets merge to form a compound wavefront, it is not perpendicular and the sound beam travels away at an angle. Varying the excitation sequence allows rapid steering of a sound beam in any direction through a sector. (C) Electronic beam focusing is realized by exciting the peripheral elements first and the centre element last (cylindrical time-gated excitation). In addition to focusing the transmitted sound beam, it is also possible to focus the returning signals so that at any one instant the transducer array is selectively receiving only those echoes coming from a specified beam direction and depth (dynamic receive focusing). This requires very complicated electronics. (D) The principle of cylindrical time-gated excitation can be used to steer and focus sound beams in any direction during both transmission and reception.

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Figure 4.9 How a two-dimensional image of the heart is created. The ultrasound beam is electronically steered through a sector arc of 80° at a uniform speed at an imaging rate of 25/s. The radial scan line data from the transducer are converted into a digital memory matrix (scan converter), which can be frozen and displayed in the horizontal TV/video format. A cursor can be moved over the image to select a scan line to produce an M-mode recording (see Figs 4.6 and 4.7).

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Figure 4.10 (A) Three-dimensional echocardiography. Instead of a single image plane as in two-dimensional echocardiography, a three-dimensional ‘volume data set’ is acquired during scanning. Different post-processing options allow visualization of the data afterwards. In this example, one basal (red rectangle) and one apical (yellow rectangle) short-axis view of the left ventricle as well as an apical long axis (red rectangle) are reconstructed from one and the same apically recorded three-dimensional volume data set. (B) Left, four-chamber view-like cut of data set; note the corrugated left ventricular endocardium in the ‘depth’ of the image (small arrow), which would not be visible on a two-dimensional image. Right, example of short-axis views of the left ventricle extracted from the three-dimensional data set. Arrow points at anterior mitral leaflet, which is open in the upper image and closed in the lower image. Also see 4.1.

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Figure 4.11 Doppler modalities. (A) Spectral Doppler analyzes the frequency shift of the echo from one sample volume position (pulsed wave Doppler, PW) or continuously and, thus, along the entire ultrasound beam (continuous wave Doppler, CW) by the ‘fast Fourier transform’. The resulting spectrum of Doppler shifts is coded in shades of grey (left). If these spectra, which represent only one point in time, are added and displayed next to each other (middle), the spectral curve becomes visible (right). (B) Colour Doppler uses an autocorrelation method to estimate velocities in a great number of sample volumes in real time. Only a mean Doppler shift is obtained, calculated from five to seven autocorrelation estimates per frame and sample volume. The mean Doppler shift is then colour coded in red and blue and superimposed on the image. A high variance between the estimates is regarded as turbulence and colour coded in green.

The most important applications of blood flow velocity analysis are:

• ♦ Calculation of (maximal and mean) gradient (Δ p) across stenotic or regurgitant orifices from instantaneous velocity (v) by the simplified Bernoulli equation:
  
  
  and of stenotic or regurgitant orifice areas by formulae based on the conservation of mass. In spite of some limitations, this allows assessment of severity of valvular stenoses, calculation of systolic right ventricular pressure from tricuspid regurgitation, (semi-) quantitation of regurgitation severity, and other measurements.
  
• ♦ Visualization of regurgitant jets and of shunt lesions by colour Doppler.
  
• ♦ Assessment of left ventricular filling and qualitative estimation of filling pressures.
  

The Doppler analysis of the high-amplitude, low-velocity signals from cardiac tissue is called tissue Doppler. It is used mainly to examine myocardial function ( Fig. 4.12). The longitudinal (apex-to-base) motion velocities of the basal segments of the left ventricle give information on global left ventricular systolic and diastolic function. Moreover, the rate of regional deformation (‘strain rate’, in 1/s or Hz) can be calculated from spatial velocity gradients and, by integration of strain rate over time, deformation (‘strain’, in per cent) itself can be computed. This deformation takes place as shortening and lengthening of the myocardium in a longitudinal direction from apical views and of thickening and thinning in a short-axis direction in parasternal views. The advantage of deformation data over velocity data lies in their truly local character, while tissue velocities are always influenced by adjacent tissue (‘tethering’) and translation movements (see Stress echocardiography, p.112 and Left ventricular function, p.116 for more detail). Recently, deformation has also been calculated by speckle tracking of the myocardium, which is not Doppler based and thus angle independent. This technique allows measurement of regional tissue velocity, deformation, and deformation rate in all directions. Tissue velocity, strain, and strain rate can be displayed either in velocity over time graphs or as colour maps.

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Figure 4.12 The Doppler-based tissue velocity and deformation modalities. (A) Principle of PW tissue Doppler. The myocardial velocity is measured by placing a PW Doppler sample volume in the myocardium (here: the basal septum in the four-chamber view, see tissue colour Doppler still frame on the left) while the echocardiography machine is set to tissue Doppler mode. The typical waves of the spectral tissue Doppler display are termed S for the systolic peak velocity, e′ for the early diastolic and A′ for the late diastolic velocity. (B) Velocity, (C) motion, (D) strain rate, and (D) strain recordings from the septal wall (see yellow circle for position of sample volume) of a healthy subject. The top row shows the colour Doppler maps of the respective parameters in the apical four-chamber view. The bottom row shows (normal) curves of the different parameters. ECG signal for timing; AVO, AVC, MVO, MVC denote aortic and mitral valve opening and closure, respectively.

The echo machine

Echocardiography machines today are fully digital devices and consist essentially of the following elements ( Fig. 4.13):

• ♦ Transducers. The typical transthoracic transducer operates with ‘broad-band’ frequency, i.e. with a range of frequencies and uses at least partially the harmonic frequencies of the reflected ultrasound to generate imaging information. It is able to produce M-mode and two-dimensional imaging, as well as incorporating all Doppler modalities (blood flow as well as tissue Doppler). The transducer surface emitting the ultrasound, which is in contact with the patient during the echocardiography exam (the transducer ‘footprint’), has to be kept small in order to fit into the intercostal spaces. Separate, dedicated three-dimensional transducers or small probes exclusively for CW Doppler are also in use. Inside a transducer lies a stacked array of piezoelectric crystals which transform ultrasound waves into electromagnetic waves. Focusing of the ultrasound beam, crucial for image quality, is achieved by acoustic lenses and electronic measures. Ultrasound gel is necessary to achieve acoustic coupling between the transducer surface and the skin of the patient.
  
• ♦ A computer to process the electromagnetic waveforms arriving from the transducer and generating images, graphs, and other displays.
  
• ♦ Digital storage capacity (hard disk) and/or interfaces to export digital data to a network and remote mass storage or to removable storage devices such as magneto-optical discs; in addition, most machines still have hard-copy printers and video recorders.
  
• ♦ Screen and keyboard for the user. The screen is usually configurable and contains the image sector as well as an ECG signal for timing, a clock, and identification data for patient and hospital. Detailed analysis of images and other data is often performed off-line after acquisition on a workstation.
  
• ♦ An ECG cable to provide a single-lead ECG signal for timing and monitoring purposes.
  

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Figure 4.13 The diversity of echocardiographic equipment. (A) State-of-the-art echocardiography machine with screen, controls, keyboard, several transducers, video recorder and printer, and wheels. (B) Laptop-type echo machine. (C) Palmtop-type echo machine. (D) Transducers with €1 coin for size comparison: left, standard transthoracic transducer, right, transthoracic 3D matrix array, transducer, bottom, standard 2D transoesophageal probe tip, top, dedicated CW Doppler probe.

All of this equipment can now be condensed into laptop computer-like portable devices powered by a rechargeable battery, or even further miniaturized to instruments that fit in a pocket (although sacrificing image quality and some options). However, even state-of-the-art echocardiography machines have wheels and can be rolled to the bedside of an intensive or emergency care patient.

Echocardiography is routinely performed as a transthoracic exam. In the course of this exam, several ‘echocardiography windows’ are utilized to give the transducer access to heart. These echocardiography windows vary from person to person somewhat in location and therefore are only broadly defined ( Fig. 4.14; 4.2, 4.3, 4.4, 4.5, 4.6, 4.7). They include

• ♦ A parasternal window, at the left sternal border, with the patient in a left lateral decubitus position; important views (cross-sections) are the parasternal long-axis view of the left ventricle and several parasternal short-axis views of left ventricle and basal cardiac structures; linear measurements such as left ventricular diameters, aortic and left atrial diameters are taken in this view, either by M-mode or from two-dimensional images.
  
• ♦ An apical window, in the region of the apical cardiac impulse, with the patient in the left lateral decubitus position slightly reclined to their back; typical views are the apical four-chamber, two-chamber, and the long-axis views.
  
• ♦ A subcostal window at the subxyphoidal angle beneath the ribcage, with the patient lying on their back; subcostal four-chamber views, as well as long-axis and short-axis views can be obtained.
  
• ♦ A suprasternal window at the suprasternal notch, with the patient on their back with their head angled backwards. This window is insufficient in many patients. The thoracic aorta, especially the aortic arch, can be visualized from here.
  
• ♦ A right parasternal window is sometimes used for Doppler interrogation of the aortic valve.
  

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Figure 4.14 (A) Routinely used echocardiographic windows: i) parasternal (PS); ii) apical (AP); iii) subcostal (SC); iv) suprasternal (SS). Note different patient positioning for each window. (Courtesy of J. Roelandt and R. Erbel). (B) Selection of normal standard echocardiographic views. Top row, left: parasternal long-axis view, middle: parasternal short-axis view at mid-papillary muscle level, right: parasternal short-axis view at aortic valve level. Bottom row, left: apical four-chamber view, middle: apical two-chamber view, right: apical long-axis view. AOA ascending aorta; AW anterior wall; INF inferior wall; IVS anterior ventricular septum; LA left atrium; LAT lateral wall; LV left ventricle; LVOT left ventricular outflow tract; MPA main pulmonary artery; PW posterior wall; RA right atrium; RV right ventricle; SE (inferior) septum. Also see 4.2, 4.3, 4.4, 4.5, 4.6, 4.7.

The examiner sits at the right or left side of the patient, with one hand holding the transducer and the other hand operating the control settings, while concentrating on the screen of the echocardiography machine. It is important to understand that the standard views and signals obtained during an echocardiography examination are largely defined by internal landmarks, e.g. for the apical four-chamber view the visualization of a maximal long axis of the left ventricle with maximal diameter of the mitral and tricuspid annulus; the external location and position of the transducer follows the requirements of the internal landmarks, not vice versa. The quality of the echocardiography recordings depends both on patient and examiner characteristics. Patients with hyperinflated lungs (e.g. suffering from obstructive lung disease or on a ventilator), with chest deformities, or very obese patients are difficult to examine, although in practically all patients at least one window is usable.

The sequence and typical elements of a standard echocardiography exam are given in Table 4.2. The duration of the exam depends on the difficulty of image generation and the pathology. The latest European recommendations stipulate an average time allowance of 30min per exam, including report writing [3]. Each echo exam must be recorded permanently, preferentially digitally or on videotape, with representative recordings from all acquired views.

The oesophagus and the gastric fundus provide an echocardiography window on the heart unobstructed by lung or bone interposition, which is in close proximity to basal structures of the heart, in particular the atria, and to the thoracic aorta [4]. Moreover, this window can be used when access to the classic transthoracic windows is not available, e.g. during cardiac surgery. Transoesophageal echocardiography (TOE) is performed via an endoscopic probe with a transducer incorporated in its tip ( Figs. 4.13 and 4.15). The tip can be flexed mechanically in different directions, and the transducer itself can be electrically rotated through a 180 degree arc to provide all possible cross-sectional plane orientations within a conical volume which has its tip at the transducer centre ( Fig. 4.16; [5, 6]). Transoesophageal transducers, due to the proximity to cardiac structures, can be operated at higher frequencies than transthoracic transducers, typically 5–7MHz. They can be equipped with all echocardiography modalities, including, recently, real-time three-dimensional imaging. The transoesophageal examination requires informed consent from the patient, since there is discomfort and a very small risk of oesophageal or pharyngeal perforation involved (~1:10,000), especially in the presence of tumours, diverticula, or strictures, as well as risks from sedation [7]. The patient is kept fasting for at least 4 hours. Under provisional light sedation and topical anaesthesia, the probe is passed blindly with active swallowing into the oesophagus and the gastric fundus. TOE has been well demonstrated to provide higher diagnostic accuracy than transthoracic echocardiography (TTE) in the diagnosis of infective endocarditis, prosthetic valve dysfunction, cardiac sources of embolism (particularly left atrial and left atrial appendage thrombi), aortic dissection, and other diseases.

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Figure 4.15 Schematic drawing of operating mode of a multiplane transoesophageal transducer. Internal rotation of the transducer allows changing the imaging planes through an arc of 180°. Modified with permission from Roelandt JRTC, Thomson IR, Vletter WB, et al. Multiplane transesophageal echocardiography: latest evolution in an imaging revolution. J Am Soc Echo 1992; 5: 361–7.

Table 4.2 Sequence and typical elements of a standard echocardiography exam

View	Data type
Parasternal long-axis view of the LV (2D + colour Doppler + M-mode)a	Loop
Parasternal short-axis view at aortic valve level (2D + colour Doppler + M-mode)a	Loop
Parasternal short-axis view at mitral valve level (2D)a	Loop
Parasternal short-axis view at mid-papillary level (2D)	Loop
Parasternal RV inflow-tract view (2D + colour Doppler)a	Loop
Parasternal RV outflow-tract view (2D + colour Doppler)a	Loop
Apical four-chamber view (2D + colour Doppler)a	Loop
Apical five-chamber view (2D + colour Doppler)a	Loop
Apical two-chamber view (2D + colour Doppler)a	Loop
Apical long-axis view (2D + colour Doppler)a	Loop
Subcostal four-chamber view (2D + colour Doppler)a atrial septum	Loop
Subcostal-inferior vena cava collapse during inspiration or sniff (+M-mode)	Loop
Suprasternal long-axis view of the aortic arch (2D + colour Doppler)a,b	Loop
Transmitral velocities (PW Doppler)	Spectral Doppler (still frame)
LV outflow tract velocities (PW Doppler)	Spectral Doppler (still frame)
Transaortic/outflow tract velocities (CW Doppler)	Spectral Doppler (still frame)
Tricuspid regurgitant velocities (CW Doppler)	Spectral Doppler (still frame)
Transpulmonary velocities (PW Doppler)	Spectral Doppler (still frame)
Tissue Doppler on mitral annulus (septal, lateral velocities)	Spectral Doppler (still frame)

aDoppler studies with colour-flow imaging may be performed at the end of the grey-scale (B-mode) imaging. M-mode optional in still frames and not necessary in both long- and short-axis views. bIn adults this projection may not always be required. LV, left ventricle; 2D, two dimensional echocardiography; PW, pulsed-wave Doppler; CW, continuous-wave Doppler. Reproduced with permission from Evangelista A, Flachskampf F, Lancellotti P, et al. European Association of Echocardiography. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur J Echocardiogr 2008; 9: 438–48.

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Figure 4.16 Typical TOE probe positions and views. Positioning of the scanning plane is indicated on the display screen: 0° indicates the transverse view, which is orthogonal to the probe, 90° shows a longitudinal view and 180° is the mirror image of 0°. (A) Upper transoesophageal views of the aortic valve in long-axis (130−150°) and short-axis (50−75°) views. (B) Upper transoesophageal views of the great vessels and atrial appendage (counter-clockwise): transverse view of the left atrial appendage and the left upper pulmonary vein (0−30°); intermediate view of ascending aorta, left atrium and right pulmonary veins (35−45°); and, with anterioflexion of the probe, transverse view of the ascending aorta, superior vena cava and main pulmonary artery with its bifurcation are obtained (0−20°). (C) Lower-middle transoesophageal views with exemplary cross-sections corresponding to (counter-clockwise) the four-chamber view of the left ventricle. From this transducer location, right heart structures can be visualized. A right atrial longitudinal view is visualized at 115−130°. (D) Transgastric views with exemplary cross-sections corresponding to (counter-clockwise) transgastric short-axis view at mid-papillary level, transgastric two-chamber view and transgastric long-axis view of the left ventricle after passing the left liver lobe. AO, ascending aorta; IVC, inferior vena cava; LA, left atrium; LAA, left atrial appendage; LV, left ventricle; LPA, left pulmonary artery; LUPV, left upper pulmonary vein; MPA, main pulmonary artery; RA, right atrium; RPA, right pulmonary artery; RLPV, right lower pulmonary vein; RUPV, right upper pulmonary vein; RV, right ventricle; SVC, superior vena cava.

While echocardiography is not able to consistently visu-alize the coronary arteries directly, its ability to identify stress-inducible ischaemia by detecting new wall motion abnormalities under stress is well established. The most common stress forms are treadmill or bicycle ergometer exercise, dobutamine infusion (in incremental doses up to 40mcg/kg/min and additional 0.25mg atropine doses up to a total of 1mg), and dipyridamole infusion [8]. Digital baseline and stress cine-loops of the left ventricle in several views are carefully compared side by side to detect new or worsening wall motion abnormalities ( Fig. 4.17). (For details of wall motion analysis see Systolic function, p.116.) If a sufficient level of stress is achieved (generally defined by achieving a ‘submaximal’ target heart rate of 85% × (220 – age)), the test can be considered valid and has a sensitivity and specificity of 80–90% compared to angiographic detection of >50% diameter stenoses of the major coronary arteries [8]. Overall, the diagnostic accuracy of stress echocardiography is very similar to tomographic nuclear perfusion scanning (single photon emission computed tomography, SPECT), in most head-to-head comparisons with minor advantages in specificity for stress echocardiography and in sensitivity for nuclear imaging.

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Figure 4.17 (A) Stress echocardiography. During physical or pharmacological stress, cineloops of the heart are captured and digitally stored. In order to detect subtle wall motion abnormalities, cineloops of the same view (here: apical four-chamber view) from different stress stages are displayed in a synchronized manner (adapted replay speed) side-by-side. In this example, apical four-chamber view loops at rest (top left), at 30mcg/kg/min dobutamine infusion (top right), and 40mcg/kg/min dobutamine infusion and additional atropine (peak stress; bottom left), and at recovery are displayed. Note different heart rates in the right lower corner of each loop. (B) Survival of 5375 patients undergoing treadmill exercise stress echocardiography according to results of the test: normal; presence of scar; presence of ischaemia; presence of scar and ischaemia combined. Reproduced with permission from Marwick TH, Case C, Vasey C, et al. Prediction of mortality by exercise echocardiography. A strategy for combination with the Duke treadmill score. Circulation 2001; 103: 2566–71.

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Figure 4.18 Use of strain analysis in dobutamine stress echocardiography. Longitudinal strain curves at baseline (left) and at peak stress (right). (A) Stress-induced ischaemia during a dobutamine stress echocardiogram results in a reduced regional systolic strain and the development of post-systolic shortening (PSS). The total strain may remain constant. (B) In normally perfused regions, the longitudinal strain profile hardly changes during a stress test. (C) ECG. AVC, aortic valve closure; MVO, mitral valve opening. Modified and reproduced with permission from Voigt JU, Exner B, Schmiedehausen K, et al. Strain rate imaging during dobutamine stress echocardiography provides objective evidence of inducible ischemia. Circulation 2003; 107: 2120–6.

A negative stress echocardiogram is an excellent predictor of a low annual mortality of ≤1% [9,10]; see Fig. 4.17. Similarly, stress echocardiography has excellent negative predictive value for peri-operative adverse events in the setting of non-cardiac surgery [11].

If image quality is insufficient, application of left heart echocardiographic contrast improves wall motion assessment and observer variability. Tissue Doppler parameters such as peak systolic velocities and magnitude and timing of systolic strain may also aid in the diagnosis of ischaemia ([12]; Fig. 4.18). Especially with pharmacologic stress (dobutamine and dipyridamole), care has to be taken to immediately recognize and treat life-threatening complications such as ventricular arrhythmias, hypotension, and others, estimated to occur in approximately 0.3–0.7% of tests [8]. Thus, proper training and emergency equipment are mandatory.

Coronary flow reserve in the left anterior descending artery may be evaluated by TOE [13], visualizing the proximal segment of the artery, or by transthoracic Doppler interrogation of the peripheral left anterior descending artery [14]. Evaluation of other coronary arteries is less established.

Compared to competing imaging modalities used for evaluating coronary artery disease, stress echocardiography has very substantial advantages:

• ♦ No radiation as in nuclear imaging or cardiac computed tomography exists, nor are contrast media of any kind routinely necessary.
  
• ♦ No restrictions as to the presence of pacemakers or underlying heart rhythm exist.
  
• ♦ Stress echocardiography can be performed almost anywhere, if necessary with portable equipment.
  
• ♦ Stress echocardiography directly detects the functional effects of myocardial ischaemia, not a perfusion imbalance (as in nuclear imaging) or the presence of coronary stenoses (as in cardiac computed tomography).
  
• ♦ Stress echocardiography costs are far lower than with any other technique.
  

On the other hand, stress echocardiography is very dependent on an experienced, well-trained operator, probably more so than other imaging techniques. Inter-observer variability, in spite of decreasing over recent years due to improved equipment and standardized protocols, remains the Achilles heel [15, 16].

Under low-dose dobutamine and also low-dose exercise, functionally impaired, but viable (hibernating or stunned) myocardium may improve its function. This can be detected by comparison of baseline and stress images and predicts recovery of function, which occurs after revascularization in the case of hibernating myocardium and spontaneously in stunned myocardium. In many cases, there is a ‘biphasic response’, where the myocardium first improves contraction under low-dose dobutamine (<20mcg/kg/min) and then at higher dosage again deteriorates, signalling an ischaemic response at the higher stress level. Dobutamine stress echocardiography has shown slightly lower sensitivity (70–80%) and higher specificity (80–90%) for the presence of dysfunctional but viable (hibernating) myocardium than nuclear SPECT in comparative studies [17]. The additional quantitative analysis of myocardial deformation (strain and strain rate) appears to be useful to optimize the detection of viable myocardium [18].

Stress echocardiography can aid clinical decision making in some situations in valvular heart disease. In severe mitral regurgitation with apparently preserved ejection fraction, exercise echocardiography may serve to identify patients who cannot increase their ejection fraction with exercise, indicating absent contractile reserve and therefore the masked onset of left ventricular impairment. In ischaemic mitral regurgitation, exercise echo can detect ‘dynamic mitral regurgitation’ with increase in severity during exercise [19]. In aortic stenosis with severely impaired left ventricular function and low transvalvular gradient, low-dose dobutamine stress echocardiography may be useful to confirm whether aortic stenosis is really severe or only apparently so due to a low stroke volume.

Echocardiography typically does not need the application of contrast agents to image cardiac structures. In some instances (e.g. ventilated or very obese patients), however, delineation of the border between blood and tissue, especially the endocardial border of the left ventricle, is insufficient for diagnostic purposes. In this case, left heart contrast agents, which consist of gas-filled small lipid-shell spheres with a diameter similar or smaller than red blood cells, can be intravenously injected as a bolus or infusion ( Fig. 4.19). The gas-shell interface provides bright ultrasound reflection, which first lights up the right heart chambers and after pulmonary passage appears in the left atrium and finally in the left ventricle. Left heart contrast has proven value for improving the delineation of the left ventricular endocardial border, thus aiding in the calculation of left ventricular volumes or the identification of wall motion abnormalities.

Moreover, left heart contrast also enters the coronary circulation and thus increases the reflectivity of the myocardium. It has therefore been used as an equivalent of nuclear perfusion tracers, especially with vasodilatory drugs like adenosine [20, 21]. Quantitative assessment of myocardial brightness and measurement of myocardial refilling kinetics after ‘destructive’ high-energy ultrasound pulses have been shown to allow quantitative inferences about vascular volume and perfusion rate. The interpretation of myocardial perfusion studies with echocardiographic contrast, however, remains difficult and cannot yet be regarded as clinical routine.

Apart from the commercially available left heart contrast media, ordinary intravenous liquids, especially agitated blood-saline mixtures, can be used to increase the visibility of right heart structures as well as Doppler signals. These microbubbles do not appreciably cross the lungs and therefore do not or only minimally show up in the left atrium or ventricle after intravenous injection. Right heart contrast is frequently used to detect small atrial shunts, e.g. patent foramen ovale, especially after a Valsalva manoeuvre, by directly observing the passage of microbubbles from the right to left atrium via the atrial septum (see Cardiogenic embolism, p.142).

After initial experimentation with three-dimensional reconstruction from spatially registered two-dimensional planes, the engineering of so-called ‘matrix transducers’ with up to approximately 3000 separate piezoelectric elements now allows real-time acquisition of a pyramidal ‘volume data set’, which contains the entire heart or parts thereof. Theoretically, acquisition of such ‘volume data’ throughout a single heartbeat for example from an apical window could provide all morphological data, and at least partially also blood flow data. The data set could then be sliced in any way desired to display the morphology ( Fig. 4.20; 4.8 and 4.9). In practice, most transducers still need several heart beats to acquire the morphological data and additional heartbeats for colour Doppler acquisition. The main drawback, however, at present is the still considerably inferior spatial and temporal resolution of three-dimensional transducers compared to two-dimensional transducers, which preclude their use for routine purposes. Nevertheless, some applications of three-dimensional echocardiography are emerging which presently already provide a net benefit over conventional two-dimensional imaging [22]. They exploit two unique three-dimensional imagery features: the ability to accurately visualize irregular cavities, e.g. the aneurysmal left ventricle, or the ability to display morphological data in en-face views which are difficult or impossible to obtain by two-dimensional echocardiography. In short, these applications are:

• ♦ Calculation of left and right ventricular volumes and ejection fraction. Three-dimensional echocardiography data provide volume calculations free of the geometric assumptions which are inherent in two-dimensional algorithms, such as Simpson’s rule for volume calculation ( Fig. 4.21). Provided image quality is sufficient, end-systolic and end-diastolic ventricular volumes as well as mass can be calculated with an accuracy and reproducibility similar to magnetic resonance tomography. Current three-dimensional software packages incorporate tools to at least partially obviate manually drawing ventricular endocardial contours, thus speeding up the analysis of volumes. Furthermore, segmental inward motion of left ventricular endocardium can be conveniently quantified and assessed with regard to synchrony or dyssynchrony.
  
• ♦ Morphologic analysis of rheumatic and degenerative mitral valve disease ( Chapter 21). Properly three-dimensional-aligned short-axis views of mitral stenosis allow accurate planimetry [23], and the location of segmental mitral prolapse or flail is nicely displayed on ‘surgeon’s view’ images from a left atrial perspective [24].
  
• ♦ En-face views of the atrial septum, especially of atrial septal defects ( Chapter 10)and occluder devices ( Fig. 4.22; 4.10 and 4.11).
  

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Figure 4.19 Left heart contrast echocardiography. (A) Microbubbles consist of a stabilizing shell (albumine, fatty acids, or phospholipids) and are filled with an inert gas or air. Intravenous injection results in a strong opacification of the heart chambers and, partially, of the myocardium (B).

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Figure 4.20 Two-dimensional (A) and three-dimensional images (B and C) of left ventricle in a patient with amyloidosis (note increased wall thickness). Parasternal images. While the three-dimensional image in (B) closely resembles the two-dimensional parasternal long axis, the same data set can be rotated to enable a view from the left atrium through the mitral valve into the left ventricle (C). LA left atrium; LV left ventricle; PE pericardial effusion. Also see 4.8 and 4.9.

Hand-held devices of laptop or palmtop computer size became available during the last decade, allowing echocardiography examinations to be performed in practically all environments (see Fig. 4.13). While quality and number of diagnostic modalities are reduced compared to state-of-the-art machines, these devices are often not inferior to a good ‘big’ echocardiography machine from 10–15 years ago. As a rule, the skills of the echocardiographer are more important than the sophistication of the machine.

Intracoronary ultrasound is covered in Chapter 8 of this book. Another form of intravascular and intracardiac ultrasound are disposable, 10 French (3.3mm diameter) ultrasound catheters (AcuNav®) with an integrated 5–10MHz transducer tip that can be introduced in the great vessels. They have been used for imaging in aortic stenting, atrial catheter ablation procedures, and other applications.

Cardiac ultrasound also has emerging therapeutic applications: with hand-held, high-intensity, focused ultrasound catheters, surgical epicardial ablation of atrial fibrillation ( Chapter 29) has been performed [25]. Catheter-based ultrasound thrombolysis has been evaluated in patients, and preliminary animal experience exists with transcutaneous ultrasound in experimentally induced myocardial infarction [26, 27].

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Figure 4.21 Left ventricular volume calculation by three-dimensional echocardiography. Three cross-sections of the same volume data set are displayed, with largely automatically traced endocardial borders throughout the cardiac cycle. With modest user input, accurate end-systolic and end-diastolic volumes, ejection fraction, and stroke volume are calculated from the full dataset, obviating any geometrical assumptions. Clockwise, apical four-chamber view, apical long-axis view, and a short-axis view of the left ventricle; bottom right, reconstructed model of left ventricular cavity.

Specific cardiovascular structures

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The assessment of left ventricular function probably represents the most frequent request from an echocardiography exam. Conceptually, it has become customary to separate systolic or pump function (which can be further subdivided into global and regional systolic function) from diastolic function, which relates to the left ventricular diastolic pressure volume relationship. The most widely accepted parameter of global systolic function is ejection fraction, which is a relatively crude parameter which may fail to reflect early and subtle disturbances of systolic function. On the other hand, there is a large group of patients suffering from symptoms of heart failure, although ejection fraction is preserved, especially in the presence of hypertension ( Chapter 13) and left ventricular hypertrophy ( Chapter 18). Such a constellation has been termed ‘heart failure with normal ejection fraction’ [34]. Echocardiography can provide—beyond the detection of hypertrophy—an estimate of elevated filling pressures in these patients, thus validating the diagnosis of heart failure with normal ejection fraction.

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Figure 4.22 En face view by transoesophageal three-dimensional echocardiography of a closure device for a patent foramen ovale in situ in the atrial septum. Also see 4.10 and 4.11.

Global systolic function is evaluated in the following ways [28]:

• ♦ Ejection fraction (EF) is calculated from end-diastolic and end-systolic left ventricular volumes. It may be visually estimated from several cross-sections, or preferentially measured by tracing the left ventricle in end-diastole and end-systole in the four-chamber view (monoplane EF), or additionally in the two-chamber view (biplane EF), enabling the calculation of left ventricular volumes and EF by the modified Simpson’s rule method (summation of discs; Fig. 4.23). If three-dimensional echo is available, volumes can be calculated from the full ‘volume data set’ without any geometric assumptions (see Fig. 4.21). The latter method can be considered the gold-standard and correlates very well with magnetic resonance volumes, although echo volumes are systematically smaller than volumes calculated by magnetic resonance or from X-ray ventriculograms. The reason lies in the different recognition of the irregular trabeculated endocardial border with these methods.
  
• ♦ End-systolic (LVESD) and end-diastolic (LVDD) left ventricular short axis diameters (by M-mode or by two-dimensional echo measured from a parasternal long-axis view, see Fig. 4.7) and the shortening fraction (LVEDD – LVESD)/LVEDD are the oldest quantitative parameters of global left ventricular function. However, they only take into account wall motion at the base of the left ventricle.
  
• ♦ The systolic excursion of the atrioventricular plane of the left ventricular, i.e. the apical displacement of the mitral annulus during systole, can serve as a measure of global systolic function. It is normally >12mm.
  
• ♦ On tissue Doppler recordings from the mitral annular region of the septal and lateral wall in the apical four-chamber view, peak systolic longitudinal velocities are normally >5cm/s. Strain values averaged over all left ventricular segments (‘global strain’) may also be used to evaluate left ventricular function.
  
• ♦ Physical exercise can be used to elicit contractile reserve measured as an increase in ejection fraction. Lack of contractile reserve implies beginning impairment of systolic function even if resting ejection fraction is still within normal range.
  

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Figure 4.23 (A) Calculation of LV volume and ejection fraction by the modified Simpson‘s rule. The ventricle is manually delineated. The method assumes rotational symmetry. Thus, the ventricular volume can be assumed to be equal the added volumes of the cylinders which fit into the delineated border. If systolic and diastolic volumes are estimated in this way, stroke volume and ejection fraction can be calculated. (B) Example of left ventricular biplane volume and ejection calculation, with normal values. Reproduced with permission from Lang R, Bierig M, Devereux R, et al. Recommendations for Chamber Quantification. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee, the Task Force on Chamber Quantification, and the European Association of Echocardiography. Eur J Echocardiogr 2006; 7: 79–108.

Regional systolic function is mainly evaluated visually in a 16-segment model of the left ventricle, where the individual segments can be assigned to typical coronary perfusion territories ( Fig. 4.24). Each segment then is visually assigned normokinetic, hypokinetic, akinetic, dyskinetic, or aneurysmatic wall motion ( Fig. 4.25). This grading can be semi-quantified by a ‘wall motion score’ of 1–4. Such wall motion scores can be displayed in maps of the left ventricle, e.g. bull’s eyes plots, and their average (sum of all wall motion scores divided by number of scored segments), the wall motion score index, can be used as a measure of global systolic function.

Deformation imaging provides truly regional strain and strain rate values and seems to be particularly useful when using speckle-tracking based techniques (‘two-dimensional strain’, ‘velocity vector imaging’). Due to considerable variation even in normals it is difficult, however, to define wall motion abnormalities quantitatively.

Practically all patients with impaired global systolic function have elevated filling pressures and hence impaired diastolic function. If heart failure symptoms occur in the presence of preserved ejection fraction, several echocardiographic parameters should be evaluated and integrated to arrive at an assessment of filling pressures ([29,30]; Figs. 4.26–4.28):

• ♦ The size of the left atrium (see Left atrium, p.123). A normal left atrial size (≤34mL/m²) excludes chronic elevation of left ventricular filling pressures. However, the left atrium also enlarges in other conditions, e.g. atrial fibrillation ( Chapter 29).
  
• ♦ The ratio E/e′ (E, the peak transmitral early diastolic flow velocity, divided by e′, peak early diastolic mitral annular tissue velocities averaged from the septal and lateral mitral annular region). A ratio <8 largely excludes elevated filling pressures, while a ratio ≥15 largely proves substantially elevated filling pressures. Between these values, other parameters have to be used to evaluate filling pressures. These include a longer duration of the retrograde pulmonary atrial wave than of the transmitral A wave ( Fig. 4.28), reduction in pulmonary systolic forward flow, a delay in the onset of e′ with relation to E, and others.
  
• ♦ A restrictive transmitral flow pattern (peak E >2 × peak A wave velocity and E wave deceleration time <150ms; Fig. 4.27c) represents an ominous sign with severely impaired prognosis; however, this is usually accompanied by systolic dysfunction. Isovolumic relaxation time, a highly preload-dependent time interval measured from cessation of aortic flow to onset of transmitral inflow, is severely shortened (<60ms). A pseudo-restrictive pattern may be observed in young, perfectly healthy individuals due to very vigorous relaxation.
  
• ♦ A transmitral flow pattern with E <A peak velocities is very frequent ( Fig. 4.27b). Isovolumic relaxation is prolonged (>100ms). It can be considered normal in patients >60 years, although some researchers view this as an expression of a genuine age-related diastolic dysfunction. It has been termed the pattern of ‘impaired relaxation’, although this implies a diagnosis impossible to conclusively make by echocardiography alone. The pattern excludes, however, substantially elevated filling pressures, since these would increase peak E wave. If E/e′ is also intermediate, a ‘diastolic stress test’ by exercise and measurement of transmitral flow and tissue Doppler parameters may show or exclude an exercise-induced substantial increase in filling pressures [31].
  

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Figure 4.24 Left ventricular 16-segment model and assignment to anterior (left anterior descending) and posterior perfusion territories (circumflex and right coronary artery). Reproduced, with permission, from Flachskampf FA. Kursbuch Echokardiographie, 4th edn., 2008. Stuttgart: Thieme.

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Figure 4.25 Schematic representation of wall motion abnormalities of the left ventricle. The innermost contour shows the endsystolic endocardial border, while the arrows depict endocardial motion from end-diastole to end-systole. In aneurysm (not shown), outward bulging persists throughout diastole, while in dyskinesia it occurs only in systole.

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Figure 4.26 Algorithm for estimation of left ventricular filling pressures in patients with normal ejection fraction. See text for details. Ar, duration of reverse pulmonary venous wave; A, duration of transmitral A wave; LA, left atrium; PAS, systolic pulmonary artery pressure (estimated from tricuspid regurgitation). Modified and reproduced with permission from Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr 2009; 10: 165–93

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Figure 4.27 Transmitral inflow patterns. (A) Normal (E early wave, A atrial wave). E wave deceleration time is indicated as time from peak E wave to end of the E wave. (B) Pattern of ‘impaired relaxation’. This pattern of E <A is frequent with left ventricular hypertrophy and other myocardial diseases. It is normal in middle or advanced age and can also be found if atrial pressure is low. (C) ‘Restrictive pattern’ with peak E more than double of peak A velocity and short E wave deceleration time (<150ms). This pattern is indicative of high filling pressures and severe left ventricular disease, but can also occur in constrictive pericarditis and in young healthy persons due to very vigorous early diastolic relaxation of the left ventricle.

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Figure 4.28 Pulmonary venous inflow patterns. (A) Normal pattern. There is a systolic (S) and diastolic (D) forward (i.e. into the left atrium) wave and a small retrograde wave (Ar) due to atrial contraction. (B) Increased left atrial pressure. There is a reduction in the S wave compared to the D wave. (C) Severely elevated left atrial pressure, with prominent systolic flow reversal and fusion of the reverse S wave with the Ar wave. This pattern occurs with severe mitral regurgitation or otherwise severely elevated left atrial pressure.

The most prevalent morphologic abnormality of the left ventricle is an increase in mass (left ventricular hypertrophy). Left ventricular mass (LVM, in g) is mostly calculated from left ventricular wall and cavity diameters, provided that no major scar or localized hypertrophy is present, by the formula:

where LVEDD is end-diastolic left ventricular diameter, PWEDD end-diastolic posterior wall thickness, and SEDD end-diastolic septal thickness (all in cm). For normal values see Table 4.3. Left ventricular mass can be determined more precisely from three-dimensional echocardiography. The aetiology of hypertrophy cannot be inferred directly from echocardiography; in the absence of hypertension, hypertrophy may be due to aortic stenosis ( Chapter 21), hypertrophic cardiomyopathy ( Chapter 18), infiltrative cardiomyopathy ( Chapter 18), or exercise training, although the latter even in professional athletes rarely leads to more than moderate increases in mass ( Chapter 32). Moderate hypertrophy initially is accompanied by a transmitral filling pattern featuring a reduced ratio of the transmitral peak E and A velocities (the maximal velocities of early and late transmitral diastolic inflow, compare Fig. 4.27), which has been termed the ‘impaired relaxation pattern’. However, this pattern also may be mimicked by decreased preload, high heart rate, and increasing age, and therefore does not necessarily imply functional myocardial impairment. Significant left ventricular hypertrophy forces the circulation to increase filling pressures to maintain stroke volume, leading to increased, left atrial size, and increasing pressures lead to ‘pseudonormalization’ of the decreased E/A ratio, which can be unmasked by a Valsalva manoeuvre, or by the finding of an increased E/e′.

Table 4.3 Echocardiographic normal values: dimensions and volumes of the left ventricle and left atrium

	Women				Men
	Reference range	Mildly abnormal	Moderately abnormal	Severely abnormal	Reference range	Mildly abnormal	Moderately abnormal	Severely abnormal
LV dimension
LV diastolic diameter	3.9–5.3	5.4–5.7	5.8–6.1	≥6.2	4.2–5.9	6.0–6.3	6.4–6.8	≥6.9
LV volume
LV diastolic volume (ml)	56–104	105–117	118–130	≥131	67–155	156–178	179–201	≥201
LV diastolic volume/BSA (ml/m2)	35–75	76–86	87–96	≥97	35–75	76–86	87–96	≥97
LV systolic volume (ml)	19–49	50–59	60–69	≥70	22–58	59–70	71–82	≥83
LV systolic volume/BSA (ml/m2)	12–30	31–36	37–42	≥43	12–30	31–36	37–42	≥43
LV mass (g)	67–162	163–186	187–210	≥211	88–224	225–258	259–292	≥293
LV mass/BSA (g/m2)	43–95	96–108	109–121	≥122	49–115	116–131	132–148	≥149
LV mass/height (g/m)	41–99	100–115	116–128	≥129	52–126	127–144	145–162	≥163
LV mass/height (g/m)2,7	18–44	45–51	52–58	≥59	20–48	49–55	56–63	≥64
Relative wall thickness (cm)	0.22–0.42	0.43–0.47	0.48–0.52	≥0.53	0.24–0.42	0.43–0.46	0.47–0.51	≥0.52
Septal thickness (cm)	0.6–0.9	1.0–1.2	1.3–1.5	≥1.6	0.6–1.0	1.1–1.3	1.4–1.6	≥1.7
Posterior wall thickness (cm)	0.6–0.9	1.0–1.2	1.3–1.5	≥1.6	0.6–1.0	1.1–1.3	1.4–1.6	≥1.7
Atrial dimensions
LA diameter (cm)	2.7–3.8	3.9–4.2	4.3–4.6	≥4.7	3.0–4.0	4.1–4.6	4.7–5.2	≥5.2
Atrial volumes
LA volume (ml)	22–52	53–62	63–72	≥73	18–58	59–68	69–78	≥79
LA volumes/BSA (ml/m2)	22 ± 6	29–33	34–39	≥40	22 ± 6	29–33	34–39	≥40

LA, left atrium; LV, left ventricle. Reproduced with permission from Lang R, Bierig M, Devereux R, et al. Recommendations for Chamber Quantification. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee, the Task Force on Chamber Quantification, and the European Association of Echocardiography. Eur J Echocardiogr 2006; 7: 79–108.

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Figure 4.29 Left ventricular remodelling. Apical four-chamber views of same patient: (A) shortly after anterior infarction, (B) 1 year after infarction. Note enlargement (both images have the same scale), relative increase in width of left ventricle (spherical remodelling), and spontaneous echocardiographic contrast in the cavity after 1 year. Also see 4.12 and 13.

In response to a loss of contractile function (e.g. after a large myocardial infarction) the left ventricle enlarges—a process termed left ventricular remodelling ( Fig. 4.29; 4.12 and 4.13). Severely enlarged left ventricles change their shape from conical to spheroid, which leads to eccentric displacement of the papillary muscles and functional mitral regurgitation. In severely dilated and hypocontractile left ventricles, thrombi may be present, especially at the apex, and spontaneous echocardiographic contrast may be visible in the cavity. This is a pattern of swirling, smoke-like echoes often detectable in regions of low blood velocity and ascribed to aggregated red blood cells (‘rouleaux’), indicating a thrombogenic milieu. Aneurysms are wall motion abnormalities with a persistent systolic and diastolic bulging and usually represent large infarct scars ( Fig. 4.30; 4.14). Such aneurysms have thin, often echo-dense walls and lack contraction. They may contain thrombus. An important differential diagnosis is the left ventricular pseudoaneurysm ( Fig. 4.31; 4.15). This is the result of a contained myocardial free wall rupture, mostly due to myocardial infarction, although traumatic pseudoaneurysms occur. Characteristics of a pseudoaneurysm include an abrupt thinning of the left ventricular wall at the border and often a relatively narrow ‘neck’, which is smaller in diameter than the largest diameter of the pseudoaneurysm. There may be paradoxical flow into the pseudoaneurysm in systole and out in diastole. For other regional wall motion abnormalities, see Stress echocardiography, p.112. Another ‘mechanical’ complication of myocardial infarction is ischaemic ventricular septal defect ( Chapter 16), which is located in the muscular portion of the septum. The hallmark of this complication is a systolic high-velocity blood jet in the right ventricle representing left-to-right shunt; the peak velocity reflects the systolic pressure difference between left and right ventricle. The morphologic defect may be difficult to clearly delineate on two-dimensional images alone. For congenital ventricular septal defect, see Chapter 10.

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Figure 4.30 Left ventricular apical akinesia with thrombus (arrow) due to an anterior myocardial infarction. Apical four-chamber view. Also see 4.14.

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Figure 4.31 Infero-posterior pseudoaneurysm (arrow) of left ventricle (LV) after inferior infarction. Note the ‘neck’ of the pseudoaneurysm, which is narrower than its largest diameter. AO, ascending aorta. Also see 4.15.

Although the right ventricle can be imaged well by echocardiography, assessment is hampered by its very irregular shape. Three-dimensional echocardiography provides the most complete and definitive possibility of assessing volumes and right ventricle EF, but is often limited by impaired image quality. Size and function therefore are usually assessed in a qualitative way. Impaired pump function most frequently is due to right ventricular infarction, cardiomyopathy, or (acute or chronic) pulmonary hypertension ( Chapter 24). Longitudinal tissue Doppler velocities and deformation imaging of the right ventricular free wall have been reported to be helpful to quantify right ventricular function.

An important aspect of right ventricle function is the maximal right ventricular systolic pressure, which corresponds, in the absence of pulmonary stenosis ( Chapters 10 and 21), to systolic pulmonary pressure. If tricuspid regurgitation is present, this value can be assessed by calculating the peak systolic gradient between right ventricle and right atrium. To this gradient an estimate of mean right atrial pressure may be added, e.g. from physical examination of the patient or by judging presence and extent of inspiratory collapse of the inferior vena cava. The estimation of peak systolic right ventricle pressure is extremely helpful to assess presence and degree of pulmonary hypertension, e.g. in pulmonary embolism ( Chapter 37).

In chronic pulmonary hypertension ( Fig. 4.32), the right ventricle enlarges and hypertrophies (end-diastolic free-wall thickness >5mm). Tricuspid regurgitation is usually present. Right ventricle function varies, but very often is impaired. The interventricular septum is shifted to the left ventricle. This is appreciable especially in short axis-views, where the septum, which normally is convex to the right ventricle side, becomes straight, giving the left ventricular cross-section the shape of a ‘D’ instead of an ‘O’. In acute pulmonary hypertension due to pulmonary embolism, the right ventricle also enlarges and is functionally impaired (except in mild pulmonary embolism). In massive pulmonary embolism, the right ventricle is acutely overloaded and dilated, with substantial tricuspid regurgitation. Systolic pulmonary pressure is elevated, but due to acute right ventricle failure often only moderately so. In some cases, transit thrombi may be seen in the right heart or lodged in the main pulmonary artery or its main branches. Paradoxical embolism at the atrial level through a patent foramen ovale is a well recognized complication in these circumstances. Because of the ease of diagnosing severe pulmonary embolism by the findings of right ventricular enlargement and dilatation together with elevated pulmonary pressures, emergency echocardiography should be performed as quickly as possible in these patients to guide management.

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Figure 4.56 Dilated cardiomyopathy. (A) All heart chambers are enlarged. Note mitral ‘tenting’ due to eccentric pull of papillary muscles with apposition of the leaflets displaced into the left ventricle. The dotted line marks the level of the mitral annulus. (B) and (C) Calculation of left ventricular volumes and ejection fraction by modified Simpson’s rule (in this case, monoplane from planimetry of the left ventricle in end-systole and end-diastole). End-systolic volume: 147mL; end-diastolic volume: 191mL; ejection fraction 23% (severely reduced).

Arrhythmogenic right ventricle cardiomyopathy ( Chapters 9 and 30) is a rare disease echocardiographically characterized by enlargement of the right ventricle and dyskinetic areas especially in the proximity of the tricuspid annulus, the apex, and the outflow tract of the right ventricle ( Fig. 4.33; 4.16). The diagnosis is not easy and many patients do not have conspicuous right ventricle abnormalities on echocardiography. For congenital heart disease affecting the right ventricle, see Chapter 10.

Left atrial function can conceptually be separated into three elements:

• ♦ a conduit function, passively conveying blood during diastole from pulmonary veins to the left ventricle;
  
• ♦ a reservoir function, accumulating blood during ventricular systole; and
  
• ♦ a booster pump function, ejecting blood by atrial contraction.
  

The best parameter of left atrial size is systolic left atrial volume, measured by monoplane or biplane modified Simpson’s rule (summation of discs; Fig. 4.34). The antero-posterior diameter of the left atrium (from parasternal views or M-mode) is a less reliable measure of size. Enlargement occurs in the following situations:

• ♦ increase in left ventricular diastolic filling pressures (impaired left ventricular function);
  
• ♦ mitral valve regurgitation or stenosis ( Chapter 21);
  
• ♦ atrial fibrillation ( Chapter 29);
  
• ♦ atrial septal defect ( Chapter 10);
  
• ♦ dilatation of the right atrium.
  

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Figure 4.57 Hypertrophic obstructive cardiomyopathy. (A) Apical long-axis view in mid-systole, showing systolic anterior motion of the mitral valve (arrow) leading almost to septal contact of the anterior leaflet tip. (B) CW Doppler signal of left ventricular outflow tract velocities with a characteristic late systolic peak velocity of 389cm/s (60mmHg). (C) M-mode recording showing systolic anterior motion of the mitral valve (arrows). Note massively thickened septum.

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Figure 4.58 Restrictive cardiomyopathy (amyloidosis). (A) Parasternal long axis; (B) magnified apical four-chamber view. Note massive thickening of left ventricular walls with bright echo texture (‘granular sparkling’), and pericardial effusion (arrow). (C) Reduced systolic and early diastolic longitudinal tissue velocities from basal septum and basal lateral wall (note scale).

In atrial fibrillation and flutter of >24–48 hours, the left atrial appendage becomes a predilection site for the formation of spontaneous echocardiographic contrast (see Left ventricular morphology, p.120) and thrombi ( Fig. 4.35; 4.17). Inspection for thrombi, especially of the left atrial appendage, is a classic domain of TOE, which should be performed before cardioversion of atrial fibrillation or flutter unless the patient has been thoroughly anticoagulated for 4–6 weeks. The occurrence of thrombi in the body of the left atrium is rarer, but well known in mitral stenosis (usually also with atrial fibrillation).

The left and right upper pulmonary veins are well assessable by TOE, while the lower veins are more difficult to visualize. Pulmonary venous inflow patterns (compare Fig. 4.28) change in response to elevation in left atrial pressure, the presence of atrial fibrillation (in both conditions, the systolic wave decreases), and the severity of mitral regurgitation, where systolic reversal of pulmonary venous inflow indicates severe regurgitation. For congenital heart disease affecting the pulmonary veins, see Chapter 10.

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Figure 4.32 Chronic severe pulmonary hypertension. The size of right ventricle (RV) and atrium (RA) far exceeds that of left ventricle and atrium. (A) Parasternal short-axis view with displacement of ventricular septum (SE) to the left ventricle, creating the ‘D sign’ as opposed to the normal circular shape of the left ventricle in short-axis views. (B) Modified apical four-chamber view. (C) Peak tricuspid regurgitant velocity (right) is 420cm/s, which by the simplified Bernoulli equation amounts to a ventriculo-atrial pressure gradient of 71mmHg. To estimate peak systolic RV and pulmonary artery pressure, an estimate of right atrial pressure can be added to that value.

Enlargement of the right atrium usually parallels left atrial enlargement, e.g. in atrial fibrillation. Tricuspid regurgitation is a frequent cause of right atrial enlargement. The orifices and proximal portions of the caval veins can be appreciated from subcostal views and particularly well by the transoesophageal sagittal view ( Fig. 4.36; 4.18). At the orifice of the inferior caval vein, the Eustachian valve is detectable, a structure of variable prominence, which may extend into the right atrium as a ‘Chiari network’ (a fenestrated membrane). Both structures are remnants of a valve of the embryonic sinus venosus. Pacemaker and implantable cardioverter/defibrillator electrodes, as well as central venous catheters are visible in the superior vena cava and right atrium, and may give origin to thrombi or endocarditic vegetations ( Chapter 22), besides causing or increasing tricuspid regurgitation.

The atrial septum is constituted by ontogenetically different components. It may contain several types of defects, the most frequent of which is the secundum defect, which occurs in the area of the fossa ovalis and may be multiple (see Chapter 10). Atrial septal defects lead to predominant left-to-right shunting, dilatation of both atria, pulmonary congestion, increase in transtricuspid velocities, and enlargement of the right ventricle. The presence of an atrial septal defect can be ascertained directly by detecting a defect in the membrane (by transthoracic, or, in particular with sinus venosus defects, by TOE) and by spectral and colour flow Doppler showing cyclic left-to-right shunting (in the absence of right atrial pressure elevation). If a shunt is present, there is also regularly at least a small right-to-left shunt, which can be proven by injecting intravenously a bolus of agitated intravenous infusion solution or blood and detecting the bubbles crossing the atrial septum to appear in the left atrium. Approximately one-fourth of the adult population has a patent foramen ovale, which constitutes another potential source of right-to-left-shunting across the fossa ovalis portion of the atrial septum. This slit-like orifice, most of the time kept shut by higher left atrial than right atrial pressure, may open during a Valsalva manoeuvre or in other instances of right atrial pressure elevation—most importantly in acute pulmonary embolism. By injection of right heart contrast, especially during TOE, and performance of a Valsalva manoeuvre, patent foramen ovale can be echocardiographically diagnosed or excluded (cf. Fig. 4.61). Closure devices, such as the Amplatzer device, for secundum atrial septal defects or patent foramen ovale, can be conveniently monitored during implantation by TOE (compare Fig. 4.22) ( Chapter 10). On follow-up, they should be inspected for residual shunt and thrombus formation.

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Figure 4.33 Arrhythmogenic cardiomyopathy of the right ventricle. Note enlarged right ventricle with aneurysmatic zones at the apex (arrow). Also see 4.16.

Frequent atrial septal anomalies are lipomatous hypertrophy of the septum, a benign condition which characteristically spares the fossa ovalis region, and atrial septal aneurysm, often defined as a deviation of the thin portion of the membranous atrial septum from the interatrial mid-line of 1cm or more to either side or both sides. This abnormality occurs in 1–2% of the population, is better diagnosed by TOE than TTE, and often coexists with atrial septal defect, septal fenestrations, and patent foramen ovale; an association with unexplained ischaemic neurologic events has been noted in the literature.

Assessment of valvular heart disease ( Chapter 21) is one of the prime strengths of echocardiography [32]. Morphologically, pathologic thickening, calcification, abnormal masses (e.g. fibroelastoma), excessive or restricted mobility, functional integrity, and congenital malformations (e.g. bicuspid aortic valve) can be detected. In infective endocarditis ( Chapter 22), new mobile mass lesions (vegetations) attached to the valve can be detected, and abscess formation in the perivalvular tissue may be observed, especially in valvular prostheses. Further sequelae of endocarditis are fistulae, perforations, or the formation of mitral pseudoaneurysms (see also Chapter 21).

Functionally, valvular dysfunction can be divided into stenosis and regurgitation. Stenotic lesions are assessed morphologically by noting reduced mobility, thickening, and calcification of valvular leaflets. In the mitral, and to a lesser degree, the aortic valve, direct planimetry of the stenotic orifice area is possible [33]. Doppler echocardiography allows calculation of maximal and mean transvalvular gradients from the simplified Bernoulli equation. The continuity equation (an expression of the conservation of mass) especially in the aortic valve permits calculation of a stenotic orifice area from stroke volume and maximal transvalvular velocities; this principle is also applicable to other valves. In the mitral valve, an estimate of stenotic valve area can be derived from the rate of decrease of the diastolic transmitral gradient, expressed as pressure half-time.

Valve regurgitation (see Table 4.4) manifests itself morphologically as incomplete leaflet closure due to leaflet prolapse or a flail leaflet, due to annular dilatation (in the mitral, aortic, and tricuspid valve), due to defects, e.g. in bacterial endocarditis ( Chapter 22), or other reasons ( Fig. 4.37). By colour Doppler, regurgitant jets are seen in the receiving chamber of the regurgitation. The overall size of these jets is loosely related to the severity of regurgitation, but also to many other factors and thus alone is not sufficient to grade severity in more than mild regurgitation. Additional Doppler-based methods to evaluate the severity of regurgitation include ( Fig. 4.38):

• ♦ The proximal jet width (‘vena contracta’) immediately after passage of the valve, which is related to the size of the regurgitant orifice.
  
• ♦ The proximal convergence zone (‘proximal isovelocity surface area’, or PISA), which at least theoretically allows calculation of regurgitant flow rate, regurgitant volume, regurgitant fraction, and regurgitant orifice area, and practically is very helpful in distinguishing moderate and severe regurgitation. This method is based on the assumption of concentric hemispheres of fluid of differing flow velocity in the upstream chamber, which are centred around the regurgitant orifice, upon which the regurgitant flow converges. By a combination of colour Doppler and CW-Doppler parameters of regurgitation severity, most importantly regurgitant orifice area (in cm²), are calculated. In spite of many limitations inherent in the theoretical basic assumptions of the method, it works relatively well if image quality is sufficient.
  
• ♦ The inflow pattern of the receiving chamber (pulmonary venous flow in mitral regurgitation and hepatic vein flow in tricuspid regurgitation).
  
• ♦ Others (see sections on individual valves).
  

Table 4.4 Echocardiographic criteria for the definition of severe native valvular regurgitation: an integrative approach

	AR	MR	TR
Specific signs of severe regurgitation	Central jet, width ≥65% of LVOTa Vena contracta >0.6 cma	Vena contracta width ≥0.7cm with large central MR jet (area >40% of LA) or with a wall improving jet of any size, swirling in LAa Large flow convergenceb Sytolic reversal in pulmonary veins Prominent flail MV or ruptured papillary muscle	Vena contracta width >0.7cm in echo Large flow convergenceb Systolic reversal in the hepatic veins
Supportive signs	Pressure half-time <200ms Holodiastolic aortic flow reversal in descending aorta Moderate or greater LV enlagementd	Dense, triangular CW, Doppler MR jet E-wave dominant mitral inflow (E > 1.2m/s)c Enlarged LV and LA sizee (particularly when normal LV function is present)	Dense, triangular CW TR signal with early peak Inferior cava dilatation and respiratory diameter variation ≤50% Prominent transtricuspid E-wave, especially if >1m/s
Quantitative parameters
R Vol, mL/beat	≥60	≥60
RF, %	≥50	≥50
ERO, cm2	≥0.30	≥0.40

AR = aortic regurgitation, CW = continuous wave, ERO = effective regurgitation orifice area, LA = left atrium, LV = left ventricle, LVOT = LV outflow tract, MR = mitral regurgitation, MS = mitral stenosis, MV = mitral valve, R Vol = regurgitation volume, RA = right atrium, RF = regurgitant fraction, RV = right ventricle, TR = tricuspid regurgitation. aAt a Nyquist limit of 50–60 cm/s. bLarge flow convergence defined as flow convergence radius ≥0.9 cm for central jets with a baseline shift at a Nyquist of 40 cm/s; cut-offs for eccentric jets are higher and should be angled correctly. cUsually above 50 years of age or in conditions of impaired relaxation, in the absence of MS or other causes of elevated LA pressure. dIn the absence of other aetiologies of LV dilatation. eIn the absence of other aetiologies of LV and LA dilatation and acute MR. Reproduced with permission from Zoghbi WA, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography: recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography: A report from the American Society of Echocardiography's Nomenclature and Standards Committee and The Task Force on Valvular Regurgitation, developed in conjunction with the American College of Cardiology Echocardiography Committee, The Cardiac Imaging Committee, Council on Clinical Cardiology, The American Heart Association, and the European Society of Cardiology Working Group on Echocardiography. Eur J Echocardiogr 2003; 4: 237–61.

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Figure 4.34 Left atrial volume calculation by summation of discs (modified Simpson’s rule) in the apical four-chamber view derived from planimetry of the left atrium in end-systole. The left atrial volume is markedly elevated (102mL). Note marked left ventricular hypertrophy.

Importantly, evaluation of the severity of regurgitation should never be based on a single number or parameter but on an ‘integrative approach’ (see Table 4.4) synthesizing all available morphologic, Doppler, and ultimately, clinical information [34].

The normal mitral valve opens quickly and completely in early diastole, with thin and pliable leaflets. The normal diastolic transmitral flow pattern is characterized by an early diastolic E wave, in response to rapid left ventricular pressure fall due to relaxation in early diastole, and a late diastolic A wave due to atrial contraction (after the P wave of the ECG; see Figs. 4.27 and 4.28). For changes of the transmitral inflow profile due to elevation of left ventricular filling pressures, see Left ventricular function, p.116. In long-standing hypertension and in advanced age, calcification of the mitral annulus—in particular posteriorly—is frequent.

Mitral stenosis ( Chapter 21) is almost always rheumatic and produces the characteristic ‘doming’ appearance of the leaflets in diastole ( Figs. 4.37 and 4.39; 4.19 and 4.20). The stenotic orifice area is best planimetered by two- or three-dimensional echocardiography. If this is not possible due to image quality, the next best method to assess orifice area A in cm² is by the empirical formula A = 220/PHT, where PHT is the pressure half-time in ms measured from the CW Doppler transmitral flow profile. This method is based on the observation that the early diastolic transmitral pressure gradient decay depends on mitral orifice area, declining rapidly with larger orifice areas and slower with smaller orifice areas. The mean diastolic transmitral gradient (by CW Doppler), although strongly heart rate dependent and affected by concomitant mitral regurgitation, is a further useful measure of severity.

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Figure 4.35 Uncommonly large thrombus (arrow) in the left atrial appendage (LAA) in a patient with atrial fibrillation. Transoesophageal image; LA left atrium; LV, left ventricle; MV mitral valve. Also see 4.17.

Mitral regurgitation ( Chapter 21) is very frequent. Minimal or mild regurgitation, especially in early systole, occurs in many apparently healthy individuals. More severe mitral regurgitation is either organic (e.g. mitral valve prolapse) or functional (e.g. in the impaired and dilated left ventricle; see Chapter 21). The mechanism can usually be identified by careful echocardiographic examination of the valve ( Fig. 4.37; Table 4.4). The most important degenerative mechanisms are prolapse and flail ( Figs. 4.40 and 4.41; 4.21 and 4.22); these terms are often used interchangeably, but in prolapse proper it is the body of the leaflet that is most prominently displaced beyond the leaflet coaptation point into the left atrium in systole, while in mitral flail leaflet it is the tip of the leaflet that moves farthest into the left atrium due to disruption of its subvalvular support (chordal rupture), invariably leading to substantial regurgitation. In functional mitral regurgitation the underlying cause is impaired regional or global left ventricular function, while the valvular apparatus itself is intact ( Fig. 4.42). However, due to displacement of the papillary muscles the leaflets are pulled into the left ventricle during systole and prevented from closing. This occurs both with global dilatation of the left ventricle (dilated or ischaemic cardiomyopathy) or with regional posterior/inferior wall motion abnormalities. The typical configuration of functional mitral regurgitation is a structurally intact valve, the leaflets of which in systole are entirely on the ventricular side of the mitral annulus, with the closure line at a distance from the line connecting the insertion of the leaflets. This appearance has been termed ‘tenting’ and is characteristic for functional mitral regurgitation. In ischaemic mitral regurgitation, it has been shown that under exercise stress, the regurgitant orifice area of mitral valves may increase, which is a negative prognostic marker [19, 35]. This increase is not due to acute ischaemia, but instead to non-ischaemic changes in ventricular and valvular geometry under stress. On the other hand, acute ischaemic regurgitation also may occur, either by acute ischaemic dilatation of the left ventricle or as a complication of myocardial infarction, by rupture of papillary muscle (usually partial rupture of the posteromedial papillary muscle) or of chordae.

While for the diagnosis of mild mitral regurgitation the observation of a small colour Doppler jet is sufficient, differentiation of moderate or large severity, besides appreciation of mitral valve and left ventricular morphology (e.g. presence of a flail leaflet or of marked tethering of the leaflets with a dilated left ventricle), often necessitates analysis of proximal jet width, proximal convergence zone, pulmonary venous flow, and sometimes further parameters. The best appreciation of regional morphologic alterations of the mitral valve, especially of prolapse or flail, is obtained by TOE. Morphologic changes are often expressed in Carpentier’s nomenclature with regard to mechanism (excessive/restricted leaflet mobility and others) and location (P1–P3 for posterior leaflet scallops, A1–A3 for anterior leaflet scallops) of the regurgitant lesion. This is important for preoperative planning of reconstructive versus replacement surgery, as well as intraoperatively to check the success of reconstructive surgery, and should be performed routinely during mitral valve repair. Mitral valve endocarditis may induce regurgitation of all degrees by perforation or rupture of mitral structures (see Chapter 22).

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Figure 4.36 Sagittal transoesophageal view of the right atrium at 108° rotation. EU, Eustachian valve; IVC, inferior vena cava; LA, left atrium; RA, right atrium; SVC, superior vena cava. Note thin part of atrial septum, the fossa ovalis, between left and right atrium. Also see 4.18.

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Figure 4.37 Schematic illustrations of typical mitral pathomorphologies in the parasternal long-axis view. (A) Posterior leaflet prolapse (arrow; systolic frame). (B) Posterior leaflet flail (arrow; systolic frame). (C) Thickening and stiffening (restricted motion) of posterior leaflet (arrow; systolic frame). (D) Functional regurgitation due to left ventricular dilatation. Note lack of closure of leaflet tips and displacement of leaflets into the left ventricle (‘tenting’; systolic frame). (E) Systolic anterior motion (arrow) in hypertrophic obstructive cardiomyopathy. Note increased septal thickness (double arrow). Systolic frame. (F) Mitral stenosis with doming (diastolic frame). Arrows indicate the reduced opening amplitude of the thickened leaflet tips.

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Figure 4.38 The principle of the proximal isovelocity surface area (PISA) method and vena contracta measurement for regurgitant volume measurement. The vena contracta or narrowest extent of the regurgitant jet as it passes through the effective regurgitant orifice correlates well with the severity of regurgitation. This method assumes that the regurgitant orifice does not alter in shape or size during regurgitation. As blood flow accelerates towards the regurgitant orifice, concentric hemispheres rings of isovelocity regions are produced and visualized with colour Doppler. The smallest hemisphere nearest the regurgitant orifice has the highest velocity. The PISA radius (r) is the radial distance between this aliasing contour (Val) and the centre of the regurgitant orifice. The regurgitant jet area consists of the laminar area with the highest velocities and a turbulent area caused by entrainment of stagnant blood volume.

Several congenital malformations of the mitral valve exist (e.g., stenosis, cleft). Hypertrophic obstructive cardiomyopathy is frequently associated with valvular malformations and with moderate or severe mitral regurgitation. Mitral valve endocarditis is characterized by the attachment of vegetations, most frequently to the atrial side of the leaflets and annulus, mitral regurgitation, and sometimes development of a mitral pseudoaneurysm. Restriction of valvular leaflet mobility, leading to progressive regurgitation, occurs in carcinoid syndrome and has been reported as a side effect of drugs such as dexfenfluramine (an appetite suppressant) and pergolide (a dopamine agonist), an effect which seems to be mediated by the release of serotonin.

The aortic valve is normally tricuspid. About 0.5% of the population have a congenitally bicuspid valve, which is prone to degeneration and the development of combined aortic regurgitation and stenosis ( Fig. 4.43; 4.23). Furthermore, these patients are at an increased risk of aortic dissection. Bicuspid valves normally can be detected during a routine echocardiographic examination. In advanced age and in long-standing hypertension, the aortic valve frequently develops focal sclerosis without significant obstruction. Minimal aortic regurgitation is common, especially in the elderly.

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Figure 4.39 (A) Rheumatic mitral stenosis with diastolic doming of the leaflets (arrow), parasternal long-axis view. The patient is in atrial fibrillation. LA, left atrium; LV, left ventricle. Note enlarged left atrium. There is also rheumatic aortic valve disease. Also see 4.19. (B) Mitral valve planimetry in the parasternal short-axis view. The stenotic orifice area (arrow) is 0.9cm2. (C) CW Doppler recording of transmitral flow in combined rheumatic mitral stenosis and regurgitation. The scale is in cm/s. The deceleration slope of the diastolic flow profile is marked with a white dotted line; from this slope, pressure half-time is calculated as the time interval from peak transmitral pressure gradient at the onset of diastole to decrease of the gradient to one half of its initial value. Because the instantaneous gradient is proportional to the square of the flow velocity, this corresponds to a decay from the initial maximal transmitral flow velocity vmax to vmax/√2. Note also systolic profile of mitral regurgitation with a peak regurgitant velocity of 6m/s, corresponding to a systolic peak pressure difference between left ventricle and left atrium of 144mmHg. (D) Schematic drawing explaining the calculation of pressure half-time. Also see 4.20.

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Figure 4.40 Mitral valve prolapse involving both leaflets. (A) Parasternal long-axis view; (B) apical long-axis view, with the level of the mitral annulus marked by a dotted line.

Aortic stenosis ( Chapter 22)is the most frequent severe valvular heart disease requiring surgical treatment in our populations. The disease begins with focal sclerosis, becoming diffuse and leading to severe thickening, immobility, and calcification of the leaflets. These characteristics are well appreciated by echocardiography. Even aortic valve sclerosis, which involves only small increments in flow velocity (<2.5m/s peak velocity), entails a distinctly impaired cardiovascular prognosis. Severe aortic valve stenosis, defined as orifice area <1.0cm² or, indexed to body surface area, <0.6cm²/m², requires careful scrutiny for symptoms or deterioration of left ventricular function, which both constitute indications for valve replacement (see Chapter 21). The most important parameters to characterize the severity of aortic stenosis by echocardiography are the maximal and mean transvalvular gradient and the aortic orifice area (AoA), which usually is calculated by the continuity equation:

where A_LVOT is the cross-sectional area of the left ventricular outflow tract (calculated from outflow tract diameter D as π × D²/4), VTI_LVOT is the time velocity integral of systolic flow in the outflow tract (measured by PW Doppler), and VTI_CW is the time velocity integral of trans-stenotic flow measured by CW Doppler ( Fig. 4.44; 4.24 and 4.25). Sometimes, especially with TOE, the stenotic orifice area can be planimetered directly. Importantly, the orifice area does not depend on stroke volume and therefore is the only reliable parameter in the presence of an impaired left ventricular function.

In some cases of severely impaired left ventricular function with questionably severe aortic stenosis, a dobutamine stress echocardiogram may provide additional functional and prognostic information.

Aortic regurgitation is the most difficult valvular lesion to grade by echocardiography. It may be due to dilatation of the ascending aorta (e.g. in Marfan’s syndrome), calcific disease of the valve, bacterial endocarditis, degenerative changes such as prolapse, rheumatic disease, and others. The severity of regurgitation may be semiquantitatively estimated by (see Fig. 4.45; 4.26; and Table 4.4):

• ♦ assessment of valve morphology and the degree of dilatation of the left ventricle;
  
• ♦ comparing the proximal jet diameter of the regurgitant jet to the diameter of the outflow in the parasternal long-axis view tract (≥65% indicating severe regurgitation);
  
• ♦ calculating the pressure half-time of the regurgitant flow signal on CW Doppler (<250ms being typical for severe regurgitation);
  
• ♦ recording a holodiastolic reverse flow signal from the descending aorta (from the suprasternal window), with end-diastolic velocities approximately >16cm/s indicating severe regurgitation.
  

An important part of the evaluation of moderate and severe aortic regurgitation is 1) the assessment of left ventricular function (diameters and ejection fraction); and 2) the assessment of the ascending aorta, especially as to diameter (see [32] and Chapter 21).

Signs of aortic valve endocarditis include vegetations, new aortic regurgitation, structural defects of aortic leaflets, and tissue invasion leading to para-aortic abscess formation and fistulae, e.g. from the aortic outflow tract to the left atrium. Such complications are especially well identified by TOE [36].

Intrinsic diseases of the tricuspid valve are relatively rare, except for tricuspid endocarditis, which occurs mainly in drug addicts and patients with long-standing disease necessitating the insertion of in-dwelling central catheters and ports. Pacemaker endocarditis may also extend to the tricuspid valve. Other structural tricuspid valve diseases are rheumatic fever, carcinoid heart disease, iatrogenic injury e.g. due to right ventricular biopsy, and others (see Chapter 10 for Ebstein’s disease).

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Figure 4.41 Posterior mitral flail leaflet (arrow) in the apical four-chamber view (A) and corresponding colour Doppler representation (B) of severe mitral regurgitant jet directed to the opposite side (arrow). Also see 4.21 and 4.22.

Tricuspid stenosis is very rare and usually accompanies rheumatic mitral valve disease. A mean transtricuspid gradient from CW Doppler >5mmHg is regarded as clinically relevant.

Trace or mild tricuspid regurgitation is almost universally present and should not be regarded as a disease. Moderate or severe tricuspid regurgitation ( Fig. 4.46; 4.27; see Table 4.4), except in the presence of a pacemaker/defibrillator electrode or in the course of infective endocarditis, almost always is the consequence of a dilatation of the right ventricle—most frequently due to pulmonary hypertension. Further causes to consider in functional tricuspid regurgitation are atrial fibrillation, a left-to-right shunt (see Chapter 10), or primary right ventricular diseases (e.g. right ventricular infarction or cardiomyopathy).

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Figure 4.42 (A) Functional (ischaemic) mitral regurgitation in a patient with ischaemic cardiomyopathy. Note tenting of the mitral valve (arrow) due to eccentric pull of the papillary muscles. (B) Colour Doppler of mitral regurgitation.

Severe tricuspid regurgitation can be identified by a large proximal convergence zone, a broad proximal jet width, and dilatation of the inferior vena cava with absent inspiratory collapse and reversal of systolic forward flow in the hepatic veins (see Table 4.4). The peak regurgitant jet velocity is used to estimate peak systolic right ventricular, and thus pulmonary artery pressure. Since the gradient calculated from the simplified Bernoulli equation represents the peak pressure difference between right ventricle and right atrium, to arrive at an estimate of absolute right ventricular or pulmonary pressure, the systolic right atrial pressure must be added. This may be accomplished by adding for the right atrial pressure either a constant (usually 10mmHg) or estimating right atrial pressure from jugular vein filling, respiratory variation in the diameter of the inferior vena cava, or hepatic vein flow pattern. Many laboratories, however, choose to only report the pressure gradient itself.

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Figure 4.43 Typical aspect of congenitally bicuspid aortic valve in the parasternal short-axis view. The arrow points at the circular shape of the opened valve. Also see 4.23.

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Figure 4.44 (A) The principle of the continuity equation. Conservation of mass dictates that the product of cross-sectional area (CSA) and averaged flow velocity or flow velocity integral (v) is equal at each cross-section of a tube, which is expressed by the continuity equation in the left upper corner of the image. Stenotic aortic area is calculated by solving the equation for CSA2. (B) Application example of the continuity equation in severe aortic stenosis. i) parasternal long-axis view of aortic stenosis (arrow); note concentric left ventricular hypertrophy. ii) zoom of aortic valve with measurement of left ventricular outflow tract diameter D at the aortic annulus level (2cm). iii) PW Doppler recording of left ventricular outflow tract velocities and velocity time integral (VTILVOT). iv) CW Doppler recording of transaortic velocities and velocity time integral (VTIAS). By the continuity equation, aortic valve area (A) is calculated as A = π × (D2/4) × VTILVOT/ VTIAS, which here results in 0.6cm2 (severe). Also see 4.24 and 4.25.

The pulmonary valve is not well visualized either by TTE or TOE. Pulmonary stenosis ( Chapter 10) is almost always congenital, and may be present with subvalvular, valvular, and supravalvular components in complex congenital heart disease such as Fallot’s tetralogy (see Chapter 10). Minimal pulmonary regurgitation is an almost universal finding even in apparently healthy individuals. More severe degrees of pulmonary regurgitation are graded by the degree of right ventricular dilatation, shortened pressure half-time of the regurgitant CW Doppler signal (<100ms indicating severe regurgitation; [37]), and cessation of regurgitation before the end of diastole.

Valve replacement is performed by inserting biologic or mechanical prostheses (see also Chapter 21). Non-biologic material of the prostheses impairs imaging by artefacts and acoustic shadowing, so that the examination is more difficult than that of native valves. TOE should be performed whenever there is a suspicion of prosthetic malfunction or endocarditis.

Prostheses differ by their design and valve mechanism. Accordingly, they present differing echocardiographic characteristics:

• ♦ Homografts or the native pulmonary valve transposed to the aortic position after a Ross procedure practically are indistinguishable from native valves.
  
• ♦ Porcine or bovine biological prostheses are relatively well imaged, including their leaflets ( Fig. 4.47; 4.28). They undergo a degenerative process over time with thickening, calcification, and increasing leaflet tissue rigidity, as well as increasing regurgitation. Tears in the leaflets of degenerated bioprostheses can lead to sudden massive regurgitation. Biological prostheses have relatively minor transvalvular gradients ( Table 4.5) and almost always at least mild transvalvular regurgitation.
  
• ♦ Mechanical prostheses nowadays are most often of the bileaflet type. The two leaflets or discs of such prostheses are mostly visualizable in the mitral position ( Fig. 4.47; 4.28), but often impossible to evaluate in the aortic position, even by TOE. These prostheses in the aortic position may have considerable transvalvular gradients despite normal mechanical function, especially if the valve size is small (19–21) and the aorta is narrow. Maximal velocities >4m/s are not rare in these conditions. The reason may be pressure recovery, which is a phenomenon due to localized high pressure gradients occurring in these prostheses due to their geometric design [38]. These pressure gradients are picked up by CW interrogation; however, they are larger than the ‘net’ gradient between left ventricle and ascending aorta, thereby leading to ‘overestimation’ of the net gradient. Unfortunately, a high transvalvular pressure gradient created by a true dysfunction, e.g. pannus or thrombus, is indistinguishable from a high pressure gradient generated by the design of the valve; the two gradients do not necessarily add, because in the case of prosthetic obstruction the ‘in-built’ gradient may be decreased [39]. Thus, in bileaflet valves (and also in other mechanical valves) with high transvalvular gradients in the aortic position, either comparison with early postoperative gradients (when the prosthesis was presumably intact) or fluoroscopy or cardiac computer tomography should be performed to exactly delineate leaflet mobility.
  

Table 4.5 Echocardiographic normal values: blood flow and tissue Doppler (adapted from [1, 52, 53])

Peak transvalvular and transprosthetic blood flow velocities (m/s). Data for prostheses are averaged over a range of sizes, except for mechanical aortic prostheses
Aortic valve	1.0–1.7
Mitral valve	0.6–1.3
Tricuspid valve	0.3–0.7
Pulmonary valve	0.6–0.9
Stented bioprostheses in the aortic position	2.8 ± 0.4
Mechanical prostheses in the aortic position: tilting disc	1.9 ± 0.2 to 3.3 ± 0.6
Mechanical prostheses in the aortic position: bileaflet	1.9 ± 0.3 to 3.1 ± 0.4
Stented bioprostheses in the mitral position	1.0 ± 0.3
Mechanical prostheses in the mitral position: tilting disc	1.3 ± 0.3
Mechanical prostheses in the mitral position: bileaflet	0.9 ± 0.2
Peak longitudinal tissue velocities (cm/s) in left ventricular basal septum by pulsed Doppler (from 54–56)
S wave	8.0 ± 2cm/s (<40 years) to 7.1 ± 1.3cm/s (> 70 years)
e′ wave	10.1 ± 2.6 (<45 years) to 6.2 ± 1.7 (>74 years)

Several typical complications of valvular prostheses must be searched for and evaluated whenever a patient with a prosthetic valve is examined echocardiographically. These include:

• ♦ Obstruction: due to thrombus, pannus (sterile tissue ingrowth), or, rarely, vegetation growth in mechanical valves; in biological prostheses, degenerative changes may lead to obstruction. The severity of obstruction is graded in accordance with assessment of stenosis in native valves. For the problem of high gradients across aortic mechanical prostheses, see earlier discussion.
  
• ♦ Regurgitation: transvalvular and paravalvular regurgitation occurs. Transvalvular regurgitation of minor degree is present in mechanical prostheses by design [40]; prosthetic dysfunction, e.g. by a thrombotically fixed disc, may lead to more severe regurgitation, and catastrophic regurgitation follows embolization of a disc. Paravalvular regurgitation is frequent and often minor. It should be ascertained whether it was present immediately after operation or appeared later, which would raise the question of endocarditis. Large paravalvular leaks leading to rocking of the whole prostheses are termed dehiscence and are associated with severe regurgitation. Three-dimensional TOE appears to be especially useful for the assessment of size of paravalvular leaks.
  
• ♦ Prosthetic endocarditis: valve prostheses are prone to infections. Typically, the infection manifests as vegetations attached to the prosthetic ring, and abscesses may develop in the immediate proximity of the prosthetic ring. This is best appreciated by TOE. Vegetations may also originate from the leaflets of biological prostheses. More rarely, vegetations may be attached to the discs of a mechanical prosthesis (see also Chapter 21).
  

The posterior pericardium is the brightest structure in the far field of parasternal echocardiographic cross-sections of the heart. The anterior pericardium is less echogenic. Pericardial fat is relatively frequent in elder patients and has an echo-lucent, but not echo-free appearance. Pericardial effusion, which is echo-free in the acute stage, can be seen in all views if circular. Small effusions are best appreciated from the subcostal window with the patient supine. The haemodynamic impact of a pericardial effusion should be examined by looking for compression of a cardiac chamber, in circular pericardial effusion the right atrium, since its inner pressure level is lowest of all chambers ( Figs. 4.48 and 4.49; 4.29, 4.30, 4.31), and the right ventricle. In rare cases of localized pericardial effusions (e.g. postoperatively) other chambers may be compressed first. The constriction created by external compression of the heart chambers leads to an exaggeration of respiratory variation of inflow and outflow patterns of the ventricles, similar to constrictive pericarditis: mitral inflow decreases with inspiration, as does aortic stroke volume, while tricuspid inflow increases ( Chapter 19). A >25% decrease in peak transmitral E wave velocity with inspiration is considered a sign of pericardial tamponade. A ‘paradoxical’ septal shift to the left in early diastole, created by the increase in transtricuspid flow, is also observed. In expiration, these changes are reversed.

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Figure 4.45 Aortic regurgitation. (A) Parasternal long-axis view showing regurgitant jet (in diastole) filling the complete left ventricular outflow tract. (B) Transoesophageal magnified long-axis view of aortic valve showing prolapse of the acoronary aortic cusp (arrow). (C) CW Doppler signal of aortic regurgitation. Diastolic velocity decay, from which pressure half-time can be measured, is marked by the white line. (D) Suprasternal PW Doppler recording of descending aortic flow, showing substantial holodiastolic flow reversal (arrow points to reversal persisting until end-diastole). ASC, ascending aorta; LA left atrium; LV left ventricle. Also see 4.26.

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Figure 4.46 Severe tricuspid regurgitation. (A) Colour Doppler recording in the apical four-chamber view. Note large proximal convergence zone. (B) PW Doppler of hepatic venous flow; note systolic flow reversal as a sign of severe tricuspid regurgitation. RA right atrium; RV right ventricle. Also see 4.27.

To prepare pericardial puncture, the subcostal view is useful to determine the location, angle, and depth of the puncture ( Fig. 4.49; 4.31). After puncture, the location of the tip of the needle or of a catheter introduced in the pericardial space may be confirmed by injecting an agitated infusion solution, which will create a bright contrast echocardiogram.

Constrictive pericarditis (see Chapter 19) is not easy to diagnose by echocardiography. Thickened (>5mm), calcified pericardium may be apparent, but often is not. The ventricles are of normal size, while the atria are enlarged. A paradoxical septal motion is almost universally present. Left and right ventricular systolic function is mostly unimpaired. The inspiratory decrease in transmitral flow and increase in transtricuspid flow, very similar to tamponade, is present in clear-cut cases. Sometimes, however, this sign is blunted by massive diuretic therapy. The transmitral flow in the typical case exhibits a tall, short E wave with short deceleration time (‘restrictive pattern’). E/e′ in this disease should not be used to predict the left ventricular filling pressures.

Myxoma is by far the most frequent originary cardiac tumour (see Chapter 20). It typically has an irregular shape, with possible calcifications and echo-lucent regions, and is mobile. Embolic complications are relatively frequent. The most frequent attachment point is the left side of the atrial septum in the fossa ovalis region. The tumour may prolapse through the mitral valve into the left ventricle during diastole ( Fig. 4.50) and obstruct left ventricular inflow. Other locations occur (right atrium, left ventricle). Fibroelastomas arise from valvular tissue, mostly from the aortic valve, but they also occur on other valves. Like myxomas, they may embolize. Typical appearance and location make the diagnosis of these two tumour types very likely, but ultimately it is impossible to predict histology from echocardiographic data. Metastatic tumours often cause pericardial effusions.

The ascending aorta can be seen over its first few centimetres from the parasternal long-axis view. Access to the aortic arch is provided by the suprasternal window, which, however, is often obstructed in elderly or emphysematous individuals. A much more complete evaluation of the thoracic aorta is possible by TOE, where almost the entire course is visible except for a ‘blind spot’ created by tracheal and left bronchial interposition at the distal ascending aorta and proximal arch. Dilatation and aneurysms, atheromatous disease, plaque-adherent thrombi, and aortic dissection or intramural haematoma can be diagnosed by TOE (see Chapter 31).

• ♦ Aortic diameters. At the aortic root, several diameters can be measured. The first and usually smallest is the diameter of the aortic annulus. A few millimetres distally, at the sinuses of Valsalva, the diameter is considerably larger. At the transition from sinuses to ascending aorta, the ‘sinotubular junction’, the normal aorta becomes narrower again, although it is still wider than at the annulus. In Marfan’s syndrome, the sinotubular junction typically is effaced, and the aorta dilates immediately distal to the aortic valve in a funnel-like shape. Normal values are given in Fig. 4.51.
  
• ♦ Atheromatosis is mainly observed in the descending aorta and the arch. Sometimes, mobile thrombi may be noted which may embolize.
  
• ♦ Aortic dissection ( Chapter 31) is diagnosed by identifying the pathognomonic dissection membrane, a thin, undulating membrane (‘intimal flap’) separating true and false lumen ( Fig. 4.52). Entry and re-entry sites may be identified by two-dimensional echocardiography and colour flow Doppler. The false lumen typically is larger, has slower flow (often spontaneous contrast or even thrombosis is present), and is convex towards the higher-pressurized, but smaller true lumen. The site of the intimal rupture and the extent of the dissection are crucial for identification of the type of dissection and thus prognosis and management. Typical concomitant signs of type A dissections (involving the ascending aorta) are aortic regurgitation and pericardial haemorrhage, portending imminent lethal tamponade. A special form of dissection is aortic intramural haematoma, which manifests as thickening of the aortic wall ( Fig. 4.53; 4.32).
  

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Figure 4.47 Mechanical bileaflet prosthesis in the mitral position with closed (A) and opened (B) discs (arrows); transoesophageal images. (C) Bioprosthesis in the aortic position in a transoesophageal short-axis view. LA left atrium; LV left ventricle; RA right atrium. Also see 4.28.

An emerging role for TOE and intravascular ultrasound is to provide imaging support for the interventional treatment of type III dissections with stents, where stent location, coverage of dissection, leaks, and other questions may be addressed by ultrasound imaging.

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Figure 4.48 Pericardial effusions. (A) Parasternal long-axis view and modest effusion (arrow). (B) Large effusion viewed from subcostal view. The arrow indicates the direction of advancement of puncture needle if pericardial tap is performed. Also see 4.29 and 4.30.

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Figure 4.49 Pericardial tamponade. (A) Apical four-chamber view with large circular effusion and compression of right atrium. (B) PW Doppler recording of transmitral flow at low sweep speed, showing inspiratory decrease in peak transmitral velocities. Also see 4.31.

The main pulmonary artery and the right pulmonary artery are reasonably well visualized from transthoracic parasternal and subcostal views and by TOE. Dilatation or the detection of thrombotic material is important in the evaluation of patients with suspected acute or chronic pulmonary hypertension.

Key echocardiographic features of frequent diseases and clinical scenarios

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The coronaries are only marginally visualized by echocardiography; the ostia of the left and right coronary are frequently identifiable, especially by TOE (see Fig. 4.53; 4.32), and the left main stem as well as the very proximal segments of the left anterior descending and sometimes the circumflex artery may be visualized by TOE. With transthoracic transducers, some centres have been able to visualize the distal left anterior descending by colour Doppler in 90% of patients or more, allowing measurement of flow velocity and—by performing a vasodilator stress test—to determine the coronary flow reserve of this artery [14]. Moreover, myocardial contrast echocardiography allows in principle to evaluate regional myocardial blood volume and flow reserve (see Contrast echocardiography, p.114). Nevertheless, at present these techniques are not widely used.

The most important sign of coronary artery disease (CAD) is therefore the impairment of regional wall motion of the left (and rarely, right) ventricle as a consequence of previous ischaemia. For this purpose, the regional function of the left ventricle is visually evaluated (see Left ventricle, p.116). Objective evaluation of regional myocardial function by quantitative parameters can be achieved using tissue velocity and deformation data (see Figs. 4.12 and 4.18). However, longitudinal myocardial velocities have location-specific normal values and are subject to the influence of neighbouring regions (‘tethering’) and are therefore difficult to use in particular when evaluating mild or moderate wall motion abnormalities. The greatest promise at presents seems to lie in regional strain and strain rate measurement, preferably based on speckle tracking algorithms (‘two-dimensional strain’; Fig. 4.54; 4.33 and 4.34). The detection of regional wall motion abnormalities at rest is not specific for CAD; cardiomyopathies, myocarditis, and other diseases may also lead to regionally variable wall motion abnormalities. On the other hand, even diffusely reduced wall motion may be due to multivessel coronary disease or post-infarct remodelling.

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Figure 4.50 (A) Apical four-chamber view shows a large myxoma prolapsing into the mitral orifice in diastole. LV, left ventricle. (B) M-mode recording shows the tumour in the mitral orifice (arrow). Note that there is an interval between mitral valve (aML and pML) opening and diastolic prolapse of the tumour corresponding to the tumour plop heard on auscultation. Ventricular filling takes place during this short interval. (C) Anatomical specimen showing the excised attachment of the tumour to the interatrial septum.

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Figure 4.51 Normal range of aortic diameters at the sinuses of Valsalva (95% confidence intervals; (A) <20 years; (B) 20–39; (C) ≥40 years). Reproduced with permission from Lang R, Bierig M, Devereux R, et al. Recommendations for Chamber Quantification. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee, the Task Force on Chamber Quantification, and the European Association of Echocardiography. Eur J Echocardiogr 2006; 7: 79–108.

Stress-inducible myocardial ischaemia can be diagnosed by stress echocardiography (see Stress echocardiography, p.112). Viability of dysfunctional myocardium due to reduced coronary perfusion or non-transmural infarction is detectable by pharmacologic or exercise stress tests. Aneurysmal wall motion abnormality, marked thinning, and increased myocardial reflectivity are signs of myocardial scar.

Acute myocardial ischaemia during an acute coronary syndrome manifests on echocardiography as an acute wall motion abnormality in the perfusion territory of the affected vessel with a severity ranging from hypokinesia to dyskinesia. This is also detectable by deformation imaging (strain and strain rate; Fig. 4.55). Acute echocardiography in the early evaluation of a suspected acute coronary syndrome, e.g. in the presence of inconclusive ECG changes and before confirmation or exclusion of the diagnosis by biomarkers, therefore is extremely useful to confirm or refute the presence and extent of ischaemia. Besides, it quickly provides critical information on potential confounding diseases such as pulmonary embolism, aortic dissection, and others. However, small wall motion abnormalities, especially in the circumflex perfusion territory, may elude echocardiographic diagnosis.

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Figure 4.52 Aortic dissection of the ascending aorta (ASC; arrows point to intimal flap). (A) Transoesophageal short-axis view of a dissection with spontaneous contrast and beginning thrombosis of the false lumen (FL). (B) Transoesophageal long-axis view of a dissection of the ascending aorta.

In the setting of a myocardial infarction, echocardiography provides data crucial for management and prognosis:

• ♦ site and extent of wall motion abnormalities, left and right ventricular systolic function and volumes, and increase in filling pressures;
  
• ♦ presence, mechanism, and severity of mitral regurgitation;
  
• ♦ presence of thrombi;
  
• ♦ presence of infarct complications such as papillary muscle rupture, ventricular septal defect, pseudoaneurysm (contained myocardial rupture), pericardial effusion.
  

Thus, every patient with a suspected or proven acute coronary syndrome should undergo echocardiography as quickly as it can be offered. In the subacute stage, stress echocardiography for ischaemia and/or viability is often helpful to determine further management in terms of coronary revascularization.

The echocardiographic hallmark of hypertension ( Chapter 13) is an increase in left ventricular mass, which is called left ventricular hypertrophy. In hypertension, several patterns of change in left ventricular morphology have been described, depending on the relation of end-diastolic wall thickness and end-diastolic left ventricular cavity diameter. The most frequent type pattern is eccentric hypertrophy, implying an increased left ventricular mass (indexed to body surface area) together with an increased left ventricular end-diastolic diameter. Concentric hypertrophy (increased indexed left ventricular mass together with a normal or decreased left ventricular diameter), carries the worst prognosis as to cardiovascular adverse events [41].

As discussed in the section on the left ventricle, left ventricular hypertrophy is frequently associated with characteristic changes of diastolic filling pressures, either at rest or during exercise. Furthermore, long standing hypertension is commonly accompanied by aortic valve sclerosis and mitral valve calcification, left atrial dilatation, aortic dilatation, and aortic atheromatosis.

Dilated cardiomyopathy ( Chapter 18) is characterized by dilatation and functional impairment—both systolic and diastolic—of the left ventricle, and in some cases also of the right ventricle ( Fig. 4.56). Parameters of systolic function, most prominently EF, are decreased, and parameters of diastolic function indicate elevated filling pressures. The presence of a ‘restrictive’ transmitral filling pattern (see Fig. 4.26c), which cannot be reversed by therapy, independently from EF implies particularly elevated filling pressures, severe myocardial disease, and impaired prognosis. Almost universally, mitral regurgitation is present with the configuration of functional regurgitation (see Mitral valve, p.126). Peak tricuspid regurgitation velocity usually identifies elevated right ventricular systolic pressure. In severe left ventricular dilatation, spontaneous echocardiographic contrast and left ventricular or left atrial thrombi are frequently seen. Early impairment of systolic and diastolic function may be detected by reduced longitudinal systolic and early diastolic myocardial velocities on tissue Doppler before EF becomes noticeably reduced [42]. Similar changes are seen in the toxic, dose-dependent cardiomyopathy induced by chemotherapy, in particular by anthrachinolones (doxorubicin and daunorubicin); see also Heart failure, p.141.

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Figure 4.53 Intramural haematoma (arrow) of ascending aorta. Note thickened aortic wall starting at the take-off of the right coronary artery (RCA). Transoesophageal long-axis view. AV, aortic valve. (Courtesy of J. Roelandt and R. Erbel.) Also see 4.32.

Hypertrophic cardiomyopathy ( Chapter 18) is often asymptomatic and is diagnosed by echocardiography based on increased wall thicknesses and increased left ventricular mass in the absence of hypertension. The location of increased wall thickness is very variable and may occur anywhere in the left ventricle, although the ventricular septum is most frequently involved. A subgroup of patients—usually with greatly increased septal thickness—develops obstruction to systolic ejection in the outflow tract. The mechanism of hypertrophic obstructive cardiomyopathy or ‘subaortic stenosis’ is believed to be a combination of increased basal septal thickness and structural changes of the mitral valve leading to systolic anterior motion (SAM) of the mitral valve in systole, a phenomenon most likely due to redundant mitral leaflet tissue being dragged or sucked into the outflow tract by vigorous ejection ( Fig. 4.57). The result is a late peaking systolic gradient occurring in the outflow tract, which is highly variable depending on load conditions, sympathetic drive, and other factors; provocative manoeuvres include exercise or the application of nitroglycerin. The CW Doppler spectrum typically is dagger-shaped with a late systolic peak; peak velocities may exceed 5m/s, but also may be barely elevated. This so-called ‘dynamic obstruction’ may also generate a mid-systolic closure movement of the aortic valve and a deceleration in mid-systolic septal tissue velocities. Similar to dilated cardiomyopathy, myocardial tissue Doppler shows reduced myocardial systolic and early diastolic peak velocities in patients with hypertrophic cardiomyopathy, although ejection fraction in these patients is usually in the high normal range. Moreover, genetic carriers of the disease without manifest hypertrophy may also be identifiable based on reduced tissue velocities [43, 44]. Furthermore, deformation parameters have been shown to be useful in distinguishing hypertrophic cardiomyopathy from hypertensive hypertrophy [45].

Echocardiography has an important further role in the follow-up of these patients under therapy and has been reported to be useful for planning of transcutaneous septal alcohol ablation by performing intracoronary echocardiographic-contrast injections into the septal branch targeted for alcohol ablation to delineate the corresponding perfusion territory [46].

Restrictive cardiomyopathy ( Chapter 18), of which cardiac amyloidosis is the most prominent form, is characterized by diffusely thickened walls (including the right ventricular wall and sometimes even the valve leaflets), a highly reflective myocardial texture (so-called ‘granular sparkling’), the very frequent presence of small pericardial effusions, enlarged atria, and signs of increased filling pressures even if EF is still preserved ( Fig. 4.58). In the end stage, the patients uniformly develop the ‘restrictive pattern’ of transmitral filling (see Fig. 4.26), portending a very grave prognosis. Tissue Doppler velocities, as well as regional deformation parameters, are impaired already early in the course of the disease. Another, rarer infiltrative form of hypertrophic cardiomyopathy is Fabry disease, which shows very variable patterns of hypertrophy which are less diffuse than in amyloidosis. Myocardial deformation parameters such as myocardial velocities, peak systolic strain, and strain rate are reduced, and the effect of causal treatment by substitution of beta-galactosidase may be documented by these parameters [47, 48].

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Figure 4.54 ‘Two-dimensional strain’ imaging using speckle tracking. Velocity and deformation parameters can be estimated in any direction within the image plane. (A) Colour-coded longitudinal strain is superimposed on an apical three-chamber view (top left). End-systolic strain is displayed per segment (bottom left). Strain curves and curved M-mode display of strain allow evaluation of the temporal course of regional deformation (top and bottom right). (B) Bull‘s eye view of the left ventricle with colour coded segmental endsystolic strain values obtained from the three apical views. The infarcted region is clearly visualized. Segmental systolic strain values are displayed. X denotes a segment not scored. Also see 4.33 and 4.34.

Another cardiomyopathy that may mimic hypertrophic cardiomyopathy is left ventricular non-compaction. This is a cardiomyopathy characterized by a two-layered left ventricular wall structure with a heavily trabecularized inner layer (the non-compacted layer) showing prominent intertrabecular spaces and a thickness at least twice as large as the compacted outer layer [49]. For arrhythmogenic right ventricular cardiomyopathy see Right ventricle, p.122.

Myocarditis is a difficult diagnosis short of myocardial biopsy evidence, and echocardiography contributes only modestly. There may be diffuse or regional wall motion abnormalities of all degrees (except for dyskinesia and aneurysms, which, however, uniquely do occur in tropical Chagas disease). Sometimes, a pericardial effusion is present, implying perimyocarditis. Tissue oedema may be present and manifest as increased wall thickness. Unfortunately, all these signs are highly unspecific, and magnetic resonance imaging is clearly superior for this indication.

After heart transplantation, there are several typical characteristics of the transplanted heart:

• ♦ The right ventricle is enlarged, there is tricuspid regurgitation of varying degree, and especially early postoperatively, significant pulmonary hypertension can be inferred from peak tricuspid regurgitant velocity.
  
• ♦ The atria are enlarged and the anastomosis between the grafted atria and the remnant of the host atria is often visible as a slight indentation in the atrial walls.
  
• ♦ Transmitral flow profiles often show the influence of competing rhythms of graft and host components of the atrium.
  
• ♦ Diagnosis of rejection, the holy grail of echo in the transplanted patient, has proven elusive. The hallmark of severe rejection is impairment in systolic left and right ventricular function. Milder forms of rejection however are difficult to diagnose. Pericardial effusion, increased wall thickness, and signs of elevated filling pressures—particularly decreased E wave deceleration and shortened isovolumic relaxation period—may be indicative. Good predictive value has been reported from single centres by intra-individual follow-up of tissue velocity and deformation parameters.
  

All patients with heart failure ( Chapter 23) should be evaluated by echocardiography [50]. To validate and refine the diagnosis of heart failure, this may include:

• ♦ Assessment of left ventricular systolic and diastolic function, including estimation of filling pressures. The latter is especially important in patients with preserved EF, where the diagnosis of heart failure is less obvious than in patients with depressed EF (see Left ventricle, p.116). The assessment includes evaluation of right ventricular function and estimation of right ventricular systolic pressure.
  
• ♦ Evaluation of concomitant valvular heart disease, in particular mitral regurgitation. Mitral regurgitation is almost uniformly present in severe left ventricular dilatation, but such functional mitral regurgitation must be distinguished from primary mitral regurgitation as the cause for left ventricular failure.
  
• ♦ Assessment for the presence of a cardiomyopathy, myocarditis, or constrictive pericarditis.
  
• Echocardiography also plays a critical role in identifying candidates for therapies and procedures which may reverse, ameliorate, or prognostically improve heart failure. The most important issues are:
  
• ♦ Measurement of EF to identify candidates for implantable defibrillator therapy (EF <35%).
  
• ♦ Diagnosis of hibernating myocardium with the potential to improve function after revascularization. Hibernating, i.e. dysfunctional, but viable myocardial regions can be identified by dobutamine or exercise stress echocardiography (see Stress echocardiography valve, p.112). The identification of hibernating myocardium predicts improvement of EF and prognosis after revascularization.
  
• ♦ Identification of candidates for cardiac resynchronization therapy (CRT; see Chapter 22). Although so far the selection of CRT candidates by echocardiography criteria has not been proven to discriminate well between potential responders and non-responders, and criteria for identifying CRT-responsive left ventricular dyssynchrony continue to evolve [51], several parameters seem to have at least moderate predictive value ( Figs. 4.59 and 4.60):
  
  • ♦ the interventricular delay, measured as the delay of onset of left ventricular ejection versus the onset of right ventricular ejection (measured from PW-Doppler of pulmonary and aortic flow), considered to be significant >40ms;
    
  • ♦ the differences in the time that it takes myocardial longitudinal systolic velocities to reach their systolic maximum (‘time to peak’) in the basal or mid segments of the left ventricle, in particular comparing septal to lateral wall segments (with a delay >65ms considered predictive);
    
  • ♦ differences in timing of systolic strain on longitudinal, radial, or circumferential strain of different wall segments;
    
  • ♦ differences in timing of maximal contraction of wall segments as calculated from three-dimensional volume sets.
    
  
  

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Figure 4.55 (A) Strain rate in acute septal myocardial infarction. (B) On admission to the emergency room, the septum shows positive longitudinal strain rate (lengthening) during ejection time (ET), indicating systolic stretching of this myocardial region. Note the marked post-systolic shortening (arrow). (C) 1 day after successful acute coronary intervention, the strain rate curve has normalized. (D) Normal curve pattern 2 weeks after the event.

The search for a cardiac source of embolism is a frequent indication for echocardiography, in particular TOE, due to its well established higher yield than TTE in identifying potential sources of cardiac embolism. The following principal pathologies should be systematically sought:

• ♦ Atrial thrombi, in particular thrombi of the left atrial appendage (see Fig. 4.35; 4.17) ( Chapter 29). This structure is known to harbour thrombi in >10% of patients with non-valvular atrial fibrillation ( Chapter 29). Even in the absence of demonstrating a thrombus, TOE can detect a thrombogenic environment as evidenced by spontaneous echocardiographic contrast and <25cm/s peak flow velocities in the appendage.
  
• 
  
  
• ♦ Infective endocarditis. Again, TOE has a higher sensitivity in detecting small vegetations than TTE. The risk of embolization from vegetations correlates with their size and mobility, and decreases with elapsed time under antibiotic treatment and with increasing echo-density. See also Chapter 22.
  
• ♦ Left ventricular thrombi occur in areas of large and severe wall motion abnormalities of the left ventricle, whether of ischaemic or cardiomyopathic origin (see Fig. 4.30; 4.14). TOE has no advantage in detecting left ventricular thrombi.
  
• ♦ Tumours, e.g. myxoma or fibroelastoma, best diagnosed or excluded by TOE ( Chapter 20).
  
• ♦ Atrial septal defect ( Chapter 10) or patent foramen ovale (see Right atrium, atrial septum, and caval veins, p.124; Fig. 4.60) as the gate for paradoxical embolism. Through this frequent anomaly, thrombi may cross from the right to the left atrium if a permanent or even transient right-to-left pressure gradient occurs, causing paradoxical embolism to the brain and other organs. While this demonstrably is not infrequent in the context of severe pulmonary embolism, the true significance of this mechanism in cryptogenic embolism remains questionable. An association with unexplained neurologic events has been reported especially for the combination of patent foramen ovale and atrial septal aneurysm.
  
• ♦ Aortic atheromatosis with superimposed thrombi of the arch, ascending aorta, or proximal portions of the descending aorta ( Fig. 4.61; 4.35). This is chiefly the domain of TOE, although large thrombi may be detectable from the suprasternal notch ( Fig. 4.62; 4.36).
  

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Figure 4.59 Evaluation of patients in heart failure who are candidates for cardiac resynchronization therapy: inter-ventricular delay. The onset of ejection of the right and left ventricle is measured against the ECG (e.g. onset QRS). The difference between both measurements is a marker of interventricular asynchrony, with a difference of >40ms considered a predictor of response to resynchronization.

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Figure 4.60 Evaluation of patients in heart failure who are candidates for cardiac resynchronization therapy: intra-ventricular asynchrony identified by tissue velocity curves. Time to peak systolic tissue velocity (Ts) is measured either with PW or from high frame rate colour tissue Doppler (as in the case shown) as the interval between onset of QRS and peak positive velocity during ejection time (ET). A difference in the time to peak systolic velocity between septal and lateral basal or mid segments > 65ms is a widely used criterion of significant intraventricular asynchrony.

In all patients with acute, life-threatening cardiovascular disease, echocardiography provides timely, crucial information and can be performed with today’s highly portable equipment virtually anywhere inside and outside the hospital. These exams have to be short and focused. As an example, in a patient with unexplained sudden severe hypotension, the following potential mechanisms should be quickly evaluated:

• ♦ impaired left ventricular function with a large severe wall motion abnormality (e.g. acute myocardial infarction);
  
• ♦ massive pulmonary embolism with an enlarged and hypokinetic right ventricle, usually with elevated right ventricular systolic pressure as detectable by the almost invariably present tricuspid regurgitation;
  
• 
  
  
• ♦ pericardial tamponade;
  
• ♦ infarct complications: right heart infarction, papillary muscle rupture with severe mitral regurgitation, ventricular septal defect, myocardial free wall rupture with tamponade;
  
• ♦ acute severe aortic or mitral regurgitation due to infective endocarditis or aortic dissection;
  
• ♦ decompensated aortic stenosis;
  
• ♦ acute aortic dissection or rupture (mostly necessitates TOE).
  

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Figure 4.61  Detection of patent foramen ovale by transoesophageal echocardiography with right heart contrast (e.g. agitated saline-blood mixture). (A) View of left (LA) and right atrium (RA) before contrast injection. The arrow points to the patent foramen ovale. (B) Contrast injection, with passage of a few bubbles from right to left atrium across the atrial septum through the patent foramen ovale (arrow). Also see 4.35.

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Figure 4.62 Mobile thrombus (arrow) in the descending aorta (AOD). Transoesophageal short-axis view. Also see 4.36.

Intraoperative TOE is mainly used to check the results of valvular heart surgery, in particular after mitral valve repair. Detection of persistent moderate or severe mitral regurgitation allows to re-operate before the sternum is closed; other complications such as new wall motion abnormalities due to damage to the circumflex artery, new systolic anterior motion of the mitral valve, and others can be detected in a timely way. A clinical benefit of intraoperative TOE has also been seen in other valvular and also revascularization procedures. Direct application of the echocardiographic transducer in a sterile pouch on the aorta may help to detect calcified sites and thus guide aortic cannulation.

During device closure of patent foramen ovale or atrial septal defect, or during percutaneous valve procedures (e.g. percutaneous aortic valve replacement), TOE can be used in the sedated patient in the catheterization laboratory to guide the procedure, detect complications, and check the final results (see Fig. 4.22; 4.10 and 4.11).

Personal perspective

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The wealth of morphologic and functional information obtained by echocardiography will keep this technique at the centre of patient evaluation in the foreseeable future, although competing imaging modalities will continue to carve out niches according to their specific strengths. Perhaps surprisingly, echocardiographic techniques and modalities continue to evolve and improve, and therefore have expanded into new territory such as the earlydiagnosis of clinically inapparent myocardial disease, the exact calculation of cavity volumes from three-dimensional datasets, the estimation of left ventricular filling pressures, and others. It is likely that three-dimensional echocardiography in the long run will supersede two-dimensional echocardiography not only for the evaluation of morphology, but also for blood flow and myocardial deformation analysis. In this context, speckle tracking as a teschnique to detect motion may come to play a similar or larger role than classic Doppler analysis.

Additional online material

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Click on image to view video 4.1 Three-dimensional echocardiography. Four-chamber view-like cut of data set; note the corrugated left ventricular endocardium in the ‘depth’ of the image (small arrow), which would not be visible on a two-dimensional image.

 

Click on image to view video 4.2 Parasternal long-axis view.

 

Click on image to view video 4.3 Parasternal short-axis view at papillary muscle level.

 

Click on image to view video 4.4 Parasternal short-axis view at aortic valve level.

 

Click on image to view video 4.5 Apical four-chamber view.

 

Click on image to view video 4.6 Apical two-chamber view.

 

Click on image to view video 4.7 Apical long-axis view.

 

Click on image to view video 4.8 Cardiac amyloidosis (1). Standard two-dimensional parasternal long axis.

 

Click on image to view video 4.9 Cardiac amyloidosis (2). Real-time three-dimensional echo.

 

Click on image to view video 4.10 En face view of left atrial side of atrial septum by transoesophageal three-dimensional echocardiography during closure of a patent foramen ovale. This clip shows the deployment of the closure device (see also 4.11).

 

Click on image to view video 4.11 View of left atrial side of atrial septum by transoesophageal three-dimensional echocardiography during closure of a patent foramen ovale. This clip shows the fully deployed closure device (see also 4.10).

 

Click on image to view video 4.12 Left ventricular remodelling (1). Shortly after anterior infarction.

 

Click on image to view video 4.13 Left ventricular remodelling (2). 1 year after infarction. Note enlargement (both clips have the same scale), relative increase in width of left ventricle (spherical remodelling), and spontaneous echocardiographic contrast in the cavity after 1 year.

 

Click on image to view video 4.14 Left ventricular thrombus. Left ventricular apical akinesia with thrombus due to an anterior myocardial infarction. Apical four-chamber view.

 

Click on image to view video 4.15 Infero-posterior pseudoaneurysm of left ventricle after inferior infarction. Note the ‘neck’ of the pseudoaneurysm, which is narrower than its largest diameter.

 

Click on image to view video 4.16 Arrhythmogenic dysplasia of the right ventricle.

 

Click on image to view video 4.17 Large thrombus in the left atrial appendage in a patient with atrial fibrillation. Transoesophageal image.

 

Click on image to view video 4.18 Sagittal transoesophageal view of the right atrium.

 

Click on image to view video 4.19 Rheumatic mitral stenosis with diastolic doming of the leaflets, parasternal long-axis view.

 

Click on image to view video 4.20 Parasternal short-axis view of stenotic mitral valve orifice.

 

Click on image to view video 4.21 Flail posterior mitral leaflet. Apical four-chamber view.

 

Click on image to view video 4.22 Corresponding colour Doppler clip of eccentric mitral regurgitant jet (also see 4.22)

 

Click on image to view video 4.23 Bicuspid aortic valve. Parasternal short-axis view.

 

Click on image to view video 4.24 Aortic stenosis (1). Parasternal long-axis view.

 

Click on image to view video 4.25 Aortic stenosis (2). Parasternal long-axis view. Image magnification of calcified valve.

 

Click on image to view video 4.26 Transoesophageal magnified long-axis view of aortic valve showing prolapse of the acoronary aortic cusp.

 

Click on image to view video 4.27 Severe tricuspid regurgitation. Apical four-chamber view.

 

Click on image to view video 4.28 Mechanical bileaflet mitral prosthesis. Transoesophageal view.

 

Click on image to view video 4.29 Pericardial effusion.

 

Click on image to view video 4.30 Large pericardial effusion, subcostal view. See also 4.31.

 

Click on image to view video 4.31 Note right atrial collapse. Four-chamber view.

 

Click on image to view video 4.32 Transoesophageal long-axis view. Note thickened aortic wall starting at the take-off of the right coronary artery.

 

Click on image to view video 4.33 Large anteroseptal wall motion abnormality after myocardial infarction (1). This clip is the basis for the strain analysis shown in the next clip (4.34).

 

Click on image to view video 4.34 ‘Two-dimensional strain’ imaging using speckle tracking. Velocity and deformation parameters can be estimated in any direction within the image plane. Top left, colour-coded longitudinal strain is superimposed on an apical three-chamber view. Bottom left, end-systolic strain is displayed per segment. Strain curves and curved M-mode display of strain allow evaluation of the temporal course of regional deformation (top and bottom right).

 

Click on image to view video 4.35 Detection of patent foramen ovale by transoesophageal echocardiography with right heart contrast.

 

Click on image to view video 4.36 Thrombus in the descending aorta. Transoesophageal short-axis view.

 
For full references and multimedia materials please visit the online version of the book (http://esctextbook.oxfordonline.com).

Further reading

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Baumgartner H, Hung H, Bermejo J, et al. Echocardiographic Assessment of Valve Stenosis: EAE/ASE Recommendations for Clinical Practice. Eur J Echocardiogr 2009; 10:1–25.
Daniel WG, Mügge A. Transesophageal echocardiography. N Engl JMed 1995; 332:1268–79.[Free Full Text]
Evangelista A, Flachskampf F, Lancellotti P, et al. European Association of Echocardiography. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur J Echocardiogr 2008; 9:438–48.[Abstract/Free Full Text]
Flachskampf FA, Decoodt P, Fraser AG, et al. Recommendations for performing transesophageal echocardiography. Eur J Echocardiogr 2001; 2:8–21.[Free Full Text]
Hung J, Lang R, Flachskampf F, et al. 3D echocardiography: a review of the current status and future directions. J Am Soc Echocardiogr 2007; 20:213–33. An update of this paper will appear in 2009.[CrossRef][Web of Science][Medline]
Lang R, Bierig M, Devereux R, et al. Recommendations for Chamber Quantification. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee, the Task Force on Chamber Quantification, and the European Association of Echocardiography. Eur J Echocardiogr 2006; 7: 79–108.
Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr 2009; 10: 165–93.[Abstract/Free Full Text]
Paulus WJ, Tschope C, Sanderson JE, et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J 2007; 28: 2539–50.[Abstract/Free Full Text]
Sicari R, Nihoyannopoulos P, Evangelista A, et al. European Association of Echocardiography. Stress echocardiography expert consensus statement: European Association of Echocardiography (EAE) (a registered branch of the ESC). Eur J Echocardiogr 2008; 9: 415–37.[Abstract/Free Full Text]
Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J 2007; 28: 230–68.[Free Full Text]
Zoghbi WA, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography: recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography: A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and The Task Force on Valvular Regurgitation, developed in conjunction with the American College of Cardiology Echocardiography Committee, The Cardiac Imaging Committee, Council on Clinical Cardiology, The American Heart Association, and the European Society of Cardiology Working Group on Echocardiography. Eur J Echocardiogr 2003; 4: 237–61.[Free Full Text]

References

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1.  1 Weyman AE. Principles and Practice of Echocardiography, 2^nd edn., 1994. Philadelphia, PA: Lea & Febiger.
2.  2 Thomas JD. The DICOM image formatting standard: What it means for echocardiographers. J Am Soc Echocardiogr 1995; 8: 319–27.[CrossRef][Medline]
3.  3 Evangelista A, Flachskampf F, Lancellotti P, et al. European Association of Echocardiography. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur J Echocardiogr 2008; 9: 438–48.[Abstract/Free Full Text]
4.  4 Flachskampf FA, Decoodt P, Fraser AG, et al. Recommendations for performing transesophageal echocardiography. Eur J Echocardiogr 2001; 2: 8–21.[Free Full Text]
5.  5 Roelandt JRTC, Thomson IR, Vletter WB, et al. Multiplane transesophageal echocardiography: latest evolution in an imaging revolution. J Am Soc Echo 1992; 5: 361–7.[Medline]
6.  6 Flachskampf FA, Hoffmann R, Verlande M, et al. Initial experience with a multiplane transesophageal echo-transducer: assessment of diagnostic potential. Eur Heart J 1992; 13: 1201–6.[Abstract/Free Full Text]
7.  7 Daniel WG, Erbel R, Kasper W, et al. Safety of transesophageal echocardiography. A multicenter survey of 10,419 examinations. Circulation 1991; 83: 817–21.
8.  8 Sicari R, Nihoyannopoulos P, Evangelista A, et al. European Association of Echocardiography. Stress echocardiography expert consensus statement: European Association of Echocardiography (EAE) (a registered branch of the ESC). Eur J Echocardiogr 2008; 9: 415–37.[Abstract/Free Full Text]
9.  9 Marwick TH, Case C, Sawada S, et al. Prediction of mortality using dobutamine echocardiography. J Am Coll Cardiol 2001; 37: 754–60.[Abstract/Free Full Text]
10. 10 Marwick TH, Case C, Vasey C, et al. Prediction of mortality by exercise echocardiography. A strategy for combination with the Duke treadmill score. Circulation 2001; 103: 2566–71.
11. 11 Poldermans D, Hoeks SE, Feringa HH. Pre-operative risk assessment and risk reduction before surgery. J Am Coll Cardiol 2008; 51: 1913–24.[Abstract/Free Full Text]
12. 12 Voigt JU, Exner B, Schmiedehausen K, et al. Strain rate imaging during dobutamine stress echocardiography provides objective evidence of inducible ischemia. Circulation 2003; 107: 2120–6.[Abstract/Free Full Text]
13. 13 Iliceto S, Marangelli V, Memmola C, et al. Transesophageal Doppler echocardiography evaluation of coronary blood flow velocity in baseline conditions and during dipyridamole-induced coronary vasodilation. Circulation 1991; 83: 61–9.[Abstract/Free Full Text]
14. 14 Caiati C, Montaldo C, Zedda N, et al. New noninvasive method for coronary flow reserve assessment: contrast-enhanced transthoracic second harmonic echo Doppler. Circulation 1999; 99: 771–8.[Abstract/Free Full Text]
15. 15 Hoffmann R, Lethen H, Marwick T, et al. Analysis of interinstitutional observer agreement in the interpretation of dobutamine stress echocardiography. J Am Coll Cardiol 1996; 27: 330–6.[Abstract]
16. 16 Hoffmann R, Marwick TH, Poldermans D et al. Refinements in stress echocardiographic techniques improve inter-institutional agreement in interpretation of dobutamine stress echocardiograms. Eur Heart J 2002; 23: 821–9.[Abstract/Free Full Text]
17. 17 Underwood SR, Bax JJ, vom Dahl J, et al.; Study Group of the European Society of Cardiology. Imaging techniques for the assessment of myocardial hibernation. Report of a Study Group of the European Society of Cardiology. Eur Heart J 2004; 25: 815–36.
18. 18 Hanekom L, Jenkins C, Jeffries L, et al. Incremental value of strain rate analysis as an adjunct to wall-motion scoring for assessment of myocardial viability by dobutamine echocardiography: a follow-up study after revascularization. Circulation 2005; 112: 3892–900.[Abstract/Free Full Text]
19. 19 Piérard LA, Lancellotti P. The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema. N Engl J Med 2004; 351: 1627–34.[Abstract/Free Full Text]
20. 20 Elhendy A, O‘Leary EL, Xie F, et al. Comparative accuracy of real-time myocardial contrast perfusion imaging and wall motion analysis during dobutamine stress echocardiography for the diagnosis of coronary artery disease. J Am Coll Cardiol 2004; 44: 2185–91.[Abstract/Free Full Text]
21. 21 Tsutsui JM, Elhendy A, Anderson JR, et al. Prognostic value of dobutamine stress myocardial contrast perfusion echocardiography. Circulation 2005; 112: 1444–50.[Abstract/Free Full Text]
22. 22 Hung J, Lang R, Flachskampf F, et al. 3D echocardiography: A review of the current status and future directions. J Am Soc Echocardiogr 2007; 20: 213–33.[CrossRef][Web of Science][Medline]
23. 23 Zamorano J, Cordeiro P, Sugeng L, et al. Real-time three-dimensional echocardiography for rheumatic mitral valve stenosis evaluation: an accurate and novel approach. J Am Coll Cardiol 2004; 43: 2091–6.[Abstract/Free Full Text]
24. 24 Pepi M, Tamborini G, Maltagliati A, et al. Head-to-head comparison of two- and three-dimensional transthoracic and transesophageal echocardiography in the localization of mitral valve prolapse. J Am Coll Cardiol 2006; 48: 2524–30.[Abstract/Free Full Text]
25. 25 Groh MA, Binns OA, Burton HG 3rd, et al. Epicardial ultrasonic ablation of atrial fibrillation during concomitant cardiac surgery is a valid option in patients with ischemic heart disease. Circulation 2008; 118(Suppl.14): S78–82.[Abstract/Free Full Text]
26. 26 Rosenschein U, Gaul G, Erbel R, et al. Percutaneous transluminal therapy of occluded saphenous vein grafts. Can the challenge be met with ultrasound thrombolysis? Circulation 1999; 99: 26–9.
27. 27 Siegel RJ, Atar S, Fishbein MC, et al. Noninvasive, transthoracic, low-frequency ultrasound augments thrombolysis in a canine model of acute myocardial infarction. Circulation. 2000; 101: 2026–9.
28. 28 Paulus WJ, Tschope C, Sanderson JE, et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J 2007; 28: 2539–50.[Abstract/Free Full Text]
29. 29 Lang R, Bierig M, Devereux R, et al. Recommendations for Chamber Quantification. A report from the American Society of Echocardiography’s Nomenclature and Standards Committee, the Task Force on Chamber Quantification, and the European Association of Echocardiography. Eur J Echocardiogr 2006; 7: 79–108.
30. 30 Nagueh S, Appleton C, Evangelista A, et al. Recommendations for the echocardiographic diagnosis of diastolic dysfunction. Eur J Echocardiogr in press.
31. 31 Burgess MI, Jenkins C, Sharman JE, et al. Diastolic stress echocardiography: hemodynamic validation and clinical significance of estimation of ventricular filling pressure with exercise. J Am Coll Cardiol 2006; 47: 1891–900.[Abstract/Free Full Text]
32. 32 Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J 2007; 28: 230–68.[Free Full Text]
33. 33 Baumgartner H, Hung H, Bermejo J, et al. Echocardiographic Assessment of Valve Stenosis: EAE/ASE Recommendations for Clinical Practice. Eur J Echocardiogr 2009; 10:1–25.
34. 34 Zoghbi WA, Enriquez-Sarano M, Foster E, et al. American Society of Echocardiography: recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography: A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and The Task Force on Valvular Regurgitation, developed in conjunction with the American College of Cardiology Echocardiography Committee, The Cardiac Imaging Committee, Council on Clinical Cardiology, The American Heart Association, and the European Society of Cardiology Working Group on Echocardiography. Eur J Echocardiogr 2003; 4: 237–61.[Free Full Text]
35. 35 Lancellotti P, Gérard PL, Piérard LA. Long-term outcome of patients with heart failure and dynamic functional mitral regurgitation. Eur Heart J 2005; 26: 1528–32.[Abstract/Free Full Text]
36. 36 Daniel WG, Mügge A, Martin RP, et al. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991; 324: 795–800.[Abstract]
37. 37 Silversides CK, Veldtman GR, Crossin J, et al. Pressure half-time predicts hemodynamically significant pulmonary regurgitation in adult patients with repaired tetralogy of Fallot. J Am Soc Echocardiogr 2003; 16: 1057–62.[CrossRef][Web of Science][Medline]
38. 38 Baumgartner H, Khan S, DeRobertis M, et al. Discrepancies between Doppler and catheter gradients in aortic prosthetic valves in vitro. A manifestation of localized gradients and pressure recovery. Circulation 1990; 82: 1467–75.
39. 39 Baumgartner H, Schima H, Kühn P. Effect of prosthetic valve malfunction on the Doppler-catheter gradient relation for bileaflet aortic valve prostheses. Circulation 1993; 87: 1320–7.[Abstract/Free Full Text]
40. 40 Flachskampf FA, Guerrero JL, O’Shea JP, et al. Patterns of normal transvalvular regurgitation in mechanical valve prostheses. J Am Coll Cardiol 1991; 18: 1493–8.[Abstract]
41. 41 Wachtell K, Dahlöf B, Rokkedal J, et al. Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Am Heart J 2002; 144: 1057–64.[CrossRef][Web of Science][Medline]
42. 42 De Backer J, Matthys D, Gillebert TC, et al. The use of tissue Doppler imaging for the assessment of changes in myocardial structure and function in inherited cardiomyopathies. Eur J Echocardiogr 2005; 6: 243–50.[Abstract/Free Full Text]
43. 43 Nagueh SF, McFalls J, Meyer D, et al. Tissue Doppler imaging predicts the development of hypertrophic cardiomyopathy in subjects with subclinical disease. Circulation 2003; 108: 395–8.[Abstract/Free Full Text]
44. 44 Ho CY, Sweitzer NK, McDonough B, et al. Assessment of diastolic function with Doppler tissue imaging to predict genotype in preclinical hypertrophic cardiomyopathy. Circulation 2002; 105: 2992–7.[Abstract/Free Full Text]
45. 45 Kato TS, Noda A, Izawa H, et al. Discrimination of nonobstructive hypertrophic cardiomyopathy from hypertensive left ventricular hypertrophy on the basis of strain rate imaging by tissue Doppler ultrasonography. Circulation 2004; 110: 3808–14.[Abstract/Free Full Text]
46. 46 Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocard contrast echocardiography. Circulation 1998; 22: 2415–21.
47. 47 Pieroni M, Chimenti C, Ricci R, et al. Early detection of Fabry cardiomyopathy by tissue Doppler imaging. Circulation 2003; 107: 1978–84.[Abstract/Free Full Text]
48. 48 Weidemann F, Breunig F, Beer M, et al. Improvement of cardiac function during enzyme replacement therapy in patients with Fabry disease: a prospective strain rate imaging study. Circulation 2003; 108: 1299–301.[Abstract/Free Full Text]
49. 49 Oechslin E, Jenni R. Isolated left ventricular non-compaction: increasing recognition of this distinct, yet ‘unclassified’ cardiomyopathy. Eur J Echocardiogr 2002; 3: 250–1.[Free Full Text]
50. 50 Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J 2008; 29: 2388–442.
51. 51 Bax JJ, Ansalone G, Breithardt OA, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? A critical appraisal. J Am Coll Cardiol 2004; 44: 1–9.[Abstract/Free Full Text]
52. 52 Hatle L, Angelsen B. Doppler ultrasound in cardiology. Physical principles and clinical applications, 2^nd edn., 1985. Philadelphia, PA: Lea & Febiger.
53. 53 Rosenhek R, Binder T, Maurer G, et al. Normal values for Doppler echocardiographic assessment of heart valve prostheses. J Am Soc Echocardiogr 2003; 16: 1116–27.
54. 54 Flachskampf FA. Kursbuch Echokardiographie, 4^th edn., 2008. Stuttgart: Thieme.
55. 55 Henein M, Lindqvist P, Francis D, et al. Tissue Doppler analysis of age-dependency in diastolic ventricular behaviour and filling: a cross-sectional study of healthy hearts (the Umeå General Population Heart Study). Eur Heart J 2002; 23: 162–71.[Abstract/Free Full Text]
56. 56 De Sutter J, De Backer J, Van de Veire N, et al. Effects of age, gender, and left ventricular mass on septal mitral annulus velocity (E’) and the ratio of transmitral early peak velocity to E’ (E/E’). Am J Cardiol 2005; 95: 1020–3.[CrossRef][Web of Science][Medline]

Contents

Front Matter

Foreword Preface Contributors Reviewers Acknowledgement to first edition contributors Symbols and abbreviations

CHAPTER 1 The Cardiovascular History and Physical Examination 

Roger Hall and Iain Simpson

[References PDF]

Summary Introduction History Examination Conclusion Key points Personal perspective Online resources Further reading References

CHAPTER 2 The Electrocardiogram 

Francisco G. Cosío, José Palacios, Agustín Pastor, and Ambrosio Núñez

[References PDF]

Summary Introduction Recording the electrical activity of the heart Chamber enlargement/hypertrophy Ischaemia and infarction Conduction disturbances Pre-excitation (also see Chapter 28) Primary repolarization disturbances Pericarditis and pericardial effusion An approach to ECG reading An approach to arrhythmia diagnosis Stress ECG Ambulatory ECG monitoring Implantable loop recorder Computer analysis of the ECG Personal perspective Online resources Further reading References

CHAPTER 3 Choice of Imaging Techniques 

Joanne D. Schuijf, Nico R. Van de Veire, Ernst E. van der Wall, and Jeroen J. Bax

[References PDF]

Summary Introduction The patient with stable chest pain presenting at the outpatient clinic The patient with chronic heart failure Personal perspective Additional online material Further reading References

CHAPTER 4 Cardiac Ultrasound 

Frank A. Flachskampf, Jens-Uwe Voigt, and Werner G. Daniel

[References PDF]

Summary Physical and technical principles of echocardiography Specific cardiovascular structures Key echocardiographic features of frequent diseases and clinical scenarios Personal perspective Additional online material Further reading References

CHAPTER 5 Cardiovascular Magnetic Resonance 

Dudley J. Pennell, Udo P. Sechtem, Sanjay Prasad, and Frank E. Rademakers

[References PDF]

Summary Basic principles Volumes and function Myocardial infarction and viability Ischaemia detection Acute coronary syndromes (also see Chapter 16) Coronary arteries Vessel wall Cardiomyopathy Valvular heart disease Congenital heart disease (also see Chapter 10) Great vessels (also see Chapter 31) Pericardium (also see Chapter 19) Tumours and masses Personal perspective Further reading References

CHAPTER 6 Cardiovascular Computed Tomography 

Pim J. de Feyter, Stephan Achenbach, and Koen Nieman

[References PDF]

Summary Introduction Basics of computed tomography Clinical applications of cardiac computed tomography Personal perspective Additional online material Further reading References

CHAPTER 7 Nuclear Cardiology 

Philipp A. Kaufmann, Paolo G. Camici, and S. Richard Underwood

[References PDF]

Summary Diagnosis of coronary artery disease Heart failure: myocardial viability and hibernation Microvascular disease ( Chapter 17) Personal perspective Further reading References

CHAPTER 8 Invasive Imaging and Haemodynamics 

Carlo Di Mario, Guy R. Heyndrickx, Francesco Prati, and Nico H.J. Pijls

[References PDF]

Summary Introduction Percutaneous techniques of cardiac catheterization Haemodynamic measurements during cardiac catheterization Invasive imaging techniques and coronary morphology Functional assessment of the coronary circulation Personal perspective Further reading References

CHAPTER 9 Genetics of Cardiovascular Diseases 

Silvia G. Priori, Carlo Napolitano, Steve E. Humphries, and James Skipworth

[References PDF]

Summary Mendelian monogenic human diseases: an overview Monogenic diseases with myocardial involvement Marfan syndrome Genetic disorders in the structurally normal heart Polygenic diseases: genetic aspects of coronary artery disease Hypertension ( Chapter 13) Personal perspective Online resources Further reading References

CHAPTER 10 Congenital Heart Disease in Children and Adults 

John E. Deanfield, Robert Yates, Folkert J. Meijboom, and Barbara J.M. Mulder

[References PDF]

Summary Introduction Nomenclature Epidemiology and incidence Aetiology and prevention Fetal circulation Pathophysiology Investigation Management Grown-up congenital heart disease Common congenital cardiac malformations Personal perspective Online resources Additional online material Further reading References

CHAPTER 11 Clinical Pharmacology of Cardiovascular Drugs 

Faiez Zannad, Pascal Bousquet, and Laurent Monassier

[References PDF]

Summary Basic concepts in clinical pharmacology Clinical trials and assessment of evidence Personal perspective Online resources Further reading References

CHAPTER 12 Prevention of Cardiovascular Disease 

Annika Rosengren, Joep Perk, and Jean Dallongeville

[References PDF]

Summary Introduction Facts and figures about CVD in Europe Prevention strategies Population strategy Modifying CVD risk at the individual level High-risk strategy Secondary prevention Smoking Physical activity Blood pressure Nutrition Obesity and problems related to obesity Lipids Psychosocial factors Gender aspects in prevention Conclusion Personal perspective Online resources Further reading References

CHAPTER 13 Hypertension 

Sverre E. Kjeldsen, Tonje A. Aksnes, Robert H. Fagard, and Giuseppe Mancia

[References PDF]

Summary Introduction Definition and classification of hypertension Diagnostic evaluation Therapeutic approach Personal perspective Online resources Further reading References

CHAPTER 14 Diabetes Mellitus and Metabolic Syndrome 

Francesco Cosentino, Lars Rydén, Pietro Francia, and Linda G. Mellbin

[References PDF]

Summary Introduction Vascular disease risk factors: from pathophysiology to clinical management Clinical presentation and management of cardiovascular disease Selected issues The metabolic syndrome Personal perspective Further reading References

CHAPTER 15 Heart and Other Organs 

Frank Ruschitzka

[References PDF]

Introduction

• Chapter 15a The Heart and the Brain

  CHAPTER 15a The Heart and the Brain 

  Hans-Christoph Diener, Heinrich Mattle, Michael Böhm, and Frank Ruschitzka

  Summary Pathophysiology of acute ischaemic stroke and diagnostic procedures Characteristics of cardioembolic stroke Treatment of acute ischaemic stroke Cryptogenic stroke and patent foramen ovale Secondary stroke prevention in patients with atrial fibrillation Secondary stroke prevention with antiplatelet drugs Secondary stroke prevention and hypertension Secondary stroke prevention in patients with coronary heart disease Secondary stroke prevention in patients with significant stenosis of brain-supplying arteries Secondary stroke prevention in heart failure Personal perspective Further reading References

• Chapter 15b Cardiovascular Problems in Chronic Kidney Disease

  CHAPTER 15b Cardiovascular Problems in Chronic Kidney Disease 

  Eberhard Ritz and Andrew Remppis

  Summary Chronic kidney disease as a cardiovascular risk factor Chronic kidney disease and cardiovascular mortality Causes of death and underlying pathology in end-stage renal disease What clinical examinations are useful or necessary in the patient with end-stage renal disease? Radiocontrast nephropathy Acute reactions and nephrogenic skin fibrosis after gadolinium Interventions to reduce the cardiovascular risk Diuretic therapy Personal perspective Further reading References

• Chapter 15c Erectile Dysfunction

  CHAPTER 15c Erectile Dysfunction 

  Graham Jackson

  Summary Introduction Cardiovascular response to sex Cardiac risk Assessing the risk of sex activity Erectile dysfunction and the cardiac patient Cardiovascular risk factors Erectile dysfunction as a predictor of occult coronary artery disease Treating erectile dysfunction in men with cardiovascular disease Drug therapy Non-drug therapy Quick guide to specific cardiac conditions and sex Conclusion Personal perspective Further reading References

CHAPTER 16 Acute Coronary Syndromes 

Christian W. Hamm, Helge Möllmann, Jean-Pierre Bassand, and Frans van de Werf

[References PDF]

Summary Introduction Incidence and prevalence of acute coronary syndromes General risk factors for acute coronary syndromes Pathophysiology of acute coronary syndromes The plaque Thrombotic response Development of myocardial infarction Diagnosis and risk stratification of acute coronary syndromes Treatment of non-ST-elevation acute coronary syndromes Treatment of ST-elevation acute coronary syndromes Personal perspective Online resources Further reading References

CHAPTER 17 Chronic Ischaemic Heart Disease 

Filippo Crea, Paolo G. Camici, Raffaele De Caterina, and Gaetano A. Lanza

[References PDF]

Summary Introduction The coronary circulation Myocardial ischaemia Coronary collateral circulation Epidemiology of chronic ischaemic heart disease Assessment of angina pectoris Stable angina: diagnosis Stable angina: risk stratification Chronic stable angina: medical treatment Chronic stable angina: myocardial revascularization Other clinical manifestations of chronic ischaemic heart disease Personal perspective Additional online material Further reading References

CHAPTER 18 Myocardial Disease 

Otto M. Hess, William McKenna, and Heinz-Peter Schultheiss

[References PDF]

Summary Definition and classification Primary myocardial disease (cardiomyopathies) Secondary myocardial diseases Personal perspective Further reading References

CHAPTER 19 Pericardial Disease 

Jordi Soler-Soler and Jaume Sagristà-Sauleda

[References PDF]

Summary Introduction Acute pericardial syndromes Pericardial effusion Constrictive pericarditis Specific types of pericardial disease Personal perspective Additional online material Further reading References

CHAPTER 20 Tumours of the Heart 

Gaetano Thiene, Marialuisa Valente, Massimo Lombardi, and Cristina Basso

[References PDF]

Summary Introduction Epidemiology, classification, and nomenclature Clinical presentation Diagnosis through interdisciplinary collaboration Benign tumours Benign tumours of paediatric age Other benign tumours Malignant tumours of the heart Malignant tumours of the pericardium Cardiac metastases Chemotherapy, radiotherapy, and cardiotoxicity in malignant cardiac neoplasms Non-neoplastic masses Surgical treatment Personal perspective Further reading References

CHAPTER 21 Valvular Heart Disease 

Alec Vahanian, Bernard Iung, Luc Piérard, Robert Dion, and John Pepper

[References PDF]

Summary Introduction Patient evaluation Aortic stenosis Aortic regurgitation Mitral stenosis Mitral regurgitation Tricuspid valve disease Prosthetic valve surgery Personal perspective Online resources Additional online material Further reading References

CHAPTER 22 Infective Endocarditis 

Werner G. Daniel and Frank A. Flachskampf

[References PDF]

Summary Definition Epidemiology Pathology and pathophysiology Risk factors Causative pathogens Symptoms and signs Diagnosis Echocardiographic signs of infective endocarditis Problems in the diagnosis of infective endocarditis Prosthetic valve endocarditis Infective endocarditis in addicts of intravenous drugs Therapy Indications, timing, and type of surgery Anticoagulation Prognosis Prophylaxis and prevention Personal perspective Additional online material Further reading References

CHAPTER 23 Heart Failure 

John McMurray, Mark Petrie, Karl Swedberg, Michel Komajda, Stefan Anker, and Roy Gardner

[References PDF]

Summary Introduction Epidemiology Aetiology: causes of heart failure Comorbidity Pathophysiology Cardiac responses to ventricular injury and reduced stroke volume Diagnosis: symptoms, signs, and investigations Treatment Heart failure with a low left ventricular ejection fraction Organization of care Education Treatment considerations related to comorbidity Devices and surgery Surgery Heart failure with preserved left ventricular ejection fraction Heart failure due to valvular heart disease Heart failure due to dilated cardiomyopathy Heart failure due to hypertrophic cardiomyopathy Acute heart failure and pulmonary oedema End-of-life considerations Acknowledgement Personal perspective Online resources Further reading References

CHAPTER 24 Pulmonary Hypertension 

Nazzareno Galiè and Alessandra Manes

[References PDF]

Summary Definition and classification of pulmonary hypertension Pathology and pathobiology of pulmonary hypertension Genetics and epidemiology Pulmonary arterial hypertension (Group 1) Pulmonary hypertension associated with left heart disease (Group 2) Pulmonary hypertension associated with lung diseases (Group 3) Chronic thromboembolic pulmonary hypertension (Group 4) Personal perspective Additional online material Further reading References

CHAPTER 25 Cardiac Rehabilitation 

Stephan Gielen, Alessandro Mezzani, Rainer Hambrecht, and Hugo Saner

[References PDF]

Summary Definition of cardiac rehabilitation within preventive cardiology Exercise testing in cardiovascular medicine Physical activity, physical fitness, and cardiovascular diseases Exercise intolerance in cardiovascular diseases Exercise-based interventions in cardiac rehabilitation and secondary prevention Comprehensive rehabilitation and risk factor management Personal perspective Further reading References

CHAPTER 26 Syncope 

Michele Brignole, Jean-Jacques Blanc, Richard Sutton, and Angel Moya

[References PDF]

Summary Definition Epidemiology Classification and pathophysiology Evaluation of a patient with T-LOC Diagnostic tests Treatment Personal perspective Further reading References

CHAPTER 27 Bradycardia 

Panos E. Vardas, Hercules E. Mavrakis, and William D. Toff

[References PDF]

Summary Introduction Anatomy and physiology of the basic rhythm of the heart Definition of bradycardia Causes of bradycardia Clinical and electrocardiographic findings in patients with bradycardia Treatment of bradycardia Personal perspective Further reading References

CHAPTER 28 Supraventricular Tachycardias 

Jerónimo Farré, Hein J.J. Wellens, José M. Rubio, and Juan Benezet

[References PDF]

Summary Introduction Atrial and atrioventricular junctional extrasystoles Supraventricular tachycardia Atrial tachycardia Atrial flutter Atrioventricular nodal reciprocating tachycardia Accessory pathways, pre-excitation syndromes, and their tachycardias Wolff–Parkinson–White syndrome Pre-excitation due to ‘Mahaim physiology’ Concealed accessory pathways Permanent junctional reciprocating tachycardia Other non-paroxysmal SVT Personal perspective Further reading References

CHAPTER 29 Atrial Fibrillation 

A. John Camm, Paulus Kirchhof, Gregory Y.H. Lip, Irena Savelieva, and Sabine Ernst

[References PDF]

Summary Epidemiology Pathophysiological changes that can cause atrial fibrillation Initial evaluation of patients with atrial fibrillation Antithrombotic therapy for atrial fibrillation Pharmacological therapy Electrical cardioversion Implantable pacemakers and defibrillators Catheter ablation of the atrioventricular node Ablation of atrial fibrillation Personal perspective Online resources Additional online material Further reading References

CHAPTER 30 Ventricular Tachycardia and Sudden Cardiac Death 

Lars Eckardt, Günter Breithardt, and Stefan Hohnloser

[References PDF]

Summary Introduction Definitions Electrocardiographic diagnosis of ventricular tachycardia Electrophysiological mechanisms of ventricular tachycardia Ventricular tachycardia: clinical presentation Broad QRS complex tachycardia: clinical approach Risk stratification Therapy of ventricular tachycardias in patients with structural heart disease Catheter ablation or surgical treatment of ventricular tachyarrhythmias Other cardiomyopathic conditions Drug-induced ventricular tachyarrhythmias Resuscitation Conclusion Personal perspective Online resources Further reading References

CHAPTER 31 Diseases of the Aorta and Trauma to the Aorta and the Heart 

Christoph A. Nienaber, Ibrahim Akin, Raimund Erbel, and Axel Haverich

[References PDF]

Summary Aneurysms of the thoracic aorta Dissection of the thoracic aorta Aortitis Aortic atheromatous disease: thrombotic or cholesterol emboli Traumatic rupture of the aorta Trauma to the heart Personal perspective Further reading References

CHAPTER 32 Sports and Heart Disease 

Domenico Corrado, Cristina Basso, Antonio Pelliccia, and Gaetano Thiene

[References PDF]

Summary Introduction Classification of sports The athlete’s heart Epidemiology of sudden death in the athlete Prevention of sudden death by preparticipation screening Interpretation of the athlete’s ECG Management of athletes with cardiovascular diseases Automatic external defibrillator programme Personal perspective Further reading References

CHAPTER 33 Pregnancy and Heart Disease 

Patrizia Presbitero, Giacomo G. Boccuzzi, Christianne J.M. Groot, and Jolien W. Roos-Hesselink

[References PDF]

Summary Cardiovascular adaptations during normal pregnancy Haemodynamic changes during pregnancy Cardiac evaluation in normal pregnancy Assessment of heart disease in pregnancy Maternal low-risk conditions Maternal high-risk conditions Congenital heart disease and pregnancy Fetal high-risk conditions Specific conditions Cardiovascular treatment during pregnancy Personal perspective Online resources References

CHAPTER 34 Non-cardiac Surgery in Cardiac Patients 

Sanne Hoeks and Don Poldermans

[References PDF]

Summary Introduction Pathophysiology of myocardial infarction Risk stratification Non-invasive testing Invasive testing Medical therapy Revascularization Conclusion Personal perspective Further reading References

CHAPTER 35 Psychological Factors and Heart Disease 

Susanne S. Pedersen, Nina Kupper, and Johan Denollet

[References PDF]

Summary Introduction Psychological impact of heart disease Psychological risk factors for poor prognosis Mechanisms linking psychological factors to adverse prognosis Pharmacological and behavioural interventions Clinical implications Conclusion Personal perspective Additional online material Further reading References

CHAPTER 36 Peripheral Arterial Occlusive Disease 

Alberto Cremonesi, Nicolas Diehm, Andrea Stella, Mauro Gargiulo, Gianluca Faggioli, Estêvão Carvalho de Campos Martins, and Fausto Castriota

[References PDF]

Summary Peripheral arterial disease Cerebral vascular disease Renal artery stenosis Personal perspective Acknowledgement Additional online material Further reading References

CHAPTER 37 Venous Thromboembolism 

Sebastian M. Schellong, Henri Bounameaux, and Harry R. Büller

[References PDF]

Summary Natural history Diagnosis Treatment Personal perspective Further reading References

CHAPTER 38 Occupational and Regulatory Aspects of Heart Disease 

Demosthenes G. Katritsis and Michael M. Webb-Peploe

[References PDF]

Summary Occupational risk factors for heart disease Regulations concerning individual risk and public safety Personal perspective Acknowledgement Online resources Further reading References

Disclaimer

Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work.

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