4 Cardiac Ultrasound

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.

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.

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

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.

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):

The most important applications of blood flow velocity analysis are:

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.

The echo machine

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

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

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.

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.

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:

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:

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].

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.

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

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 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′.

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.

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.

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:

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:

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.

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.

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):

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.

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).

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.

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):

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).

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).

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.

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:

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

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.

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).

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.

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.

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.

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.

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

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.

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].

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:

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:

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:

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:

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).