Textbook of Cardiovascular Medicine
3rd Edition

Chapter 49
Transthoracic Echocardiography
Richard A. Grimm
James D. Thomas
Overview and History
Echocardiography (cardiac ultrasound) remains the most powerful diagnostic tool in cardiology (1). Although technically demanding, its diagnostic accuracy, cost effectiveness, availability, and noninvasive nature have made it the largest cardiovascular expense item in the Medicare budget.
Modalities of Echocardiography
M-mode echocardiography was the first form of cardiac ultrasound (Fig. 49.1), in which a single beam is directed toward the heart and reflected signals are displayed on a strip chart or oscillograph at high data rates (200 Hz in most contemporary machines). Two-dimensional echocardiography (Fig. 49.2) is created by sweeping an ultrasound beam back and forth through an arc either mechanically or by phased-array transducer.
Echocardiographic Evaluation of the Ventricles
Left Ventricle
Left ventricular (LV) evaluation is probably the single most important clinical application of echocardiography. A combined M-mode, two-dimensional, and Doppler evaluation of the LV can provide reliable information about overall systolic function, regional wall motion, and ventricular mass and geometry (2).
Evaluation of Global Systolic Function
Reliable determinations of LV function require the qualitative and quantitative evaluation of images taken from several standard windows. Typically, the LV is first viewed in the parasternal long-axis and short-axis planes (Fig. 49.2). From these planes, M-mode tracings are generated. If quantitation of M-mode tracings is used clinically, the American Society of Echocardiography recommends obtaining these from the parasternal short-axis view in the two-dimensional M-mode image (3,4) (Fig. 49.3).
M-Mode Evaluation
Standard M-mode measurements are shown in Figure 49.4. Fractional shortening by M-mode imaging is given by LV diameter at end diastole (LVEDd) minus LV diameter at end systole (LVESd)/LVEDd where EDd is the LV minor axis in diastole and ESd in systole. Normally, fractional shortening is approximately 50% and is considered clearly abnormal when it falls to less than 30% (5,6). Another M-mode measurement is the E-point septal separation (7,8), which is a marker of LV dysfunction when it exceeds 7 mm.
Apical Window Imaging
After the parasternal images, the LV is displayed along its long axis from the apical impulse location. The standard examination typically includes the apical four- and two-chamber views (orthogonal to each other, Fig. 49.2) and the apical long-axis
P.807

view (9,10).
FIGURE 49.1. M-mode echocardiogram displaying motion along a single scan line within the heart. Here, the transducer (T) is swept from the left ventricular level (left) to the mitral valve level (middle) and up to the left atrial level (right). A, aorta; ANT, anterior; Ao, aorta; ECG, electrocardiogram; LA, left atrium; LV, left ventricle; MV, mitral valve; P, pericardium; PE, pericardial effusion; POST, posterior; RV, right ventricle; RVW, right ventricular wall. (From
Cheitlin MD, Sokolow M, McIlroy MB. Clinical cardiology, 6th ed. Norwalk, CT: Appleton & Lange, 1993.
)
The four-chamber view (9) displays the midseptum and inferolateral LV wall as well as the right ventricle (RV) at its widest point, including the moderator band. At the cardiac base, the mitral valve (MV) and the tricuspid valve (TV) are shown, with the TV displaced approximately 1 cm more apically than the MV by the membranous septum. The atria are shown partitioned by the interatrial septum. Posterior transducer angulation reveals the coronary sinus and papillary muscles. Anterior angulation shows the LV outflow tract. To enhance endocardial definition, ultrasonic contrast agents that cross the lungs intact (unlike agitated saline contrast) can be used. Contrast augmentation is gained by displaying the second harmonic of the transmitted ultrasound carrier frequency.
The shape of a healthy LV is a truncated ellipsoid with the long axis roughly twice the length of the short axis. As the heart decompensates, it assumes a more globular shape (11). Diastolic wall thickness is viewed in absolute terms (approximately 1 cm is normal, >1.2 cm is considered hypertrophied) and relative to LV cavity size, with a radius-to-thickness ratio that is typically about 2:1. The distribution of hypertrophy is important. In secondary hypertrophy (e.g., from hypertension or outflow obstruction), the increase in wall thickness is uniform or concentric, whereas it is typically confined to the septum in asymmetric hypertrophy. Regional LV function is assessed by evaluating segmental thickening and wall excursion. Myocardial texture is also informative. Scar formation results in a thin bright segment, and infiltrative disease yields increased reflectance in approximately half of such cases. Geometric uniformity is another useful feature and becomes important after infarction. LV remodeling in its extreme form involves an entire region in an aneurysm that is distinguished from simple dysfunction by deformity throughout the cardiac cycle. Generally, all endocardial segments should move inward synchronously, with incoordinate contraction suggesting at least moderate LV dysfunction. However, dyssynchronous contraction can also be seen with left bundle branch block (12) or RV apical pacing. Finally, the longitudinal motion of the heart can be observed by the descent of the cardiac base (annular plane) toward the nearly fixed cardiac apex (13). A decrease in this parameter is often the first sign of nascent cardiomyopathy.
Quantitation of Left Ventricular Function
Although automated methods of measurement have been developed for assessing LV function (14), the standard method remains manual border tracing (15,16,17). Ejection fraction (EF) is commonly estimated by visual inspection, but this approach is prone to error and interobserver variability.
M-mode measurements of LV function (18,19,20,21) are limited because they use a single LV short-axis dimension, generally assuming a long-axis–to–short-axis ratio of 2:1 to extrapolate information to three dimensions. Unfortunately, many pathologic states introduce regional asymmetry or alter the ratio toward unity. Because volume is a cube function of dimension, errors are compounded. In contrast, two-dimensional volumes and mass compare favorably with those that are obtained from angiography and autopsy, but only if care is taken to optimize data acquisition and analysis (3).
The best apical images are obtained with the patient lying in the left recumbent position and during unforced suspended expiration. A foreshortened ventricle can be avoided by
P.808

maximizing the visualized long axis.
FIGURE 49.2. Two-dimensional echocardiography. Four standard views. A: Parasternal long axis. B: Parasternal short axis. C: Apical four chamber. D: Apical two chamber. AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
The biplane method of disks (referred to less precisely as the modified Simpson rule) most closely predicts angiographic volumes (10,15,16,17). The single-plane area length is also suitable, provided the ventricle is symmetric (22) (Fig. 49.5). These algorithms are applied to orthogonal apical two- and four-chamber views. The apical four-chamber view (10) should display the true LV apex, by showing neither the aorta nor the coronary sinus while maximizing RV size. The two-chamber view should not include any portion of the RV, aorta, or right atrium (RA) (Fig. 49.2).
LV mass computed from two-dimensional images is more reproducible and anatomically more rational than with M-mode imaging but is still limited by relatively wide standard deviations (±35 g for 95% confidence intervals) (23). The truncated ellipsoid and area-length methods are both recommended by the American Society of Echocardiology for mass determination (3,24).
FIGURE 49.3. Quantitation of left ventricular size. Measurement sites recommended by the American Society of Echocardiography. A: Parasternal long-axis view. B: Parasternal short-axis view. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (From reference 3.)
Wall Thickness and Left Ventricular Mass
Hypertrophy is defined anatomically as an increase in the mass of the ventricular myocardium, but wall thickness often serves as its surrogate. Initially obtained from M-mode imaging (25), wall thickness is usually determined from two-dimensional images with normal values from 0.6 to 1.1 cm. Wall thickness should be measured at the onset of the QRS complex (rather than in diastasis), because atrial contraction may thin the wall considerably. Analogously, if filling volume is greatly reduced (e.g., in cardiac tamponade), the wall becomes thickened despite normal mass, and a dilated ventricle may have increased
P.809

mass with normal thickness. To overcome the shortcomings of simple wall thickness, actual mass can be estimated. However, M-mode formulas (18,26,27,28) suffer the same theoretic limitation as the cube method of estimating LV volume, especially in hearts with asymmetric thickening (29). Despite this, the Framingham Heart Study has used M-mode methods to yield valuable insight into the electrocardiographic (ECG) criteria for hypertrophy (27,30,31) and the adverse prognosis of ventricular hypertrophy (32).
FIGURE 49.4. Standard measurements from an M-mode echocardiogram. Shown are sweeps at the aortic level (A), mitral valve level (B), and left ventricular level (C). AML, anterior mitral leaflet; Ao, aortic root diameter; AoV, opening of aortic valve; EF, E to F slope (rate of closure of mitral valve); LA, end-systolic left atrial diameter; LVEDd, left ventricular diameter at end diastole; LVESd, left ventricular diameter at end systole; PML, posterior mitral leaflet; PW, posterior wall thickness; SEPTUM, septal thickness.
FIGURE 49.5. Left ventricular (LV) volume determination. The biplane method of disks (top) requires orthogonal two- and four-chamber apical views and is more accurate in asymmetric hearts than the single-plane method shown at the bottom. In symmetric ventricles, the single-plane method is almost as accurate as the biplane method. (From reference 3.)
Most two-dimensional methods for determining LV mass (3,23,24,33) are similar because they combine a short-axis estimation of wall thickness with an estimation of ventricular length. The difference between the endocardial and epicardial volumes multiplied by the specific gravity of myocardium (1.05 g/mL) yields myocardial mass. Even two-dimensional methods have relatively wide 95% confidence bounds (±25 g) (23,33,34).
Two-Dimensional Echocardiography in Ischemic Heart Disease
Myocardial infarction produces regional akinesis within seconds of coronary occlusion. The presence of scarring (thinning and increased brightness) indicates an old infarction. The interface between contracting and akinetic tissue forms a visually distinctive “hinge point.” The diffuse hypokinesis of ischemic cardiomyopathy can be difficult to distinguish from primary myocardial disease.
To localize segmental wall motion abnormalities in a standardized format, the American Heart Association has recommended dividing the ventricle into 17 segments (35). Grading of these segments generates a wall motion score index that has been shown to have prognostic value (36). A diastolic deformity, sharply demarcated, indicates aneurysm formation. Hypokinesis without wall thinning suggests ischemia rather than completed infarction, but the specificity of this is not high.
P.810

Echocardiography is valuable in the assessment of chest pain (37,38,39,40,41), because a normal echocardiogram makes cardiac ischemia unlikely. The reliability and speed in detecting ischemic hypokinesis have led to the use of echocardiography in conjunction with exercise and pharmacologic stress testing (see Chapter 50).
Complications of Myocardial Infarction: Recognition by Echocardiography
Many of the complications of myocardial infarction can be diagnosed by a bedside echocardiogram. LV thrombi occur frequently in the setting of extensive anteroapical infarction and rarely in inferior infarction. They can appear within days of the infarction and typically are highly mobile. Older thrombi tend to have smooth surfaces and a texture like liver, and they may have a layered appearance. The more mobile and irregular the surface of the thrombus, the higher is the risk of embolization (42,43,44,45). Thrombi can be difficult to differentiate from apical trabeculations, which may be pronounced in cardiomyopathy (46).
Postinfarction aneurysms are characterized by a wall motion abnormality with a diastolic deformity. The ability of echocardiography to delineate aneurysm is well described (47,48,49).
Pseudoaneurysms, which result from frank wall rupture or cardiorrhexis, are actually composed of pericardium, which confines the rupture. Because only small ruptures in the wall are compatible with survival, pseudoaneurysms tend to have narrow necks, in contrast to the more open neck of true aneurysms (see Chapter 105). Pseudoaneurysms typically form at the inferoposterior base of the heart, are usually accompanied by pericardial effusion (50), and carry a poor prognosis if they are not repaired.
Abrupt myocardial rupture into the pericardial sac is rapidly fatal, although slower accumulations can allow time for surgery. Most postinfarction pericardial effusions are the result of either local inflammation (early) or Dressler syndrome (late). The incidence of pericardial effusions has ranged from 6% (51) to 37% (52) after infarction, and the correlation with physical signs of pericarditis is poor. Ventricular septal defect is a contained cardiorrhexis (53,54,55,56,57), typically at the anteroapex for left coronary infarction and the inferior base for right coronary infarction.
Mitral regurgitation (MR) is regularly encountered as a periinfarction complication (11,53). Papillary muscle rupture is always disabling and may be rapidly fatal (58,59). Because of cross support of the chordae, free motion of the liberated papillary muscle can sometimes be inapparent. Therefore, any patient with severe heart failure and unexpectedly good ventricular function after infarction should have papillary muscle rupture considered. Less severe MR is also commonly seen after myocardial infarction, typically owing to the abnormal wall motion displacing or undermining the papillary muscle (see Chapter 51).
RV infarction can be seen in approximately 40% of inferior infarctions (60,61), with injury ranging from subclinical depression to severe RV dysfunction causing a low-output state with high mortality. RV infarction is characterized by ventricular enlargement, decreased descent of the base, and inferior vena cava (IVC) plethora (60,61). Elevation of right-sided filling pressures can cause right-to-left shunting through a patent foramen ovale and can be easily documented by the passage of saline microbubbles across the interatrial septum.
Cardiomyopathies: Their Recognition by Echocardiography
Dilated, hypertrophic, and restrictive cardiomyopathies can be characterized by two-dimensional echocardiography. Congestive cardiomyopathy shows spheric cavitary dilatation (LV volume often >250 mL), normal wall thickness, and poor wall thickening and endocardial motion. M-mode echocardiography displays MV septal E-point separation, poor MV and aortic valve (AV) opening, and decreased systolic aortic root motion. Involvement of the right side of the heart is important because it implies pulmonary hypertension and RV cardiomyopathy, which independently worsen prognosis (62,63). In spite of an EF of less than 30%, cardiac output (stroke volume × heart rate) may be normal because of tachycardia and the large end-diastolic volume.
Early signs of cardiomyopathy are a decrease in the descent of the cardiac base (13), an increase in sphericity (13), and a rise in end-systolic volume index (64,65). This latter value is highly useful in detecting early cardiomyopathy because the end-systolic volume tends to be more sensitive to contractility than the preload volume (22). An end-systolic volume index that exceeds 30 mL/m2 indicates significant global dysfunction. In a study of valve disease, patients whose end-systolic volume index exceeded 60 mL/m2 (64) had a much poorer outcome than did other patients. Similarly, in ischemic cardiomyopathy, the value of 45 mL/m2 segregates patients with poor outcome.
Hypertrophic Cardiomyopathies
Primary hypertrophic cardiomyopathies are characterized by increased LV mass without apparent cause, such as hypertension or aortic stenosis (AS), and they can be asymmetric or symmetric (66,67,68,69). In asymmetric septal hypertrophy (ASH), the increased wall thickness is typically localized in the basal septum (67), and although it is clearly heritable, there is variable expressivity among affected family members. An unusual variation of ASH is apical hypertrophy (so-called Yamaguchi disease) (70,71). When dynamic outflow tract obstruction accompanies ASH, hypertrophic obstructive cardiomyopathy is present (72,73,74). Findings that are consistent with obstruction may be noted echocardiographically at rest or with provocation by amyl nitrite, exercise, or inotropic stimulation (66). Fully developed hypertrophic obstructive cardiomyopathy consists of ASH, systolic anterior motion of the MV, crowding of the LV outflow tract by the MV apparatus and septum, partial midsystolic closure or notching of the AV, and MV annular calcification.
Secondary LV hypertrophy (LVH) is most commonly the result of hypertension and conveys a poor prognosis (32). The sensitivity of M-mode echocardiography for detecting LVH is clearly superior to that of ECG (30), but two-dimensional echocardiography has superior reproducibility.
Restrictive Cardiomyopathy
Restrictive cardiomyopathies are more difficult to diagnose than hypertrophic or congestive states, but echocardiography remains the most effective diagnostic test. The most common restrictive state is the small, stiff heart of diabetes (75). It is clinically inapparent in the majority of diabetic patients but may lead to pulmonary congestion in association with regional ischemia.
Amyloid heart disease is rare (76,77,78) and carries a poor prognosis (79). Amyloid infiltration is characterized echocardiographically by increased LV wall thickness and a peculiar glittering appearance of the myocardium. Superficially, amyloid heart disease can resemble typical LVH (76). Contractile function is nearly normal or mildly depressed, and the left atrium (LA) is usually enlarged. The presence of these findings along with typical clinical signs or symptoms (e.g., low ECG voltage, neuropathy) should prompt a gingival or rectal biopsy.
Unclassified Cardiomyopathy
Ventricular noncompaction is a rare form of ventricular dysplasia that results from intrauterine arrest in endomyocardial morphogenesis (80,81). It involves the LV or the LV and RV, most commonly in
P.811

association with other congenital malformations, but occasionally in isolation (82). The myocardium is characterized by numerous prominent, excessive trabeculations with deep intertrabecular recesses. Noncompaction most commonly affects the apical, midinferior, and midlateral segments (83).
Left Ventricular Masses
Nonthrombotic LV masses are quite rare, but approximately 25% are malignant (33% angiosarcomas, 20% rhabdomyosarcomas, 10% mesotheliomas, and 11% fibrosarcomas with melanomas reported) (84). In the pediatric population, the most common tumors are rhabdomyomas associated with tuberous sclerosis. Nonmalignant lesions include myxomas and fibroelastomas, and both have considerable embolic potential. Myxomas can occur anywhere in the LV cavity, whereas fibroelastomas usually occur on the MV or valvular apparatus.
Endomyocardial fibrosis is a disease of impoverished persons living in North Africa and South America. It is associated with restriction of LV and RV filling by obliteration of one or both cardiac apices by a thrombotic fibrocalcific process (85). The disease can also occur in relation to eosinophilia and eosinophilic leukemia. In addition to the unique appearance of the apices, the atria are strikingly enlarged, with MR and TV regurgitation (TR) complicating the picture. Its recognition depends on a high degree of clinical suspicion and a characteristic echocardiographic appearance. In South America, a surgical approach has been developed that debulks fibrotic material from the apex and restores LV compliance.
Right Ventricle
RV imaging is an essential portion of a comprehensive echocardiographic evaluation, because occult right-sided heart disease may occur as a result of a left-sided pathologic process.
Right Ventricular Wall Thickness, Contractile Function, and Size
RV wall thickness, assessed from the parasternal or subcostal windows, should be only 3 to 4 mm, with 5 mm considered hypertrophied (4,25,86). It has been described as a pyramid with a triangular base. The tomographic nature of echocardiography makes imaging this irregularly shaped organ in a single plane or volumetric measurement impractical (86,87,88,89,90,91). The normal RV size is considerably less than LV size, whether imaged from the parasternal long axis, the parasternal short axis, or the apical four-chamber view (Fig. 49.2). In the last view, the LV should form the cardiac apex. If the RV even shares the apex, RV dilatation should be suspected.
RV volume and EF can be estimated by the area-length algorithm applied from the apical four-chamber or subcostal views (89,90,91). This correlates reasonably well (r = 0.83) with radionuclide scanning for EF (88), although absolute volumes are significantly underestimated. The four-chamber area-length RV-to-LV volume ratio should be approximately 0.6, but it increases to greater than 1.1 in cor pulmonale (92).
Descent of the RV base toward the fixed apex (2.0±0.2 cm in normal hearts) is easily seen in the subcostal and four-chamber views and, if depressed, is a sensitive indicator of RV systolic dysfunction (91). Doppler tissue imaging has yielded similar results in normal subjects (93).
Segmental Abnormalities of the Right Ventricle
The most common segmental RV abnormality results from RV infarction, usually in the setting of inferior wall myocardial infarction (60), and it may lead to a lethal low-output syndrome even when LV damage is not extensive. In RV infarction, there is cavity enlargement (61), with midanterior and inferior wall akinesis or even aneurysm by two-dimensional imaging. The degree of RV dilatation and IVC plethora provides clues to the hemodynamic severity of RV infarction (60).
Right Ventricular Tumors and Masses
RV masses can be primary, metastatic, or embolic (94,95). Generally, the same masses that affect the LV can also involve the RV. Myxomas are the most common benign RV tumors. Primary malignant tumors are very rare and are usually angiosarcomas. Metastatic melanoma can occur, but usually very late in the course of the disease. More commonly, tumors reach the right side of the heart by propagating through the venae cavae.
The most important propagating masses are embolic thrombi from the lower extremities (96). These thrombi, which may present as a localized mobile RV mass, are generally less reflective than malignant masses. RV enlargement and pulmonary hypertension suggest multiple pulmonary emboli. These masses may remain in the right side of the heart, embolize to the lungs, or rarely cross a patent foramen ovale (97). These thrombi generally have an ominous prognosis and require aggressive medical or surgical intervention.
Conditions Associated with Right Ventricular Dilatation
RV volume overload without pulmonary hypertension is seen in atrial septal defect (ASD), TV insufficiency, and pulmonary insufficiency. RV contractile function is usually preserved, and wall thickness remains normal. In ASD, the pulmonary artery is also enlarged. If the right pulmonary artery is of normal caliber, pulmonary hypertension and left-to-right shunts of any magnitude are unlikely. Similarly, the short-axis basal precordial view is the best window for evaluating the size of the main pulmonary artery.
An ASD can be further confirmed by saline contrast injection, which shows a negative contrast jet in the RA or right-to-left shunt flow in the LA. Sometimes the defect itself can be seen, especially with color Doppler, which may also show discrepant flow through the RV and LV outflow tracts (88). Congenital absence of the pericardium may cause RV enlargement (98) as a result of rotation of the heart, but with a small pulmonary artery, low pulmonary pressure, and a normal contrast study. RV enlargement may also be caused by severe TR, most commonly the result of LV dysfunction, rheumatic disease, endocarditis, and primary pulmonary hypertension. Chronically elevated pulmonary vascular resistance leads to cor pulmonale with a dilated apex-forming RV (92), mild to moderate RV hypertrophy (RVH), and a dilated IVC that is unresponsive to respiration. A patent foramen ovale (20% to 30% of patients) may show right-to-left shunting with contrast injection. The cause usually is chronic obstructive lung disease or other primary pulmonary disease states.
Echocardiographic features of primary pulmonary hypertension are similar to those of cor pulmonale but with greater RVH and septal flattening, often preceding IVC plethora. Pulmonary hypertension from congenital heart disease (atrial or ventricular septal defect) may cause severe RVH, but right-sided heart failure may be minimal early in the disease course. In the end stage, it may be difficult to distinguish ASD/ Eisenmenger complex from primary pulmonary hypertension with a patent foramen ovale.
Isolated RV dilatation may be seen in arrhythmogenic RV dysplasia (parchment ventricle or Uhl disease) (99). Features of RV dysplasia include a thin RV wall, increased epicardial fat, aneurysms of the RV free wall, and a prominent moderator band with complex attachment to the septum and RV free wall. Spontaneous fatal ventricular arrhythmias may be seen
P.812

in patients with this condition. In Ebstein anomaly, the septal leaflet of the TV is displaced (>1 cm) toward the RV apex, leaving an “atrialized ventricle” behind the valve. Contraction during systole may cause right-to-left shunting across a patent foramen and cyanosis (100,101).
Echocardiography of the Left Atrium
The LA serves reservoir, conduit, and booster pump functions for blood that enters the LV. It is commonly involved in pathologic processes, including dilation, thromboembolic and neoplastic disease, extrinsic compression, and fibrillation, each of which is well assessed by echocardiography.
Left Atrial Volume and Function
The standard parasternal M-mode image yields the anterior-to-posterior dimension of the LA (Fig. 49.4), typically the smallest, perhaps because of confinement between the sternum and the spine (102). This dimension is the least sensitive to enlargement but, when increased, is highly specific.
Because this single anterior-to-posterior dimension may underestimate overall LA size, volume estimates are preferred, requiring two sector scans, preferably orthogonal apical planes. The area-length formula has shown good correlation (r = 0.82 - 0.98) with angiography and contrast computed tomographic scanning (102,103), with some underestimation (≤23%) but good reproducibility (95% confidence interval, 10 mL). In the healthy young heart, only 10 mL atrial transport occurs with atrial contraction, the rest entering by passive flow early in diastole. With aging, the amount of active atrial transport more than doubles.
Atrial fibrillation causes progressive LA enlargement (104), which may be prevented by cardioversion (105). In rheumatic disease, LA diameter is predictive of atrial fibrillation (106) and the restoration of atrial function after cardioversion (107). However, the recurrence of lone atrial fibrillation appears to be independent of atrial diameter (108).
Left Atrial Thrombi, Masses, and Tumors
LA thrombi are common but must be large to be identified by transthoracic echocardiography (TTE). This is especially true of the LA appendage, which usually requires transesophageal echocardiography (TEE) (109).
The most common LA tumor is myxoma, a benign mass that most often arises from the inferior limb of the fossa ovalis. It can present with embolism or obstruction to MV inflow. Myxomas may be encapsulated or highly mobile and amorphous, with the latter at highest risk for peripheral emboli. Encapsulated myxomas may have clear spaces (cysts) and highly reflective patches (bone). Attachment is typically by a stalk to the interatrial septum and may be biatrial. Malignant LA tumors include fibrosarcoma, liposarcoma, and osteogenic sarcoma that may metastasize through the pulmonary vein.
Echocardiography of the Cardiac Valves
Echocardiography images the cardiac valves as does no other modality. It provides high temporal and spatial resolution while relating valve structure to surrounding structures. Doppler imaging is also critical to valve interrogation, as discussed in detail in Chapter 51.
Mitral Valve
Historically, the MV was the first structure to be identified by echocardiography (110,111,112,113). An integrated investigation of the MV includes an M-mode tracing, several two-dimensional views, a Doppler evaluation, and, if needed, TEE (109).
The anterior MV leaflet is highly mobile and quite echogenic, whereas the posterior leaflet is somewhat less apparent (Fig. 49.2). By M-mode examination, an M-shaped pattern of MV motion is seen, reflecting first passive rapid filling and second atrial contraction, with near closure during diastasis, although blood may still pass from pulmonary veins to LV using the atrium as a conduit (114). Final closure results from atrial inflow deceleration and isovolumic LV contraction (Fig. 49.4).
By two-dimensional imaging in the short-axis plane (Fig. 49.2), the MV is an ovoid orifice. In the long-axis plane, it resembles clapping hands moving freely in diastole, but forming a stable coaptation plane in systole. The MV and annulus descend with the cardiac base to assist LA filling.
Normal MV leaflets are thin (<2 mm), although somewhat thicker at points of chordal attachment to the free margin (primary chordae) and leaflet body (secondary chordae). The papillary muscles can be seen in the short-axis view at 4 and 8 o’clock with highly variable anatomy. From the apical four-chamber view, posterior angulation (typically showing the coronary sinus) is necessary to show the papillary muscles and chordae. Normal chordae appear fragmented unless they are thickened and fused by fibrosis or calcification. The mitral annulus has been shown to be saddle shaped and highly dynamic by three-dimensional imaging.
Mitral Stenosis
From the earliest days of echocardiography (111), mitral stenosis (MS) has been recognized by altered motion of the valve resulting from commissural fusion and chordal shortening. MS severity can be assessed on M-mode imaging by measuring the delay in diastolic closure (E-F slope). A normal value is greater than 60 mm per second; a slope of less than 10 mm per second indicates severe MS (115). By two-dimensional echocardiography, the leaflets dome into the ventricle throughout diastole. In short axis, the MV orifice can be reliably measured by direct planimetry (115,116), with an area of less than 1 cm2 defining severe MS. Doppler quantitation methods are discussed in Chapter 51.
Indirect signs of MS severity include chordal shortening, leaflet calcification, LA enlargement, LV underloading, and right-sided heart involvement (pulmonary hypertension). Progression cannot be accurately predicted, although disease in patients with mild MS and aortic insufficiency progresses slightly faster (117).
Mitral Regurgitation
Regurgitant lesions may be structurally more subtle than stenotic lesions, and Doppler (see Chapter 51) plays an even more dominant role in imaging. Nevertheless, careful structural interrogation is critical to evaluating MR, particularly as it relates to feasibility of surgical repair.
Rheumatic Mitral Regurgitation
In rheumatic disease, the posterior leaflet is fixed and shortened, allowing the anterior leaflet to override it on closure and resulting in posteriorly directed MR. The degree of malcoaptation is predictive of MR
P.813

severity (118).
Mitral Valve Prolapse
The original clinical, auscultatory, and angiographic descriptions of MV prolapse (MVP) (119,120) were rapidly supplemented by echocardiographic studies (121,122,123), which contributed to an “epidemic” of MVP by overly liberal diagnostic criteria.
Although MVP has a classic appearance on M-mode imaging (midsystolic or pansystolic posterior motion), up to 23% of healthy asymptomatic women may be diagnosed by these criteria (123). Two-dimensional echocardiography yielded a similar diagnostic prevalence until Levine et al. (124) demonstrated that the MV annulus was saddle-shaped (nonplanar). Thus, leaflets may appear to close above the annulus in the apical four-chamber view (cutting through the low points of the annulus), while being normally oriented in a long-axis view (through the high points of the annulus). Current diagnosis of MVP rests on this long-axis displacement, although anatomic variability dictates that the full anterior leaflet and each of the three posterior scallops be thoroughly interrogated.
MVP is also associated with myxomatous leaflet thickening and redundancy, with the tips sometimes being club-like, with a ground-glass appearance extending onto the chordae. The degree of MV deformity has been related to chest pain, arrhythmias, endocarditis, systemic emboli, and chordal rupture (125). Extreme MVP may be difficult to differentiate from frank chordal rupture or endocarditis.
Aortic Valve
Normal Aortic Valve
M-mode echocardiography of the AV and root demonstrates leaflet closure at the midpoint of the aortic root and opening throughout systole to the walls of the aortic root, producing a box-like M-mode waveform. Fine systolic vibrations can be seen and correspond to a normal flow murmur. Failure to achieve or sustain full opening implies decreased stroke volume. Abrupt early closure may be caused by fixed subvalvular stenosis, and subsequent reopening in later systole may imply dynamic subvalvular obstruction. The coapted leaflets move parallel to the aortic root in diastole, with vibrations suggesting valve disruption or endocarditis. Eccentricity on closure typically indicates a congenital bicuspid valve.
Two-dimensional imaging of the normal AV demonstrates three thin leaflets, opening as a circular orifice and closing as a three-pointed star with slight central thickening. The left coronary cusp is adjacent to the LA appendage, the left main coronary artery, and the pulmonary valve and artery. The right lies just posterior to the RV outflow tract, close to the septal attachment of the TV. The noncoronary cusp sits above the RA and the interatrial septum. Aortic diameter is largest at the sinuses of Valsalva and should not exceed 3.5 cm.
Aortic Stenosis
In severe AS, the M-mode image shows dense persistent echoes with little systolic separation (126). Aortic sclerosis without AS shows dense echoes, but at least one leaflet will move rapidly or will vibrate, indicating a peak systolic gradient of less than 50 mm Hg.
Cusp separation by two-dimensional imaging is helpful if it is less than 8 mm or more than 12 mm, but it is poorly predictive between 8 and 12 mm (127). Leaflet doming, poststenotic aortic dilatation, and LVH predict significant AS, although none approaches the utility of Doppler-derived pressure gradient and valve area (127,128,129,130).
The severe calcification of senile AS is nonspecific regarding the underlying disease. In younger patients, bicuspid valves show eccentric opening and only two moving leaflets. On closure of the valve, three commissures may be seen as a result of raphe formation between two leaflets, usually the left and right. Patients with rheumatic AS show commissural fusion and leaflet retraction, generally associated with rheumatic MV disease.
Subvalvular and Supravalvular Stenosis
Fixed subvalvular stenosis is occasionally encountered in the adult population (131,132,133), often with prior ventricular septal defect. The subvalvular membrane is a narrow ridge in the distal septum. Because the narrowing may be difficult to appreciate by inspection, Doppler imaging remains the definitive quantitative modality. Dynamic subvalvular stenosis is discussed earlier in relation to the normal aortic valve. Supravalvular AS is rarely seen in adults. Features include narrowing above and affixed to the valve leaflets, aortic insufficiency, enlarged coronary arteries (sometimes obstructed), and severe hypertrophy (134).
Aortic Regurgitation
Aortic regurgitation (AR) can be seen with diastolic fluttering of the anterior MV leaflet by M-mode echocardiography (135), a sign largely supplanted by Doppler imaging. With severe acute AR, M-mode images may show early closure of the MV (136), thus indicating precarious hemodynamics and a need for urgent pharmacologic or surgical intervention (136). Henry et al. (137) suggested that an LV end-systolic dimension of greater than 55 mm predicts poor operative results, a concept challenged by Fioretti et al. (138), perhaps because of improvements in myocardial preservation at surgery. Assessment of AR severity by two-dimensional echocardiography has not been adequately studied (139). Posteriorly directed AR may reverse the diastolic curvature of the anterior mitral leaflet (140), but no two-dimensional sign replaces a quantitative Doppler examination (135,141) (see Chapter 51).
Senile calcification typically results in mild AR. Rheumatic disease causes leaflet retraction and a central AR jet. Bicuspid AVs may have significant AR as a result of leaflet prolapse, usually of a conjoined anterior leaflet. Endocarditis may cause acute severe AR, recognized as mobile echoes prolapsing into the LV outflow tract. TEE has greatly improved detection of aortic vegetations (142). AR can arise from subaortic membrane jets that undermine valve integrity. Myxomatous disease can cause AV prolapse. In Marfan disease, isolated dilation of the sinuses of Valsalva causes traction on the aortic commissures and a central jet of AR (143). Other aortic diseases that are associated with AR include dissection, sinus of Valsalva aneurysms, aortoannular ectasia, and aneurysms resulting from atherosclerosis, syphilis, and ankylosing spondylitis. As discussed in Chapter 52, TEE is preferred for emergency diagnosis (109).
Tricuspid Valve
The TV has anterior, septal, and posterior leaflets; the latter two are somewhat variable in size and position. Two-dimensional imaging can be recorded from the parasternal long- and short-axis and apical four-chamber views for anatomic and Doppler evaluation. The TV is apically displaced by the membranous septum, and this is useful in identifying the TV in congenital heart disease. TEE offers relatively little advantage, especially for measuring TR velocity (144).
Tricuspid Insufficiency
Contemporary echocardiography confirms Sir James Mackenzie’s claim, made in 1908, that TR is ubiquitous. Present in 80% of normal subjects and in nearly all cardiac patients,
P.814

this “abnormality” usually is just a convenient means to estimate pulmonary artery pressure (145). Pathologic TR causes RV and RA enlargement, paradoxic septal motion, and systolic IVC pulsation from retrograde flow. M-mode imaging shows paradoxic septal motion, with anterior systolic motion of the septum related to the exaggerated RV stroke volume. By two-dimensional imaging, RV dilatation can be seen, although quantitation is imprecise (92), and hyperdynamic function can be seen as a result of the augmented stroke volume (13,146). RA enlargement is common and is related to TR duration and to the severity and the presence of atrial fibrillation. With severe TR, the normal leftward bulging of the interatrial septum is reversed (147).
The most common cause of significant TR is RV failure from high LV filling pressures, with annular dilatation and failure of leaflet coaptation (148). Rheumatic TR rarely exists without MV involvement. It is characterized by leaflet thickening, commissural fusion and calcification, and chordal shortening. Myxomatous MV disease may be accompanied by TV prolapse (149), but severe TR is uncommon unless there is chordal rupture (150). RV biopsy may cause iatrogenic chordal rupture (151). Endocarditis (usually related to intravenous drug use) causes bulky prolapsing vegetations and flail leaflets (152). Metastatic liver carcinoid causes TV leaflet shortening with more regurgitation than stenosis (153). Ebstein anomaly commonly causes severe TR (100).
Tricuspid Stenosis
TV stenosis may result from rheumatic disease, carcinoid syndrome, or prolapsing RA tumors. Because two-dimensional planimetry is not reliable, Doppler imaging is the mainstay of quantitation.
Pulmonary Valve and Artery
Pulmonary valve disorders are common in congenital disease but are rarely acquired. M-mode and two-dimensional imaging are limited to leaflet inspection (often difficult) and pulmonary artery dilatation. The M-mode image in pulmonary stenosis (PS) shows an exaggerated diastolic “a wave” caused by powerful RA contraction opening or doming the pulmonary valve. By two-dimensional imaging, PS is characterized by systolic leaflet doming, variable leaflet thickening, poststenotic dilation of the main pulmonary artery with decreased pulsations, and variable RVH. PS must be distinguished from subpulmonic stenosis and double-chamber RV that results from prior ventricular septal defect.
Trivial pulmonary regurgitation (PR) is present in most healthy persons. Severe PR rarely occurs from prior tetralogy of Fallot repair, endocarditis (154), or carcinoid (153). Moderate PR can result from pulmonary hypertension (Graham Steell murmur).
Infective Endocarditis
Echocardiography is essential to the diagnosis and management of patients with infective endocarditis (IE). Early studies of echocardiography and IE used the criteria of Von Reyn et al. (155) for diagnosis. Newer echocardiographic criteria for diagnosing IE have been prospectively tested by the Duke Endocarditis Service (156,157). In these studies, echocardiography increased the sensitivity for detecting IE from 51% to 80%, although TEE was required to visualize the vegetations in 41% of cases.
Two-Dimensional Imaging
In a meta-analysis of 16 early studies (641 patients), O’Brien and Geiser (158) reported a mean sensitivity of 79% for two-dimensional detection of vegetations and 52% for M-mode imaging, with vegetations as small as 3 mm reported by two-dimensional imaging (159). More recently, however, the reported sensitivity of TTE has dropped to 62% despite equipment improvement (142,160,161,162,163,164,165), a finding reflecting less biased case selection and the fact that these studies used TEE (sensitivity of 92%).
Sanfilippo et al. (166) retrospectively studied 204 patients with IE and showed that larger (>10 mm) mobile noncalcified vegetations were predictive of antibiotic failure, congestive heart failure, embolization, surgery, and death. Size was highly predictive of complications: 10% for 6-mm vegetations, 50% at 11 mm, and almost 100% at 16 mm. DiSalvo and colleagues also reported that vegetation size (>10 mm) and mobility by TEE predicted embolic events on multivariate analysis among 178 patients with IE (167).
Transesophageal Echocardiography
TV IE (usually Staphylococcus aureus) typically occurs in intravenous drug users (168) and typically causes large vegetations.
Pericardial Disorders
Echocardiography detects virtually all pericardial effusions (169), and it is the diagnostic test of choice providing important hemodynamic data as well (170). Normally, less than 20 mL pericardial fluid is present (171), and it is barely detected during systole by M-mode imaging. The high temporal resolution of M-mode imaging is valuable in assessing pericardial motion and RA and RV dynamics. The parietal pericardium is highly echogenic.
Two-Dimensional Echocardiography
Two-dimensional echocardiography and Doppler imaging are key in assessing pericardial disease, with small effusions first seen above the RA. The normal systolic torsion of the heart is lost when inflammation causes adhesions between the pericardial layers. Pericardial fat may mimic effusion (172), typically seen anterior to the heart. D’Cruz and Hoffman (173) have described an ellipsoid formula for estimating effusion size, although effusions typically are graded as small (separation seen throughout the cardiac cycle), medium, and large (typically >2 cm circumferentially). Although transudates, exudates, and blood appear similar, septations suggest chronicity.
Tamponade
Tamponade is a continuum of hemodynamic embarrassment, often associated with large effusions (174,175,176,177,178,179,180,181), although a small, rapid accumulation can be life-threatening. Characteristic echocardiographic features are listed in Table 49.1. The heart is usually small, unless previously enlarged (175), and respirophasic ventricular interdependence is seen. The RV enlarges with inspiration and the LV with expiration, the echocardiographic equivalent of pulsus paradoxus (146,175). RV diastolic collapse and RA invagination (for more than one third of the cardiac cycle) are seen (175,176,178,179). Central venous pressure (CVP) can be estimated from IVC dynamics (177). If CVP is normal, the IVC is greater than 17 mm and decreases by more than 5 mm during inspiration. With elevated CVP, typical of tamponade, the IVC exceeds 20 mm and respiratory change is blunted (177,182), a sign that is less useful with mechanical
P.815

ventilation (183).
TABLE 49.1 Normal values for left and right ventricular volume, left ventricular mass, and left and right atrial volume derived from several studies
END-DIASTOLIC VOLUME LEFT VENTRICLE (TWO- AND FOUR-CHAMBER APICAL VIEWS/BIPLANE METHOD OF DISKS)
Male: 111 mL index 58 mL/m2 [80 (45)]
Female: 80 mL index 50 mL/m2 [66 (103)]
END-SYSTOLIC VOLUME LEFT VENTRICLE (TWO- AND FOUR-CHAMBER APICAL VIEWS/BIPLANE METHOD OF DISKS)
Male: 34 index 18 mL/m2 [30 (19)]
Female: 29 index 18 mL/m2 [32 (21)]
EJECTION FRACTION
61 ± 10%
END-DIASTOLIC VOLUME RIGHT VENTRICLE (BASED ON NORMAL RATIO OF LEFT VENTRICLE TO RIGHT VENTRICLE OF 0.6)
Male: 67 mL
Female: 48 mL
LEFT VENTRICULAR MASS (TRUNCATED ELLIPSOID)
Male: 135 g index 71 g/m2 [96 (61)]
Female: 99 g index 62 g/m2 [89 (54)]
Volume-to-mass ratio: 83
LEFT ATRIAL VOLUME (TWO- AND FOUR-CHAMBER APICAL VIEWS/BIPLANE METHOD OF DISKS)
Male: 38 mL index 21 mL/m2
Female: 32 mL index 21 mL/m2
LEFT ATRIAL VOLUME FOUR-CHAMBER VIEW (SINGLE-PLANE AREA LENGTH)
Male: 38 mL
Female: 34 mL
LEFT ATRIAL VOLUME TWO-CHAMBER VIEW (SINGLE-PLANE AREA LENGTH)
Male: 46 mL
Female: 36 mL
RIGHT ATRIAL VOLUME FOUR-CHAMBER VIEW (SINGLE-PLANE AREA LENGTH)
Male: 39 mL
Female: 27 mL
Pleural versus Pericardial Effusion
Left pleural effusions can be distinguished by their posterior location, passing behind the descending aorta. Large bilateral pleural effusions may occasionally cause tamponade that is responsive to drainage (184).
Pericardial Thickening and Constriction
Pericardial thickening is common, although constriction is rare. Thickening and adhesion are distinguished from simple effusion by the parallel (rather than damped) motion of the epicardium and visceral pericardium with the parietal pericardium. Pericardial constriction is a continuum of hemodynamic impairment, which may overlap with tamponade and (when the visceral layer is primarily involved) may have a component of restriction. By M-mode imaging, a septal notch may be seen in early diastole around the time of the pericardial knock (between S2 and S3) (185,186). Two-dimensional echocardiography may show extensive adhesion and a diastolic septal bounce (182), which may resemble left bundle branch block or RV pacing. One usually sees IVC plethora (177,182), unless the patient is severely dehydrated. In the four-chamber view, the ventricles appear elongated, and the atria are globally enlarged. Malignancy often causes pericardial effusions and pericardial studding, and a frank mass effect may be seen.
Congenital Abnormalities
Complete absence of the pericardium causes RV enlargement and paradoxic septal motion (187). Partial absence may cause LV herniation through the defect with coronary compression and myocardial infarction. Pericardial cysts are difficult to localize by echocardiography because of their lateral position (188).
Aorta and Great Vessels
Despite the primacy of TEE, TTE is useful in assessing the great vessels. The aortic root and ascending aorta are well seen in the parasternal long- and short-axis views. Coronary artery ostia can be visualized, sometimes allowing for diagnosis of coronary anomalies and Kawasaki disease.
Aortic Aneurysm
Symmetric sinus of Valsalva aneurysms (189,190) may be seen in Marfan syndrome. Echocardiographic enlargement of the root beyond 55 mm should generally prompt surgery. Ascending aortic dilatation may be poststenotic or atherosclerotic in origin, requiring high parasternal and right parasternal imaging to observe. The descending thoracic aorta can be seen in the long- and short-axis parasternal views posterior to the atrioventricular groove. The left and right pulmonary arteries may be seen in the short-axis view. In the apical views, posterior angulation often produces long- (two-chamber) and short- (four-chamber) axis views of the thoracic aorta. Atheroma and aneurysms of the abdominal aorta may be seen subcostally to the left of and deep to the IVC (191). Thoracic aortic dissection with effusion can also be imaged from the left paraspinal window, although TEE is the preferred method to assess the aorta (192).
Great Veins
The IVC is seen subcostally. It crosses the diaphragm just after receiving the confluence of the hepatic veins. Its size and response to respiration predict RA pressure (193,194). If the vessel loses 50% of its initial expiratory diameter during deep inspiration (while the patient is lying supine with knees bent), RA pressure is considered normal.
Controversies and Personal Perspectives
TTE is the single most useful imaging test in cardiology. Its use has grown tremendously over the last 10 years. However,
P.816

this examination is not performed and interpreted uniformly, an issue that has attracted unfavorable attention to the potential overuse of echocardiography in the United States. Of particular concern is the lack of quantitation in many echocardiographic reports. Echocardiography is quantitative in nature. Calibration marks are included, and the Digital Imaging and Communications in Medicine (DICOM) standard allows them to be stored digitally. Nonetheless, echocardiograms too often are interpreted in general categoric terms.
TABLE 49.2 Two-dimensional echocardiographic findings in tamponade
Large effusion
RA expiratory collapse
RV expiratory compression or collapse
IVC plethora with diminished respiratory response
Left atrial compression
Small chamber volumes
Reciprocal size changes between right and left ventricles and excursion between mitral and tricuspid valves
Sensitivity, specificity, and positive and negative predictive values
  Sensitivity Specificity PPV NPV
Size (large vs. moderate) 97 45 99
RV compression 48 95 38 99
RA compression 55 88 10 99
IVC plethora 97 66 7 99
IVC, inferior vena cava; NPV, negative predictive value; PPV, positive predictive value; RA, right atrial; RV, right ventricular.
In addition to the emerging echocardiographic technologies such as three-dimensional imaging and contrast echocardiography, newer applications such as its role in selection and device optimization for patients undergoing cardiac resynchronization therapy and guidance of interventional procedures have helped to maintain the dominance of echocardiography as a cardiac diagnostic modality. Three-dimensional reconstruction has been available commercially for several years and is a valuable tool in quantifying chamber size and in visualizing cardiac structures. Nevertheless, it has failed to penetrate the clinical arena completely, in part because of the prolonged acquisition and display times. The development of real-time three-dimensional acquisition has addressed this limitation, and examination times have become shorter as structural data can be captured in a data set from a single cardiac cycle.
Advances in echocardiography have resulted in improvements in image quality, especially for patients whose echocardiographic examination was previously suboptimal. Intravenous contrast agents are now available for LV opacification and endocardial border detection. Guidelines for the use of ultrasonic contrast in echocardiography have been published (195). Intravenous contrast agents should be used to provide additional diagnostic information for the detection of cardiac disease in patients whose hearts are difficult to image. These agents have been shown to be especially beneficial in obese patients, those with lung disease, and individuals who are receiving mechanical ventilation.
In the midst of the tremendous success of resynchronization therapy for heart failure, echocardiography has emerged as the diagnostic modality of choice for identifying potential candidates as well as for optimizing devices following pacemaker implantation (196). The unique ability of Doppler echocardiography to evaluate structure, function, and electrical mechanical event timing in real time has made cardiac ultrasound the clear-cut front runner in evaluating these patients. Furthermore, the portability (TTE, intracardiac echocardiography, or TEE) and improved image quality have made echocardiography the diagnostic modality of choice to assist with atrial fibrillation ablation procedures, percutaneous balloon MV valvuloplasty, and device closures of ASDs, patent foramen ovale, and the LA appendage, as well as for guidance of percutaneous MV repairs.
The Future
The field of echocardiography will continue to be under intense pressure as cost containment leads to decreased reimbursement. This may seem paradoxic, because the value of the test should grow enormously as contrast, three-dimensional, improved quantification methods, and digital technologies mature. Additionally, increasing applications for procedural guidance and monitoring will enhance the utility of the test. Although videotape may still be used, digital storage, which allows retrieval throughout the hospital, permits transmission anywhere in the world, and eliminates repetition of tests, will be the standard. Adherence to international formatting standards is mandatory.
References
1. Feigenbaum H. Evolution of echocardiography. Circulation 1996;93:1321–1327.
2. Qin JX, et al. The development of real time three-dimensional echocardiography is ideally suited for assessment of LV size and function and compares very well to cardiac MRI: validation of real time three dimensional echocardiography for quantifying left ventricular volumes in the presence of a left ventricular aneurysm: in vitro and in vivo studies. J Am Coll Cardiol 2000;36:900–907.
3. Schiller NB, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography: American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358–367.
4. Schnittger, I, et al. Standardized intracardiac measurements of two-dimensional echocardiography. J Am Coll Cardiol 1983;2:934–938.
5. Feigenbaum H. Echocardiography, 5th ed. Philadelphia: Lea & Febiger, 1994.
6. Weyman A. Principles and practice of echocardiography, 2nd ed. Philadelphia:Lea & Febiger, 1994.
7. Massie BM, et al. Mitral-septal separation: new echocardiographic index of left ventricular function. Am J Cardiol 1977;39:1008–1016.
8. Child JS, Krivokapich J, Perloff JK. Effect of left ventricular size on mitral E point to ventricular septal separation in assessment of cardiac performance. Am Heart J 1981;101:797–805.
P.817

9. Silverman NH, Schiller NB. Apex echocardiography: a two-dimensional technique for evaluating congenital heart disease. Circulation 1978;57:503–511.
10. Silverman NH, et al. Determination of left ventricular volume in children: echocardiographic and angiographic comparisons. Circulation 1980;62:548–557.
11. Van Dantzig JM, et al. Pathogenesis of mitral regurgitation in acute myocardial infarction: importance of changes in left ventricular shape and regional function. Am Heart J 1996;131:865–871.
12. Dillon JC, Chang S, Feigenbaum H. Echocardiographic manifestations of left bundle branch block. Circulation 1974;49:876–880.
13. Simonson JS, Schiller NB. Descent of the base of the left ventricle: an echocardiographic index of left ventricular function. J Am Soc Echocardiogr 1989;2:25–35.
14. Lang RM, et al. Echocardiographic quantification of regional left ventricular wall motion with color kinesis. Circulation 1996;93:1877–1885.
15. Schiller NB, et al. Left ventricular volume from paired biplane two-dimensional echocardiography. Circulation 1979;60:547–555.
16. Folland ED, et al. Assessment of left ventricular ejection fraction and volumes by real-time, two-dimensional echocardiography: a comparison of cineangiographic and radionuclide techniques. Circulation 1979;60:760–766.
17. Starling MR, et al. Comparative accuracy of apical biplane cross-sectional echocardiography and gated equilibrium radionuclide angiography for estimating left ventricular size and performance. Circulation 1981;63:1075–1084.
18. Corya BC, et al. M-mode echocardiography in evaluating left ventricular function and surgical risk in patients with coronary artery disease. Chest 1977;72:181–185.
19. Fortuin NJ, Hood WP Jr, Craige E. Evaluation of left ventricular function by echocardiography. Circulation 1972;46:26–35.
20. Kisslo J, et al. Ultrasound assessment of left ventricular function following aortocoronary saphenous vein bypass grafting. Circulation 1973;48(suppl III):III156–III161.
21. McDonald IG, Feigenbaum H, Chang S. Analysis of left ventricular wall motion by reflected ultrasound: application to assessment of myocardial function. Circulation 1972;46:14–25.
22. Sagawa K, et al. End-systolic pressure/volume ratio: a new index of ventricular contractility. Am J Cardiol 1977;40:748–753.
23. Kuecherer HF, et al. Echocardiography in serial evaluation of left ventricular systolic and diastolic function: importance of image acquisition, quantitation, and physiologic variability in clinical and investigational applications. J Am Soc Echocardiogr 1991;4:203–214.
24. Schiller NB. Considerations in the standardization of measurement of left ventricular myocardial mass by two-dimensional echocardiography. Hypertension 1987;9(suppl):II33–II35.
25. Sahn DJ, et al. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978;58:1072–1083.
26. Troy BL, Pombo J, Rackley CE. Measurement of left ventricular wall thickness and mass by echocardiography. Circulation 1972;45:602–611.
27. Devereux RB, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986;57:450–458.
28. Devereux RB, et al. Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Coll Cardiol 1984;4:1222–1230.
29. Teichholz LE, et al. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy. Am J Cardiol 1976;37:7–11.
30. Devereux RB, et al. Electrocardiographic detection of left ventricular hypertrophy using echocardiographic determination of left ventricular mass as the reference standard: comparison of standard criteria, computer diagnosis and physician interpretation. J Am Coll Cardiol 1984;3:82–87.
31. Casale PN, et al. Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. J Am Coll Cardiol 1985;6:572–580.
32. Levy D, et al. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322:1561–1566.
33. Byrd BFD, et al. Accuracy and reproducibility of clinically acquired two-dimensional echocardiographic mass measurements. Am Heart J 1989;118: 133–137.
34. Collins HW, Kronenberg MW, Byrd BFD. Reproducibility of left ventricular mass measurements by two-dimensional and M-mode echocardiography. J Am Coll Cardiol 1989;14:672–676.
35. Cerqueira M, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. Circulation 2002;105:539–542.
36. Nishimura RA, et al. Prognostic value of predischarge 2-dimensional echocardiogram after acute myocardial infarction. Am J Cardiol 1984;53:429–432.
37. Gibson RS, et al. Value of early two dimensional echocardiography in patients with acute myocardial infarction. Am J Cardiol 1982;49:1110–1119.
38. Kan G, et al. Early two-dimensional echocardiographic measurement of left ventricular ejection fraction in acute myocardial infarction. Eur Heart J 1984;5:210–217.
39. Kumar A, Minagoe S, Chandraratna PA. Two-dimensional echocardiographic demonstration of restoration of normal wall motion after acute myocardial infarction. Am J Cardiol 1986;57:1232–1235.
40. Roberts CS, et al. Early and late remodeling of the left ventricle after acute myocardial infarction. Am J Cardiol 1984;54:407–410.
41. Stamm RB, et al. Echocardiographic detection of infarct-localized asynergy and remote asynergy during acute myocardial infarction: correlation with the extent of angiographic coronary disease. Circulation 1983;67:233–244.
42. Haugland JM, et al. Embolic potential of left ventricular thrombi detected by two-dimensional echocardiography. Circulation 1984;70:588–598.
43. Reeder GS, Tajik AJ, Seward JB. Left ventricular mural thrombus: two-dimensional echocardiographic diagnosis. Mayo Clin Proc 1981;56:82–86.
44. Visser CA, et al. Two dimensional echocardiography in the diagnosis of left ventricular thrombus: a prospective study of 67 patients with anatomic validation. Chest 1983;83:228–232.
45. Visser CA, et al. Long-term follow-up of left ventricular thrombus after acute myocardial infarction: a two-dimensional echocardiographic study in 96 patients. Chest 1984;86:532–536.
46. Keren A, Billingham ME, Popp RL. Echocardiographic recognition and implications of ventricular hypertrophic trabeculations and aberrant bands. Circulation 1984;70:836–842.
47. Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study. Am J Cardiol 1984;53:1542–1546.
48. Matsumoto M, et al. Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course. Circulation 1985;72:280–286.
49. Wong M, Shah PM. Accuracy of two-dimensional echocardiography in detecting left ventricular aneurysm. Clin Cardiol 1983;6:250–254.
50. Kaul S, et al. Atypical echocardiographic and angiographic presentation of a postoperative pseudoaneurysm of the left ventricle after repair of a true aneurysm. J Am Coll Cardiol 1983;2:780–784.
51. Wunderink RG. Incidence of pericardial effusions in acute myocardial infarctions. Chest 1984;85:494–496.
52. Kaplan K, et al. Frequency of pericardial effusion as determined by M-mode echocardiography in acute myocardial infarction. Am J Cardiol 1985;55: 335–337.
53. Lindower P, Embrey R, Vandenberg B. Echocardiographic diagnosis of mechanical complications in acute myocardial infarction. Clin Intensive Care 1993;4:276–283.
54. Drobac M, et al. Ventricular septal defect after myocardial infarction: diagnosis by two-dimensional contrast echocardiography. Circulation 1983;67:335–341.
55. Recusani F, et al. Ventricular septal rupture after myocardial infarction: diagnosis by two-dimensional and pulsed Doppler echocardiography. Am J Cardiol 1984;54:277–281.
56. Keren G, et al. Diagnosis of ventricular septal rupture from acute myocardial infarction by combined 2-dimensional and pulsed Doppler echocardiography. Am J Cardiol 1984;53:1202–1203.
57. Eisenberg PR, Barzilai B, Perez JE. Noninvasive detection by Doppler echocardiography of combined ventricular septal rupture and mitral regurgitation in acute myocardial infarction. J Am Coll Cardiol 1984;4:617–620.
58. Nishimura RA, et al. Papillary muscle rupture complicating acute myocardial infarction: analysis of 17 patients. Am J Cardiol 1983;51:373–377.
59. Nishimura RA, Shub C, Tajik AJ. Two dimensional echocardiographic diagnosis of partial papillary muscle rupture. Br Heart J 1982;48:598–600.
60. Goldberger JJ, et al. Right ventricular infarction: recognition and assessment of its hemodynamic significance by two-dimensional echocardiography. J Am Soc Echocardiogr 1991;4:140–146.
61. Sharpe DN, et al. The noninvasive diagnosis of right ventricular infarction. Circulation 1978;57:483–490.
62. Unverferth DV, et al. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984;54:147–152.
63. Lewis JF, et al. Discordance in degree of right and left ventricular dilation in patients with dilated cardiomyopathy: recognition and clinical implications. J Am Coll Cardiol 1993;21:649–654.
64. Borow KM, et al. End-systolic volume as a predictor of postoperative left ventricular performance in volume overload from valvular regurgitation. Am J Med 1980;68:655–663.
65. White HD, et al. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 1987;76:44–51.
66. Abbasi AS, et al. Echocardiographic diagnosis of idiopathic hypertrophic cardiomyopathy without outflow obstruction. Circulation 1972;46:897–904.
67. Maron BJ, et al. Patterns of inheritance in hypertrophic cardiomyopathy: assessment by M-mode and two-dimensional echocardiography. Am J Cardiol 1984;53:1087–1094.
68. Maron BJ. Asymmetry in hypertrophic cardiomyopathy: the septal to free wall thickness ratio revisited. Am J Cardiol 1985;55:835–838.
69. Nair CK, et al. Echocardiographic and electrocardiographic characteristics of patients with hypertrophic cardiomyopathy with and without mitral anular calcium. Am J Cardiol 1987;59:1428–1430.
70. Maron BJ, et al. Hypertrophic cardiomyopathy with ventricular septal hypertrophy localized to the apical region of the left ventricle (apical hypertrophic cardiomyopathy). Am J Cardiol 1982;49:1838–1848.
71. Kereiakes DJ, et al. Apical hypertrophic cardiomyopathy. Am Heart J 1983;105:855–856.
P.818

72. Maron BJ, et al. Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy. Circulation 1983;68:282–293.
73. Spirito P, Maron BJ. Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography. Am J Cardiol 1984;54:1039–1046.
74. Yock PG, Hatle L, Popp RL. Patterns and timing of Doppler-detected intracavitary and aortic flow in hypertrophic cardiomyopathy. J Am Coll Cardiol 1986;8:1047–1058.
75. Bouchard A, et al. Noninvasive assessment of cardiomyopathy in normotensive diabetic patients between 20 and 50 years old. Am J Med 1989;87:160–166.
76. Sedlis SP, et al. Cardiac amyloidosis simulating hypertrophic cardiomyopathy. Am J Cardiol 1984;53:969–970.
77. Siqueira-Filho AG, et al. M-mode and two-dimensional echocardiographic features in cardiac amyloidosis. Circulation 1981;63:188–196.
78. Nicolosi GL, et al. Prospective identification of patients with amyloid heart disease by two-dimensional echocardiography. Circulation 1984;70:432–437.
79. Klein AL, et al. Prognostic significance of Doppler measures of diastolic function in cardiac amyloidosis: a Doppler echocardiography study. Circulation 1991;83:808–816.
80. Allenby PA, et al. Dysplastic cardiac development presenting as cardiomyopathy. Arch Pathol Lab Med 1988;112:1255–1258.
81. Jenni R, et al. Persisting myocardial sinusoids of both ventricles as an isolated anomaly: echocardiographic, angiographic, and pathologic anatomical findings. Cardiovasc Intervent Radiol 1986;9:127–131.
82. Agmon, Y, et al. Noncompaction of the ventricular myocardium. J Am Soc Echocardiogr 1999;12:859–863.
83. Oechslin EN, et al. Long-term follow-up of 34 adults with isolated left ventricular noncompaction: a distinct cardiomyopathy with poor prognosis. J Am Coll Cardiol 2000;36:493–500.
84. Ports TA, et al. Echocardiography of left ventricular masses. Circulation 1978;58:528–536.
85. Acquatella H, et al. Value of two-dimensional echocardiography in endomyocardial disease with and without eosinophilia: a clinical and pathologic study. Circulation 1983;67:1219–1226.
86. Cooper MJ, et al. Comparison of M-mode echocardiographic measurement of right ventricular wall thickness obtained by the subcostal and parasternal approach in children. Am J Cardiol 1984;54:835–838.
87. Jiang L, et al. Three-dimensional echocardiography: in vivo validation for right ventricular volume and function. Circulation 1994;89:2342–2350.
88. Silverman NH, Hudson S. Evaluation of right ventricular volume and ejection fraction in children by two-dimensional echocardiography. Pediatr Cardiol 1983;4:197–203.
89. Levine RA, et al. Echocardiographic measurement of right ventricular volume. Circulation 1984;69:497–505.
90. Starling MR, et al. A new two-dimensional echocardiographic technique for evaluating right ventricular size and performance in patients with obstructive lung disease. Circulation 1982;66:612–620.
91. Kaul S, et al. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J 1984;107:526–531.
92. Himelman RB, et al. Improved recognition of cor pulmonale in patients with severe chronic obstructive pulmonary disease. Am J Med 1988;84:891–898.
93. Isaaz K, et al. Quantitation of the motion of the cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr 1993;6:166–176.
94. Ports TA, Schiller NB, Strunk BL. Echocardiography of right ventricular tumors. Circulation 1977;56:439–447.
95. Lee CC, Celik C, Lajos TZ. Excision of papillary fibroelastoma arising from the septal leaflet of the tricuspid valve. J Card Surg 1995;10:589–591.
96. Nellessen U, et al. Impending paradoxical embolism from atrial thrombus: correct diagnosis by transesophageal echocardiography and prevention by surgery. J Am Coll Cardiol 1985;5:1002–1004.
97. Higgins JR, Strunk BL, Schiller NB. Diagnosis of paradoxical embolism with contrast echocardiography. Am Heart J 1984;107:375–377.
98. Payvandi MN, Kerber RE. Echocardiography in congenital and acquired absence of the pericardium: an echocardiographic mimic of right ventricular volume overload. Circulation 1976;53:86–92.
99. Marcus FI, Fontaine G. Arrhythmogenic right ventricular dysplasia/cardiomyopathy: a review. Pacing Clin Electrophysiol 1995;18:1298–314.
100. Ports TA, Silverman NH, Schiller NB. Two-dimensional echocardiographic assessment of Ebstein’s anomaly. Circulation 1978;58:336–343.
101. Silverman NH, et al. Pathologic elucidation of the echocardiographic features of Ebstein’s malformation of the morphologically tricuspid valve in discordant atrioventricular connections. Am J Cardiol 1995;76:1277–1283.
102. Schabelman S, et al. Left atrial volume estimation by two-dimensional echocardiography. Cathet Cardiovasc Diagn 1981;7:165–178.
103. Kircher B, et al. Left atrial volume determination by biplane two-dimensional echocardiography: validation by cine computed tomography. Am Heart J 1991;121:864–871.
104. Sanfilippo AJ, et al. Atrial enlargement as a consequence of atrial fibrillation: a prospective echocardiographic study. Circulation 1990;82:792–797.
105. Welikovitch L, et al. Change in atrial volume following restoration of sinus rhythm in patients with atrial fibrillation: a prospective echocardiographic study. Can J Cardiol 1994;10:993–996.
106. Diker E, et al. Prevalence and predictors of atrial fibrillation in rheumatic valvular heart disease. Am J Cardiol 1996;77:96–98.
107. Mattioli AV, et al. Restoration of atrial function after atrial fibrillation of different etiological origins. Cardiology 1996;87:205–211.
108. Rostagno C, et al. Left atrial size changes in patients with paroxysmal lone atrial fibrillation: an echocardiographic follow-up. Angiology 1996;47:797–801.
109. Schiller NB, Foster E, Redberg RF. Transesophageal echocardiography in the evaluation of mitral regurgitation: the twenty-four signs of severe mitral regurgitation. Cardiol Clin 1993;11:399–408.
110. Edler I. Ultrasound cardiogram in mitral valve disease. Acta Chir Scand 1956;111:230.
111. Edler I. Ultrasonic cardiogram in mitral stenosis. Acta Med Scand 1957; 159:85.
112. Edler I. Ultrasound cardiography in mitral valve stenosis. Am J Cardiol 1967;19:18–31.
113. Fagard R, et al. Noninvasive assessment of seasonal variations in cardiac structure and function in cyclists. Circulation 1983;67:896–901.
114. Gutman J, et al. Normal left atrial function determined by 2-dimensional echocardiography. Am J Cardiol 1983;51:336–340.
115. Nichol PM, Gilbert BW, Kisslo JA. Two-dimensional echocardiographic assessment of mitral stenosis. Circulation 1977;55:120–128.
116. Wann LS, et al. Determination of mitral valve area by cross-sectional echocardiography. Ann Intern Med 1978;88:337–341.
117. Sagie A, et al. Doppler echocardiographic assessment of long-term progression of mitral stenosis in 103 patients: valve area and right heart disease. J Am Coll Cardiol 1996;28:472–479.
118. Wann LS, et al. Cross-sectional echocardiographic detection of rheumatic mitral regurgitation. Am J Cardiol 1978;41:1258–1263.
119. Allen H, Harris A, Leatham A. Significance and prognosis of an isolated late systolic murmur: a 9- to 22-year follow-up. Br Heart J 1974;36:525–532.
120. Barlow JB, Pocock WA. Mitral valve prolapse, the specific billowing mitral leaflet syndrome, or an insignificant non-ejection systolic click (editorial). Am Heart J 1979;97:277–285.
121. Kerber RE, Isaeff DM, Hancock EW. Echocardiographic patterns in patients with the syndrome of systolic click and late systolic murmur. N Engl J Med 1971;284:691–693.
122. Dillon JC, et al. Use of echocardiography in patients with prolapsed mitral valve. Circulation 1971;43:503–507.
123. Markiewicz W, et al. Mitral valve prolapse in one hundred presumably healthy young females. Circulation 1976;53:464–473.
124. Levine RA, et al. The relationship of mitral annular shape to the diagnosis of mitral valve prolapse. Circulation 1987;75:756–767.
125. Nishimura RA, et al. Echocardiographically documented mitral-valve prolapse: long-term follow-up of 237 patients. N Engl J Med 1985;313:1305–1309.
126. Chin ML, et al. Aortic valve systolic flutter as a screening test for severe aortic stenosis. Am J Cardiol 1983;51:981–985.
127. Godley RW, et al. Reliability of two-dimensional echocardiography in assessing the severity of valvular aortic stenosis. Chest 1981;79:657–662.
128. Stoddard MF, Hammons RT, Longaker RA. Doppler transesophageal echocardiographic determination of aortic valve area in adults with aortic stenosis. Am Heart J 1996;132:337–342.
129. Teirstein P, et al. Doppler echocardiographic measurement of aortic valve area in aortic stenosis: a noninvasive application of the Gorlin formula. J Am Coll Cardiol 1986;8:1059–1065.
130. Yeager M, Yock PG, Popp RL. Comparison of Doppler-derived pressure gradient to that determined at cardiac catheterization in adults with aortic valve stenosis: implications for management. Am J Cardiol 1986;57:644–648.
131. Choi JY, Sullivan ID. Fixed subaortic stenosis: anatomical spectrum and nature of progression. Br Heart J 1991;65:280–286.
132. Kitchiner D, et al. Morphology of left ventricular outflow tract structures in patients with subaortic stenosis and a ventricular septal defect. Br Heart J 1994;72:251–260.
133. Kleinert S, Geva T. Echocardiographic morphometry and geometry of the left ventricular outflow tract in fixed subaortic stenosis. J Am Coll Cardiol 1993;22:1501–1508.
134. Braunstein PW Jr, et al. Repair of supravalvar aortic stenosis: cardiovascular morphometric and hemodynamic results. Ann Thorac Surg 1990;50: 700–707.
135. Landzberg JS, et al. Etiology of the Austin Flint murmur. J Am Coll Cardiol 1992;20:408–413.
136. Botvinick EH, et al. Echocardiographic demonstration of early mitral valve closure in severe aortic insufficiency: its clinical implications. Circulation 1975;51:836–847.
137. Henry WL, et al. Observations on the optimum time for operative intervention for aortic regurgitation. I. Evaluation of the results of aortic valve replacement in symptomatic patients. Circulation 1980;61:471–483.
138. Fioretti P, et al. Echocardiography in chronic aortic insufficiency: is valve replacement too late when left ventricular end-systolic dimension reaches 55 mm? Circulation 1983;67:216–221.
139. Vandenbossche JL, et al. Relation of left ventricular shape to volume and mass in patients with minimally symptomatic chronic aortic regurgitation. Am Heart J 1988;116:1022–1027.
P.819

140. Robertson WS, et al. Reverse doming of the anterior mitral leaflet with severe aortic regurgitation. J Am Coll Cardiol 1984;3:431–436.
141. Pflugfelder PW, et al. Comparison of cine MR imaging with Doppler echocardiography for the evaluation of aortic regurgitation. AJR Am J Roentgenol 1989;152:729–735.
142. Shively BK, et al. Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis. J Am Coll Cardiol 1991;18:391–397.
143. Freed C, Schiller NB. Echocardiographic findings in Marfan’s syndrome. West J Med 1977;126:87–90.
144. San Roman JA, et al. Transesophageal echocardiography in right-sided endocarditis. J Am Coll Cardiol 1993;21:1226–1230.
145. Schiller NB. Pulmonary artery pressure estimation by Doppler and two-dimensional echocardiography. Cardiol Clin 1990;8:277–287.
146. Ho GM, Eisenberg MJ, Schiller NB. Variation of blood flow in the thoracic aorta during cardiac tamponade. Am Heart J 1994;128:190–193.
147. Kusumoto FM, et al. Response of the interatrial septum to transatrial pressure gradients and its potential for predicting pulmonary capillary wedge pressure: an intraoperative study using transesophageal echocardiography in patients during mechanical ventilation. J Am Coll Cardiol 1993;21:721–728.
148. Sagie A, et al. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. J Am Coll Cardiol 1994;24:446–453.
149. Werner JA, Schiller NB, Prasquier R. Occurrence and significance of echocardiographically demonstrated tricuspid valve prolapse. Am Heart J 1978;96:180–186.
150. Bonmassari R, Nicolosi GL, Disertori M. Tricuspid insufficiency with rupture of the chordae tendineae caused by closed thoracic trauma: evaluation by transesophageal echocardiography: description of a case. G Ital Cardiol 1994;24:763–768.
151. Tucker PA, et al. Flail tricuspid leaflet after multiple biopsies following orthotopic heart transplantation: echocardiographic and hemodynamic correlation. J Heart Lung Transplant 1994;13:466–472.
152. Hausen B, et al. Tricuspid valve regurgitation attributable to endomyocardial biopsies and rejection in heart transplantation. Ann Thorac Surg 1995;59:1134–1140.
153. Himelman RB, Schiller NB. Clinical and echocardiographic comparison of patients with the carcinoid syndrome with and without carcinoid heart disease. Am J Cardiol 1989;63:347–352.
154. Winslow T, et al. Pulmonary valve endocarditis: improved diagnosis with biplane transesophageal echocardiography. J Am Soc Echocardiogr 1992;5:206–210.
155. Von Reyn CF, et al. Infective endocarditis: an analysis based on strict case definitions. Ann Intern Med 1981;94:505–518.
156. Bayer AS, et al. Evaluation of new clinical criteria for the diagnosis of infective endocarditis. Am J Med 1994;96:211–219.
157. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings: Duke Endocarditis Service. Am J Med 1994;96:200–209.
158. O’Brien JT, Geiser EA. Infective endocarditis and echocardiography. Am Heart J 1984;108:386–394.
159. Gilbert BW, et al. Two-dimensional echocardiographic assessment of vegetative endocarditis. Circulation 1977;55:346–353.
160. Mugge A, et al. Echocardiography in infective endocarditis: reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol 1989;14:631–638.
161. Jaffe WM, et al. Infective endocarditis, 1983–1988: echocardiographic findings and factors influencing morbidity and mortality. J Am Coll Cardiol 1990;15:1227–1233.
162. Burger AJ, et al. The role of two-dimensional echocardiology in the diagnosis of infective endocarditis (published erratum appears in Angiology 1991;42:765). Angiology 1991;42:552–560.
163. Daniel WG, et al. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:795–800.
164. Sochowski RA, Chan KL. Implication of negative results on a monoplane transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol 1993;21:216–221.
165. Shapiro SM, et al. Transesophageal echocardiography in diagnosis of infective endocarditis. Chest 1994;105:377–382.
166. Sanfilippo AJ, et al. Echocardiographic assessment of patients with infectious endocarditis: prediction of risk for complications. J Am Coll Cardiol 1991;18:1191–1199.
167. DiSalvo G, et al. Echocardiography predicts embolic events in the infective endocarditis. J Am Coll Cardiol 2001;37:1069–1076.
168. Hecht SR, Berger M. Right-sided endocarditis in intravenous drug users: prognostic features in 102 episodes. Ann Intern Med 1992;117:560–566.
169. Feigenbaum H, Zaky A, Grabhorn LL. Cardiac motion in patients with pericardial effusion: a study using reflected ultrasound. Circulation 1966;34:611–619.
170. Eisenberg MJ, et al. Diagnostic value of chest radiography for pericardial effusion. J Am Coll Cardiol 1993;22:588–593.
171. Horowitz MS, et al. Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974;50:239–247.
172. Rifkin RD, et al. Combined posteroanterior subepicardial fat simulating the echocardiographic diagnosis of pericardial effusion. J Am Coll Cardiol 1984;3:1333–1339.
173. D’Cruz IA, Hoffman PK. A new cross sectional echocardiographic method for estimating the volume of large pericardial effusions. Br Heart J 1991;66:448–451.
174. Eisenberg MJ, et al. Prognostic value of echocardiography in hospitalized patients with pericardial effusion. Am J Cardiol 1992;70:934–939.
175. Schiller NB, Botvinick EH. Right ventricular compression as a sign of cardiac tamponade: an analysis of echocardiographic ventricular dimensions and their clinical implications. Circulation 1977;56:774–779.
176. Schiller NB. Echocardiography in pericardial disease. Med Clin North Am 1980;64:253–282.
177. Himelman RB, et al. Inferior vena cava plethora with blunted respiratory response: a sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 1988;12:1470–1477.
178. Armstrong WF, et al. Diastolic collapse of the right ventricle with cardiac tamponade: an echocardiographic study. Circulation 1982;65:1491–1496.
179. Singh S, et al. Right ventricular and right atrial collapse in patients with cardiac tamponade: a combined echocardiographic and hemodynamic study. Circulation 1984;70:966–971.
180. Kronzon I, Cohen ML, Winer HE. Diastolic atrial compression: a sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 1983;2:770–775.
181. D’Cruz IA, Constantine A. Problems and pitfalls in the echocardiographic assessment of pericardial effusion. Echocardiography 1993;10:151–166.
182. Himelman RB, Lee E, Schiller NB. Septal bounce, vena cava plethora, and pericardial adhesion: informative two-dimensional echocardiographic signs in the diagnosis of pericardial constriction. J Am Soc Echocardiogr 1988;1:333–340.
183. Jue J, Chung W, Schiller NB. Does inferior vena cava size predict right atrial pressures in patients receiving mechanical ventilation? J Am Soc Echocardiogr 1992;5:613–619.
184. Klopfenstein HS, Wann LS. Can pleural effusions cause tamponade-like effects? Echocardiography 1994;11:489–492.
185. Tei C, et al. Atrial systolic notch on the interventricular septal echogram: an echocardiographic sign of constrictive pericarditis. J Am Coll Cardiol 1983;1:907–912.
186. Gibson TC, et al. An echocardiographic study of the interventricular septum in constrictive pericarditis. Br Heart J 1976;38:738–743.
187. Felner JM, Churchwell AL, Murphy DA. Right atrial thromboemboli: clinical, echocardiographic and pathophysiologic manifestations. J Am Coll Cardiol 1984;4:1041–1051.
188. Hynes JK, et al. Two-dimensional echocardiographic diagnosis of pericardial cyst. Mayo Clin Proc 1983;58:60–63.
189. Eisenberg MJ, et al. The clinical spectrum of patients with aneurysms of the ascending aorta. Am Heart J 1993;125:1380–1385.
190. Dev V, et al. Echocardiographic diagnosis of aneurysm of the sinus of Valsalva. Am Heart J 1993;126:930–936.
191. Eisenberg MJ, Geraci SJ, Schiller NB. Screening for abdominal aortic aneurysms during transthoracic echocardiography. Am Heart J 1995;130:109–115.
192. Banning AP, et al. Transoesophageal echocardiography as the sole diagnostic investigation in patients with suspected thoracic aortic dissection. Br Heart J 1994;72:461–465.
193. Popp RL, Yock PG. Noninvasive intracardiac pressure measurement using Doppler ultrasound (editorial). J Am Coll Cardiol 1985;6:757–758.
194. Simonson JS, Schiller NB. Sonospirometry: a new method for noninvasive estimation of mean right atrial pressure based on two-dimensional echographic measurements of the inferior vena cava during measured inspiration. J Am Coll Cardiol 1988;11:557–564.
195. Mulvagh SL, et al. Contrast echocardiography: current and future applications. J Am Soc Echocardiogr 2000;13:331–342.
196. Bax J, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? J Am Coll Cardiol 2004;44:1–9.