Members of the Chamber Quantification Writing Group are: Roberto M. Lang, MD, FASE, Michelle Bierig, MPH, RDCS, FASE, Richard B. Devereux, MD, Frank A. Flachskampf, MD, Elyse Foster, MD, Patricia A. Pellikka, MD, Michael H. Picard, MD, Mary J. Roman, MD, James Seward, MD, Jack S. Shanewise, MD, FASE, Scott D. Solomon, MD, Kirk T. Spencer, MD, FASE, Martin St John Sutton, MD, FASE, and William J. Stewart, MD

http://www.botonimarco.it/files/chamberquantification.pdf

Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology.

To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p

Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings

Quantification of cardiac chamber size, ventricular mass and function ranks among the most clinically important and most frequently requested tasks of echocardiography. Over the last decades, echocardiographic methods and techniques have improved and expanded dramatically, due to the introduction of higher frequency transducers, harmonic imaging, fully digital machines, left-sided contrast agents, and other technological advancements. Furthermore, echocardiography due to its portability and versatility is now used in emergency rooms, operating rooms, and intensive care units. Standardization of measurements in echocardiography has been inconsistent and less successful, compared to other imaging techniques and consequently, echocardiographic measurements are sometimes perceived as less reliable. Therefore, the American Society of Echocardiography, working together with the European Association of Echocardiography, a branch of the European Society of Cardiology, has critically reviewed the literature and updated the recommendations for quantifying cardiac chambers using echocardiography. This document reviews the technical aspects on how to perform quantitative chamber measurements of morphology and function, which is a component of every complete echocardiographic examination.

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Recommendations for chamber quantification

This report is the continuation of two earlier reports that defined human arterial intima and precursors of advanced atherosclerotic lesions in humans. This report describes the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions. These, with the earlier definitions of precursor lesions, led to the histological classification of human atherosclerotic lesions found in the second part of this report. The Committee on Vascular Lesions also attempted to correlate the appearance of lesions noted in clinical imaging studies with histological lesion types and corresponding clinical syndromes. In the histological classification, lesions are designated by Roman numerals, which indicate the usual sequence of lesions progression. The initial (type I) lesion contains enough atherogenic lipoprotein to elicit an increase in macrophages and formation of scattered macrophage foam cells. As in subsequent lesion types, the changes are more marked in locations of arteries with adaptive intimal thickening. (Adaptive thickenings, which are present at constant locations in everyone from birth, do not obstruct the lumen and represent adaptations to local mechanical forces). Type II lesions consist primarily of layers of macrophage foam cells and lipid-laden smooth muscle cells and include lesions grossly designated as fatty streaks. Type III is the intermediate stage between type II and type IV (atheroma, a lesion that is potentially symptom-producing). In addition to the lipid-laden cells of type II, type III lesions contain scattered collections of extracellular lipid droplets and particles that disrupt the coherence of some intimal smooth muscle cells. This extracellular lipid is the immediate precursor of the larger, confluent, and more disruptive core of extracellular lipid that characterizes type IV lesions. Beginning around the fourth decade of life, lesions that usually have a lipid core may also contain thick layers of fibrous connective tissue (type V lesion) and/or fissure, hematoma, and thrombus (type VI lesion). Some type V lesions are largely calcified (type Vb), and some consist mainly of fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).

A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association

An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.

Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.

The relation of minor and major axes of the left ventricle was determined in 100 left ventriculograms performed in the right anterior oblique projection. This relation taken over a wide range of volumes was used to derive a theoretically correct equation for determination of ventricular volume by echocardiography. The final equation was: V =[7.0/2.4 +d] (D3), where V = volume and D = the echocardiographically measured internal dimension. In 12 patients without asynergy, this equation accurately and directly calculated end-systolic and end-diastolic volumes whether the left ventricle was small or large. However, in 12 patients exhibiting left ventricular asynergy the correlation between angiographically and echocardiographically determined volumes was poor. Thus, caution is recommended in the use of time-motion echocardiography to calculate ventricular volumes in patients with coronary artery disease and possible left ventricular asynergy.

Problems in echocardiographic volume determinations: Echocardiographic-angiographic correlations in the presence or absence of asynergy

CONGESTIVE heart failure has usually been considered to be a global affection of the myocardium in which disturbance of contraction in one or both ventricles is generalized. On the other hand, abnormal myocardial contraction may be caused by local areas of malfunctioning myocardium interacting with other areas of completely normal muscle. The possibility that unco-ordinated contraction of the heart results from such a combination of normal and abnormal muscle has received little attention. In 1925 Wiggers1 described the pattern of left ventricular contraction as a "series of sequential fractionate contractions of muscle bundles." He suggested that disturbance in this temporal . . .

Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure.

In a study group of 2,457 consecutive patients undergoing cardiac catheterization, 30 patients had coronary arterial ectasia, an irregular dilatation of major vessels up to seven times the diameter of branch vessels. The frequency of hypertension, abnormal electrocardiogram and history of myocardial infarction was greater than that in a control group with obstructive coronary artery disease. Patients with ectasia did not differ from patients with obstructive disease in sex, age, prevalence of angina or presence of metabolic abnormalities. Six deaths occurred in the group with ectasia during a mean follow-up period of 24 months (annual rate of 15 percent). Extensive destruction of the musculoelastic elements was evident, resulting in marked attenuation of the vessel wall. The short-term prognosis in this group is the same as in medically treated patients with three vessel obstructive coronary artery disease.

Clinical significance of coronary arterial ectasia

Ventricular asynergy, local disturbances in ventricular wall motion which disrupt the normal coordinated pattern of left ventricular contraction, is described in a group of patients. There are four distinct types of asynergy: (1) akinesis, or local absence of wall motion; (2) dyskinesis, or local expansile or paradoxical wall motion; (3) asyneresis, or geometric distortion or inequality of wall motion; and (4) asynchrony, or a disturbed temporal sequence of contraction. These local abnormalities are closely related to anatomic, electrocardiographic and biochemical zones of ischemia in coronary heart disease and are also seen in cardiomyopathy and with ectopic excitation and activation of the left ventricle. Although often associated with clinical and more frequently, laboratory evidence of cardiac failure, asynergy sometimes occurs in the absence of cardiac enlargement. Such morphologic abnormalities provide a functional basis for the hemodynamic disturbances seen in coronary heart disease and so poorly explained at postmortem examination. Thus, ventricular asynergy represents a dynamic abnormality appreciated only in life as a derangement of the integrated function of the left ventricle and represents an important cause of cardiac failure.

Implications of left ventricular asynergy

Thirteen patients with left ventricular aneurysm due to coronary heart disease were studied by left heart and coronary sinus catheterization, including cineventriculography and measurement of ventricular mechanics and energetics at rest, and in some subjects, during either isoproterenol infusion or supine leg exercise. Eight patients had an aneurysm estimated to comprise greater than 20% of the left ventricular surface area, associated with increased left ventricular end-diastolic volume and pressure and mean systolic force. Average isometric rate of pressure rise and mean fiber shortening velocity and distance were uniformly decreased. Five patients had an aneurysm, estimated to comprise less than 15% of the left ventricular surface, associated with normal or nearly-normal left ventricular end-diastolic volume and pressure and mean systolic force. Average isometric rate of pressure rise was normal, but fiber shortening velocity and distance were moderately depressed. Stroke output and cardiac output were...

Michael V. Herman

Papers

Problems in echocardiographic volume determinations: Echocardiographic-angiographic correlations in the presence or absence of asynergy

Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure.

Clinical significance of coronary arterial ectasia

Implications of left ventricular asynergy

A Hemodynamic Study of Left Ventricular Aneurysm