The rapid technological developments of the past decade and the changes in echocardiographic practice brought about by these developments have resulted in the need for updated recommendations to the previously published guidelines for cardiac chamber quantification, which was the goal of the joint writing group assembled by the American Society of Echocardiography and the European Association of Cardiovascular Imaging. This document provides updated normal values for all four cardiac chambers, including three-dimensional echocardiography and myocardial deformation, when possible, on the basis of considerably larger numbers of normal subjects, compiled from multiple databases. In addition, this document attempts to eliminate several minor discrepancies that existed between previously published guidelines.

https://biblio.ugent.be/publication/5953422/file/5953443.pdf

Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.

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.

We have presented recommendations for the optimum acquisition of quantitative two-dimensional data in the current echocardiographic environment. It is likely that advances in imaging may enhance or supplement these approaches. For example, three-dimensional reconstruction methods may greatly augment the accuracy of volume determination if they become more efficient. The development of three-dimensional methods will depend in turn on vastly improved transthoracic resolution similar to that now obtainable by transesophageal echocardiography. Better resolution will also make the use of more direct methods of measuring myocardial mass practical. For example, if the epicardium were well resolved in the long-axis apical views, the myocardial shell volume could be measured directly by the biplane method of discs rather than extrapolating myocardial thickness from a single short-axis view. At present, it is our opinion that current technology justifies the clinical use of the quantitative two-dimensional methods described in this article. When technically feasible, and if resources permit, we recommend the routine reporting of left ventricular ejection fraction, diastolic volume, mass, and wall motion score.

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.

Background. Left ventricular dilatation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, long-term therapy with the angiotensin-converting—enzyme inhibitor captopril attenuated ventricular dilatation and remodeling. We investigated whether captopril could reduce morbidity and mortality in patients with left ventricular dysfunction after a myocardial infarction. Methods. Within 3 to 16 days after myocardial infarction, 2231 patients with ejection fractions of 40 percent or less but without overt heart failure or symptoms of myocardial ischemia were randomly assigned to receive double-blind treatment with either placebo (1116 patients) or captopril (1115 patients) and were followed for an average of 42 months. Results. Mortality from all causes was significantly reduced in the captopril group (228 deaths, or 20 percent) as compared with the placebo group (275 deaths, or 25 percent); the reduction in risk was 19 percent (95 percent conf...

Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. results of the survival and ventricular enlargement trial

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/pdf/acc-aha-2005-guideline-update-for-the-diagnosis-and-4hik65ngbe.pdf

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.

/pdf/hemodynamic-determinants-of-the-time-course-of-fall-in-3kqolpaenr.pdf

Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.

Background Platelet glycoprotein IIb/IIIa is a membrane receptor for fibrinogen and von Willebrand factor, and it has an important role in platelet aggregation. It is known to be involved in the pathogenesis of acute coronary syndromes. Previously, we found a high frequency of a particular polymorphism, Pl A2 , of the gene encoding glycoprotein IIIa in kindreds with a high prevalence of premature myocardial infarction. Methods To investigate the relation between the Pl A2 polymorphism and acute coronary syndromes, we conducted a case–control study of 71 case patients with myocardial infarction or unstable angina and 68 inpatient controls without known heart disease. The groups were matched for age, race, and sex. We used two methods to determine the Pl A genotype: reverse dot blot hybridization and allele-specific restriction digestion. Results The prevalence of Pl A2 was 2.1 times higher among the case patients than among the controls (39.4 percent vs. 19.1 percent, P = 0.01). In a subgroup of patients w...

/pdf/a-polymorphism-of-a-platelet-glycoprotein-receptor-as-an-2brtz3wf66.pdf

A Polymorphism of a Platelet Glycoprotein Receptor as an Inherited Risk Factor for Coronary Thrombosis

To assess the early topographic changes after acute transmural myocardial infarction, we studied 28 patients during the first two weeks after infarction by serial two-dimensional echocardiography. Regional end-diastolic segment lengths and wall thicknesses for anterior and posterior left ventricular walls were calculated. Eight patients showed infarct expansion, with disproportionate dilatation and transmural thinning in the infarcted zone, that was significantly different (P less than 0.005) from changes in non-infarcted regions. This regional expansion led to an overall left ventricular dilatation in these eight patients of 25 per cent compared to 5 per cent in the 20 patients without infarct expansion. Although the eight patients with regional expansion did not have significantly higher peak creatine kinase or Killip classification, they had a significantly greater eight-week mortality (four of eight versus none of 20, P less than 0.004). Thus, regional cardiac dilatation may be an early, lethal consequence of transmural infarcts, and appears to be an important mechanism of acute cardiac dilatation after myocardial infarction.

Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography.

To study endocardial wall motion and thickness as indexes of infarction, we used two-dimensional echocardiography to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Thirteen dogs were studied 48 hours after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 msec at 1-cm intervals from apex to base in an open-chest, anesthetized preparation were analyzed with a computer-aided contouring system for quantification of segmental %EM and %Th at 16 equally spaced points per slice. Slices corresponding to each two-dimensional echocardiographic cross section were examined pathologically for evidence of infarction.Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM both yielded clear separation with little overlap (−12.5% infarcted vs 37.4% normal for thickness; −11.3 vs 25.7% for motion, p ≪ 0.001 for both). Endocardial motion was less precise than thickening, however, in distinguishing infarct from either distant normal zones or zones directly adjacent to infarct.Although wall thickening was useful in separating out true subendocardial infarct, change in systolic thickening was not accurate in detecting the transmural extent of infarction. In 827 individual two-dimensional echocardiographic segments with varying degrees of transmural involvement, segments with 1–20% extent of transmural infarction showed reduced thickening compared with noninfarcted segments (39.9 vs 15.2%, p < 0.001), whereas myocardial segments with 21–100% transmural infarction showed systolic thinning (−8.9 to − 13.3%). There was no significant augmentation in the severity of systolic thinning as the extent of transmural infarction increased from 21% to 100%.We conclude that: (1) Wall motion abnormalities are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. (2) There is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. (3) There is no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21% to 100%. This \"threshold\" phenomenon may therefore preclude accurate estimation of infarct size by two-dimensional echocardiography. (4) Evidence of any systolic thickening indicates less than 20% transmural extent of infarction.

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

James L. Weiss

Papers

Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.

A Polymorphism of a Platelet Glycoprotein Receptor as an Inherited Risk Factor for Coronary Thrombosis

Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography.

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Leftward septal displacement during right ventricular loading in man.