Evaluation of myocardial function in cardiomyopathic states.
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Biomedical subjects
Publications and source records attributed to W H Gaasch.
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In this report we have emphasized the significant influence of loading conditions on LV relaxation. Changes in inotropic state, ischemia, hypertrophy, and a host of other factors were not discussed herein. Ventricular asynchrony is likewise beyond the scope of this review, but it should be recognized that complex loading interactions among fibers within the LV wall influence relaxation and filling in ventricles that contract and relax nonsynchronously. Intact heart and isolated muscle experiments indicate that changes in preload do not influence relaxation rates when systolic pressure or total load remains constant. It appears, therefore, that the relaxation changes that occur with volume loading are primarily due to changes in systolic pressure or load. Indeed, an increase in systolic pressure may cause a substantial decrease in isovolumic relaxation rate, especially if there is a slow rise and a late peak in LV pressure. By contrast, an abrupt increase in late systolic load augments relaxation rate. Intact heart studies indicate that an abrupt load increment near the end of ejection results in premature and more rapid isovolumic relaxation, while an increase in left atrial pressure increases the filling rate; isolated muscle studies indicate that a load increment at the end of isometric relaxation causes an increase in isotonic relaxation rate. Thus, loading conditions during the periods of ejection, isovolumic relaxation, and filling can influence relaxation parameters and should be considered in clinical and experimental studies of LV relaxation.
The popular diet drugs, fenfluramine and dexfenfluramine, were withdrawn from the market in the United States after the publication of an association of these drugs with valvulopathy in a small series of patients, spontaneous reports to the Food and Drug Administration, and echocardiographic surveys that suggested a valvulopathy prevalence of 32.8% among diet drug users. Subsequent publications suggested that there is an association of these agents with valvulopathy, but that the prevalence seems lower than initially suspected. This review examines the available prevalence data and attempts to account for some of the variability in these data. Potential pathophysiologic mechanisms are discussed and management guidelines for these patients are provided. This is an area of ongoing study and more information about the natural history of these lesions will certainly be forthcoming. A review of the data reveals that the withdrawal of these agents was prudent and likely prevented further harm.
This report presents a method for determining the time course of circumferential LV wall stress and fiber shortening velocity (endocardial as well as midwall) using simultaneous recordings of LV dimensions by echography and LV pressure (micromanometer). The values for max VCF, VCF at peak stress, mean VCF, and peak stress are in general agreement with those observed with previous methods; the separation between normal and abnormal LV function appears to be good. The method permits frequent observations to be performed in a single patient, which is of particular value during acute interventions. Data from a small number of interventions suggest that VCF in man is relatively insensitive to acute changes in preload, is inversely affected by changes in afterload and appears sensitive to inotropic stimulation. Although VCF seems to be a good index of LV performance, its sensitivity to afterload might, at times, limit its usefulness.
Perfusion deficits on lung scanning in narcotic addicts are frequently demonstrable. To determine the angiographic and hemodynamic correlates of these deficits, right heart catheterization with selective pulmonary angiography was carried out in 7 addicts with abnormal lung scans, and one with normal scan. Four had angiographic abnormalities corresponding to the regions of perfusion defects on lung scan. These consisted of large vessel cut-offs, intraluminal filling defects and/or considerably reduced vascularity. Three subjects had normal angiograms in the presence of abnormal perfusion scans. One subject had normal angiogram and scan. All eight patients had normal pulmonary artery pressures and calculated pulmonary vascular resistances. This study demonstrates that (1) angiographic abnormalities in larger pulmonary arteries may be found in narcotic addicts with perfusion defects on lung scanning, and (2) these findings may be present without significant hemodynamic alterations.