Human myocardial histologic characteristics in congestive heart failure

Abstract

The purpose of this study was to identify the histologic characteristics of human myocardium in congestive heart failure (CHF) by cellular hypertrophy, nuclear area, endocardial thickness, and percentage of fibrosis and to correlate histologic findings to cause, severity, and duration of disease. Right ventricular endomyocardial biopsies from 109 patients were quantitatively analyzed. Ten patients with normal cardiac history, physical examination results, and cardiac function served as the control group. The remaining patients were divided into the following groups: those treated with doxorubicin (n = 18), and those with chest pain with normal coronary arteries (n = 8), familial CHF (n = 3), CHF associated with myotonic dystrophy (n = 3), peripartal CHF (n = 2), valvular CHF (n = 9), alcohol-induced CHF (n = 13), postviral CHF (n = 6), or idiopathic CHF (n = 36). Linear regression analyses showed a strong correlation between cell diameter and nuclear area (r = .70, p < .001) and weaker correlations between amount of fibrosis and cell diameter (r = .30, p < .005) and fibrosis and nuclear area (r = .29, p < .005). Results of function studies and histologic measurements (e.g., echocardiographically measured change in the minor-axis dimension of the left ventricle with systole and cell diameter) correlated poorly (r = -.33, p < .005). Duration of dyspnea did not correlate with any histologic factor. Within the normal group there was a direct correlation of cell diameter with age (r = .67, p < .05). Analysis of covariance revealed that the doxorubicin-treated patients had significantly less cellular hypertrophy but more fibrosis than the other patients. In those with alcohol-induced CHF the opposite pattern of more hypertrophy and less fibrosis was observed. The idiopathic and valvular CHF groups did not differ from each other or from the other groups. The results of this study demonstrate that fibrosis and hypertrophy tend to be worse in patients with severe CHF and that some myocardial insults (especially that of doxorubicin) induce a characteristic response to the injury.