Different pathophysiology of cardiac hypertrophy in hypertension and hypertrophic cardiomyopathy.

In order to investigate differences in the pathophysiology of cardiac hypertrophy between patients with arterial hypertension and hypertrophic cardiomyopathy, DNA synthesis by cardiac myocytes and the effects of an angiotensin-converting enzyme inhibitor were examined in these two groups of patients. DNA synthesis and the cell cycle were investigated by flow cytometry using autopsy materials from patients with hypertension and hypertrophic cardiomyopathy. The hypertension group (n=10) included four men and six women aged 61+/-10 years (heart weight: 470+/-79 g, mean+/-s.d.); the cardiomyopathic group (n=10) included eight men and two women aged 61+/-23 years (heart weight: 615+/-211 g). The percentage of cells in G2M phase of the cell cycle was significantly decreased in the myocardium from patients with hypertrophic cardiomyopathy compared with that from hypertensive patients (cardiomyopathy v hypertension: 1.1+/-0.6 v 7.7+/-2.6%, mean+/-s.d.). Captopril, an angiotensin-converting enzyme inhibitor, was administered for 12 months to patients with hypertension (n=20) and hypertrophic cardiomyopathy (n=15). Regression of cardiac hypertrophy was assessed by echocardiography. Long-term administration of captopril achieved regression of cardiac hypertrophy in the hypertensive patients, but not in the patients with hypertrophic cardiomyopathy. In the hypertensive patients, the left ventricular mass was 234+/-9 g before treatment and 198+/-26 g after treatment (mean+/-s.d., P<0. 01). In cardiomyopathic patients, on the other hand, there was no significant difference of left ventricular mass after treatment (before v after, 305+/-85 v 285+/-90 g, mean+/-s.d.). These results suggest that the mechanism of cardiac hypertrophy differs between patients with hypertension and hypertrophic cardiomyopathy.