A 57-year-old womanwas admitted to our hospital be-

Changes in two of the elements of myocardial subcellular organelles relating to cardiac energetics, ventricular myosin isozymes and mitochondrial DNA mutations, were examined using left ventricular tissue samples obtained at autopsy from patients with ischemic heart disease. Myosin isozymes were examined in tissues from nine patients with ischemic heart disease and 12 control patients with cancer but no heart disease. Extracted myosin was separated by pyrophosphate gel electrophoresis. The relative concentration of each component was determined by densitometry. Mitochondrial DNA mutations were evaluated in tissues from ten patients with myocardial infarction and 11 control patients with cancer but no heart disease. DNA was extracted and mitochondrial DNA mutations were detected by the polymerase chain reaction. Two bands were revealed by pyrophosphate gel electrophoresis. These contained VM-A, which exhibited faster electrophoretic mobility and was present in lower concentrations, and VM-B, which had a lower mobility and a higher concentration, respectively. SDS polyacrylamide gel electrophoresis showed that these two components contained the heavy chain and light chains 1 and 2 of myosin. VM-A concentrations tended to be higher in patients with ischemic heart disease than in controls. A 7.4-kb deletion was detected between the D-loop and the ATPase 6 genes of mitochondrial DNA from the myocardium of 6 out of 10 patients with myocardial infarction. The relative amounts of the two myosin isozymes could be altered by ischemic heart disease, although the functional significance of these components is unclear. The changes in the two myosin isozymes might be an adaptive change to disordered energy metabolism, but this change was small. The myocardial mitochondrial DNA deletions in patients with myocardial infarction were thought to result from ischemic damage.

The effect of long-term administration of delapril, an angiotensin converting enzyme inhibitor, and candesartan, an angiotensin II receptor blocker, on cardiac hypertrophy was investigated in spontaneously hypertensive rats (SHR). Delapril (2 mg/kg/ day) and candesartan (2 mg/kg/day) were administered for 5 weeks to 15-week-old male SHR. Echocardiographic estimation of cardiac morphology and function revealed cardiac hypertrophy in SHR compared with Wistar-Kyoto rats (WKY) which were used as normal controls. Both treated groups revealed regression of cardiac hypertrophy estimated by echocardiography. Heart to body weight ratio of treated SHR was also smaller than that of untreated SHR. Plasma BNP and ANP concentrations were increased in untreated SHR and decreased in the treated groups. Histological examination was performed using light microscopy and the area of fibrosis was estimated by computer. Reduction of the fibrotic area was observed in SHR treated with delapril and candesartan, although the latter was not statistically significant. Immunohistochemical examination using anti-collagen monoclonal antibody showed a decrease of type I collagen in treated SHR as compared with untreated SHR. It is concluded that both angiotensin converting enzyme inhibitor and angiotensin II receptor blocker sufficiently reduce blood pressure in SHR associated with regression of cardiac remodeling.