Angiotensin converting enzyme inhibition and ventricular remodeling in heart failure.

The prevention or attenuation of the development of heart failure by the angiotensin converting enzyme inhibitor captopril was examined in two animal models, spontaneously hypertensive rats and rats with myocardial infarction produced by coronary artery ligation. In 24-month-old female spontaneously hypertensive rats with marked left ventricular hypertrophy, cardiac output was reduced despite an increase in ventricular volume, resulting in a greatly reduced ejection fraction. Treatment with captopril from 14 to 24 months of age maintained forward output and prevented ventricular dilatation so that ejection fraction remained normal; left ventricular hypertrophy regressed to levels observed in six-month-old spontaneously hypertensive rats. In rats with moderate and large infarcts three months after ligation, left ventricular filling pressures were elevated, forward output was reduced, and ventricular volumes were greatly increased. Long-term therapy with captopril maintained filling pressures within normal limits and maintained forward output from a lesser dilated left ventricle to yield an ejection fraction that was elevated compared with that in untreated rats. Thus, the potentially deleterious remodeling of the left ventricle in heart failure, an extensive increase in mass and chamber volume, can be favorably altered by long-term angiotensin converting enzyme inhibition (captopril) with salutary effects on hemodynamics.