Renin, Aldosterone and Cardiac Decompensation: Studies With an Oral Converting Enzyme Inhibitor in Heart Failure
ROBERT
C. TARAZI,
MD,
FACC
FETNAT M. FOUAD, MD JOANNE K. CEIMO, MD EMMANUEL L. BRAVO, MD Cleveland,
Ohio
From the Research Division, Cleveland Clinic Foundation, Cleveland, Ohio. Manuscript received August 3, 1979; revised manuscript received and accepted August 14, 1979. Address for reprints: Robert C. Tarazi, MD, Research Division, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106.
Congestive heart failure is frequently associated with stimulation of the renin-angiotensin system; the resulting increase in peripheral resistance and secondary aldosteronism, in turn, adds to the cardiac load and thus helps perpetuate decompensation. An oral converting enzyme inhibitor (captopril) was therefore tried in six normotensive patients with heart failure resistant to digitalis, diuretic agents and vasodilator therapy. After an oral dose of 25 to 50 mg, cardiac output and stroke volume increased (P
ROBERT
C. TARAZI,
MD,
FACC
FETNAT M. FOUAD, MD JOANNE K. CEIMO, MD EMMANUEL L. BRAVO, MD Cleveland,
Ohio
From the Research Division, Cleveland Clinic Foundation, Cleveland, Ohio. Manuscript received August 3, 1979; revised manuscript received and accepted August 14, 1979. Address for reprints: Robert C. Tarazi, MD, Research Division, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106.
Congestive heart failure is frequently associated with stimulation of the renin-angiotensin system; the resulting increase in peripheral resistance and secondary aldosteronism, in turn, adds to the cardiac load and thus helps perpetuate decompensation. An oral converting enzyme inhibitor (captopril) was therefore tried in six normotensive patients with heart failure resistant to digitalis, diuretic agents and vasodilator therapy. After an oral dose of 25 to 50 mg, cardiac output and stroke volume increased (P
