TY - JOUR
T1 - Angiotensin inhibition in severe heart failure
T2 - Acute central and limb hemodynamic effects of captopril with observations on sustained oral therapy
AU - Faxon, David P.
AU - Halperin, Jonathan L.
AU - Creager, Mark A.
AU - Gavras, Haralambos
AU - Schick, Edgar C.
AU - Ryan, Thomas J.
N1 - Funding Information:
From Evans Memorial Department of Clinical Research, Department Medicine, Boston University Medical Center, Boston, Mass. This work was supported by National Heart, Lung and Blood Institute Grant No. 5P50.HL18318-04 and by a grant-in-aid from the Squibb Institute for Medical Research, Princeton, N. J. for publication Oct. 15, 1980; accepted Jan. 16, 1981. requests: David P. Faxon, M.D., Section of Cardiology, 75 East Newton St., Boston, MA. 02118. *This work was done during Dr. Halpeti’s tenure of the Howard Sprague Fellowship of the American Heart Association, Massachusetts Affiliate, and American Heart Association, Northeast Massachusetts Division, No. 13-404-789.
PY - 1981/5
Y1 - 1981/5
N2 - The systemic, pulmonary, and limb circulatory responses to the angiotensin-converting enzyme inhibitor, captopril, were determined in 10 patients with severe, chronic heart failure. Immediate effects include sustained reductions in arterial pressure and pulmonary capillary wedge pressure and improvement in cardiac output, as reported with other vasodliator drugs. Calf vascular resistance did not change despite substantial lowering of total systemic vascular resistance, indicating that arteriolar dilatation occurred on a selective basis. Transient reduction in mean right atrial pressure paralleled slight calf venodillatation, but effects upon the resistance vasculature predominated. Plasma renin activity and norepinephrine concentrations increased after therapy in the acute phase as plasma aldosterone levels consistently fell. During maintenance oral treatment over 7 to 15 months (median, 11.5 months), patients displayed symptomatic benefit, improved functional capacity, and greater exercise tolerance. No major adverse reactions developed. These findings suggest that angiotensin converting enzyme inhibition with captopril in congestive heart failure patients improves cardiocirculatory function through selective arteriolar dilatation. The reordering of regional blood flow which appears to result from release of angiotensin-mediated vasoconstriction, as well as the suppression of aldosterone, may underlle the prolonged benefit observed in these patients. This oral vasodilator appears to represent an effective adjunct for the treatment of advanced, chronic heart failure refractory to conventional measures.
AB - The systemic, pulmonary, and limb circulatory responses to the angiotensin-converting enzyme inhibitor, captopril, were determined in 10 patients with severe, chronic heart failure. Immediate effects include sustained reductions in arterial pressure and pulmonary capillary wedge pressure and improvement in cardiac output, as reported with other vasodliator drugs. Calf vascular resistance did not change despite substantial lowering of total systemic vascular resistance, indicating that arteriolar dilatation occurred on a selective basis. Transient reduction in mean right atrial pressure paralleled slight calf venodillatation, but effects upon the resistance vasculature predominated. Plasma renin activity and norepinephrine concentrations increased after therapy in the acute phase as plasma aldosterone levels consistently fell. During maintenance oral treatment over 7 to 15 months (median, 11.5 months), patients displayed symptomatic benefit, improved functional capacity, and greater exercise tolerance. No major adverse reactions developed. These findings suggest that angiotensin converting enzyme inhibition with captopril in congestive heart failure patients improves cardiocirculatory function through selective arteriolar dilatation. The reordering of regional blood flow which appears to result from release of angiotensin-mediated vasoconstriction, as well as the suppression of aldosterone, may underlle the prolonged benefit observed in these patients. This oral vasodilator appears to represent an effective adjunct for the treatment of advanced, chronic heart failure refractory to conventional measures.
UR - http://www.scopus.com/inward/record.url?scp=0019497057&partnerID=8YFLogxK
U2 - 10.1016/0002-8703(81)90220-9
DO - 10.1016/0002-8703(81)90220-9
M3 - Article
C2 - 7013458
AN - SCOPUS:0019497057
SN - 0002-8703
VL - 101
SP - 548
EP - 556
JO - American Heart Journal
JF - American Heart Journal
IS - 5
ER -