Left ventricular performance after intravenous infusion of captopril in patients with congestive heart failure
Arcidiacono, G.; Asmundo, G.O.; Battaglia, E.; Bordignon, E.; Calogero, A.E.; Cuscunà, S.; Floridia, S.; Vigo, G.; Ossino, A.M.; Gurgone, G.
Minerva Cardioangiologica 43(11-12): 481-484
1995
ISSN/ISBN: 0026-4725 PMID: 8710137 Document Number: 446552
Although oral administration of captopril, an angiotensin-converting enzyme inhibitor, is effective for the treatment of congestive heart failure (CHF), the effect of its intravenous (iv) administration is not well known. Ten patients (age range 48-72 years), with CHF belonging to the second and third NYHA class, were given an iv bolus of 25 mg of captopril. Before and 30 minutes after the infusion of captopril, a number of parameters of the left ventricular function were evaluated by echocardiography IREX 3 M-B Mode. Eight patients showed a significant improvement of left ventricular performance indices. In fact, the ejection fraction (13.8%, p < 0.05), the cardiac output (24%, p < 0.001), the circumferential shortness fraction (29.9%, p < 0.05), and the fraction shortening (16.0%, p < 0.005) increased significantly, whereas the end-systolic diameter (21%, p < 0.001), the endsystolic stress (23.8%, p < 0.01) and the left ventricle ejection time (4.8%, p < 0.05) decreased significantly. Systolic and diastolic blood pressure values also underwent a significant reduction by 17% and 11% (p < 0.01 and p < 0.05 respectively). No evident correlation between the improvement of the left ventricular function and the basal renin rates was noticed. A significant improvement of parietal kinesis was observed especially in those segments which showed movement abnormalities (hypokinesia and akinesia) and in many cases this was detected by M-B Mode echocardiography. Our findings may be the result of the following factors: 1) reduction of parietal stress; 2) increased district coronary flow; 3) inhibition of tissue renin-angiotensin-aldosterone system; and 4) "scavenging" action exerted by the SH group of captopril.