PMID- 12390293 OWN - NLM STAT- MEDLINE DCOM- 20030422 LR - 20190826 IS - 0305-1870 (Print) IS - 0305-1870 (Linking) VI - 29 IP - 12 DP - 2002 Dec TI - Effects of the angiotensin-converting enzyme inhibitor alacepril on exercise capacity and neurohormonal factors in patients with mild-to-moderate heart failure. PG - 1060-5 AB - 1. Alacepril is a long-acting, sulphydryl-containing angiotensin-converting enzyme inhibitor. Data are limited regarding the effects of alacepril on exercise tolerance in patients with chronic heart failure (CHF). The aim of the present study was to determine the effects of chronic alacepril treatment on exercise capacity and neurohormones in patients with CHF. 2. The effects of 12 weeks treatment with alacepril on clinical, echocardiographic and cardiopulmonary exercise variables were studied in 18 CHF patients (mean age: 63 +/- 2 years; New York Heart Association (NYHA) class I n = 6, class II n = 10, class III n = 2) in a cross-over fashion. Resting levels of plasma noradrenaline, renin-angiotensin system activity and natriuretic peptides were evaluated. 3. Treatment with alacepril significantly improved NYHA functional class and decreased cardiothoracic ratio (60.1 +/- 2.0 vs 58.1 +/- 1.9% for baseline vs alacepril, respectively; P < 0.01). Cardiac dimensions by echocardiogram were decreased after alacepril therapy. Peak Vo2 (17.7 +/- 1.2 vs 19.5 +/- 1.3 mL/min per kg; P < 0.01) and anaerobic threshold (11.7 +/- 0.6 vs 13.2 +/- 0.9 mL/min per kg; P < 0.01) increased with alacepril treatment. Plasma noradrenaline and plasma angiotensin II levels were not altered, but plasma aldosterone (77.7 +/- 13.5 vs 51.7 +/- 9.7 pg/mL; P < 0.01), atrial natriuretic peptide (ANP; 86.5 +/- 20.3 vs 43.6 +/- 7.6 pg/mL; P < 0.05) and brain natriuretic peptide (BNP; 222.7 +/- 59.3 vs 117.7 +/- 34.3 pg/mL; P < 0.05) levels decreased after alacepril treatment. 4. These results suggest that treatment with alacepril improves functional status and exercise capacity in patients with mild-to-moderate CHF. Neurohormones were favourably influenced by alacepril therapy, with significant decreases in plasma aldosterone, ANP and BNP levels. FAU - Kinugawa, Toru AU - Kinugawa T AD - First Department of Internal Medicine, Tottori University Faculty of Medicine, Yonago, Japan. kinugawa@grape.med.tottori-u.ac.jp FAU - Osaki, Shuichi AU - Osaki S FAU - Kato, Masahiko AU - Kato M FAU - Ogino, Kazuhide AU - Ogino K FAU - Shimoyama, Masaki AU - Shimoyama M FAU - Tomikura, Yoko AU - Tomikura Y FAU - Igawa, Osamu AU - Igawa O FAU - Hisatome, Ichiro AU - Hisatome I FAU - Shigemasa, Chiaki AU - Shigemasa C LA - eng PT - Journal Article PL - Australia TA - Clin Exp Pharmacol Physiol JT - Clinical and experimental pharmacology & physiology JID - 0425076 RN - 0 (Angiotensin-Converting Enzyme Inhibitors) RN - 0 (Neurotransmitter Agents) RN - 9G64RSX1XD (Captopril) RN - X39TL7JDPF (alacepril) SB - IM MH - Aged MH - Angiotensin-Converting Enzyme Inhibitors/*pharmacology/therapeutic use MH - Captopril/*analogs & derivatives/*pharmacology/therapeutic use MH - Cross-Over Studies MH - Exercise Test/*drug effects/statistics & numerical data MH - Female MH - Heart Failure/*blood/drug therapy MH - Humans MH - Male MH - Middle Aged MH - Neurotransmitter Agents/*blood MH - Patients/statistics & numerical data MH - Statistics, Nonparametric EDAT- 2002/10/23 04:00 MHDA- 2003/04/23 05:00 CRDT- 2002/10/23 04:00 PHST- 2002/10/23 04:00 [pubmed] PHST- 2003/04/23 05:00 [medline] PHST- 2002/10/23 04:00 [entrez] AID - 3779 [pii] AID - 10.1046/j.1440-1681.2002.03779.x [doi] PST - ppublish SO - Clin Exp Pharmacol Physiol. 2002 Dec;29(12):1060-5. doi: 10.1046/j.1440-1681.2002.03779.x.