title: Both a calcium antagonist and ACE inhibitor reverse hypertrophy in hypertension but a calcium antagonist also depresses contractility.
abstract: The aim of this study was to compare the effects of a calcium antagonist, nicardipine SR, with an angiotensin-converting enzyme (ACE) inhibitor, alacepril, on the regression of left ventricular hypertrophy (LVH) and function. Twenty patients with LVH, aged 42-78 years, were treated with nicardipine SR or alacepril. Ten patients were treated with nicardipine SR (40-80 mg) for 21 months, and the other 10 patients were treated with alacepril (25-100 mg) for 18 months. All patients underwent echocardiography to assess left ventricular structure and function before and after the treatment. After nicardipine SR or alacepril treatment, blood pressure was decreased significantly from 176.0 +/- 13.9/97.0 +/- 5.3 mmHg to 140.0 +/- 14.0/77.4 +/- 7.2 mmHg and from 168.2 +/- 22.3/99.0 +/- 5.5 mmHg to 138.4 +/- 12.5/85.2 +/- 9.7 mmHg, respectively (both p < 0.01), whereas heart rate did not change (73.8 +/- 14.6 beats/min vs. 69.9 +/- 13.5 beats/min and 71.6 +/- 9.7 vs. 65.8 +/- 8.1 beats/min, respectively). The left ventricular mass index decreased significantly from 133.2 +/- 11.7 g/m2 to 114.4 +/- 15.7 g/m2 with nicardipine SR and from 137.1 +/- 14.8 g/m2 to 99.3 +/- 23.0 g/m2 with alacepril (both p < 0.01). The fractional shortening, peak shortening rate, and peak lengthening rate all improved significantly after each treatment. The end-systolic wall stress/left ventricular end-systolic volume index, as an index of left ventricular contractility, was decreased significantly after treatment with nicardipine SR but was not changed after treatment with alacepril. In conclusion, both nicardipine SR and alacepril similarly reduced LVH and improved left ventricular systolic and diastolic function. However, alacepril did not alter left ventricular contractility, whereas nicardipine SR decreased left ventricular contractility.
authors.affiliation: Second Department of Internal Medicine, Ehime University, School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sumimoto
authors.forename: T
authors.initials: T
authors.lastname: Ochi
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Joh
authors.forename: S
authors.initials: S
authors.lastname: Muneta
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000009:adverse effects* / Q000627:therapeutic use*; D002216:Captopril / Q000031:analogs & derivatives / Q000627:therapeutic use; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects*; D009529:Nicardipine / Q000627:therapeutic use; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D002216:Captopril; D009529:Nicardipine; C046835:alacepril