Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics
Print ISSN : 0300-9173
Effect of Antihypertensive Treatment in Elderly Hypertensive Patients with Cardiac Hypertrophy
Noriko NaganoMasahiro NaganoHaruhiko IwatsuboTakeshi HataHiroshi MikamiToshio Ogihara
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1992 Volume 29 Issue 6 Pages 457-462


In elderly hypertensive patients effect of antihypertensive treatment with Ca antagonist or ACE inhibitor on the heart were examined. Twenty-four elderly hypertensive patients with cardiac hypertrophy, aged 65-79 years old (mean±SEM, 71±1) were treated with Ca antagonist (nifedipine or nicardipine) or ACE inhibitor (captopril or enalapril) for 3 months. Thirteen patients had essential hypertension (EH: SBP≥160mmHg and DBP≥95mmHg, 70±1 years) and 11 had isolated systolic hypertension (ISH: SBP≥160mmHg and DBP <95mmHg, 74±2 years). Blood pressure (BP) and heart rate were measured every two weeks. In all patients, M-mode echocardiography was performed to measure left ventricular mass index (LVMI) and ejection fraction (EF), and the sympathetic nervous (plasma norepinephrine and epinephrine) and the renin-angiotensin system (plasma renin activity and aldosterone concentration), were assessed before and after 3 months of treatment. BP significantly decreased from 174±3/97±1 to 149± 4/84±2mmHg in EH and from 167±3/82±2 to 144± 4/74±2mmHg in ISH. LVMI was significantly reduced from 204±14 to 174±16g/m2 in EH and from 179±14 to 156±12g/m2 in ISH. EF showed no significant changes in either group. In ISH, the change in LVMI was significantly correlated with the change in systolic BP (r=0.74, p<0.05). In EH, there was no significant relation between BP and LVMI changes. The changes in circulatory hormones and those in LVMI did not correlate. In these elderly hypertensive patients, the antihypertensive treatment with Ca antagonist or ACE inhibitor decreased BP sufficiently with monotherapy, and reduced cardiac hypertrophy without any deterioration of left ventricular function in either EH or ISH. It was suggested that the reduction of systolic pressure load might contribute to the reversal of cardiac hypertrophy in ISH.

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