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Effects of long-term treatment with sustained-release nicardipine on left ventricular hypertrophy and function in patients with essential hypertension.

作者信息

Sumimoto T, Hiwada K, Ochi T, Matsubara W, Joh T, Imamura Y

机构信息

Second Department of Internal Medicine, Ehime University School of Medicine, Japan.

出版信息

J Clin Pharmacol. 1994 Mar;34(3):266-9. doi: 10.1002/j.1552-4604.1994.tb03997.x.

DOI:10.1002/j.1552-4604.1994.tb03997.x
PMID:8021336
Abstract

The effects of long-term treatment with sustained-release nicardipine (nicardipine SR) on left ventricular hypertrophy and function were studied. Ten uncomplicated essential hypertensive patients with left ventricular hypertrophy, aged 61 +/- 7.6 years old, were treated with nicardipine SR alone for an average of 20 months (range: 12-26 months). All patients underwent echocardiography for assessment of left ventricular diameters and function before and after the treatment. At the end of the treatment, systolic and diastolic blood pressures significantly decreased from 176.0 +/- 13.9 to 140.0 +/- 14.3 mm Hg and from 97.0 +/- 5.3 to 77.4 +/- 7.2 mm Hg, respectively (each P < 0.01), while heart rate did not change (73.8 +/- 14.6 vs. 69.9 +/- 13.5 beats/min). The left ventricular mass index significantly decreased from 132.1 +/- 14.4 to 114.4 +/- 15.7 g/m2 (P < 0.01) due to significant reductions in both interventricular septal thickness (P < 0.01) and left ventricular posterior wall thickness (P < 0.05). The ejection fraction (EF), fractional shortening (FS), peak shortening rate (PSR), and peak lengthening rate (PLR) were also improved significantly by the treatment (EF and FS, P < 0.05; PSR and PLR, P < 0.01). Significant inverse relationships existed between end-systolic wall stress and peak shortening or lengthening rate before the treatment (r = 0.80, P < 0.05; r = 0.86, P < 0.05, respectively). These relationships were unchanged after the treatment. Nicardipine SR reduced left ventricular hypertrophy and improved both left ventricular systolic and diastolic functions without causing any consistent augmentation of intrinsic left ventricular function in essential hypertensive patients with left ventricular hypertrophy.

摘要

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