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Ultrasonic tissue characterization of end-stage dilated cardiomyopathy.

作者信息

Davison G, Hall C S, Miller J G, Scott M, Wickline S A

机构信息

Washington University School of Medicine, St. Louis, MO, USA.

出版信息

Ultrasound Med Biol. 1995;21(7):853-60. doi: 10.1016/0301-5629(95)00036-q.

Abstract

The clinical use of angiotensin-converting enzyme (ACE) inhibitors now represents the standard of care for the treatment of chronic congestive heart failure. We utilized ultrasonic tissue characterization to define potentially salutary effects of treatment with ACE inhibitors on the material properties of the heart and its potential influence on cardiac remodeling at the cellular level. Ten 1-month-old cardiomyopathic (CM) Syrian hamsters were treated with captopril (2 g/L water ad libitum), and 10 CM and 5 normal hamsters were maintained untreated for 9 months. Hearts were excised, and backscattered radio-frequency data were acquired from 1200 independent sites from each specimen with a high-resolution 50-MHz acoustic microscope for calculation of integrated backscatter. Treatment with captopril elicited relative decreases in left ventricular (LV) wet weight, LV calcium concentration and integrated backscatter (IB) in treated as compared with untreated cardiomyopathic hearts without affecting LV collagen concentration. The IB from hearts of treated cardiomyopathic hamsters was significantly less in both grossly normal regions of myocardium (P < 0.02) and scar tissue regions (P = 0.0005) as compared with IB from hearts of untreated hamsters. The reduced integrated backscatter from hearts of treated cardiomyopathic hamsters indicates direct alterations in the material properties of cardiomyopathic hearts after captopril therapy. The lower IB from scar tissue in the treated animals was associated with decreased scar tissue calcification, which represents a novel therapeutic effect of captopril. This is the first report that delineates direct effects of ACE inhibitors on the material properties of both scar tissue and grossly normal myocardium at the cellular level in experimental dilated cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

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