Abstract

The aim of the present study was to investigate the effects of converting enzyme inhibition by captopril on ECG parameters in aged rats. Four-month-old male rats received captopril dissolved in tap water (0.5 mg/l) or tap water for 2 or 20 months. At the end of treatment, under anesthesia, RR and PR interval, P wave and QRS duration, QT and corrected QT interval were measured in all animals. On the following day, chronic ECG (lead II) recordings were performed to quantify supraventricular (SVPB) or ventricular premature beats (VPB). After sacrifice, the hearts were removed and weighed. RR interval was similar in young and untreated aged rats, but significantly larger in aged rats treated with captopril. P wave and QRS length did not differ among groups. PR interval was significantly larger in old than in young rats and was not affected by captopril. Corrected QT interval was larger in aged than in young rats (117 +/- 4 vs 64 +/- 6 ms, P<0.05) and was reduced by captopril (71 +/- 6 ms, P<0.05). VPB were absent in young rats and highly frequent in untreated old animals (8.4 +/- 3.0/30 min). Captopril significantly reduced VPB in old rats (0.3 +/- 0.1/30 min, P<0.05). The cardiac hypertrophy found in untreated aged rats was prevented by captopril (3.44 +/- 0.14 vs 3.07 +/- 0.10 mg/g, P<0.05). The beneficial effects of angiotensin converting enzyme inhibition on the rat heart during the aging process are remarkable.

Highlights

  • Several electrocardiographic (ECG) indices have been proposed to identify patients at risk of sudden death, including the QT interval length and/or dispersion [1,2,3]

  • Untreated aged rats were significantly heavier than untreated young rats (512 ± 22 vs 460 ± 15 g, P

  • The remarkable attenuation of the pressor response produced by angiotensin I demonstrated the efficacy of angiotensin converting enzyme (ACE) blockade by captopril

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Summary

Introduction

Several electrocardiographic (ECG) indices have been proposed to identify patients at risk of sudden death, including the QT interval length and/or dispersion [1,2,3]. Other vasoactive peptides can be modified by ACE inhibitors, especially bradykinin, which is potentiated by ACE blockage [12,13] These effects elicit a decrease in arterial pressure in several experimental models of hypertension and clinical forms of human hypertension as well [12,13]. These drugs improve cardiac performance in patients with congestive heart failure, reducing cardiovascular risk and mortality [12,13]

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