Circulation, Vol 90, 2457-2467, Copyright © 1994 by American Heart Association
KC Wollert, R Studer, B von Bulow and H Drexler
BACKGROUND--Chronic treatment with high doses of angiotensin-converting
enzyme (ACE) inhibitors prolongs survival after myocardial infarction.
Since the plasma renin-angiotensin system (RAS) is not consistently
activated in the chronic phase after myocardial infarction, the beneficial
effects of ACE inhibition have been attributed, in part, to inhibition of
an activated tissue RAS. However, a relation between tissue ACE inhibition
and long-term efficacy (ie, concerning left ventricular [LV] hypertrophy
and survival) has not been established. The present study was designed to
evaluate the impact of low-dose ACE inhibition (predominant inhibition of
plasma ACE) and high-dose ACE inhibition associated with substantial tissue
ACE inhibition) on reversal of LV hypertrophy and 1-year mortality after
myocardial infarction in the rat. METHODS AND RESULTS--Infarcted rats were
randomized to placebo, low-dose lisinopril, or high-dose lisinopril (each,
n = 80) and compared with sham-operated animals (n = 40). In a separate
group of animals, tissue ACE activity was determined after 6 weeks of
therapy, demonstrating that both regimens were effective with regard to
both plasma and pulmonary ACE inhibition; however, only high- dose
lisinopril inhibited renal ACE. Neither dose affected LV ACE activity and
ACE mRNA levels as determined by competitive polymerase chain reaction,
whereas LV ANF mRNA levels were significantly reduced by high-dose
lisinopril. High-dose lisinopril reduced arterial blood pressure and
normalized right ventricular and LV weight and resulted in a substantial
reduction of 1-year mortality, whereas the low dose did not (1 year
mortality: placebo, 56.3%; low dose, 53.3%; high dose, 22.9%, P < .0001
versus low dose and versus placebo). CONCLUSIONS-- Hemodynamically
effective ACE inhibition is required for reduction of LV hypertrophy and
long-term mortality after myocardial infarction in the rat. Sustained
inhibition of renal ACE during long-term therapy may contribute to the
beneficial effect of high-dose lisinopril. Low-dose lisinopril, although
exerting sustained inhibition of the plasma ACE, does not improve survival
after myocardial infarction.
ARTICLES
Survival after myocardial infarction in the rat. Role of tissue angiotensin-converting enzyme inhibition
Medizinische Klinik III, Universitat Freiburg, Germany.
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