MINIREVIEW
Heart Failure and Angiotensin
Converting Enzyme inhibition: Problems and Perspectives
F. ŠIMKO, J. ŠIMKO
Department of Pathophysiology, Medical Faculty,
and Center of Human Genetics, Faculty Hospital, Bratislava,
Slovak Republic
Received December 22, 1997
Accepted July 22, 1998
Summary
Heart failure has become the most widely studied syndrome in
cardiology over the recent years. Despite the encouraging
achievements by angiotensin converting enzyme (ACE) inhibitors,
the mortality of patients with chronic heart failure remains
high. There are several factors which can potentially be
responsible for the fact that about 80% of patients with a
failing heart defy protection by ACE inhibitors: different
activation of tissue and systemic renin-angiotensin system (RAS)
in a particular heart disease and the distinct ability of
various ACE inhibitors to block cardiac ACE, alternative
pathways for angiotensin II formation (chymase), genetic
polymorphism of the RAS system and the complexity of
neuroendocrine activation. Moreover, chronic heart failure can
provoke disturbances in the reactivity of peripheral vessels and
metabolism of striated muscles. These factors may then
potentiate the vicious circle of heart failure. New therapeutic
approaches, which could further reduce the mortality in patients
with heart failure involve angiotensin II type 1 receptor
antagonists, beta-blockers, aldosterone antagonists and blockers
of the endothelin receptor. A number of questions associated
with functions of the RAS still remain open and their solution
could be of substantial benefit for patients with a failing
heart.
Key words
Heart failure - ACE inhibitors - Angiotensin II receptor
antagonists - Beta-blockers - Local angiotensin II - Chymase -
Neurohumoral activation
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