December 27, 2001; revised July 4, 2002; accepted August 12, 2002 Chronic heart failure (HF) is a common and debilitating condition with high rates of mortality and morbidity. The prevalence of symptomatic HF in the general European population ranges from 0.4%-2% and is expected to increase as the population ages.1 Commonly, symptom generation in chronic HF was attributed to central hemodynamic alterations, but other factors, such as skeletal muscle changes, may also play a role. The purpose of the present review is to summarize the available data on the widespread abnormalities which skeletal muscle develops in the course of chronic HF, and to discuss how such alterations may be generated and their role in the onset of the typical symptoms of this condition.

Angiotensin‐converting enzyme (ACE) is a zinc metallopeptidase, with primary known functions of converting angiotensin I into the vasoactive and aldosterone‐stimulating peptide angiotensin II and inactivating bradykinin. There is high variability among individuals in ACE concentrations, mainly due to the presence of a genetic polymorphism. The ACE gene has, in fact, insertion/deletion polymorphism in intron 16, consisting of a 287‐base pair Alu repeat sequence, with three genotypes: insertion polymorphism, insertion/deletion polymorphism, and deletion polymorphism. The genetic effect accounts for 47% of the total variance of serum ACE. The determination of this polymorphism has allowed researchers to study the implications of the ACE gene in many case‐control studies of cardiovascular disease, including myocardial infarction and hypertrophic and dilated cardiomyopathy. We review the current knowledge about the ACE gene polymorphism and its implications in heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Interpretation of the results of studies about the role of this polymorphism are controversial. The repetition of epidemio‐genetic studies and the creation of adequate experimental studies will help to definitively establish the pathogenetic role of the permanent increase in ACE expression associated with the deletion polymorphism genotype.

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