Angiotensin-Converting Enzyme in the Human Heart

TLDR

An insertion/deletion polymorphism of the ACE gene is linked to altered plasma ACE levels and increased risk of myocardial infarction, cardiomyopathy, left‑ventricular hypertrophy, and coronary artery disease. The study measured cardiac ACE activity and genotype in 71 autopsy subjects who died of noncardiac disorders. Cardiac ACE activity was significantly higher in individuals with the DD genotype than in those with ID or II genotypes, independent of sex, age, and tissue‑collection time, indicating that elevated ACE activity may raise angiotensin II levels and contribute to cardiovascular risk.

Abstract

Background An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with differences in the plasma levels of ACE as well as with myocardial infarction, cardiomyopathy, left ventricular hypertrophy, and coronary artery disease. Methods and Results We determined the cardiac ACE activity and the ACE genotype in 71 subjects who died of noncardiac disorders. Cardiac ACE activity was significantly higher ( P <.01) in subjects with the ACE DD genotype (12.7±1.9 mU/g wet wt) compared with subjects with the ID (8.7±0.8 mU/g) and the II (9.1±1.0 mU/g) genotypes. This difference was independent of sex, age, and the time required for tissue collection. Conclusions Cardiac ACE activity is highest in subjects with the DD genotype. Elevated cardiac ACE activity in these subjects may result in increased cardiac angiotensin II levels, and this may be a mechanism underlying the reported association between the ACE deletion polymorphism and the increased risk for several cardiovascular disorders.