Association between a Deletion Polymorphism of the Angiotensin-Converting-Enzyme Gene and Left Ventricular Hypertrophy

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Abstract
The report by Schunkert et al. (June 9 issue)1 was intriguing, but it did not elaborate on why the effect of the DD genotype of the angiotensin-converting-enzyme (ACE) gene on the development of left ventricular hypertrophy was stronger in normotensive subjects than in hypertensive patients. On this subject, we previously reported2 that the association between plasma ACE activity and the ACE genotypes is observed in normotensive subjects, but not in hypertensive patients, and that plasma ACE activity in hypertensive patients with the II, ID, and DD genotypes is similar to that in normotensive subjects with the DD genotype. Since angiotensin II is known to cause cardiac-cell hypertrophy, the strong effect of the DD genotype on left ventricular hypertrophy in normotensive subjects, but not in hypertensive patients, may result in the clear association between the DD genotype and plasma ACE activity without confounding by high blood pressure, which is a strong causative factor of left ventricular hypertrophy.