F. Perticone et al., DELETION POLYMORPHISM OF ANGIOTENSIN-CONVERTING ENZYME GENE AND LEFT-VENTRICULAR HYPERTROPHY IN SOUTHERN ITALIAN PATIENTS, Journal of the American College of Cardiology, 29(2), 1997, pp. 365-369
Objectives. This study sought to evaluate the possible association of
polymorphism of the angiotensin converting enzyme (ACE) gene with bloo
d pressure and left ventricular mass index (LVMI). Background. The ren
in-angiotensin system seems to be involved in the pathogenesis of esse
ntial hypertension, Moreover, recent epidemiologic observations demons
trate that many subjects with left ventricular hypertrophy have normal
blood pressure levels, suggesting that factors other than hemodynamic
overload may contribute to the hypertrophy. Methods. The study includ
ed 140 untreated hypertensive out-patients who underwent ambulatory bl
ood pressure monitoring, echocardiographic evaluation and analysis for
insertion (I)/deletion (D) polymorphism in intron 16 of the ACE gene
by polymerase chain reaction, Blood pressure was measured at 24 h, and
LVMI was calculated by the Devereux formula, in each patient. Resuls.
Left ventricular mass index values (mean +/- SD) mere 137 +/- 28 g/m(
2) in patients with the DD genotype, 125 +/- 27 g/m(2) in those with t
he ID genotype and 115 +/- 27 g/m(2) in those with II genotype, The fr
equencies of the DD, ID and II genotypes were 45.71% (n = 64), 46.42%
(n = 65) and 7.85% (n = 11), respectively, and were in Hardy-Weinberg
equilibrium, The strongest association between left ventricular mass a
nd DD genotype in our cohort appeared to be an independent cardiovascu
lar risk factor (DD vs, ID: odds ratio [OR] 2.497, 95% confidence inte
rval [CI] interval 1.158 to 5.412, p < 0.05; DD vs. II: OR 6.577, 95%
CI 1.169 to 28.580, p < 0.02). Conclusions. Our data show that the LVM
I was significantly enhanced in patients with the DD genotype. (C) 199
7 by the known College of Cardiology.