J. Mayet et al., LEFT-VENTRICULAR HYPERTROPHY, BLOOD-PRESSURE AND ACE GENOTYPE IN UNTREATED HYPERTENSION, Journal of human hypertension, 11(9), 1997, pp. 595-597
It has been suggested that the deletion polymorphism of the angiotensi
n-converting enzyme (ACE) genotype may be important in the development
of left ventricular hypertrophy (LVH). In order to test this hypothes
is we investigated the interaction between blood pressure (BP), LVH an
d ACE genotype in 86 previously untreated hypertensive patients, Each
underwent two-dimensional and Doppler echocardiography and ACE genotyp
ing. There were no significant differences in BP, the parameters of le
ft ventricular structure (including left ventricular mass index) or di
astolic function between the three genotype groups, Additionally, ther
e were no significant differences in the relationship between systolic
BP and left ventricular mass index among the three genotype groups (I
I genotype, r=0.46, P=0.02; ID genotype, r=0.42, P=0.01; DD genotype,
r=0.34, P=0.10; F=0.38). In contrast to some previous studies, we have
found in this group of previously untreated hypertensive subjects no
evidence to suggest that the deletion polymorphism of the ACE genotype
is important in the development of LVH.