The relationship between blood pressure and left ventricular mass in essential hypertension is observed only in the presence of the angiotensin-converting enzyme gene deletion allele.
An insertion/deletion polymorphism in the angiotensin-converting enzyme (ACE) gene accounts for approximately 50% of the variance in plasma ACE concentration: deletion homozygotes (DD) have the highest, and insertion homozygotes (II) the lowest ACE concentrations. ACE is responsible for the generation of angiotensin II, which is implicated in the development of left ventricular hypertrophy, an independent risk factor for morbidity and mortality in hypertension. The aim of this study was to investigate the contribution of ACE genotype to the development of left ventricular hypertrophy in patients with essential hypertension. Eighty-five patients with essential hypertension underwent echocardiographic assessment of left ventricular mass index (LVMI) and determination of ACE genotype from leukocyte DNA by polymerase chain reaction. There was no significant difference in LVMI among the genotypes (II, ID, DD). Analysis of covariance modelled for LVMI showed a significant interaction with systolic blood pressure (p = 0.036) but not diastolic blood pressure (p = 0.453). The relationship between LVMI and systolic blood pressure was strongest in the deletion homozygotes (p = 0.002, R2 = 0.47), and also present in the heterozygotes (p = 0.013, R2 = 0.40). No relationship was seen in the insertion homozygotes (p = 0.914, R2 = 0.23). These findings suggest that the effect of blood pressure on LVMI in essential hypertension is expressed only in the presence of the ACE gene deletion allele.
Prasad
N
N
Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee, UK.
O'Kane
K P
KP
Johnstone
H A
HA
Wheeldon
N M
NM
McMahon
A D
AD
Webb
D J
DJ
MacDonald
T M
TM
D000483:Alleles; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000235:genetics; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D017384:Sequence Deletion; D013599:Systole
D007703:Peptidyl-Dipeptidase A