The DD genotype of the ACE insertion/deletion polymorphism was associated with an increased risk of left ventricular hypertrophy (OR 5.80) compared to the II genotype in hypertensive patients.
Cross-Sectional (n=155)
No
Is the ACE gene insertion/deletion polymorphism associated with altered 24-h blood pressure profiles and left ventricular hypertrophy in treated non-diabetic hypertensive individuals?
The ACE DD genotype is associated with higher systolic blood pressure and a greater prevalence of left ventricular hypertrophy in treated hypertensive patients.
Effect estimate: OR 5.80 (95% CI 1.50-22.44)
Absolute Event Rate: 46.5% vs 13%
p-value: p=0.011
BACKGROUND: The absence of nocturnal blood pressure dipping (ND) identified by 24-h ambulatory blood pressure monitoring (ABPM) correlates with a worse cardiovascular prognosis. The renin-angiotensin system influences blood pressure levels and the occurrence of target organ damage (TOD). Thus, the aim of this study was to correlate the angiotensin-converting enzyme gene (ACE) insertion/deletion (I/D) polymorphism with the 24-h blood pressure profile and TOD in hypertensive individuals. METHODS: 155 non-diabetic hypertensive individuals on antihypertensive treatment underwent ABPM. Peripheral blood samples were drawn for biochemistry and genetic analysis of the ACE I/D polymorphism by polymerase chain reaction. ND was defined as ≥10 % differences in the mean systolic blood pressure (BP) during wakefulness and sleep. RESULTS: There were no differences in clinical or biochemical variables or TOD in respect to ND status, except for higher BP levels during sleep (p < 0.001) in non-dippers. There was significant difference in the prevalence of left ventricular hypertrophy (LVH) between ACE genotypes (II: 13.0 %; ID: 34.1 %; DD: 46.5 %; p value = 0.024) with an increased risk in carriers of the DD genotype (OR = 5.80; IC 95 % 1.50-22.44; p value = 0.011). Carriers of the D allele had higher systolic BP during wakefulness and by ABPM (p < 0.05), higher left ventricular mass (117.3 ± 50.0 vs. 100.3 ± 25.7; p value = 0.017) and higher prevalence of LVH (37.4 vs. 12.5 %; OR = 4.14; 95 % IC: 1.17-14.65; p value = 0.028), compared to the II genotype. CONCLUSIONS: The DD genotype is associated with a higher prevalence of LVH. The presence of the D allele appears to be associated with higher mean 24-h and wake systolic BP measured by ABPM in hypertensive patients under antihypertensive treatment.
Cosenso‐Martin et al. (Thu,) conducted a cross-sectional in Hypertension (n=155). ACE DD genotype vs. ACE II genotype was evaluated on Left ventricular hypertrophy (OR 5.80, 95% CI 1.50-22.44, p=0.011). The DD genotype of the ACE insertion/deletion polymorphism was associated with an increased risk of left ventricular hypertrophy (OR 5.80) compared to the II genotype in hypertensive patients.