Angiotensin-converting enzyme insertion/deletion polymorphism, 24-h blood pressure profile and left ventricular hypertrophy in hypertensive individuals: a cross-sectional study

Abstract

BackgroundThe 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.Methods155 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.ResultsThere 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.ConclusionsThe 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.

Left Ventricular Myocardial Hypertrophy as a Result of Arterial Hypertension Among Mountain Shoria Population. The Role of Genetic Polymorphism

“…(по кодоминантному типу наследования) в когорте некоренного этноса и в 5 раз -у носителей гетерозиготного генотипа I / D в когорте мужчин-шорцев. Целый ряд исследований свидетельствует о большей предрасположенности к развитию ГЛЖ у больных АГ при наличии у них генотипа D / D гена АСЕ[8,[21][22][23]]. Достоверное увеличение частоты обнаружения генотипа D / D у пациентов с ГЛЖ наблюдали Т. Ishigami и соавт.…”

Relationship of renin‐angiotensin system polymorphisms with ambulatory and central blood pressure in patients with hypertension

“…While there have been arguments about these results, several authors support this conclusion. A study by Cosenso‐Martin and colleagues demonstrated that the presence of the D allele appears to be associated with higher mean 24‐hour and daytime SBP in patients with hypertension. Bautista and associates reported that SBP and DBP were 4.58 and 3.32 mm Hg higher in DD homozygous individuals than in carriers of the I allele, and the DD genotype appears to be an independent risk factor for development of hypertension.…”

Hypertension and Cerebral Microangiopathy (Cerebral Small Vessel Disease): Genetic and Epigenetic Aspects of Their Relationship

“…A combination of II+ID alleles of the I/D polymorphism with a daily intake of more than 2,300 mg of salt was found to be associated with HT and subsequent obesity [47]. The D allele of I/D polymorphism was found to be associated with diastolic and systolic HT, daily variability of HT, and injury to target organs [48][49][50][51][52]. The D/D genotype was shown to play a significant role in the development of CMA-associated cerebral lesions [53,54] and in the prediction of the risk of this lesion [55].…”

“…Inhibition of the NOS1 gene in the medulla oblongata and hypothalamus is associated with the pathogenesis of systemic hypertension [57]. A genome-wide association study for Lacunes [35,41], WMH [41] Loss of white matter tract microstructure [46] Not verified [42,45] Found [37,8] Not verified [39,40] AGT rs4762 Not verified [42] Found [37,38] Not verified [39,40] AGT -20A>C WMH [45] Found [45] ACE I/D Alu-sequences WMH [52][53][54][55] Not verified [46] Found [47][48][49][50][51][52] CYP11B2 rs1799998 WMH, expansion of perivascular spaces [36,56] [55,67,68] Found [65,66] PLAT rs2020918 LI [71,72] No data FGB rs1800790 LI [73] No data IL1B rs16944 LI [78], WMH [81] No data IL6 rs1800795 LI [79], WMH [80] Not verified [ [87] No data REVIEWS ischemic stroke risk factors iditified NOS1 as a potential candidate gene…”