ASSOCIATION OF ANGIOTENSINOGEN M235T AND ANGIOTENSIN CONVERTING ENZYME I/D POLYMORPHISMS WITH HYPERTENSION-MEDIATED CARDIAC, CAROTID DAMAGE AND DYSLIPIDEMIA

Abstract

Objective: Uncontrolled essential hypertension (EHT) may cause left ventricular hypertrophy (LVH), carotid atherosclerosis (ATS) and increased intima media thickness (cIMT). The renin-angiotensin aldosterone system polymorphism could be associated with uncontrolled EHT. We analyze the relationship of M235T (angiotensinogen-AGT gene) and I/D (angiotensin converting enzyme-ACE gene) polymorphisms with carotid ATS, LVH and dyslipidemia as possible risk factors for ischemic cardiac events in EHT. Design and method: We included 153 patients with EHT. We collected data concerning BMI, triglyceride (TG), LDL cholesterol (LDL-C) levels. We performed cardiac and carotid ultrasound for LVH, carotid ATS presence, cIMT value. Genotype was determined using PCR and restriction fragment length polymorphism. Statistical analysis was performed using the EpiInfo7 software. Results: 69.93% of hypertensive patients were carriers of the M235T-AGT polymorphism, of which 67.3% were heterozygous. The prevalence of I/D-ACE in hypertensive patients was 62.6%, of which 59.4% was represented by carriers of the homozygous DD genotype. 7.84% of patients with EHT were homozygous for both genetic variations. 75.7% of carriers of the M235T-AGT polymorphism had LDL-hypercholesterolemia (HC), 44.8% had hypertriglyceridemia (HTG). Patients with HTG, carriers of the M235T-AGT, had a 2.58-fold increased risk (p < 0.007) to develop EHT. The presence of LVH, carotid ATS and c-IMT>1 mm was in 65.4%, 46.7% and 44% of hypertensive patients positive for the M235T-AGT polymorphism. Hypertensive patients with carotid ATS, carriers of the M235T-AGT polymorphism, had a 1.8-fold (p < 0.05) increased risk to develop ESH. The presence of c-IMT>1 mm showed a correlation trend without statistical significance (OR-1.7, p < 0.06). 69.2% of hypertensive patients, carriers of the I/D-ACE polymorphism, had LDL-HC, 37.3% had HTG. We evidenced the presence of LVH, carotid ATS and c-IMT>1 mm in 67%, 39.5% and 39.5% of hypertensive patients positive for the M235T-AGT polymorphism. Hypertensive patients with LDL-HC, carriers of the M235T-AGT polymorphism, had a 0.3-fold increased risk (p < 0.005) to develop EHT. LVH showed a correlation trend without statistical significance (OR-1.67, p < 0.06). Conclusions: Patients with EHT, carriers of the M235T-AGT polymorphism, presented HTG and carotid ATS as potential risk factors for ischemic cardiac events. Association between I/D-ACE polymorphism and LDL-HC is a protective factor for EHT.