The role of clinical and genetic factors in the progression of hypertrophy of the left ventricular myocardial in arterial hypertension

Abstract

Introduction. A special position among the structural changes of the heart is occupied by left ventricular myocardial hypertrophy (LVH), which refers to the subclinical signs of heart damage in arterial hypertension (AH). Currently, the role of not only demographic, neuroendocrine, but also genetic factors in the development and progression of LVH is no longer in doubt.Aim. To assess the role of clinical and genetic factors in the progression of LVH in patients with hypertension based on the results of a dynamic 5-year follow-up of a cohort of Shors.Materials and methods. The survey of the indigenous population in Gornaya Shoria was carried out in two time periods: onetime (from 2013 to 2017) and prospective (from 2018 to 2020). The study included the adult population (18 years and older) – a total of 901 people – by continuous method. A group of patients with hypertension was identified – 367 people (40.7%). LVH was assessed by electrocardiography and/or echocardiography. The prospective stage of the study included patients with hypertension who had not previously received antihypertensive therapy (263 people). The control and correction of blood pressure numbers was carried out annually, the dynamics of LVH was assessed after five years.Results. Clinical predictors of negative dynamics of LVH were established: obesity (OR = 3.61), abdominal obesity (OR = 4.11), impaired carbohydrate metabolism (OR = 2.83), low high-density lipoprotein cholesterol (OR = 2.05). Genetic markers also demonstrated their involvement in the progression of LVH: allele D of the ACE gene, allele C of the AGTR1 gene, and 4a of the eNOS gene (OR = 9.69; OR = 6.72; OR = 6.37, respectively).Conclusion. The associations of clinical and genetic factors with LVH identified in the Shor cohort can be considered as predictors of myocardial remodeling in hypertension. The data obtained support the hypothesis that polymorphisms of the renin-angiotensin-aldosterone system and endothelial function can influence the phenotype, creating new approaches to the possible prediction of unfavorable outcomes.