Genetic predictors of myocardial remodeling and cardiac performance in hypertension

The objective of the study is to analyze the clinical, physiological and genetic aspects of left ventricular myocardial remodeling in hypertensive disease, considering the average daily load on myocardial muscles and to clarify the correlation of candidate gene polymorphism (ACE, AGT, NOS3 and ADRA2B) with various types of myocardial remodeling. Materials and methods. We examined 255 patients with hypertension (stage 1-2) with and without left ventricular hypertrophy (LVH). The study enrolled 158 women (aged 64±10), and 97 men (aged 60±10). Hypertrophy was diagnosed for not less than 6 months. No regular therapy was conducted. The protocol included patient intake, taking height and weight measurements, blood pressure and heart rate check, daily monitoring of blood pressure and ECG, biochemical blood test, echocardiography, and genetic analysis. Results. Patients with LVH, compared with patients without LVH, demonstrated a significant decrease in myocardial work (both overall performance and intensity of the myocardium), increasing in severity: from eccentric to concentric hypertrophy and concentric remodeling. Patients with LVH have decreased ability to maintain daily average blood pressure in the wall of the main arteries. We considered correlation of candidate gene polymorphism (ACE, AGT, NOS3 and ADRA2B) with a specific type of myocardial remodeling. According to the occurrence of genotypes II and ID (ACE gene), hypertensive patients with remodeled myocardium significantly differ from the controls represented by a population sample of Novosibirsk residents. Hypertensive patients with the alleles of the ACE II and ADRA2B II genes are prone to concentric remodeling of the myocardium. Conclusion. Different types of structural myocardial changes, which are observed in some patients with essential hypertension, are caused by a genetic predisposition to specific remodeling of the heart muscle in response to an increased hemodynamic load.