Background. Left ventricular mass (LVM) is increased in 20-25% of untreated hypertensive patients and influences cardiovascular morbidity and mortality. It is kept under control by mineralocorticoids, angiotensin II, genetic and emodynamics factors. Association of the renin angiotensin aldosterone system (RAA) genes and sodium sensitivity with LVM has been reported by many authors but it remains controversial for the small sample size of the cohorts studied and for the study design (methodology and stratification, genetic heterogeneity).
Aim of the study. To assess the cardiovascular events as a function of genotype (RAA system genes and sodium sensitivity) and of LVM on a large cohort of untreated, genetically homogeneus esssential hypertensive patients. We studied on 473 patients
Methods. n=473 untreated, genetically homogeneous essential hypertensive patients were studied (age: 47.3 ± 9.8 old); M/F: 257/172; BP at the time of first visit: 156 mmHg ). All patients’ data were recorded on electronic file.
Results. The A1166C polymorphism of the AT1R gene was found associated with LVM. No association between the genes under study and cardiovascular events was found even when they were analysed as a function of cardiac mass.
Conclusions. our data confirm that LVM is a determinant of cardiovascular damage and indicate that association studies do not have the potential to reveal the genetic component of cardiovascular events
