Determinants of left ventricular hypertrophy in hypertensive subjects that have never been treated: role of the sodium intake

Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.