Association between transforming growth factor-beta(1) and left ventricular mass and diameter in hypertensive patients.

Angiotensin II influences development of left ventricular hypertrophy (LVH) by stimulating cardiomyocyte hypertrophy, fibroblast proliferation, and collagen synthesis. Because pro-fibrotic actions of angiotensin may be mediated by increased production of transforming growth factor-beta(1) (TGF-beta(1)), we assessed whether serum TGF-beta(1) levels might reflect involvement in LVH development. We analyzed relationships between left ventricular mass and levels of renin, aldosterone, and TGF-beta(1) in 67 hypertensive subjects (mean age 64 +/- 11.3 years) with electrocardiographic evidence of LVH. Levels were obtained after a 2-week washout of antihypertensive medications; two-dimensional echocardiography was subsequently performed. Linear regression analysis showed a correlation between TGF-beta(1) and LV mass (r = 0.36, P = .002). This was apparently explained by the correlation between TGF-beta(1) and left ventricular diastolic internal diameter (r = 0.42, P < .001), because no correlation between TGF-beta(1) levels and LV wall thickness was found. In multivariate analysis, the correlation between TGF-beta(1) and internal diameter remained significant (r = 0.39, P = .0014). There were no racial differences in levels of TGF-beta(1) or left ventricular geometry, and no correlations between age, blood pressure, renin, aldosterone, and left ventricular mass or dimensions. These findings indicate that serum TGF-beta(1) levels are related to left ventricular structure in hypertensive subjects, suggesting its possible involvement in the process of hypertensive left ventricular remodeling.