HDCN Article Review/Hyperlink

Rossi GP, Sacchetto A, Visentin P, Canali C, Graniero GR, Palatini P, Pessina AC

Changes in left ventricular anatomy and function in hypertension and primary aldosteronism

Hypertension (May) 27:1039-1045 1996

The role of the renin-angiotensin system in the pathogenesis of cardiac hypertrophy has been the subject of intense investigation over the past 5 years. One hypothesis is that angiotensin II may directly stimulate myocardial cell hypertrophy directly, as experimental models have shown, thereby leading to left ventricular hypertrophy. These observations have led to the hypothesis that reducing left ventricular hypertrophy by interfering with angiotensin II formation or blockade of the AII type 1 receptor may in turn reduce mortality in subjects with left ventricular hypertrophy, a powerful risk factor for sudden cardiac death. Indeed, a major clinical trial utilizing the AII type I receptor blocker losartan, is now underway. Recent observations also suggest the possibility that aldosterone may directly influence cardiac function through growth promoting effects on cardiac connective tissue, specifically cardiac fibroblasts which produce collagen type III.

In this regard, Rossi and colleagues compared cardiac mass (2D echocardiograph) and estimates of left ventricular filling (color doppler) in 34 patients with primary aldosteronism (PA) and 34 patients with essential hypertension (EH) matched for age, sex, BMI, degree and duration of hypertension and potassium intake. They also measured these parameters before and one year after surgical correction in 19 patients and after 1 year of medical therapy alone in 6 patients with PA. They found that patients with PA had greater degree of left ventricular hypertrophy and lower intracardiac flow velocity as compared to EH patients. Moreover, impaired ventricular diastolic filling was noted in PA patients and the atrial contribution to LV filling was noted to be increased in PA as compared to EH patients. After one year, LV mass was significantly reduced in post-surgically treated but not in medically treated PA patients. The increased LVH and reduced flows were positively correlated with plasma aldosterone concentration, diastolic and systolic blood pressures.

The authors concluded that hyperaldosteronism with suppression of the renin-angiotensin system is associated with increased degree of LVH and impaired diastolic function. They speculate that high concentration of aldosterone may contribute to this effect possibly by altering cardiac extracellular matrix through changes in fibroblast and collagen.

Comment: The study raises the intriguing possibility that aldosterone could alter cardiac function independent of angiotensin II as previous studies have suggested. It is noteworthy that patients with PA had longer mean duration of hypertension (111 vs 77 months, NS) and that sodium excretion rates were not compared. It is possible that differences in duration of hypertension and/or differences in volume could have produced these effects. Still, the comparison of post-op versus medically treated patients showing the regression of LVH in the former but not in the latter is quite interesting. It will be interesting to see if indeed aldosterone emerges as an important hormone in cardiac remodeling in humans. (Robert D. Toto, M.D., University of Texas Southwestern Medical Center)