Cardiac Consequences of Aldosterone Excess In Human Hypertension

The evaluation of target organ damage (TOD) is a “must” in the clinical assessment of the hypertensive patient.1 The presence of TOD, and particularly of left ventricular hypertrophy (LVH), increases substantively the risk of future cardiovascular events and therefore is a compelling indication for an aggressive lowering of blood pressure (BP).1 In this issue of the American Journal of Hypertension Matsumura et al2 report on their investigation of LVH in two curable forms of hypertension—renovascular hypertension (RVH) and primary aldosteronism (PA). They provide additional evidence supporting the concept that cardiac remodeling in hypertension is not simply the outcome of the raised hemodynamic (after-)load, but deeply involves endocrine and autocrine–paracrine factors. By examining with echocardiography the changes of the left ventricle (LV) occurring in RVH and PA patients, the researchers confirmed earlier reports that patients with these forms of hypertension feature prominent cardiac alterations. They found that patients with RVH had excess LVH, as compared to patients with primary (essential) hypertension (PH), thus confirming the findings of Suzuki et al3 and Vensel et al.4 Moreover, in keeping with data from our laboratory,5 they observed that LVH was especially exaggerated in the patients with PA, as compared to matched PH patients. As a common denominator, patients with RVH and PA share the hyperaldosteronism, either due to autonomous aldosterone production or secondary to activation of the renin-angiotensin system (RAS); however, they exhibit contrasting degrees of activation of the RAS. Therefore, these findings collectively suggest that exposure of the heart to excess aldosterone independent of RAS is crucial for inducing excess LV remodeling and LVH. The observation of a direct correlation between the LV mass index and plasma aldosterone,2 which confirms previous results,6 further supports this suggestion.