Response to Hyperaldosteronism and Left Ventricular Hypertrophy
We would like to thank Sechi et al1 for their interest in our recently published study “Rapid Reversal of Left Ventricular Hypertrophy and Intracardiac Volume Overload in Patients With Resistant Hypertension and Hyperaldosteronism: A Prospective Clinical Study”2 and insightful comments.
As they rightly point out, the lack of difference in left ventricular (LV) mass is perplexing. We believe that this might be related to this study group (both high-aldosterone patients and normal-aldosterone patients) being on multiple antihypertensive medications, including long-term renin angiotensin aldosterone system blockers. There is no doubt that the rapid regression of LV mass was related in part to the blood pressure reduction. However, reduction in intracardiac volumes, particularly in the patients with high aldosterone in our study group, is likely to have provided supplemental LV mass regression in addition to blood pressure effect, as clearly demonstrated by an equal decrease in blood pressure in both groups but an increased regression in cardiac volumes and LV mass in the high aldosterone group. MRI is more accurate than 2D echocardiography in measuring cardiac volumes, thus facilitating detection of subtle but significant alterations in intracardiac volume status, as shown in our study.
Numerous studies have shown that LV hypertrophy is an important predictor of major cardiovascular events, and LV mass regression had served as an important surrogate end point in various antihypertensive studies. Our study findings clearly demonstrate a significant decrease in LV mass with the use of aldosterone antagonist in all patients with resistant hypertension although more so in the high-alodsterone group, thus demonstrating benefit of aldosterone blockade regardless of underlying aldosterone status. Whether this reduction in LV mass translates to reduction in cardiovascular events in this high-risk population remains to be studied.
Sources of Funding
This study was supported by NHLBI SCCOR P50 HL077100 (D.A.C.), R01-HL79040 (D.A.C.), T32 HL007457 (K.G.) and GCRC Grant M01-RR00032.
Sechi LA, Colussi G, Catena C. Hyperaldosteronism and left ventricular hypertrophy. Hypertension. 2010; 56: e26.
Gaddam K, Corros C, Pimenta E, Ahmed M, Denney T, Aban I, Inusah S, Gupta H, Lloyd SG, Oparil S, Husain A, Dell'Italia LJ, Calhoun DA. Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: a prospective clinical study. Hypertension. 2010; 55: 1137–1142.