Impact of mineralocorticoid receptor antagonists on changes in cardiac structure and function of left ventricular dysfunction: a meta-analysis of randomized controlled trials.

Background-A comprehensive evaluation of the benefits of mineralocorticoid receptor antagonists on cardiac remodeling is lacking. We aimed to evaluate the impact of mineralocorticoid receptor antagonists on changes in cardiac structure and function of left ventricular dysfunction. Methods and Results-Articles were identified by online searches in PubMed, EMBASE, Cochrane, and ClinicalTrials.gov databases before June 2012, by hand searches of reviews and relevant journals, and by contact with the authors. Qualified articles were restricted to randomized controlled trials. There were, respectively, 12, 4, and 3 qualified trials that randomized 572, 647, and 407 patients to spironolactone, canrenoate, and eplerenone, and 531, 655, and 395 patients to placebo or active treatment, respectively. Overall, under mineralocorticoid receptor antagonist treatment there was improvement in left ventricular ejection fraction (weighted mean difference, 2.97; 95% confidence interval [ 95% CI], 2.26-3.67; P<0.0005), left ventricular end-systolic and end-diastolic volume index (weighted mean difference, -5.64; 95% CI, -7.94 to -3.34; P<0.0005 and weighted mean difference, -7.46; 95% CI, -11.63 to -3.3; P<0.0005), serum amino-terminal peptide of procollagen type-III (weighted mean difference, -1.12; 95% CI, -1.49 to -0.74; P<0.0005), B-type natriuretic peptide (weighted mean difference, -67.06; 95% CI, -91.24 to -42.88; P<0.0005), peak velocities of early mitral inflow (E; weighted mean difference, -9.57; 95% CI, -12.98 to -6.17; P<0.0005), and E wave deceleration time (weighted mean difference, 7.08; 95% CI, 4.07-10.09; P<0.0005). There was low probability of heterogeneity and publication bias. Conclusions-Our findings demonstrate that mineralocorticoid receptor antagonist treatment may exert beneficial effects on the reversal of cardiac remodeling and improvement of left ventricular function.