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Obesity predisposes to LV dysfunction and heart failure and myocardial fibrosis might be an important contributor. We sought the effects of spironolactone on LV function and serological fibrosis markers: procollagen type III amino-terminal propeptide (PIIINP) and procollagen type I carboxy-terminal propeptide (PICP) in patients with obesity.Methods: We recruited 113 pts (age 58±8 yrs) with BMI ≥30, without any comorbidities, who were randomized to spironolactone 25mg/d or placebo for 6 months. Each pt underwent baseline and follow-up echo with evaluation of LV systolic (strain and strain rate, SR) and diastolic function (tissue E velocity, Em and E/e' ratio), myocardial reflectivity (calibrated integrated backscatter, cIB) and serum PICP and PIIINP estimation.Results: In the group assigned to spironolactone, significant improvement in strain SR, Em, E/e' and cIB was noted with simultaneous decrease in PICP and PIIINP. No corresponding alterations were found with placebo. In multivariable analysis, the independent correlates of LV systolic function improvement (increase in strain) were: baseline strain (β=-0.43, p<0.001), change in cIB (β=0.26, p<0.02) and baseline PICP (β=0.24, p<0.04). LV diastolic improvement (increase in Em) was independently predicted by baseline Em (β=-0.44, p<0.001) and baseline PICP (β=0.35, p<0.002). Change in PICP was associated with improvement in E/e' (β=0.25, p<0.04).Conclusion: In patients with obesity,aldosterone antagonism improves LV function and myocardial acoustic properties, and reduces circulating procollagen levels. The degree of benefit on myocardial performance is determined by baseline LV dysfunction and fibrosis intensity, as well its response to therapy.