Abstract 14448: Favourable Effect of Aldosterone Antagonism on Left Ventricular Function and Structure and Collagen Synthesis in the Metabolic Syndrome
Aim: Myocardial fibrosis might be an important contributor to the myocardial impairment associated with the metabolic syndrome (MS). We sought the effects of spironolactone on left ventricular (LV) structure and function in relation to the serological fibrosis markers: procollagen type III amino-terminal propeptide (PIIINP) and procollagen type I carboxy-terminal propeptide (PICP) in patients with the MS.
Methods: We enrolled 79 pts (age 59±11 yrs) satisfying the IDF criteria of MS with a normal stress echo who were randomized to spironolactone 25mg/d or placebo for 6 months. Each pt underwent baseline and follow-up echo with measurement 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 assessment.
Results: In the group allocated to spironolactone, strain SR, Em, E/E′ and cIB improved significantly with concomitant decrease in PICP and PIINP. No analogous changes were seen in the placebo group. In multivariable analysis, the independent associates of LV systolic function improvement (increase in negative strain) were: baseline negative strain (β=0.47, p<0.0001), treatment with spironolactone (β= -0.38, p<0.0001) and change in PICP (β= -0.19, p<0.03). Correlates of LV diastolic function improvement (increase in Em) were baseline Em (β=0.47, p<0.0001), treatment with spironolactone (β= -0.21, p<0.03), change in PICP (β= -0.23, p<0.02) and patient age (β=0.22, p<0.04).
Conclusion: In the MS patients, treatment with spironolactone improves LV function and myocardial acoustic properties, and diminishes serum procollagen levels reflecting the intensity of collagen synthesis. The beneficial effect of aldosterone antagonism on cardiac performance is determined by baseline LV function and the degree of collagen anabolism reduction as indicated by the decrease in circulating PICP.
- © 2010 by American Heart Association, Inc.