Background: Many studies proved the prognostic importance of aortic stiffness as an independent predictor of cardiovascular morbidity and all-cause mortality. The decrease of arterial compliance has a high prevalence in patients with heart failure and affects both hemodynamics and prognosis. Aortic stiffness is partially caused by excessive activation of the renin-angiotensin-aldosterone system. Spironolactone, a mineralcorticoid receptor antagonist (MRA), has been shown to decrease aortic stiffness and fibrosis in experimental models. However, there are few studies that describe the effects of MRA on aortic stiffness in patients with nonischemic dilated cardiomyopathy.
Aims: To evaluate the effect of spironolactone on aortic stiffness in patients with nonischemic dilated cardiomyopathy.
Materials and methods: We randomized (1 : 1) 102 patients with nonischemic dilated cardiomyopathy with New York Heart Association class I-II to receive spironolactone 25 mg/day (up to 100 mg/day) or placebo, in addition to recommended therapy. Aortic stiffness index, aortic strain, aortic distensibility and aortic dimensions were assessed at baseline and after 6 months. All measures were obtained with echocardiography M-mode at 3 cm above the aortic valve on parasternal long axis view and simultaneous brachial arterial pressure with sphygmomanometer.
Results: Ascending aorta diameters, aortic stiffness index, aortic distensibility and aortic strain were similar at randomization in the two groups. After 6 months of therapy in the treated group, we found a reduction of aortic stiffness index (7.2 ± 3.5 versus 9.6 ± 4.8 mmHg; P = 0.03) and an increase of aortic distensibility (3.77 ± 1.0 versus 2.92 ± 0.55 mmHg; P = 0.01) and systolic aortic strain (10.0 ± 5.0 versus 8.0% ± 2.1%; P = 0.01). There were no difference in systolic arterial pressure, diastolic arterial pressure and differential pressure in the two groups.
Conclusion: Therapy with spironolactone is effective in reducing aortic stiffness in patients with nonischemic dilated cardiomyopathy. This effect could improve hemodynamics supporting the use of MRAs in patients with low New York Heart Association class (I-II).