Low vitamin D status associated with dilated cardiomyopathy.

In recent years, a growing body of evidence supports that vitamin D plays a crucial role in various cardiovascular diseases. Cardiac muscle cells have vitamin D receptors as well as calcitriol-dependent Ca(2+) binding protein. Therefore, the vitamin D may have an effect on cardiac function. In this research, we investigated the association between vitamin D status and dilated cardiomyopathy (DCMP). We compared serum 25-hydroxy-vitamin D3 (25OHD3) concentrations in 39 patients (mean age 50.4 ± 11.7 years, 15 women) with DCMP and in 35 healthy controls (mean age 54.6 ± 13.2 years, 17 women). Parathyroid hormone (PTH), calcium (Ca++), phosphorus, lipid profile, albumin and echocardiographic parameters (left-ventricular (LV) ejection fraction, LV fractional shortening, LV-end-diastolic and end-systolic dimensions) were measured in all study participants. The mean serum 25OHD3 concentrations in patients with the DCMP were significantly lower in compared to healthy controls (24.1 ± 10.4 ng/mL versus 41.4 ± 20.9 ng/mL, P < 0.0001). PTH concentrations were significantly higher in patients with DCMP in comparison with healthy controls (90.6 ± 29.8 pg/mL versus 49.1 ± 18 pg/mL, P < 0.0001). Additionally, we observed a significant negative correlation between 25OHD3 concentrations and PTH concentrations, LV end-diastolic dimensions, LV end-systolic dimensions (r = -0.66; P < 0.0001, r = -0.49; P < 0.0001, r = -0.50; P < 0.0001, respectively). Moreover, 25OHD3 was positively correlated with LV ejection fraction, LV fractional shortening, stroke volume, cardiac output, cardiac index (r = 0.46; P < 0.001, r = 0.44; P < 0.001, r = 0.25; P = 0.03, r = 0.37; P < 0.001, r = 0.25; P = 0.03; respectively). Our findings support that vitamin D has a potential role both in the development of DCMP and LV remodeling.