Low vitamin D levels affect left ventricular wall thickness in severe aortic stenosis

BACKGROUND: Vitamin D [25(OH)D] deficiency and degenerative aortic stenosis represent emerging conditions, linked to a progressive ageing of the population and increased frailty. Previous studies have associated lower levels of 25 (OH)D to the pathogenesis of atherosclerosis and vascular calcifications. However, few studies have evaluated, so far, the impact of vitamin D deficiency in patients with aortic stenosis, which was therefore the aim of present study. METHODS: Consecutive patients with severe degenerative aortic stenosis undergoing nonurgent coronary angiography were included. Aortic stenosis was defined as aortic valve area (AVA) less than 1 cm and/or mean gradient more than 40 mmHg. Indexed area and stroke volume or dobutamine stress evaluation were performed when indicated. Fasting samples were collected at admission for 25 (OH)D levels assessment. RESULTS: We included 137 patients with severe degenerative aortic stenosis (48.9% men, mean age 78.4 ± 6.4 years) who were divided according to vitamin D median values (≥12.4 ng/ml). Patients with lower vitamin D had a more frequent history of coronary artery bypass graft (P = 0.02) and received more often angiotensin-converting enzyme-inhibitors (P = 0.03). Among them, 38.7% had vitamin D levels less than 10 ng/ml and only five patients were in therapy with vitamin D supplementation. We observed no significant relationship between vitamin D levels and echocardiographic parameters for the severity of aortic stenosis (AVA, peak and mean gradients, volumes, ejection fraction) except for a greater wall thickness in patients with lower vitamin D levels (r = -0.34, P = 0.03). Results did not change when excluding patients with renal failure or treated with vitamin D supplementation. CONCLUSION: Among patients with severe degenerative aortic stenosis, vitamin D deficiency is common. We found a significant association between left ventricular wall thickness and vitamin D levels, suggesting a potential role of this hormone in modulating hypertrophic remodelling in these patients. However, future larger studies are certainly needed to confirm our findings and to define their prognostic implications.