Vitamin D is now believed to have a significant role in cardiac signal transduction and regulation of gene expression, and thus influences normal cardiomyocyte function. It has been reported to provide cardioprotection through its anti-inflammatory, anti-apoptotic and anti-fibrotic actions; and to prevent cardiac remodeling, Ca{}^{2+}-handling defects, and abnormal electrophysiological patterns. A vitamin D deficient state has been associated in the pathogenesis of heart failure; however, while many clinical studies report a benefit of vitamin D to heart function, other clinical studies are inconsistent with these findings. These uncertainties have led to a discord in the recommendation of vitamin D supplementation for the treatment of heart failure or as a preventive agent in patients deemed to be at risk for cardiac dysfunction. Accordingly, this article is intended to describe some of the mechanisms/sites of action of vitamin D in different animal models of heart failure, as well as to review the clinical observations and challenges in the interpretation and understanding of the clinical relevance of vitamin D in relation to heart function.