Mineral metabolism in heart disease

Abstract

Strong experimental and clinical evidence points towards a substantial contribution of mineral metabolism disorders to the initiation and progression of cardiovascular disease. Vice versa, recent work suggests that cardiovascular disease may also cause mineral metabolism alterations. Experimental studies suggest that hyperphosphatemia, elevated plasma levels of phosphaturic hormones--parathyroid hormone and fibroblast growth factor-23 (FGF-23)--and hypovitaminosis D exert detrimental effects on vascular tissue and on the myocardium. Accordingly, in longitudinal clinical cohort studies, individuals with high plasma levels of phosphate, parathyroid hormone and FGF-23, and with low vitamin D levels, face worst cardiovascular prognosis.Notably, recent evidence suggests that cardiovascular disease may not only follow but also induce mineral metabolism disorders: severe derangements in mineral metabolism were observed in patients with acute heart failure, who face a tremendous increase in plasma FGF-23. Unfortunately, few prospective studies have been completed hitherto that specifically target components of the mineral metabolism for cardiovascular disease prevention or treatment. A bidirectional interaction exists between mineral metabolism disorders and cardiovascular disease. However, clinical evidence for a cardiovascular benefit of therapeutic interventions into mineral metabolism is outstanding.