Cardiovascular consequences of hypophosphatemia.

INTRODUCTION: Few studies have been conducted to evaluate the effect of hypophosphatemia on cardiovascular consequences. The goal of this review was to determine whether hypophosphatemia is associated with cardiovascular consequences and to increase its awareness as a new clinical entity and a reversible cause of cardiovascular consequences. EVIDENCE ACQUISITION: We searched MEDLINE and PubMed through September 2016 for primary studies that reported the relationship between hypophosphatemia and cardiovascular consequences including cardiomyopathy and arrhythmia. EVIDENCE SYNTHESIS: A total of 937 articles were initially obtained. Of these articles, 921 publications were excluded according to the inclusion and exclusion criteria. Sixteen articles were included in this review. These articles included 3 prospective cohort studies, 1 retrospective cohort study, 7 case series or case reports, 2 case-control studies, 1 pre- vs. post-test in a single group, and 2 animal studies. CONCLUSIONS: The mechanisms of hypophosphatemia in cardiomyopathy and arrhythmia have been reported to be a depletion of adenosine triphosphate in myocardial cells and decreased 2,3-diphosphoglycerate in erythrocytes. Left ventricular performance seems to improve when severe hypophosphatemia is corrected, but not in those with mild to moderate hypophosphatemia. However, analyses of the relationship between cardiac function and hypophosphatemia using clinical end points have not been conducted. The association between hypophosphatemia and arrhythmia remains unclear, but anecdotal reports exist in the literature.

Native bivalvular endocarditis by Gemella haemolysans requiring venovenous extracorporeal membrane oxygenation.

A 24-year-old otherwise healthy man presented with a 3-week history of malaise, headache, fever and rigors after he was treated with oral clindamycin for left parotitis and Gemella haemolysans bacteraemia. He developed G. haemolysans infective endocarditis, septic emboli and heart failure due to progressive bivalvular disease. He underwent urgent mechanical aortic valve replacement and mitral valve repair, which required venovenous extracorporeal membrane oxygenation, to support severe respiratory failure. This is the first documented case of G. haemolysans infective endocarditis affecting native aortic and mitral valves in a healthy adult.

Hypophosphatemia-induced Cardiomyopathy.

Relatively few studies have been conducted to evaluate the effect of hypophosphatemia on cardiac function. The goal of this review was to determine whether there is an association between hypophosphatemia and cardiac function and to increase awareness of hypophosphatemia-induced cardiomyopathy as a new clinical entity and a reversible cause of heart failure. We searched MEDLINE and PubMed from 1971 until March 2015 for primary studies, which reported the relationship between hypophosphatemia and cardiac function. A total of 837 articles were initially obtained. Of these articles, 826 publications were excluded according to the inclusion and exclusion criteria. In all, 11 articles were included in this review. These articles included 7 case series or case reports, 1 case-control study, 1 pretest versus posttest in a single group and 2 animal studies. In conclusion, the mechanisms of hypophosphatemia in cardiomyopathy have been reported to be a depletion of adenosine triphosphate in myocardial cells and decreased 2,3-diphosphoglycerate in erythrocytes. After correction of hypophosphatemia, left ventricular performance seems to improve in patients with severe hypophosphatemia, but not in those with mild-to-moderate hypophosphatemia. However, analyses of the relationship between cardiac function and hypophosphatemia using clinical end points have not been conducted.