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Published on: August 8, 2022
Hypophosphatemia-induced Cardiomyopathy
Nobuhiro Ariyoshi1, Masayuki Nogi1, Akika Ando1
1Department of Internal Medicine, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii.
Insights
Hypophosphatemia, a condition of low phosphate levels, can impact heart function, potentially causing cardiomyopathy. Severe cases may show improved cardiac performance after phosphate correction, highlighting its role in heart failure.
Area of Science:
- Cardiology
- Electrophysiology
- Critical Care Medicine
Background:
- Limited research exists on hypophosphatemia's cardiac effects.
- Hypophosphatemia may be an underrecognized cause of heart failure.
Purpose of the Study:
- To review the association between hypophosphatemia and cardiac function.
- To raise awareness of hypophosphatemia-induced cardiomyopathy as a reversible cause of heart failure.
Main Methods:
- Systematic literature search of MEDLINE and PubMed (1971-March 2015).
- Inclusion of 11 primary studies (case reports, case-control, animal studies).
Main Results:
- Hypophosphatemia may cause cardiomyopathy via ATP depletion and reduced erythrocyte 2,3-DPG.
- Left ventricular function may improve after correcting severe hypophosphatemia.
- No significant improvement in mild-to-moderate hypophosphatemia.
Conclusions:
- Hypophosphatemia is a potential cause of reversible cardiomyopathy.
- Further clinical studies are needed to analyze cardiac function and hypophosphatemia.
- Recognition of hypophosphatemia is crucial for managing heart failure.
Abstract:
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.
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