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Published on: February 17, 2018
HYPOCALCEMIC CARDIOMYOPATHY - A RARE HEART FAILURE ETIOLOGY IN ADULT
I Parepa1, L Mazilu2, A Suceveanu2
1"Ovidius" University of Constanta, Faculty of Medicine - Constanta, Romania.
Insights
Hypoparathyroidism-induced hypocalcemia can cause heart failure and dilated cardiomyopathy in adults. Prompt treatment with calcium and vitamin D significantly improves cardiac function.
Area of Science:
- Cardiology
- Endocrinology
Background:
- Heart failure and dilated cardiomyopathy (DCM) are infrequently linked to hypoparathyroidism-induced hypocalcemia in adults.
- A 40-year-old female with diabetes and a history of thyroidectomy presented with syncope and heart failure symptoms.
Observation:
- The patient exhibited signs of severe left ventricular systolic dysfunction (ejection fraction 15%) and diastolic dysfunction.
- Initial heart failure treatment provided minimal improvement, while hypocalcemia symptoms (low serum calcium and parathormone) became apparent.
Findings:
- Serum calcium levels were critically low (total 3.6 mg/dL, ionic 2.2 mg/dL), with suppressed parathormone (10 pg/mL) and elevated phosphatemia (6.4 mg/dL).
- Parenteral calcium and oral vitamin D therapy led to the resolution of hypocalcemia and significant cardiac function improvement.
Implications:
- This case highlights a rare cause of heart failure in adults, refractory to standard therapies but responsive to calcium repletion.
- Awareness of hypoparathyroidism as a potential cause of cardiac dysfunction is crucial for accurate diagnosis and effective treatment.
Introduction:
Heart failure and dilated cardiomyopathy (DCM) in adults are rarely caused by hypoparathyroidism induced hypocalcemia.
Case Report:
Female patient, 40 years old, diabetic, with previous history of thyroidectomy for Graves' disease, was hospitalized for syncope and symptoms of heart failure. ECG revealed sinus tachycardia, long QT, negative T from V1 up to V4. Chest X-ray, cardiac ultrasound and contrast cardiac MRI confirmed dilated left chambers, severe systolic dysfunction of the left ventricle (left ventricle ejection fraction=15%) due to diffuse hypokinesia and restrictive type of diastolic dysfunction. Patient status insignificantly improved with specific heart failure depletion treatment but important signs of hypocalcemia occurred. Low levels of total and ionic serum calcium were detected (total serum calcium 3.6 mg/dL, ionic calcium=2.2 mg/dL) along with low serum levels of parathormone (10 pg/mL) and high level of phosphatemia (6.4 mg/dL). After one month of parenteral treatment with calcium and oral vitamin D, hypocalcemic signs disappeared and heart failure significantly improved.
Conclusion:
This rare adult condition is refractory to heart failure conventional therapy but promptly responds to restoration of normocalcemia. It is important to be aware of this pathophysiological setting, in order to treat it correctly.
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