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Hypocalcemic cardiomyopathy-different mechanisms in adult and pediatric cases
Beena Bansal1, Manish Bansal, Pankaj Bajpai
1Divisions of Endocrinology and Diabetes (B.B.), Cardiology (M.B., H.K.G.), and Pediatric Cardiology (P.B.), Medanta, the Medicity, Sector 38, Gurgaon, Haryana 122001, India.
Insights
Hypocalcemic cardiomyopathy (CMP) is a rare, reversible heart failure cause. Mechanisms differ in infants (vitamin D deficiency) versus adults (hypoparathyroidism), impacting treatment strategies for this treatable condition.
Area of Science:
- Cardiology
- Endocrinology
- Pediatrics
Background:
- Hypocalcemic cardiomyopathy (CMP) is a rare but reversible cause of heart failure.
- Mechanisms of hypocalcemia-induced CMP differ between pediatric and adult populations.
- Understanding these differences is crucial for effective diagnosis and treatment.
Observation:
- A 47-year-old female with severe left ventricular systolic dysfunction presented with hypocalcemia (3.5 mg/dL) and low parathyroid hormone (PTH) (11.8 pg/mL).
- An infant presented in cardiogenic shock with hypocalcemia (4.5 mg/dL) and compensatory hyperparathyroidism (PTH 670 pg/mL).
- Both patients experienced complete cardiac function recovery with calcium and calcitriol supplementation.
Findings:
- Adult hypocalcemic CMP is typically linked to hypoparathyroidism, with or without vitamin D deficiency.
- Pediatric hypocalcemic CMP is commonly associated with maternal vitamin D deficiency and secondary hyperparathyroidism.
- Prompt diagnosis and treatment of hypocalcemia can reverse CMP in both age groups.
Implications:
- Highlights the distinct etiologies of hypocalcemic cardiomyopathy in infants and adults.
- Emphasizes the importance of assessing calcium and PTH levels in unexplained heart failure.
- Suggests tailored therapeutic approaches based on the underlying cause of hypocalcemia.
Background:
Hypocalcemic cardiomyopathy (CMP) is a rare but potentially reversible cause of heart failure. However, the mechanism of hypocalcemia seems to differ between infants and adults. Although severe vitamin D deficiency alone is the usual cause of hypocalcemic CMP in infants, in adult patients significant cardiac dysfunction usually occurs as a result of hypoparathyroidism, either isolated or in combination with vitamin D deficiency. We present two cases of hypocalcemic CMP-one adult and one pediatric-to highlight these differences.
Case Presentation:
The first patient was a 47-year-old female who presented with progressive dyspnea and fatigue and was found to have severe left ventricular (LV) systolic dysfunction (LV ejection fraction, 25%). Her serum calcium level was 3.5 mg/dL, serum phosphorus level was 5.7 mg/dL, and serum 25-hydroxyvitamin D level was 14.1 ng/mL, along with a serum PTH level of 11.8 pg/mL. Her LV ejection fraction normalized completely over 6 months with calcium and calcitriol treatment. In contrast, the second patient was an infant who had presented in cardiogenic shock. Investigations revealed serum calcium of 4.5 mg/dL, serum phosphorus of 11.9 mg/dL, 25-hydroxyvitamin D of 8.9 ng/mL, and serum PTH level of 670 pg/mL. Calcium and calcitriol supplementation resulted in rapid and complete clinical and hemodynamic recovery.
Conclusion:
Hypocalcemia is a rare but treatable cause of dilated CMP. In infants, hypocalcemia is usually due to maternal vitamin D deficiency and is accompanied by compensatory hyperparathyroidism. In contrast, in adult patients, hypocalcemic CMP is usually a result of hypoparathyroidism, with or without concomitant vitamin D deficiency.
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