Beena Bansal1, Manish Bansal, Pankaj Bajpai, Hardeep Kaur Garewal. 1. Divisions 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.
Abstract
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.
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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