Marked Improvement of Left Ventricular Function after Calcium Supplementation in a Patient with Severe Hypocalcemia Secondly to Idiopathic Hypoparathyroidism

Abstract

Hypocalcemia is a rare cause of cardiomyopathy. We report a case of cardiomyopathy associated with hypocalcemia secondary to idiopathic hypoparathyroidism.A 82-year-old woman was admitted, because of exertional dyspnea and leg edema. Chest X-ray showed pleural effusion and cardiomegaly. Echocardiography revealed global hypokinesia with mild dilatation of the left ventricle, moderate mitral regurgitation, moderate tricuspid regurgitation, and left ventricular (LV) systolic dysfunction with an ejection fraction (EF) of 32%. On physical examination, Trousseau's sign were positive. Coronary angiography performed on twelfth day of admission showed no fixed stenosis. Laboratory tests showed serum total calcium 5.2 mg/dl (normal 8.2-10.0 mg/dl) and serum phosphate 5.2 mg/dl (normal 2.5-4.5 mg/dl). The serum parathormone (i-PTH) level was 49 pg/ml (normal 10-65 pg/ml). A low serum calcium level, high serum phosphate level and relative decrease of i-PTH level were all consistent with the diagnosis of hypoparathyroidism. She had treatment of heart failure and calcium supplementation by intravenous calcium, long-term oral calcium and vitamin-D preparation. Her symptoms and signs of heart failure rapidly improved, but LV function did not improve at the time of discharge. Repeat echocardiography done at six month and one year of follow-up showed dramatic improvement in the LV functions (EF=63% on one-year follow-up). In concludion, hypoparathyroidism with severe hypocalcemia is an important cause of left venitcular dysfunction and heart failure. Hypocalcemia is a rare cause of cardiomyopathy. We report a case of cardiomyopathy associated with hypocalcemia secondary to idiopathic hypoparathyroidism. A 82-year-old woman was admitted, because of exertional dyspnea and leg edema. Chest X-ray showed pleural effusion and cardiomegaly. Echocardiography revealed global hypokinesia with mild dilatation of the left ventricle, moderate mitral regurgitation, moderate tricuspid regurgitation, and left ventricular (LV) systolic dysfunction with an ejection fraction (EF) of 32%. On physical examination, Trousseau's sign were positive. Coronary angiography performed on twelfth day of admission showed no fixed stenosis. Laboratory tests showed serum total calcium 5.2 mg/dl (normal 8.2-10.0 mg/dl) and serum phosphate 5.2 mg/dl (normal 2.5-4.5 mg/dl). The serum parathormone (i-PTH) level was 49 pg/ml (normal 10-65 pg/ml). A low serum calcium level, high serum phosphate level and relative decrease of i-PTH level were all consistent with the diagnosis of hypoparathyroidism. She had treatment of heart failure and calcium supplementation by intravenous calcium, long-term oral calcium and vitamin-D preparation. Her symptoms and signs of heart failure rapidly improved, but LV function did not improve at the time of discharge. Repeat echocardiography done at six month and one year of follow-up showed dramatic improvement in the LV functions (EF=63% on one-year follow-up). In concludion, hypoparathyroidism with severe hypocalcemia is an important cause of left venitcular dysfunction and heart failure.