Hypocalcemia is a curable cause of myocardial dysfunction and clinical congestive cardiac failure, with only stray reports available in literature. We describe 15 infants presenting with severe left ventricular dysfunction, who were found to have hypocalcemia with or without hypomagnesemia. Vitamin D deficiency was identified as the main cause of hypocalcemia. These children improved on supplementation of vitamin D and calcium.

Key words: Child, Congestive cardiac failure, Myocardial dysfunction, Hypocalcemia, Vitamin D deficiency.

Medical records of 94 children admitted with a diagnosis of left ventricular dysfunction without any structural heart defect over 7 years (June 2001-October 2008), were retrospectively analyzed. Sixteen percent (n=15, 12 males) had hypocalcemia as the main cause of ventricular dysfunction and included in this retrospective analysis.

Chest radiograph revealed cardiomegaly in all cases. Twelve lead ECG showed sinus tachycardia, normal frontal QRS axis for age and prolonged corrected QT interval. Serum calcium was low while alkaline phosphatase was high in all infants. Serum parathyroid hormone level (Chemiluminescent Immunoassay) was elevated (secondary hyperparathyroidism) in all cases except in one case, who was found to be hypoparathyroid. Serum vitamin D (25 hydoxy) assayed in 12 cases (Chromatography Radioreceptor H3 assay), was low in 6 cases and near normal in 4. Maternal serum calcium, alkaline phosphatase and serum phosphorus were within normal limit in all cases. Maternal serum vitamin D level was found to be low in one case. Hemoglobin ranged between 8 and 10 g/dL. Screening for inborn errors of metabolism, including carnitine level, was done in 4 infants and was normal. Myocardial biopsy was not done in any of the patient. Echocardiography revealed dilated left ventricle (Z score +3-4), severely decreased left ventricle ejection fraction (LVEF), fractional shortening (FS), normal coronaries and no structural heart defect in all cases. All cases received decongestive therapy (digoxin, frusemide and ACE inhibitor). Calcium was started as continuous intravenous infusion (dose 100-200 mg/kg/day) till serum calcium normalized, after which we switched to oral calcium in the same dose. Injection vitamin D (cholecalciferol) was given intramuscularly (600 000 IU) followed by oral maintenance dose of 400 unit/d for 6 months. Injection magnesium sulfate (50%) (0.1 mL/kg) was given intramuscularly to all infants on day 1 and day 2 of the treatment. Serum calcium levels normalized in 2-4 days in all, except in one infant who had hypoparathyroidism. In this baby, resistant hypocalcemia was treated with oral 1,25-dihydroxycholecalciferol, which led to normalization of serum calcium level. One infant had recurrent hypocalcemia along with tonic spasm leading to aspiration and death, after initial normalization of calcium level. Ten children received packed cell transfusion (15mL/kg) for low hemoglobin level (8-8.9 g/dL).

Fourteen infants were discharged after normalization of their calcium levels and QTc interval. There was a definite improvement in their LVEF and it normalized over 8-12 weeks.

Fifteen out of 94 (16%) babies with severe left ventricular dysfunction had severe hypocalcemia. Primary cause of hypocalcemia in our series was found to be vitamin D deficiency. Vitamin D levels were at lower limit of normal, but they were definitely low for that degree of hypocalcemia(14). All infants except one responded dramatically to therapeutic doses of vitamin D and calcium. Clinical findings, investigations, and response to treatment with vitamin D and calcium strongly support hypocalcemia as a cause for myocardial dysfunction. However, contribution of coexistent hypomagnesemia for left ventricular dysfunction can not be ruled out.

Available literature has only case reports of hypocalcemia as the cause of cardiomyopathy in pediatric age group in available literature. Vitamin D deficiency, vitamin D dependent resistant rickets, or idiopathic factors have been implicated for hypocalcemia(1-3). Maiya, et al.(9) reported 16 cases of cardiomyopathy in children associated with vitamin D deficiency leading to hypocalcemia over a period of 6 years. In adults with ventricular dysfunction, hypoparathyroidism was found to the main reason for hypocalcemia(4-8). Hypomagnesaemia was not mentioned as an association in these reports. There is one prospective study investigating cardiac function in patients with rickets(10). All patients were asymptomatic though echocardiographic abnormalities were noted.

Possible explanations of myocardial dysfunction in patients with hypocalcemia are well described in the literature(1-10). The reason for vitamin D deficiency(9) in developing countries is possibly nutritional. In addition, deficiency may occur in dark skinned infants or in breast fed infants of mothers unexposed to sunlight. This problem may thus be more dispersed in this part of the world or a particular ethnic group in more developed countries. We conclude that serum calcium and magnesium levels must be estimated in all children presenting with cardiomyopathy.

Contributors: All the authors were involved in all aspects of the study. MT would be the guarantor for the study.

Funding: None.

Competing interests: None stated.

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