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Dilated cardiomyopathy is an important cause of heart failure in children. Often it requires transplantation, but on rare occasions it is curable by micronutrient supplements.
A girl aged 4½ months was referred in shock with acute heart failure and respiratory distress. She was of West African descent but had been born in the UK and breastfed from birth. Echocardiogram revealed a poorly functioning dilated heart (fractional shortening 6.5%; Table 1). She was admitted to the paediatric intensive-care unit where treatment included inotropic agents, furosemide and captopril. Intravenous antibiotics were also administered for suspected chest infection. Laboratory investigations revealed a severe normocytic anaemia (haemoglobin 6.8 g/dL), abnormal clotting (international normalized ratio 2.04) and a blood picture typical of vitamin D deficiency (low calcium [1.37 mmol/L], low phosphate, low vitamin D, raised parathyroid hormone and raised alkaline phosphatase). Radiographs showed bony changes consistent with rickets. Her dilated cardiomyopathy was therefore attributed to nutritional vitamin D deficiency.
In addition to supportive treatment for her cardiac failure and transfusion for the anaemia she received ergocalciferol and Calcium-Sandoz. By day 11 serum calcium was within normal limits (2.52 mmol/L); phosphate remained low. At the time of her discharge on day 17 the echocardiogram showed persisting left ventricular dilatation, although ventricular function was improving (fractional shortening 17.8%). Subsequently all her biochemical results became normal, and fifteen months after discharge her left ventricular dilatation had completely resolved (fractional shortening 34%). She is now well without medication.
This boy, aged 8 months and likewise of West African descent, presented in a similar way with shock, acute heart failure and respiratory distress; he also had a low blood glucose. Echocardiogram showed a dilated heart with fractional shortening 7.6% (see Table 1). Blood tests showed a normocytic anaemia (haemoglobin 8.3 g d/L), metabolic acidosis and deranged clotting (international normalized ratio 2.9). The biochemical picture was similar to that in case 1, with low calcium (1.55 mmol/L, vitamin D and raised parathyroid hormone). This infant had originally been breastfed at night and formula-fed during the day. However, from the age of 4½ months his diet had consisted mainly of African meats and rice with very few dairy products.
Serum calcium did not improve with calcium supplementation, so he was started on 1-alphacalcidol, later changed to ergocalciferol. His anaemia worsened and he required a blood transfusion. 21 days after admission he was stable enough for discharge home, although his heart remained enlarged with poor functioning (fractional shortening 11%). Thereafter he made excellent progress, with normal biochemistry values at one month and normal cardiac function at twelve months (fractional shortening 30%). Because of persistent mild left ventricular dilatation, his cardiac medications were continued.
Vitamin D deficiency is commonly due to inadequate nutrition and insufficient exposure to ultraviolet. The most prominent biochemical feature is hypocalcaemia, and this can adversely affect ventricular contraction.1 In treatment of rickets (often due to vitamin D deficiency), calcium with or without vitamin D supplementation may be more effective than vitamin D alone.2 There are not many reports on dilated cardiomyopathy associated with vitamin D deficiency in infants.3-7 Other nutritional deficiencies to be considered8 are those of carnitine, selenium and taurine—carnitine in particular, because depletion can diminish ventricular contractility9 and oral supplementation of L-Carnitine is effective.10
Dilated cardiomyopathy caused by nutritional deficiencies seems to have a better prognosis than idiopathic dilated cardiomyopathy. Appropriate treatment can lead to complete resolution. Thus, in an infant with cardiac failure, a nutritional cause deserves early consideration.