Osman Yilmaz1, Hasim Olgun2, Murat Ciftel1, Omer Kilic3, Ibrahim Kartal4, Nebahat Y Iskenderoglu4, Fuat Laloglu5, Naci Ceviz2. 1. 1Department of Pediatric Cardiology,Erzurum District Training and Research Hospital,Erzurum,Turkey. 2. 2Department of Pediatrics,Division of Pediatric Cardiology,Ataturk University Medical Faculty,Erzurum,Turkey. 3. 3Department of Pediatric Infectious Diseases,Erzurum District Training and Research Hospital,Erzurum,Turkey. 4. 4Department of Pediatrics,Erzurum District Training and Research Hospital,Erzurum,Turkey. 5. 5Department of Neonatal Intensive Care Unit,Nenehatun Obstetrics and Gynecology Hospital,Erzurum,Turkey.
Abstract
INTRODUCTION: Dilated cardiomyopathy is usually idiopathic and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia. Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may decline in patients with hypocalcaemia. MATERIALS AND METHODS: Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology clinic. Echocardiography was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Maternal lifestyle and living conditions were investigated, and the maternal 25-OH vitamin D3 blood level was measured. RESULTS: We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3-12 months. Laboratory results were consistent with advanced-stage rickets. Severe hypocalcaemia was detected in all patients. The maternal 25-OH vitamin D3 levels were low. Echocardiography revealed increased pre-treatment left ventricle end-systolic and end-diastolic diameters for age and reduced ejection fraction and fractional shortening. After clinical improvement, the patients were discharged. CONCLUSIONS: Severe hypocalcaemia associated with rickets must always be kept in mind among the causes of dilated cardiomyopathy and impaired cardiac function in infants. If diagnosed and treated in time, dilated cardiomyopathy and severe heart failure related to rickets respond well.
INTRODUCTION:Dilated cardiomyopathy is usually idiopathic and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia. Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may decline in patients with hypocalcaemia. MATERIALS AND METHODS:Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology clinic. Echocardiography was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Maternal lifestyle and living conditions were investigated, and the maternal 25-OH vitamin D3 blood level was measured. RESULTS: We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3-12 months. Laboratory results were consistent with advanced-stage rickets. Severe hypocalcaemia was detected in all patients. The maternal 25-OH vitamin D3 levels were low. Echocardiography revealed increased pre-treatment left ventricle end-systolic and end-diastolic diameters for age and reduced ejection fraction and fractional shortening. After clinical improvement, the patients were discharged. CONCLUSIONS:Severe hypocalcaemia associated with rickets must always be kept in mind among the causes of dilated cardiomyopathy and impaired cardiac function in infants. If diagnosed and treated in time, dilated cardiomyopathy and severe heart failure related to rickets respond well.
Authors: Stefan Pilz; Nicolas Verheyen; Martin R Grübler; Andreas Tomaschitz; Winfried März Journal: Nat Rev Cardiol Date: 2016-05-06 Impact factor: 32.419