Congestive heart failure due to hypocalcemia: First manifestation of hypoparathyroidism in an infant

Citation
A. Koch et al., Congestive heart failure due to hypocalcemia: First manifestation of hypoparathyroidism in an infant, Z KARDIOL, 88(1), 1999, pp. 10-13
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
ZEITSCHRIFT FUR KARDIOLOGIE
ISSN journal
03005860 → ACNP
Volume
88
Issue
1
Year of publication
1999
Pages
10 - 13
Database
ISI
SICI code
0300-5860(199901)88:1<10:CHFDTH>2.0.ZU;2-0
Abstract
Hypocalcemia is a relatively uncommon reversible cause of congestive heart failure. There are a few reports of hypocalcemic children who developed con gestive heart failure associated with hypoparathyroidism. In all these pati ents, however, cardiac failure did not occur before the age of nine years. In addition, other striking non-cardial manifestations of hypoparathyroidis m, e.g., convulsive seizures, had been present prior to cardiac symptoms. We report on a 3.7 year old girl with mitral insufficiency and severe cardi ac failure due to hypocalcemia secondary to familial hypoparathyroidism. Th e infant's mother was suffering from idiopathic hypoparathyroidism, but her own history lacked any evidence for parathyroid hormone deficiency. On adm ission, she presented with fatigue, dyspnea, and pedal edema. Liver edge wa s palpable 4 cm below the right costal margin, and a 3/6 systolic murmur wa s heard. A chest x-ray showed cardiac enlargement; electrocardiogram demons trated a prolonged QTc interval of 0.46 s. The echocardiography revealed a cleft in the mitral valve with mitral insufficiency and markedly reduced co ntractility of the left ventricle. Laboratory studies demonstrated a low to tal serum calcium level of 1.3 mmol/1; serum magnesium level was slightly d ecreased (0.5 mmol/1), and parathyroid hormone level was not detectable. Pa rtial monosomy of chromosome 22 was excluded. Ophthalmological examination, audiometry, and renal ultrasonogram were normal. Oral calcium supplementation and anticongestive therapy with metildigoxin, furosemid, and captopril was initiated but no improvement of the heart fail ure occurred. However, normalization of serum calcium level by calcium infu sions caused prompt clearing of the clinical symptoms, complete normalizati on of liver size, reduction of cardiac enlargement (thoracic ratio decrease d from 0.68 to 0.57), and marked improvement in contractility (left ventric ular shortening fraction increased from 21% to 34%). The QTc interval decre ased to 0.39 a. The successful treatment following normalization of serum c alcium level proved the superiority of hypocalcemia over mitral valve insuf ficiency in the etiology of the cardiac failure. To our knowledge, this is the first report of congestive heart failure due to hypocalcemia as the first manifestation of hypoparathyroidism in childho od. Hypocalcemia should be kept in mind in any congestive heart failure in chil dren with or without underlying cardiac malformation.