Reversible dilated cardiomyopathy caused by idiopathic hypoparathyroidism
A 50-year-old female suffering from dyspnea (New York Heart Association class IV) and orthopnea was admitted to our cardiology clinic at Hallym University Kangdong Sacred Heart Hospital, Seoul, Korea. She had been treated with neurotonics due to dizziness for 2 months, and dyspnea had developed 5 days before admission.\nOn admission, the patient's blood pressure was 100/60 mmHg, and her pulse rate was 82 beats per minute. No heart murmur was detected, but rales were heard on both sides of the lung field. Physical examination did not reveal neurological dysfunction with regard to muscle tone and sensitivity. Neither pitting edema nor neck vein distension was observed. Electrocardiography showed a prolonged QT interval (432 ms) with nonspecific ST-T changes. Chest X-ray revealed prominent cardiomegaly with pulmonary congestion (). Echocardiography indicated decreased left ventricular function.\nThe ejection fraction of the left ventricle (LV) was 36.5%, and the diastolic and systolic dimensions of the LV were 59 and 47 mm, respectively. Moderate mitral and tricuspid valvular regurgitations were identified with global hypokinesia. Serum levels of creatine kinase-MB and troponin-I were within the respective normal ranges, whereas the brain natriuretic peptide level was 1,855.1 pg/mL (reference range, 0 to 100).\nBased on her symptoms and the results of several previous studies, we made a diagnosis of congestive heart failure and began initial treatment with furosemide injection. The patient had no history of hypertension, diabetes mellitus, or smoking. In addition, we could not find any influence of neurotonics taken before admission on the patient's heart.\nAdditional studies were performed to determine the etiology of congestive heart failure. Laboratory studies revealed reduced total serum calcium of 3.7 mg/dL (reference range, 8.4 to 10.2), magnesium of 1.7 mg/dL (reference range, 1.9 to 2.5), and ionized calcium of 0.6 mmol/L (reference range, 1.12 to 1.3). The phosphorus and creatinine levels were 8.5 mg/dL (reference range, 2.5 to 4.6) and 1.5 mg/dL (reference range, 0.6 to 1.2), respectively. Hormone analysis was performed and showed free T4 and thyroid stimulating hormone to be within the respective normal ranges, while intact parathyroid hormone (PTH-intact, terminal) level was 8.17 pg/mL (reference range, 15 to 68). The vitamin D level was 10.1 ng/mL (reference range, 11 to 70). Coronary angiography did not detect significant stenotic lesions on the coronary arteries.\nWe made a diagnosis of DCM caused by severe hypocalcemia, and treatment was started with intravenous calcium and oral vitamin D3 and calcitriol. Concurrently, we sought to determine the cause of severe hypocalcemia, and a neck sonogram was ordered to rule out parathyroid infiltrating disease. However, no abnormalities were observed. Rheumatoid factor and fluorescent antinuclear antibody test were also assessed to rule out autoimmune disease; their serum levels were within the respective normal ranges ().\nThe patient was finally diagnosed with idiopathic hypoparathyroidism-induced DCM, and the treatment described above was continued in addition to conventional heart failure management. The patient responded to this regimen with remarkable improvement of dyspnea, and chest X-ray showed a reduction of cardiomegaly with clearance of pulmonary edema (). Calcium levels reached the normal range; the initial ionized calcium level was 0.6 mmol/L, and increased to 0.89 mmol/L after 5 days of calcium supplementation. The prolonged QT interval was also reduced (). Discharge treatment included oral calcium, vitamin D3, and congestive heart failure medications.\nFollow-up visits revealed progressive improvement of myocardial function; the LV ejection fraction was 46% by the first month and 51% by the third month. In addition, the LV diastolic and systolic dimensions were decreased to 53 and 37 mm, respectively (). Calcium and vitamin treatments were maintained, and aspirin, an angiotensin receptor blocker and statin medications were added. The patient is currently well on this therapy.