Takotsubo Cardiomyopathy Associated with Severe Hypocalcemia Secondary to Idiopathic Hypoparathyroidism
A 69-year-old woman presented to the emergency department of our institution with a three-day history of exertional dyspnea and chest discomfort that had progressed to dyspnea at rest. She complained of a six-year history of numbness in both hands and leg cramps. She was diagnosed as having hypocalcemia secondary to idiopathic primary hypoparathyroidism and was treated with calcium lactate and calcitriol. One year earlier, she had suffered from intermittent cognitive dysfunction with memory loss and was diagnosed with senile dementia. Thereafter, she was irregularly given medication to treat hypoparathyroidism. One month before the present admission, calcium lactate and calcitriol had been discontinued. On arrival, physical examination revealed low blood pressure (90/60 mm Hg), tachycardia with a heart rate of approximately 102 beats per minute, and tachypnea with a respiration rate of 25 per minute. Her body temperature was 36.4℃ and oxygen saturation on room air was 90%. Chest auscultation revealed rales in the bilateral lung field without murmur. Spasm and cramps of both extremities were noted but the remainder of the physical and neurological examination yielded no remarkable results. Initial electrocardiogram showed sinus tachycardia, negative T waves in leads V 1-4 and a slightly prolonged QT interval (corrected QT interval=490 msec). Chest X-ray showed cardiac enlargement with pulmonary congestion and both pleural effusion. Laboratory testing indicated the following results: total serum calcium concentration, 5.0 mg/dL (reference range: 8.0-10.5 mg/dL), with free ionized calcium, 2.8 mg/dL (reference range: 4.0-4.5 mg/dL); serum phosphorous, 6.1 mg/dL; albumin, 3.7 g/dL; creatinine, 0.9 mg/dL; magnesium, 1.9 mg/dL; PTH, 170 pg/mL (reference range: 180-560 pg/mL); intact PTH, 10.7 pg/mL (reference range: 6.2-29.0 pg/mL) and 25-OH vitamin D, 9.3 ng/mL (reference range: 6.9-69.5 ng/mL). N-terminal pro-B-type natriuretic peptide was 12968 pg/mL; creatine phosphokinase, 1029 IU/L; Myoglobin, 91.78 ng/mL; Troponin-T, 0.234 ng/mL, and thyroid function was within the normal range. Initial echocardiography demonstrated a contractile pattern with preserved basal segment, akinesia of the apical segment and severe hypokinesia of the middle segment of the LV, compatible with takotsubo cardiomyopathy (). The ejection fraction was estimated to be 32%. Initial treatment with administration of furosemide, spironolactone, angiotensin II receptor blocker and intravenous calcium gluconate with close monitoring of serum free ionized calcium levels was started. On the fourth day of admission, we performed coronary angiography and a left ventriculogram. The former revealed normal coronary arteries () and the latter showed markedly improved LV contractility excluding residual localized akinesia of the mid to apical antero-septal wall, demonstrating the resolving course of the takotsubo cardiomyopathy (). The clinical symptoms and signs of congestive heart failure and the objective parameters of LV systolic function obtained by serial echocardiography improved rapidly after correction of the hypocalcemia (). On the twelfth day of admission, the echocardiographic findings showed complete resolution of the regional wall motion abnormalities of the LV with an ejection fraction of 65% () and the patient was discharged with no symptoms and signs of either heart failure or hypocalcemia. During the ensuing 18 month follow-up period, repeated echocardiograms showed normal ventricular contractility and there were no further episode of heart failure with the maintenance of daily alfacalcidol and calcium carbonate.