INTRODUCTION: Hypocalcemic cardiomyopathy (HC) is a rare and potentially reversible cause of heart failure (HF). Primary hypoparathyroidism, due to accidental damage to the parathyroid glands during thyroid surgery, is one of the most common causes of hypocalcemia. Identifying this etiology is crucial.
CASE REPORT: A 54 y.o. patient affected by arterial hypertension and hypothyroidism, presented to our hospital with HF. He underwent total thyroidectomy 20 years earlier. An echocardiogram revealed a dilated cardiomyopathy with systolic dysfunction (LVEF 22%), reduced right ventricular function and elevation in pulmonary artery pressure. ECG showed sinus rhythm, QTc 470 msec. BNP was increased (1888 pg/ml) and troponin value normal. Blood calcium and phosphorus values were not performed on admission. Intravenous diuretic therapy led to good clinical response and disease-modifying therapy (bisoprolol, sacubitril/valsartan, eplerenone) was started and uptitrated. Coronary CT excluded significant coronary lesions. Cardiac MRI showed increased native T1-T2 values and an intramyocardial ‘patchy’ distribution of late gadolinium enhancement involving the interventricular septum. Endomyocardial biopsy excluded the presence of viral DNA/RNA and signs of active inflammation. After few days an episode of dysarthria, spatial/temporal disorientation and muscle spasms was reported. Urgent brain CT was performed, which excluded acute ischemic or hemorrhagic events, but diffuse basal ganglia calcification. Blood tests revealed severe hypocalcemia in the setting of primary hypoparathyroidism (total calcium 1.57 mmol/L, ionized calcium 0.61 mmol/L, PTH 8,8 pg/ml). Trousseau ‘s sign (‘obstetrician’s hand”) was positive, suggesting the presence of latent tetany. Hypocalcemia was corrected with calcium carbonate and calcitriol administration. On ECG QTc was 522 msec with subsequent normalization. In the following days, progressive neurological improvement was reported. After a week he was discharged in good status. At follow-up we observed a progressive improvement in biventricular systolic function with complete normalization of LVEF and ventricular volumes at 9 months.
CONCLUSION: HC must be suspected when a patient presents with myocardial dysfunction, neuro-muscular signs and QT prolongation on ECG. Diuretics administration may aggravate hypocalcemia by increasing urinary calcium excretion. Normalization of calcium concentration could lead to complete recovery.
