Abstract
Myocardial calcification is rare. It can be broadly dystrophic, metastatic, or idiopathic. We describe a case of myocardial calcification due to endstage renal disease from uncontrolled tertiary hyperparathyroidism. Description: A 27 year old African-American male with end-stage renal disease (ESRD) on hemodialysis, tertiary hyperparathyroidism s/p subtotal parathyroidectomy, and uncontrolled hypertension, presented to the cardiology clinic as a referral from his nephrologist to further evaluate progressively worsening dyspnea .The patient had a history of focal segmental glomerulosclerosis with two failed cadaveric renal transplants. He had high serum calcium and PTH level for a prolonged time following his second renal transplant .The patient's graft function failed from tertiary hyperparathyroidism and he is on hemodialysis thrice weekly for last three years.The patient first started having exertional dyspnea six months ago,limiting his ability to perform daily activities. He slept on two pillows, but denied PND. He denied any other cardiac symptoms. He was admitted to the hospital a month ago for worsening dyspnea. The impression then, was volume overload secondary to missed hemodialysis sessions.CT chest and abdomen done during admission showed a diffuse calcification of the left ventricle, mitral valve, and a small pericardial effusion .There was no evidence of pulmonary granulomatous lesions, malignancy, calcification of other major organs. Nuclear stress test showed no inducible ischemia . AFB, fungal cultures and CMV titres were negative.The patient was hypertensive during his clinic visit. EKG showed sinus rhythm, with left ventricular hypertrophy (LVH). .TTE showed a concentric LVH with prominent hyperechoic myocardium with an EF of 50%Discussion : Myocardial calcification is rare. It can occur by two mechanisms: dystrophic or metastatic. Dystrophic calcification occurs in dead and damaged tissues with normal calcium and phosphate balance. Metastatic calcification occurs with derangement of calcium and phosphorus metabolism.Metastatic calcification is rarely isolated to single organ but not the case for our patient.Fairly exhaustive investigations to rule out other etiologies were unrevealing. Infectious causes were ruled out. We believe that the myocardial calcification in our patient can be explained by the altered calcium and phosphate metabolism with tertiary hyperparathyroidism . His persistently elevated calcium-phosphorus product despite subtotal parathyroidectomy is a continuing risk factor. Uncontrolled tertiary hyperparathyroidism causing myocardial calcification appears to be irreversible and can lead to graft failure- an important consideration for transplant patients.
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