Myocardial calcifications are often discovered incidentally and result from dystrophic or metastatic deposition of calcium. Dystrophic calcification represents the sequelae of local tissue damage with necrosis, most commonly from myocardial ischemia. Unlike dystrophic calcification, metastatic calcification is the result of abnormal calcium homeostasis, including renal failure, hyperparathyroidism, and vitamin D deficiency. Myocardial calcifications are not entirely a benign finding because they can lead to heart failure, arrhythmias, and sudden cardiac death. A 67-year-old woman with hypertension presented to the clinic for evaluation of an incidental finding on an abdominal computed tomography she had for an acute episode of abdominal pain and diarrhea. The abdominal computed tomography was unremarkable except for a renal cyst, but high-density material in the distribution of the left ventricular myocardium was found (Figure) . She denied smoking, chest pain, or dyspnea on exertion. Her only medication was hydrochlorothiazide. Transthoracic echocardiogram showed normal biventricular systolic function, extensive calcification of the interventricular septum, severe posterior mitral annular calcification without mitral valve stenosis, and mild calcification of the pericardium. Cardiac magnetic resonance imaging demonstrated extensive myocardial calcification involving the basal and mid septum and basal anterolateral free wall, with associated myocardial thickening and hypokinesis (Figure). Her laboratory analyses showed elevated serum calcium at 10.9 mg/dL (ionized calcium 1.36 mg/dL), elevated intact parathyroid hormone at 76 pg/mL, and reduced 24-h urinary calcium at 12.4 mg. A thyroid ultrasound and parathyroid scan with single-photon emission computed tomography showed a possible parathyroid adenoma. Hydrochlorothiazide was discontinued, and she underwent parathyroidectomy without complications. Repeat echocardiogram 2 years after the surgery showed persistent calcifications, mild mitral stenosis, and no evidence of constrictive physiology.
Cardiovascular complications from hyperparathyroidism are unusual. Clinical manifestations secondary to calcium deposition can be absent in some cases, but in other cases heart failure, arrhythmias, mitral or aortic calcific stenosis, and coronary disease can develop. Additionally, parathyroid hormone itself can affect cardiomyocytes by activating G-protein signaling, resulting in calcium influx into cardiac cells. This influx does not lead to contractile dysfunction, but it is thought to trigger several indirect effects on the myocardium, including activation of protein kinase C, which causes myocardial hypertrophy. Incidental myocardial calcifications should alert physicians about an underlying abnormal calcium homeostasis and warrant further investigation. A review of systems could reveal symptoms such as weakness or constipation, and laboratory analyses including total serum calcium, serum phosphorus, creatinine, parathyroid hormone, and urinary calcium in 24 hours should be performed. A transthoracic echocardiogram is useful to characterize the hemodynamic consequences of myocardial and valvular calcifications. The results of these tests will guide the clinician about further management and timely referral to the appropriate specialties. In cases of primary hyperparathyroidism, parathyroidectomy can prevent further detrimental structural and functional changes in the cardiovascular system and reverse cardiac hypertrophy.
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-Kenneth Hoang, MD, Katia Bravo-Jaimes, MD, Daniel Ocazionez, MD
