Abstract #1088796: Non-Ischemic Cardiomyopathy in Setting of Functional Hypoparathyroidism Secondary to Hypomagnesemia

Abstract

Magnesium (Mg) is involved in many biochemical reactions and low levels can have negative effects on the entire cardiovascular system. These can occur directly or indirectly via dysfunction in calcium homeostasis. We present a case of severe hypomagnesemia leading to functional hypoparathyroidism in the setting of newly diagnosed cardiomyopathy (CMO) and the importance of aggressive electrolyte repletion as a mainstay in the management of heart failure. 71 year-old male with history of squamous cell lung cancer status post cisplatin-based chemoradiation, CKD, DM2, and GERD presented with dyspnea on exertion and recurrent hypocalcemia. Two months prior, he was diagnosed with non-ischemic CMO with ejection fraction (EF) of 10% in the setting of TSH >100. On admission, he had Mg 0.5 mg/dL (1.6-2.5 mg/dL), calcium (Ca) 6.9 mg/dL (8.4-10.4 mg/dL), ionized calcium (iCa) 3.0 mg/dL (4.4-5.4 mg/dL), phosphorous 5.4 (2.5-4.5 mg/dL) and inappropriately normal parathyroid hormone (PTH) of 50 pg/mL (15-65 pg/mL). Since prior admission TSH and free T4 had improved to 26.96 and 1.3, respectively after adding levothyroxine. On exam, he had tachycardia, bilateral rhonchi, and pitting edema in the lower extremities. NT-BNP was 16,474 and EKG showed sinus tachycardia with lateral T-wave inversions. Chvostek sign was negative, with no perioral numbness or paresthesia. Electrolytes were repleted aggressively. He was discharged on oral Ca and Mg supplements in addition to heart failure medical therapy. Labs on discharge showed improvement in Mg to 2.0 mg/dL, iCa 3.8 mg/dL, phosphorous 3.3 mg/dL, and PTH of 89 pg/mL. Seven months later, his EF% doubled on echocardiogram. Follow up EF% did not recover further despite euthyroidism due to noncompliance with Ca and Mg supplements. Hypomagnesemia is a potential cause of CMO and medications are a significant risk factor that must be considered. Our patient was exposed to cisplatin, chronic PPI use and loop diuretics, which can all chronically decrease Mg stores in the body. Low Mg leads to defects in cyclic AMP generation in the parathyroid gland, which causes decreased PTH secretion and low Ca. This is evidenced by the inappropriately normal PTH in our patient despite low Ca levels. Of note, he had history of hypothyroidism but low EF persisted despite appropriate repletion and normalization of T4 levels. Previous cases have reported hypocalcemia-induced CMO, but few have described the hypomagnesemia as an underlying cause of this finding. This case underlines the importance of monitoring and repletion of Mg and Ca in addition to goal-directed medical therapy for optimized heart failure management.