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Abstract

Cardiac complications are common in systemic lupus erythematosus (SLE), but drug-induced cardiomyopathy remains underdiagnosed. Hydroxychloroquine (HCQ) cardiotoxicity is rare, and the few reports of HCQ-associated cardiogenic shock have followed acute overdose rather than chronic therapeutic use. A 36-year-old woman with SLE on long-term HCQ and heart failure with mildly reduced ejection fraction (EF) presented with exertional dyspnea, lower extremity edema, and retrosternal chest pain. Echocardiography showed a new EF of 20% to 25%, and computed tomography demonstrated pulmonary edema. The patient’s lactate levels rose despite intravenous furosemide, consistent with Society for Cardiovascular Angiography and Interventions stage C cardiogenic shock. Right heart catheterization showed elevated biventricular filling pressures and a cardiac index of 2.29 L/min/m². An intra-aortic balloon pump normalized lactate, but device-related thrombocytopenia prompted removal on hospital day 5. Rheumatology found no evidence of active lupus and recommended holding HCQ because the corrected QT interval was approximately 600 ms. Cardiac magnetic resonance imaging showed no active myocarditis. Endomyocardial biopsy (EMB) demonstrated scattered myocytes containing myelinoid bodies, consistent with HCQ cardiotoxicity. The patient’s symptoms improved, and she was discharged on guideline-directed medical therapy after discontinuing HCQ. At 21 months of follow-up, she was New York Heart Association class I, with an EF of 55% to 60% and a corrected QT interval of 461 ms. Chronic therapeutic HCQ exposure can cause cardiotoxicity severe enough to require mechanical circulatory support. HCQ toxicity should be considered in patients with prolonged exposure and otherwise unexplained cardiogenic shock, and EMB should be pursued early when noninvasive imaging is nondiagnostic.

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