MS2 UTHealth McGovern Medical School Houston, Texas, United States
Background: Systemic lupus erythematosus (SLE) is known to cause cardiac complications. Drug-induced cardiomyopathy, however, is often underdiagnosed. We report a patient with a history of SLE on hydroxychloroquine (HCQ) and heart failure who presented with a reduced ejection fraction (EF) and cardiogenic shock later found to have HCQ-induced cardiotoxicity.
Methods: A 36-year-old female with a history of SLE on HCQ and heart failure with reduced EF presented to the hospital with exertional shortness of breath, swelling in her lower extremities, and retrosternal chest pain. Her echo demonstrated a new reduction in EF to 20-25%. Computed tomography pulmonary embolism study showed pulmonary edema. She was started on treatment for heart failure exacerbation with a furosemide drip, however, her labs showed rising lactate levels, concerning for SCAI class C cardiogenic shock. She was taken to the catheterization lab where right heart catheterization demonstrated elevated biventricular filling pressures and low cardiac index. Intra-aortic balloon pump (IABP) was placed and the patient’s lactate eventually normalized. She had an acute thrombocytopenia caused by the IABP prompting removal, and platelet levels recovered. Rheumatology did not believe she was in an active lupus flare and recommended holding her HCQ due to prolonged QTc. Cardiac magnetic resonance imagining suggested autoimmune myocardial disease versus prior myocarditis, however no active myocarditis was seen. Finally, EMB showed scattered myocytes containing myelinoid bodies suggestive of HCQ-induced cardiotoxicity. The patient had continual symptom improvement and was discharged with guide-line directed therapy and holding of her HCQ for lupus therapy.
Outcome: Prolonged HCQ therapy may lead to more severe presentations than previously known, so timely recognition of HCQ-induced cardiotoxicity is critical. Risk factors for HCQ-induced cardiotoxicity include older age, female sex, previous history of cardiovascular conditions, and long-term HCQ use. Patients with HCQ-induced cardiotoxicity often present with symptoms of heart failure, conduction abnormalities, and arrhythmias. Notably, this case is distinct in the severity of presentation with cardiogenic shock. Diagnostic tests include electrocardiograms, echocardiography, and cardiac magnetic resonance imaging (CMRI), which can show distinct findings suggestive of HCQ-induced cardiomyopathy. Invasive tests, such as EMB, may be required for definitive diagnosis. Treatment of HCQ-induced cardiotoxicity includes immediate discontinuation of HCQ and guideline-directed therapy when appropriate. Close follow-up for cardiac monitoring should be initiated in an outpatient setting.
Conclusion: This report emphasizes the importance of recognition and intervention of HCQ-induced cardiotoxicity. Routine monitoring with electrocardiograms and echocardiograms may be beneficial in high-risk patients, followed by CMRI for abnormalities. Early EMB should be considered for definitive diagnosis given prompt discontinuation of HCQ may lead to earlier restored cardiac function.
