A CONFOUNDING CASE OF NON-ISCHEMIC CARDIOMYOPATHY: ACQUIRED MYOCARDITIS FROM COVID-19 AND SYSTEMIC LUPUS ERYTHEMATOSUS LEADING TO CLINICAL HEART FAILURE

ABSTRACT

CASE We report a 50-year-old Caucasian female with a history of systemic lupus erythematosus (SLE) in remission and chronic kidney disease (CKD) stage 5. The patient presented with dyspnea on exertion and orthopnea for two weeks. Six weeks ago, she was diagnosed with COVID-19 after presenting to the ED for substernal chest pain, myalgias, and fatigue. During this admission, she denied any current joint pain, chest pain, or rashes. She denies a history of alcohol or illicit drug use. EKG in the ED showed T-wave inversions in lead I and aVL, stable from prior EKG. The brain natriuretic peptide level was elevated at 3,500 pg/ml. There was no transaminitis, and kidney function was at baseline. Chest x-ray showed pulmonary vascular congestion and cardiomegaly. A transthoracic echocardiogram showed a left ventricular ejection fraction of 15-20% with severe global hypokinesis. The patient had a full cardiomyopathy workup. We ruled out ischemic cardiomyopathy with a negative coronary angiogram. Non-ischemic cardiomyopathy (NICMO) workup was initiated, with a focus on viral or autoimmune myocarditis. While a cardiac MRI would have been the gold standard to assess for myocardial scarring, the patient's CKD status prohibited this possibility. Similarly, an endomyocardial biopsy was not performed due to its low sensitivity for diagnosing viral or autoimmune myocarditis. Without evidence of infiltrative disease, or other exposures, it was deemed that the patient's recent history of COVID-19 infection, in conjunction with underlying SLE, were the causes of her new-onset NICMO. The patient's dyspnea responded to intravenous bumetanide. We initiated guideline-directed medical therapy with carvedilol and isosorbide-dinitrate. She continues regular follow-up in the outpatient heart failure clinic. IMPACT/DISCUSSION: Classification and evaluation of NICMO can be broad, and thus the clinical picture plays an essential role in the workup. Acquired cardiomyopathy from prior myocarditis was the most likely etiology of our patient's new-onset NICMO. Our patient had no clinical symptoms of myocarditis prior to her exposure to COVID-19, making it unlikely that SLE was the sole driving factor. There is a known association between COVID-19 and myocarditis. A few proposed mechanisms for COVID-19 induced myocarditis include upregulation of cytokines, particularly interleukin-6, and downregulation of ACE2, leading to microvascular and cardiac pericyte dysfunction. Cytokine release from COVID-19 coupled with subclinical SLE could have acted synergistically to cause this patient's condition. Given the increasing incidence of COVID-19 infections, internists must consider COVID-19 exposures during the workup of new-onset heart failure. CONCLUSION: The workup for NICMO in the COVID-19 era must include detailed history taking for sick contacts and prior history of COVID-19 diagnosis. More research is needed to determine if COVID-19 infection can increase the risk of NICMO in patients with a known history of SLE.