Abstract Introduction COVID-19 infection has been associated with multiple cardiovascular complications, including acute coronary syndromes, myocarditis, venous thromboembolism, and arrhythmias. However, infiltrative cardiac diseases in the setting of post-COVID syndromes remain underrecognized. We report a case of cardiac sarcoidosis diagnosed several years after COVID-19 infection, highlighting the potential autoimmune and inflammatory sequelae of long COVID and the need to consider sarcoid involvement beyond the lungs. Case Presentation A 39-year-old man with a history of long COVID, hypertension, type 2 diabetes mellitus (non-insulin-dependent), and obstructive sleep apnea presented with new-onset palpitations. He was found to be in sustained monomorphic ventricular tachycardia requiring emergent synchronized cardioversion. His cardiac history was notable for symptomatic bradycardia two years earlier, for which a dual-chamber pacemaker had been implanted. At that time, transthoracic echocardiography demonstrated normal left ventricular function, and coronary angiography revealed no obstructive coronary artery disease. During the current admission, repeat echocardiography and angiography again showed no abnormalities, but electrocardiographic findings raised concern for arrhythmogenic right ventricular cardiomyopathy. He was transferred to a tertiary care center, where cardiac MRI demonstrated findings suggestive of cardiac sarcoidosis. He was discharged with a wearable cardioverter-defibrillator (WCD) and scheduled for an implantable cardioverter-defibrillator (ICD) upgrade. Before this could be performed, he re-presented with recurrent ventricular tachycardia, was started on amiodarone, and subsequently underwent lead extraction with upgrade to a biventricular ICD. FDG-PET imaging confirmed active cardiac sarcoidosis. Discussion Retrospective review revealed that several months prior to his initial bradycardia, the patient experienced a prolonged post-COVID illness consistent with long COVID. Despite normal echocardiographic and angiographic findings at that time, inflammatory or infiltrative etiologies were not considered. This case supports the hypothesis that post-COVID immune dysregulation may trigger or unmask autoimmune processes such as sarcoidosis. While pulmonary sarcoidosis remains the most common form, cardiac involvement may occur in isolation or as part of a systemic inflammatory response to viral antigens. Early recognition of cardiac sarcoidosis during the active inflammatory phase is essential to initiate corticosteroid or immunomodulatory therapy and prevent irreversible fibrosis, conduction abnormalities, and arrhythmic complications. Clinicians should maintain a high index of suspicion for infiltrative cardiac diseases in patients presenting with unexplained arrhythmias or conduction disturbances following COVID-19 infection. Given the widespread prevalence of SARS-CoV-2, further research is warranted to elucidate the mechanisms linking long COVID to autoimmune cardiac disorders such as sarcoidosis and to define their long-term pulmonary and systemic implications. This abstract is funded by: None
Gandhamaneni et al. (Fri,) studied this question.