Post-operative atrial fibrillation (POAF) is a persistent and serious surgical complication that occur in 20-55% of cardiac surgery cases. POAF may lead to adverse health outcomes such as stroke, thromboembolism, cardiac arrest, and mortality, and may develop long-term. Patients have a 2-fold increase in mortality risk and spend about 3.7 more days in the hospital and $16,000 more in medical costs during their visit. The mechanisms and risk factors of POAF are still poorly understood, yet a strong foundation of how a disease process occurs is needed to provide the most effective treatment. Current mechanisms that are postulated to contribute to POAF include an increase in sympathetic tone, oxidative stress, local and systemic inflammation, a trigger that induces atrial substrate changes, a driver to sustain POAF, and electrolyte disturbances such as hypomagnesemia. While needing more research, current risk factors include age, male sex, history of myocardial infarction or heart failure, hypertension, diabetes, obesity, and COPD. Treatments mostly include prophylaxis of repurposed drugs such as beta-blockers, statins, oral anticoagulants, antiarrhythmics, and Vitamin D and electrolyte supplementation. Autonomic denervation has also been a promising preventative measure for patients undergoing cardiac surgery. This critical review article provides an up-to-date and comprehensive summary of the pathophysiology of POAF, current clinical risk factors and management for POAF and discusses new pathways for further investigation.

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SARS-CoV-2 is a +ssRNA helical coronavirus responsible for the global pandemic caused by coronavirus disease 19 (COVID-19). Classical clinical symptoms from primary COVID-19 when symptomatic include cough, fever, pneumonia or even ARDS; however, they are limited primarily to the respiratory system. Long-COVID-19 sequalae is responsible for many pathologies in almost every organ system and may be present in up to 30% of patients who have developed COVID-19. Our review focuses on how long-COVID-19 (3 –24 weeks after primary symptoms) may lead to an increased risk for stroke and thromboembolism. Patients who were found to be primarily at risk for thrombotic events included critically ill and immunocompromised patients. Additional risk factors for thromboembolism and stroke included diabetes, hypertension, respiratory and cardiovascular disease, and obesity. The etiology of how long-COVID-19 leads to a hypercoagulable state are yet to be definitively elucidated. However, anti-phospholipid antibodies and elevated D-dimer are present in many patients who develop thromboembolism. In addition, chronic upregulation and exhaustion of the immune system may lead to a pro-inflammatory and hypercoagulable state, increasing the likelihood for induction of thromboembolism or stroke. This article provides an up-to-date review on the proposed etiologies for thromboembolism and stroke in patients with long-COVID-19 and to assist health care providers in examining patients who may be at a higher risk for developing these pathologies.