Delve into the surprising cardiac effects of COVID-19. Learn how viral infection can lead to arrhythmias and the role of a hyperactive immune response. The prevalence of bradycardia among severe cases raises questions about long-term impacts. Atrial fibrillation emerges as a major concern, increasing the risk of strokes. Discover how inflammation may cause cardiac tissue fibrosis, contributing to ongoing arrhythmias even after recovery. This informative discussion shines a light on the hidden risks associated with the virus and the importance of monitoring.
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Inflammation Drives Cardiac Issues
COVID-19 causes cardiac issues mainly through inflammatory responses, not direct viral invasion.
This inflammation can lead to arrhythmias, myocarditis, and fibrosis of cardiac tissue.
insights INSIGHT
Atrial Fibrillation Risks in COVID-19
Atrial fibrillation is the most common arrhythmia linked to COVID-19 and worsens patient outcomes.
It raises stroke risk, necessitating anticoagulation and close monitoring.
insights INSIGHT
Fibrosis and Sinus Node Dysfunction
Inflammatory injury causes cardiac myocyte fibrosis, which prolongs arrhythmias after infection.
Sinus node dysfunction can mimic POTS with fluctuating heart rates due to autonomic issues.
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What factors are considered in a COVID-19 infection?
The viral load: Understood as the impact of SARS-CoV-2 viral particles infecting host cell tissue itself (utilizing ACE-2 receptors).
Pro-Inflammatory Response: Post-infection, the body's downstream systemic cytokine release (can be both normal or hyperactive, aka “cytokine storm”).
What cardiac impacts have been observed with COVID-19?
Arrhythmias: The mechanism of COVID-19 infection and arrhythmias is believed to be multifactorial. However, evidence suggests T-cell-mediated toxicity and cytokine storm may contribute to cardiac myocyte damage, precipitating proarrhythmias instead of direct viral entry.
Bradycardia: Increased prevalence in patients with severe COVID-19 infection, but not associated with increased adverse outcomes.
Atrial Fibrillation: Most common cardiac complication and risk factor for worsened outcomes in patients with COVID-19. Biggest associated risk is strokes, and may require heightened monitoring and anticoagulation therapy to mitigate stroke risk.
Fibrosis of Cardiac Tissue: Similar to arrhythmias, believed to be inflammation-mediated in COVID-19. Fibrosis of cardiac tissue increases the risk that any arrhythmias that develop during infection may persist after the infection has resolved.
Ventricular damage: Also inflammation mediated by an active infection and contributes to myocarditis.
No evidence suggests that COVID-19 vaccination contributes to myocarditis.
Sinus node dysfunction induced by inflammation that may lead to or be similar to Postural Orthostatic Tachycardia Syndrome (POTS).
Big takeaway?
Patients who have had or currently have COVID-19 are at an increased risk of developing arrhythmias and sustaining them post-infection. However, a majority of patients will recover.
Due to atrial fibrillation being the most prevalent arrhythmia associated with COVID-19 infection, increased monitoring and potential anticoagulation therapy are required.
References
Gopinathannair R, Olshansky B, Chung MK, Gordon S, Joglar JA, Marcus GM, et al. Cardiac Arrhythmias and Autonomic Dysfunction Associated With COVID-19: A Scientific Statement From the American Heart Association. Circulation. 2024 Nov 19;150(21):e449–65.
Khan Z, Pabani UK, Gul A, Muhammad SA, Yousif Y, Abumedian M, et al. COVID-19 Vaccine-Induced Myocarditis: A Systemic Review and Literature Search. Cureus. 14(7):e27408.
Summarized by Dan Orbidan, OMS1 | Edited by Dan Orbidan & Jorge Chalit, OMS3
Emergency Medical Minute