Atrial fibrillation (Afib) is a common heart rhythm disorder characterized by a rapid, irregular heartbeat that increases the risk of stroke and heart failure. Respiratory infections, such as influenza, have long been recognized for placing stress on the cardiovascular system, occasionally triggering or worsening arrhythmias. The SARS-CoV-2 virus, which causes COVID-19, affects multiple organ systems, including the heart. This has raised important questions about how COVID-19 specifically interacts with and potentially exacerbates Afib.
The Direct Impact of COVID-19 on Atrial Fibrillation
COVID-19 infection is a significant trigger for both the exacerbation of pre-existing Afib and the onset of new Afib (NOAF), even in patients with no prior history. In hospitalized individuals, the incidence of NOAF ranges from 3% to 10% in general wards, and up to 16% to 44% in Intensive Care Unit (ICU) patients. This indicates a strong correlation between the severity of the viral illness and the likelihood of developing a heart rhythm disturbance.
The appearance of NOAF during hospitalization is considered a marker of a more severe illness and is associated with poorer clinical outcomes. Patients who develop NOAF often experience longer hospital stays, an increased need for ICU care, and a higher risk of in-hospital death. For those with pre-existing Afib, the infection can lead to increased frequency or severity of episodes, making rhythm control more challenging.
Biological Mechanisms of Cardiac Injury
The underlying cause of cardiac instability is multifactorial, involving systemic reactions to the virus rather than solely direct viral damage. A primary mechanism is the profound systemic inflammation, often termed a “cytokine storm,” that the body mounts in response to the infection. Pro-inflammatory markers, such as Interleukin-6 (IL-6), can directly affect the electrical properties of the heart muscle, creating an unstable environment in the atria that promotes disorganized electrical signals.
The virus also utilizes the Angiotensin-Converting Enzyme 2 (ACE2) receptor to enter cells, which are highly abundant in heart tissue. Interaction with ACE2 can disrupt the balance of the renin-angiotensin system, potentially leading to cardiac hypertrophy and fibrosis.
Another element is the respiratory failure and pneumonia caused by COVID-19, which often result in hypoxia (low oxygen levels). This places stress on the heart to compensate. This metabolic stress, combined with fever, increases the heart’s workload and can make the atria more electrically irritable, triggering Afib.
Acute Management and Monitoring for Afib Patients with COVID
Patients with pre-existing Afib who contract COVID-19 should consult their cardiologist for a review of their current medication regimen. This is particularly important because certain COVID-19 treatments, including some antiviral drugs, can interact with common antiarrhythmic and anticoagulant medications. These drug-drug interactions can alter the effectiveness or safety profile of Afib medications, potentially leading to severe bradycardia, dangerous heart rhythms, or an increased risk of bleeding.
Monitoring for specific symptoms of worsening Afib is crucial during the acute phase of illness. Signs such as a rapid or irregular heart rate, new or increased shortness of breath, significant fatigue, or lightheadedness warrant immediate medical attention. Maintaining proper hydration and electrolyte balance is also necessary, as fever and illness can cause fluid loss and electrolyte shifts that destabilize the heart’s electrical system. If Afib becomes uncontrolled or leads to hemodynamic instability, immediate emergency care is necessary to stabilize the heart rhythm.
Long-Term Cardiovascular Considerations
Even after the respiratory symptoms of COVID-19 resolve, the cardiovascular consequences can persist, falling under the umbrella of “Long COVID.” Studies show that individuals who had COVID-19 are significantly more likely to develop Afib in the year following the infection compared to those with other respiratory infections. The inflammatory damage and electrical changes induced by the acute illness may linger, contributing to a persistent or newly chronic form of Afib.
This post-COVID Afib requires extended cardiac follow-up and monitoring, even if the patient was previously in a normal rhythm. The presence of new or persistent Afib elevates the risk of thromboembolic events, specifically stroke, because the irregular pumping of the atria can allow blood clots to form. Appropriate anticoagulation strategies may need to be implemented to mitigate this long-term risk.
Disclaimer
The information contained in this article is for informational purposes only and is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.