Atrial fibrillation (Afib) is the most common heart rhythm disorder, characterized by a rapid, irregular heartbeat originating in the heart’s upper chambers. This disorganized electrical activity disrupts the orderly flow of blood and significantly increases the risk of stroke and heart failure. The SARS-CoV-2 virus caused a global pandemic with complications extending far beyond the respiratory system. Scientific investigation has established a clear relationship between COVID-19 infection and the development of new-onset atrial fibrillation.
Documenting the Link: Clinical Evidence
Large-scale clinical data confirms that a COVID-19 infection increases the likelihood of developing new-onset Afib, meaning the arrhythmia appears for the first time following the viral illness. Studies involving thousands of hospitalized patients showed that approximately 5.4% of those without a prior history developed it during their hospital stay. The incidence rate is notably higher in cases of severe infection, reaching up to 10% to 18% in critically ill or elderly patients.
The risk increase is most dramatic immediately following the acute infection. One large study demonstrated that the risk of Afib was up to twelve times greater in the first month after a COVID-19 diagnosis compared to uninfected individuals. This association highlights that the virus, or the intense physiological reaction to it, creates an environment conducive to this serious arrhythmia. New-onset Afib during hospitalization is consistently associated with a worse prognosis and higher rates of major adverse cardiovascular events.
How SARS-CoV-2 Triggers Arrhythmia
The connection between the SARS-CoV-2 virus and Afib is explained by biological processes that disrupt the heart’s electrical stability. The primary mechanism involves systemic inflammation, often referred to as a cytokine storm, where the body’s immune response becomes overly aggressive. Elevated levels of inflammatory markers, such as C-reactive protein and Interleukin-6, can directly destabilize the atrial tissue, creating a substrate for irregular electrical signaling.
The virus also has the potential to cause direct myocardial injury, though this is less frequent than systemic inflammation. SARS-CoV-2 binds to the Angiotensin-Converting Enzyme 2 (ACE2) receptor on the surface of heart muscle cells. This binding, along with the subsequent immune response, can lead to localized damage, fibrosis, and electrical disturbances within the atrial tissue, initiating the irregular rhythm.
Severe respiratory distress caused by the infection leads to significant hypoxia, or low oxygen levels, throughout the body. The resulting strain on the heart, coupled with increased sympathetic nervous system activation, promotes electrical instability and the onset of new arrhythmias. This physiological stress is exacerbated by factors like fever and sepsis, which increase the heart’s workload. The combination of inflammation, direct damage, and physiological stress creates a highly arrhythmogenic state in the acute phase of the illness.
Identifying Vulnerable Patients
While COVID-19 can trigger Afib in previously healthy individuals, certain patient characteristics significantly increase the risk. Advanced age is consistently identified as a major factor, with older patients showing a much higher prevalence of new-onset Afib compared to younger cohorts. This reflects that older hearts are generally more susceptible to inflammatory and electrical disturbances.
Pre-existing cardiovascular conditions, such as hypertension, heart failure, and coronary artery disease, also make the heart more vulnerable to the inflammatory stress of the virus. Patients with metabolic disorders like diabetes and obesity are similarly at heightened risk due to the underlying inflammatory state these conditions often entail.
Beyond pre-existing health, the severity of the COVID-19 infection itself is the strongest predictor of developing Afib. Individuals requiring intensive care unit admission, mechanical ventilation, or those who develop acute respiratory distress syndrome are disproportionately affected. This suggests that Afib is frequently a complication of the overall systemic collapse and severe inflammatory cascade associated with critical illness.
Acute Complication vs. Persistent Risk
The onset of Afib related to COVID-19 is divided into two categories based on the timing of its presentation and prognosis. Acute Afib occurs during the peak severity of the illness, typically while the patient is hospitalized and critically ill. This form is often transient, driven by acute factors like fever, sepsis, and extreme physiological stress, and may resolve as the patient recovers.
Even this short-lived arrhythmia is a serious event, associated with higher rates of major adverse cardiovascular events and in-hospital mortality. Clinicians often treat this acute form aggressively to stabilize the patient. The rhythm may return to normal once the systemic inflammation subsides.
A more concerning form is persistent or late-onset Afib, which emerges weeks or months after the initial infection, often as a feature of Long COVID. Studies show that survivors have an increased overall risk of Afib for months following the acute phase, even among those who were not hospitalized. This persistent risk is linked to ongoing, low-grade inflammation, microvascular dysfunction, or permanent scarring in the atrial tissue. Because late-onset Afib may require chronic management and long-term anticoagulation, continued cardiac monitoring and follow-up are important for all COVID-19 survivors who experience cardiac symptoms.