Atrial Fibrillation (AFib) is an irregular heart rhythm where the heart’s upper chambers beat chaotically and rapidly. Chemotherapy refers to drugs used to treat cancer, often by destroying quickly dividing cells. There is a documented relationship between receiving chemotherapy and the development or worsening of AFib. This connection is a recognized aspect of cardiotoxicity, which describes damage to the heart caused by cancer treatment. Understanding this link is important for patients, as it allows for proactive management of potential cardiac issues.
The Connection Between Chemotherapy and AFib
Chemotherapy-related AFib can occur during drug administration, shortly after the treatment cycle, or months later. The incidence of new-onset AFib varies widely depending on the specific cancer, patient age, and the type of drug regimen used. Studies suggest that in certain patient populations, such as those with thoracic cancers or specific lymphomas, the incidence can range from 1% up to 12% or higher. This variability underscores that the risk is not uniform across all patients.
A patient’s pre-existing heart health is a significant factor in determining the likelihood of developing this arrhythmia during therapy. Patients who already have underlying conditions like hypertension, diabetes, or coronary artery disease are generally at higher risk. While the overall incidence is relatively low, the potential for AFib to cause stroke or heart failure means that this connection must be taken seriously.
How Chemotherapy Affects Heart Rhythm
The mechanism by which chemotherapy disrupts heart rhythm is categorized as cardiotoxicity, involving several physiological pathways. Direct myocardial injury is a primary cause, where the chemotherapy agent damages heart muscle cells (cardiomyocytes). This damage can lead to structural changes, such as fibrosis or scarring, which interfere with the heart’s normal electrical signaling pathways. An altered structure creates an environment where electrical impulses circle abnormally, triggering AFib.
Chemotherapy also induces systemic effects that destabilize the heart’s electrical system without immediate structural damage. These effects include increased systemic inflammation and oxidative stress. These processes alter the function of ion channels within heart cells, making them more excitable and prone to arrhythmia.
Furthermore, many chemotherapy regimens can inadvertently cause severe dehydration or lead to electrolyte imbalances, such as low levels of potassium (hypokalemia) or magnesium (hypomagnesemia). These mineral deficiencies are known to destabilize the electrical activity of the heart, acting as triggers for AFib onset.
Specific Drug Classes That Increase Risk
Several classes of chemotherapy and targeted therapy drugs have a higher documented association with cardiotoxicity, including the induction of AFib. Anthracyclines, such as doxorubicin, are a long-standing class of agents known to cause dose-dependent toxicity to the heart muscle. This damage is often cumulative, meaning the total lifetime dose increases the risk of both structural heart failure and rhythm disturbances. The risk of AFib induction is pronounced when these drugs are administered rapidly or in high doses.
Targeted therapies, which are newer cancer treatments, also carry specific cardiac risks. Tyrosine Kinase Inhibitors (TKIs) can interfere with signaling pathways in the heart that regulate electrical stability. Certain platinum-based chemotherapy agents, like cisplatin, are also linked to cardiovascular complications, often by contributing to systemic inflammation and electrolyte changes. The risk associated with these agents is not always immediate; some targeted therapies can cause AFib shortly after starting treatment, while others may become apparent only after many cycles.
Screening, Monitoring, and Treatment
Managing the risk of chemotherapy-induced AFib begins with a thorough pre-treatment assessment to identify high-risk individuals. This initial screening typically involves a baseline electrocardiogram (ECG) to check electrical activity and an echocardiogram to assess the heart’s structure and pumping function. Identifying pre-existing conditions like a history of AFib, heart failure, or uncontrolled hypertension allows oncologists and cardiologists to tailor the treatment plan. This multidisciplinary approach, known as cardio-oncology, helps determine if prophylactic measures or alternative drug regimens are necessary.
During the treatment phase, patients are advised to be vigilant for symptoms that may indicate an irregular rhythm. Common signs include a sudden onset of palpitations, a racing or fluttering heart, shortness of breath, or unexplained dizziness and fatigue. Regular monitoring, which may include periodic ECGs or portable heart monitors, is often implemented, particularly when patients are receiving high-risk agents. This proactive surveillance helps detect AFib early, before it leads to serious complications.
If AFib is confirmed during chemotherapy, the immediate treatment focuses on two main goals: controlling the heart rate and preventing stroke. Medications such as beta-blockers or calcium channel blockers are commonly used to slow the ventricular response and restore a more regular rhythm. Because AFib increases the risk of blood clot formation, anticoagulation therapy (blood thinners) is often initiated to prevent a stroke. In some cases, the treating oncologist may temporarily interrupt or reduce the dose of the offending chemotherapy agent until the heart rhythm is stabilized.