Can Chemotherapy Cause Atrial Fibrillation (AFib)?

Chemotherapy can cause atrial fibrillation, and the link is well established across multiple drug classes. A large study of women with early-stage breast cancer found that those who received chemotherapy had a roughly 23% higher rate of developing AFib compared with those who did not, and the association held regardless of which specific agents were used. The relationship between cancer treatment and irregular heart rhythm turns out to be more layered than a simple drug side effect, though, involving inflammation, tissue damage, electrolyte disruption, and in some cases, the cancer itself.

How Often It Happens

The overall rate of treatment-induced arrhythmias varies widely depending on the drug, the cancer type, and the patient’s heart health going in. One study tracking about 5,000 cancer patients found that roughly 12% developed a new arrhythmia during or after treatment, with AFib being among the most common types.¹ A systematic review and meta-analysis that pooled data from over 14,700 cancer patients identified twelve distinct risk factors that predicted who would develop arrhythmias after chemotherapy.² That number probably understates the true prevalence, because many episodes of AFib are brief, cause no symptoms, and go undetected unless the patient happens to be on a monitor at the time.

The breast cancer data is particularly telling because the study population was large and closely tracked. Women who received chemotherapy for early-stage breast cancer had a statistically higher rate of AFib, and the increased risk was not limited to any single chemotherapy agent. Neither anthracyclines nor trastuzumab specifically accounted for the association, suggesting that chemotherapy in general, rather than one particular drug, raises the odds.³

Which Drugs Carry the Highest Risk

Not all chemotherapy drugs are equal when it comes to heart rhythm problems. The evidence points to several classes that deserve special attention.

Anthracyclines, the workhorse drugs used in many breast cancer, lymphoma, and sarcoma regimens, are among the best-studied offenders. Doxorubicin, the most widely used anthracycline, causes direct damage to atrial heart cells. Research has shown it triggers cell death, tissue shrinkage, and disrupts the gap-junction proteins that help electrical signals travel smoothly between cells. This combination of structural and electrical damage sets the stage for chaotic rhythms.⁴ When researchers compared anthracyclines head-to-head with newer targeted therapies, patients on anthracyclines had about a 40% higher risk of developing a new arrhythmia within the first six months.¹

BTK inhibitors, particularly ibrutinib, stand out in a different way. Ibrutinib is used primarily for blood cancers and has one of the most clearly defined AFib risks of any cancer drug. Researchers traced the problem to ibrutinib’s off-target inhibition of a specific kinase called CSK. When that kinase is blocked, it leads to atrial enlargement, fibrosis, and inflammation in the heart’s upper chambers. Pharmacovigilance data showed that drugs blocking CSK were reported to cause AFib at dramatically higher rates than cancer drugs that do not affect that target.⁵ Among patients on ibrutinib who already had cardiovascular disease, the rate of new AFib was about 17%, nearly three times higher than in ibrutinib patients without pre-existing heart problems.⁶

Immune checkpoint inhibitors, which unleash the immune system to fight cancer, can also trigger AFib, though through a different mechanism. In at least one documented case, a biopsy of the heart’s electrical conduction system showed patches of immune cells (T-lymphocytes) infiltrating the tissue that controls heart rhythm. That inflammatory invasion can disrupt the signals that keep the heartbeat regular.⁷ Other drug families linked to AFib include alkylating agents, antimetabolites, and angiogenesis inhibitors, though the evidence is thinner for some of these compared with anthracyclines and BTK inhibitors.⁸

How Chemotherapy Disrupts Heart Rhythm

The mechanisms fall into two broad categories: direct electrical interference and indirect structural damage. Some drugs act on ion channels or intracellular signaling pathways in heart cells, essentially scrambling the electrical signals that keep the heart beating in rhythm.⁹ Others cause their damage more slowly, through chronic oxidative stress that kills heart cells and triggers waves of inflammation and scarring.¹⁰

Fibrosis, or scarring of the atrial tissue, is one of the most important downstream effects. When healthy heart muscle is replaced by scar tissue, electrical signals can no longer travel through the chamber in an orderly fashion. They start circling and fragmenting, creating the chaotic rhythm that defines AFib. Inflammation accelerates this process. Research has identified specific inflammatory pathways, including the NLRP3 inflammasome, that promote both atrial fibrosis and electrical instability in cancer patients.¹¹ Cancer itself can drive some of these same inflammatory pathways, which means the tumor and its treatment sometimes work together to push the heart toward arrhythmia.

For doxorubicin specifically, molecular-level studies have shown that the drug binds tightly to certain regulatory proteins in heart cells, with binding energies strong enough to suggest stable, spontaneous interactions. This helps explain why the cardiac effects can persist long after the drug is cleared from the bloodstream.¹² Encouragingly, laboratory studies have shown that dexrazoxane, a cardioprotective agent sometimes given alongside anthracyclines, and certain antioxidants can prevent the atrial remodeling by reducing oxidative stress.⁴

When AFib Tends to Appear

Timing varies, and that unpredictability is part of what makes the problem difficult to manage. Some patients develop arrhythmias during or immediately after their first infusion. Others do not experience rhythm problems until months into treatment. A review of cardiac toxicity from chemotherapy described two distinct windows: an acute phase, where transient rhythm disturbances show up during or right after a dose, and a delayed phase, where the more common pattern of left ventricular dysfunction and possible arrhythmias develops months after treatment begins.¹³

Case reports illustrate the acute end of the spectrum. One patient with rhabdomyosarcoma developed AFib with a dangerously fast heart rate soon after his second cycle of chemotherapy. His rhythm was controlled with a beta-blocker, which is often the first-line treatment in these situations.¹⁴ But for drugs like ibrutinib, which patients take continuously for months or years, AFib can surface at any point during long-term use, sometimes well after the first year. The distinction matters because acute episodes may resolve when the offending drug is paused, while arrhythmias from cumulative structural damage tend to be more persistent.

Who Is Most Vulnerable

Certain patients walk into chemotherapy with a substantially higher risk of developing AFib. The meta-analysis of nearly 15,000 patients identified twelve risk factors, and several of them are conditions that oncologists can screen for before treatment begins.² High blood pressure, for instance, was associated with a roughly 63% increased risk of developing an arrhythmia during treatment, and a history of heart failure more than doubled the risk.¹ Men faced a modestly higher risk than women in the same study.

Electrolyte imbalances deserve particular attention because they are so common during chemotherapy. Nausea, vomiting, diarrhea, and reduced food intake can all deplete potassium, magnesium, and calcium, the minerals that keep heart cells firing in rhythm. The meta-analysis found that patients with electrolyte or acid-base disturbances had nearly double the risk of arrhythmia compared with patients whose levels stayed normal.² This is one of the more actionable findings, since electrolytes can be monitored and corrected throughout treatment.

Pre-existing cardiovascular disease is an especially strong predictor for patients on ibrutinib. Among those with a known history of coronary artery disease, heart failure, or significant valve disease, about one in six developed new atrial arrhythmias, and these patients also had higher mortality rates.⁶ For oncologists choosing between ibrutinib and newer alternatives with a cleaner cardiac profile, a patient’s heart history can tip the balance.

Why Managing AFib in Cancer Patients Is Unusually Complicated

Treating AFib in someone who also has active cancer is a clinical minefield. The two biggest challenges are anticoagulation and drug interactions, and both are harder to navigate than in a typical AFib patient.

AFib raises stroke risk because blood can pool and clot in the heart’s upper chambers. The standard treatment is blood thinners, but cancer patients often have competing bleeding risks. Some tumors bleed easily. Chemotherapy can drop platelet counts, making clotting harder. Certain cancer surgeries create wounds that need to heal. Physicians are frequently reluctant to prescribe anticoagulants in these circumstances, and the standard risk-prediction scores used for the general AFib population do not account for the bleeding hazards unique to active cancer.¹⁵ The decision about whether and how to thin the blood requires individualized assessment that weighs stroke risk against bleeding risk, accounts for the specific cancer and treatment plan, and gets revisited regularly as the situation changes. Real-world data confirm that patients with both AFib and active cancer experience high rates of both blood clots and bleeding, underscoring how difficult this balancing act is.¹⁶

Drug interactions add another layer. Many targeted cancer therapies are metabolized by the same liver enzymes that process common heart-rhythm drugs. Using both at the same time can push levels of either drug too high or too low, creating a risk of dangerous side effects or ineffective treatment. This has been flagged as a growing concern as the number of targeted cancer therapies expands.¹⁷ Sometimes the cancer treatment itself needs to be adjusted, paused, or switched to a different agent to accommodate AFib management, which introduces its own risks if the cancer treatment is interrupted at a critical time.

The Role of Cardio-Oncology

The overlap between cancer and heart disease has grown prominent enough to spawn its own subspecialty. Cardio-oncology teams now exist at most major cancer centers, staffed by cardiologists who understand the cardiac effects of specific cancer drugs and oncologists who know which treatment modifications are safe without compromising cancer outcomes. For patients at elevated risk of AFib, baseline cardiac assessment before starting chemotherapy, including an electrocardiogram and sometimes an echocardiogram, can establish what the heart looks like before treatment begins. That baseline makes it much easier to spot changes early.

Monitoring during treatment varies by regimen and risk level. Patients on anthracyclines often get periodic imaging to watch for drops in heart pumping function. Those on ibrutinib may have more frequent rhythm checks, especially if they have cardiovascular risk factors. The practical message for patients is straightforward: report any new palpitations, racing heartbeat, dizziness, or unusual fatigue to your oncology team right away. Many chemotherapy-induced AFib episodes are treatable, and catching them early opens up more management options.

Catheter Ablation in Cancer Patients

For AFib that does not respond well to medications, catheter ablation is a standard procedure that uses targeted energy to silence the abnormal electrical circuits in the heart. The question of whether this works as well in cancer patients as it does in the general population has not been thoroughly answered. Data on its effectiveness and safety in patients with a cancer history remain limited, and the procedure carries its own risks, including the need for anticoagulation around the time of the ablation.¹⁸ That said, there is nothing about cancer that categorically rules ablation out, and it may be a reasonable option for selected patients whose AFib is persistent and interfering with quality of life or the ability to continue cancer treatment. These decisions are best made jointly by the oncologist and cardiologist.

Can AFib Outlast the Cancer Treatment

This is a question many patients ask, and the honest answer is: sometimes. For AFib triggered by an acute event, like a transient electrolyte imbalance or the immediate stress of an infusion, the arrhythmia often resolves once the trigger is corrected. Stopping or switching the offending drug may be enough. But when AFib results from structural changes to the heart, particularly fibrosis and scarring caused by cumulative anthracycline exposure, the damage can be permanent. Chronic oxidative stress, repeated bouts of inflammation, and sustained overproduction of pro-fibrotic signals remodel the atrial tissue in ways that do not fully reverse.¹⁰ These patients may need long-term rhythm or rate control, along with ongoing decisions about anticoagulation, well beyond the end of their cancer treatment.

The distinction between reversible and irreversible AFib is not always clear in the moment. A patient who develops AFib during their third cycle of chemotherapy may not know for weeks or months whether it will persist after treatment ends. Follow-up cardiac monitoring after completing chemotherapy is increasingly recognized as important, especially for patients who received high cumulative doses of anthracyclines or prolonged courses of ibrutinib. Cancer survivorship care plans are starting to incorporate cardiac surveillance, but practice varies widely, and many patients still fall through the cracks once active treatment ends.

Protective Strategies Under Investigation

The finding that antioxidants and dexrazoxane can prevent doxorubicin-induced atrial remodeling in laboratory settings has sparked interest in protective strategies that could be given alongside chemotherapy.⁴ Dexrazoxane is already approved for use in certain clinical settings to protect against anthracycline-related heart damage, but its use has been inconsistent, partly due to earlier concerns (now largely allayed) that it might reduce the anticancer effectiveness of the chemotherapy. Whether it specifically prevents AFib in humans, as opposed to the better-studied outcome of reduced heart-pumping problems, remains an open question that clinical trials have not yet definitively answered.

For BTK inhibitor-related AFib, the clearest protective strategy is choosing a different drug. Newer-generation BTK inhibitors like acalabrutinib and zanubrutinib were designed to be more selective, hitting the intended cancer target with less off-target activity on the kinases involved in heart rhythm. Early comparative data suggest these alternatives carry a lower AFib risk than ibrutinib, though they are not completely free of cardiac effects. For patients who need a BTK inhibitor and have significant cardiac risk factors, the choice of agent matters more than any add-on protective measure.

1
PubMed Central. Incidence of Cancer Treatment-Induced Arrhythmia Associated With Novel Targeted Chemotherapeutic Agents
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JAMA Network Open. Association of Early-Stage Breast Cancer and Subsequent Chemotherapy With Risk of Atrial Fibrillation
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PubMed. Anthracycline-Induced Atrial Structural and Electrical Remodeling Characterizes Early Cardiotoxicity and Contributes to Atrial Conductive Instability and Dysfunction
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PubMed Central. Ibrutinib-Mediated Atrial Fibrillation Attributable to Inhibition of C-Terminal Src Kinase
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PubMed Central. Pre-existing cardiovascular disease increases risk of atrial arrhythmia and mortality in cancer patients treated with Ibrutinib
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PubMed Central. Cardiac adverse events of immune checkpoint inhibitors in oncology patients: A systematic review and meta-analysis
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PubMed Central. Anticancer Therapy-Induced Atrial Fibrillation: Electrophysiology and Related Mechanisms
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PubMed Central. Cancer, Inflammation, and Thrombosis: Drivers of Atrial Fibrillation in Oncology Patients
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PLoS One. An integrated multi-omics study of key mediators and therapeutic targets for doxorubicin-induced atrial fibrillation
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PubMed Central. Chemotherapy-Induced Atrial Fibrillation With Rapid Ventricular Response in a Patient With Pleomorphic Rhabdomyosarcoma: A Case Report and Approach to Management
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PubMed Central. Anticoagulation for atrial fibrillation in active cancer
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PubMed Central. Efficacy and safety of catheter ablation for atrial fibrillation in patients with history of cancer