Atrial fibrillation (AFib) is an electrical problem: the upper chambers of the heart beat irregularly, sometimes too fast, and often inefficiently. Most treatment plans aim to manage three overlapping goals: preventing stroke, controlling heart rate or rhythm, and addressing the underlying conditions that make AFib more likely in the first place.
High blood pressure sits near the top of that list. Hypertension places constant strain on the heart, promotes structural changes in the atria, and significantly increases the risk of developing and sustaining AFib over time. But the relationship between blood pressure medications, heart structure, and the heart’s electrical system is complex.
Over the next several paragraphs, you’ll see how different drugs work, what they’re designed to do, and why careful monitoring is necessary.
Blood Thinners
Not all medications used in treating AFib are trying to “fix the rhythm.” Some manage symptoms, some address upstream risk factors, and others protect against downstream complications. Blood thinners fall squarely into the third category: they don’t change the heart’s rhythm, and they don’t lower blood pressure. Instead, their job is to reduce the risk of serious complications that can result from AFib – most importantly, stroke.
AFib causes the atria, the upper chambers of the heart, to beat irregularly. This prevents blood from flowing smoothly, allowing it to pool and form clots; if a clot travels to the brain, it can cause a stroke. Hypertension itself increases stroke risk by stressing the blood vessels and promoting clot formation, creating a dangerous combination with AFib. Blood thinners, also called anticoagulants or antiplatelet medications, help prevent these clots from forming, significantly reducing the chance of a cerebrovascular event.
Anticoagulants, such as warfarin or direct oral anticoagulants (DOACs), interfere with the blood’s ability to clot, lowering stroke risk by 50% or more.1 Warfarin also requires regular blood testing and avoidance of some dietary items, like grapefruit. Antiplatelet drugs prevent blood platelets from clumping together. Aspirin is a common antiplatelet that’s used for stroke, heart attack, and AFib prevention in patients with a history or high risk of cardiovascular disease; however, it’s not recommended outside of those parameters.2 And while it is an over-the-counter medication, it still necessitates consulting with a physician in patients with cardiovascular and bleeding risks. DOACs are favored for most AFib patients due to better stroke prevention.
Because they reduce the blood’s ability to clot, these medications increase the risk of bleeding; even a minor injury can lead to more serious bleeding than usual. It doesn’t complicate or worsen AFib, but it does mean patients need to use extra caution with activities, procedures, and other medications, which can complicate day-to-day life.
Blood thinners are usually prescribed based on a patient’s stroke risk, which can be measured with what’s called the CHA₂DS₂-VASc score. This score considers factors such as age, high blood pressure, diabetes, heart failure, previous stroke or vascular disease, and sex. The higher the score, the more likely a blood thinner is recommended.1
Beta-Blockers
Beta-blockers are often the first medications used to manage how AFib feels day to day. These drugs don’t control rhythm, but they do help regulate the heart rate and reduce the strain AFib places on the heart.
Beta-blockers work by blocking the effects of adrenaline on the heart. This slows the heart rate, reduces how forcefully the heart contracts, and lowers blood pressure. In AFib, where the heart may beat rapidly and irregularly, this can significantly improve symptoms like palpitations, shortness of breath, fatigue, or exercise intolerance.
The benefits of beta-blockers include better symptom control, reduced risk of tachycardia-induced cardiomyopathy (heart muscle weakening from sustained fast rates), and lower blood pressure (a major upstream AFib risk factor). In patients with hypertension, coronary artery disease, or prior heart attacks, beta-blockers can serve dual purposes: managing AFib-related heart rate and protecting overall cardiovascular health.
Despite their benefits, beta-blockers aren’t always a good fit for some individuals and can cause excessive fatigue, dizziness or lightheadedness, and/or bradycardia (heart rates that are too slow). Because they blunt the heart’s ability to increase rate, beta-blockers may worsen symptoms rather than improve them in those with already slow resting heart rates or conduction system disease.
Beta-blockers can also interact with other medications, including some rhythm-control drugs, so careful dose titration, close monitoring, and follow-ups are essential to a plan of care.
Beta-blockers do not correct the underlying electrical chaos of AFib, but they make AFib more tolerable and safer by controlling how fast the ventricles (the two lower chambers of the heart) respond. For many patients, beta-blockers become a more long-term therapy solution. For others, they may be used temporarily while additional treatments, such as antiarrhythmic drugs or ablation, are considered.
Various Channel Blockers
Some medications influence AFib by altering how electrical signals travel through the heart rather than acting on adrenaline or clot formation. These drugs work by blocking specific ion channels involved in cardiac conduction, slowing the transmission of electrical impulses from the atria to the ventricles. Different channel blockers affect the heart in different ways, and their usefulness depends heavily on a patient’s underlying heart function, blood pressure, and tolerance of side effects.
Calcium Channel Blockers
Calcium channel blockers (CCBs) are another class of medications commonly used to control heart rate in patients with AFib, though not all CCBs are effective for AFib. Like beta-blockers, they control rate versus rhythm, but through a different mechanism. Instead of blocking the effects of adrenaline on the heart, they slow how quickly electrical signals travel from the atria to the ventricles, helping prevent excessively fast heart rates during AFib episodes. By slowing conduction through the AV node, these medications allow the ventricles to beat at a more controlled pace.
Calcium channel blockers also relax blood vessels, which lowers blood pressure and reduces overall cardiac workload in patients who also have hypertension or angina (chest pain related to reduced blood flow to the heart).
Like any medication, calcium channel blockers aren’t appropriate for everyone. Because they reduce the force of heart contraction, they can worsen symptoms in patients with certain types of heart failure and lead to fluid retention (edema) or worsening shortness of breath.
Sodium Channel Blockers
Sodium channel blockers are a group of medications used for rhythm control rather than simply slowing the heart rate. These drugs work by reducing how quickly electrical signals fire and spread through atrial heart tissue, making it harder for irregular rhythms to start or persist.
Because of how they affect cardiac conduction, sodium channel blockers are most often prescribed to patients with paroxysmal AFib and otherwise healthy heart structures. For this type of patient, they can be effective at reducing episode frequency and improving symptoms.
AFib exists on a spectrum, and the type of AFib determines which medications are going to be safe and effective:
- Paroxysmal AFib episodes start and stop on their own, usually within 7 days.
- Persistent AFib episodes last longer than 7 days and typically require treatment to restore normal rhythm.
- Long-standing persistent AFib lasts longer than 12 months and is harder to convert (restore to a normal heart rhythm).
- Permanent AFib is continuous, and rhythm restoration is no longer pursued, focusing instead on rate control and stroke prevention.
Sodium channel blockers are generally avoided in persistent or permanent AFib, as well as in patients with significant structural heart disease or coronary artery disease, because they can increase the risk of dangerous arrhythmias rather than reduce them.
Potassium Channel Blockers
Potassium channel blockers are another class of rhythm-control medications that prolong the heart’s electrical recovery phase. This helps stabilize the rhythm by preventing premature or abnormal electrical impulses that can trigger AFib. Potassium channel blockers are often used in patients with persistent AFib, particularly when other rhythm-control strategies have failed or aren’t appropriate.
These medications can also cause complications. By altering electrical repolarization, they can sometimes provoke other dangerous arrhythmias, particularly in the ventricles. Some can also have different organ-specific toxicities, affect kidney function, or interact with electrolyte levels, so initiation and dose adjustments often require close monitoring, sometimes even hospitalization at the start of therapy.
Diuretics
Diuretics sit in upstream risk factor management – but with downstream electrical consequences if mismanaged. They are commonly prescribed to treat high blood pressure and heart failure, both of which are major contributors to AFib development and progression, and work by helping the body eliminate excess fluid and sodium, reducing blood volume and easing the workload on the heart. By lowering pressure inside the heart and blood vessels, diuretics can help reduce atrial stretch, a structural change that makes AFib more likely.
However, diuretics also illustrate how treating AFib risk factors requires careful balance. Many diuretics, particularly thiazide and loop diuretics, can lower potassium levels. Low potassium (hypokalemia) alters the heart’s electrical stability and can increase the risk of abnormal rhythms, including AFib. To reduce arrhythmia and the risk of life-threatening cardiovascular events, doctors often pair thiazide diuretics with potassium-sparing medications.
ACE Inhibitors and ARBs
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) relax blood vessels, reduce vascular resistance, and decrease hypertensive strain placed on the heart over time. In this regard, they help in AFib management by targeting high blood pressure, the most common risk factor for developing AFib.
They are also thought to help by limiting structural remodeling of the atria (including fibrosis and enlargement) that makes AFib harder to control once it develops.
ACE inhibitors and ARBs don’t correct abnormal rhythms or relieve palpitations, but by addressing the underlying conditions that promote AFib, they help create a more stable electrical environment over time.
Complications of these drugs can cause an excessive drop in blood pressure, dizziness, or fatigue in some patients, especially when combined with other blood pressure medications. While diuretics tend to lower potassium levels, ACE inhibitors and ARBs can have the opposite effect and raise potassium; either too little or too much potassium can disrupt the heart’s electrical stability and increase the risk of arrhythmias, including AFib. ACE inhibitors may also trigger a persistent dry cough or, rarely, swelling of the lips or throat (angioedema), and both drugs can affect kidney function in some individuals.
Medications affect heart rate, rhythm, blood pressure, and electrolyte balance in different ways, and individual responses can vary widely. Working closely with a cardiology team, including an electrophysiologist for specialized rhythm management, is the best way to maximize benefits, minimize complications, and align treatment plan adjustments with a patient’s overall cardiovascular health.
Dr. Tordini is a part of Florida Medical Clinic, Orlando Health.
- Vyas, V., Vyas, V., Sharma, A., & Ashok Kumar, P. (2025). Anticoagulation for Stroke Prevention in Patients with Atrial Fibrillation: A Review of the Literature and Current Guidelines. Reviews in cardiovascular medicine, 26(6), 39233. https://doi.org/10.31083/RCM39233.
- American Heart Association Newsroom. (2022, April 26). New USPSTF guidance: Continue to take low-dose aspirin if you have a history of heart attack, AFib, stroke or vascular stenting. American Heart Association. https://newsroom.heart.org/news/new-uspstf-guidance-continue-to-take-low-dose-aspirin-if-you-have-a-history-of-heart-attack-afib-stroke-or-vascular-stenting.
