Wikipedia Deep Dive

Atrial fibrillation

17 min read

Your heart is supposed to beat in a steady, predictable rhythm. But for more than 33 million people worldwide, the upper chambers of their heart have gone rogue, quivering chaotically instead of contracting in an organized way. This condition, called atrial fibrillation, is the most common serious heart rhythm disorder on the planet—and half the people who have it don't even know what put them at risk.

A Heart That Won't Keep Time

Picture your heart as a four-room house. The two upper rooms, called the atria, are supposed to squeeze blood down into the two lower rooms, the ventricles, which then pump that blood out to your body. This happens roughly once per second, give or take, coordinated by electrical signals that ripple through your heart muscle in a precise sequence.

In atrial fibrillation—often shortened to AFib or simply AF—that electrical coordination falls apart in the upper chambers. Instead of one organized signal telling the atria when to contract, hundreds of chaotic electrical impulses fire simultaneously. The result? The atria don't really contract at all. They quiver. They fibrillate, like a bag of worms, to use the unsettling but accurate description cardiologists sometimes employ.

This matters for two big reasons.

First, when the atria can't squeeze properly, blood doesn't move through them efficiently. It pools. It stagnates. And stagnant blood has a dangerous tendency to clot. If one of those clots breaks loose and travels to the brain, you have a stroke. Atrial fibrillation dramatically increases stroke risk—it's one of the leading causes of preventable strokes worldwide.

Second, all those chaotic electrical signals bombarding the lower chambers create a heart rate that's both too fast and maddeningly irregular. A healthy heart at rest beats 60 to 100 times per minute in a steady rhythm. In uncontrolled atrial fibrillation, the heart might race at 150 beats per minute, then drop to 90, then spike again—all within seconds. Your heart becomes an unreliable engine, and over time, this can wear it out completely, leading to heart failure.

What It Feels Like (Or Doesn't)

Here's something that surprises many people: atrial fibrillation often announces itself with absolutely nothing. No symptoms at all. Many people discover they have it only during a routine physical exam, when a doctor checks their pulse and notices something wrong, or during an electrocardiogram done for an unrelated reason.

When symptoms do occur, they can range from mildly annoying to genuinely frightening.

Palpitations are the classic complaint—that unsettling sensation of your heart racing, pounding, fluttering, or skipping beats. Some people describe it as a fish flopping in their chest. Others feel like their heart is trying to escape through their ribcage.

Fatigue hits hard because an irregular heart can't pump blood efficiently. Your muscles don't get the oxygen they need, so climbing stairs or walking to the mailbox leaves you winded. Some people feel dizzy or lightheaded. A few lose consciousness entirely, fainting without warning when their brain suddenly doesn't receive enough blood flow.

Shortness of breath is common, especially when lying flat, because blood backs up into the lungs when the heart can't keep up with demand. Some people wake gasping in the middle of the night, a deeply alarming experience that sends many to emergency rooms fearing a heart attack.

The cruelest irony is that some people discover they have atrial fibrillation only after it has already caused catastrophic damage—they arrive at the hospital with stroke symptoms, and doctors find the arrhythmia that caused it.

Where the Chaos Begins

For decades, doctors knew that atrial fibrillation existed but struggled to understand exactly why certain hearts developed it while others didn't. A major breakthrough came in the 1990s when researchers discovered that the chaos often starts in a surprisingly specific location: the pulmonary veins.

The pulmonary veins are the blood vessels that carry oxygen-rich blood from your lungs back to your heart, specifically into the left atrium. Where these veins connect to the atrium, there are sleeves of heart muscle tissue that extend into the veins themselves. These muscle sleeves can develop abnormal electrical activity, firing off rapid bursts of signals that overwhelm the heart's normal pacemaker.

Think of it like a room full of people trying to have a conversation while someone in the corner keeps shouting random words at machine-gun speed. Eventually, nobody can follow what anyone else is saying, and chaos ensues.

This discovery revolutionized treatment. If the pulmonary veins are the source of the problem, doctors reasoned, why not electrically isolate them from the rest of the heart? This procedure, called pulmonary vein isolation or catheter ablation, uses either extreme heat or extreme cold delivered through a thin tube threaded into the heart to create scar tissue around the pulmonary vein openings. The scar tissue acts as an electrical barrier, preventing the rogue signals from escaping into the atrium.

But the pulmonary veins aren't the only troublemakers. The heart contains clusters of nerve cells called ganglionated plexi—essentially little relay stations for the autonomic nervous system, the part of your nervous system that controls unconscious functions like heart rate. These nerve clusters can also trigger atrial fibrillation and are sometimes targeted during ablation procedures.

There's also a structure called the left atrial appendage, a small pouch attached to the left atrium that's particularly prone to forming blood clots during atrial fibrillation. And the ligament of Marshall, a remnant of embryonic development that contains both nerve tissue and muscle fibers, can serve as yet another source of abnormal electrical activity.

As atrial fibrillation progresses from occasional episodes to a more constant presence, something troubling happens. The left atrium itself begins to change, developing its own capacity to generate chaotic electrical signals independent of the pulmonary veins. The disease, in essence, rewires the heart. This is why treating atrial fibrillation early often yields better results than waiting—the longer the chaos continues, the more entrenched it becomes.

Who Gets Atrial Fibrillation?

Age is the single biggest risk factor. Atrial fibrillation is rare in young people—fewer than one in a thousand people under 50 have it. But after 60, the numbers climb steeply. About four percent of people in their 60s and early 70s have atrial fibrillation. By age 80, that figure reaches 14 percent. Among people who live past 90, atrial fibrillation becomes more the rule than the exception.

This dramatic age-related increase reflects the cumulative wear and tear that decades of living inflict on the heart. Blood pressure gradually stiffens artery walls. The heart muscle itself becomes less elastic. The electrical conduction system accumulates subtle damage. Eventually, the conditions become ripe for chaos.

High blood pressure is the most common modifiable risk factor, present in somewhere between half and 90 percent of people with atrial fibrillation. The connection makes physiological sense. Chronically elevated blood pressure forces the heart to work harder, causing the muscle to thicken and stiffen. The left atrium, which receives blood from the lungs and must push it into the increasingly resistant left ventricle, enlarges under the strain. Enlarged, stiffened atrial tissue conducts electricity abnormally, setting the stage for fibrillation.

Heart valve problems, particularly those affecting the mitral valve between the left atrium and left ventricle, dramatically increase risk. When this valve doesn't close properly—a condition called mitral regurgitation—blood leaks backward into the atrium with each heartbeat, causing it to stretch and enlarge. When the valve is too narrow—mitral stenosis—blood backs up behind it, again distending the atrium. In developing countries, rheumatic fever, a complication of untreated strep throat, remains a major cause of valve damage and subsequent atrial fibrillation.

Other cardiac conditions contribute as well: coronary artery disease, heart failure, cardiomyopathy (diseases of the heart muscle itself), and congenital heart defects. People born with structural heart abnormalities tend to develop atrial fibrillation younger than others, and their arrhythmias often originate from the right atrium rather than the typical left-sided location.

Beyond the heart, the lungs play a surprising role. Chronic obstructive pulmonary disease, or COPD, increases risk, as does obesity and sleep apnea. The connection with sleep apnea is particularly striking—repeated episodes of nighttime oxygen deprivation appear to directly promote atrial fibrillation, with more severe oxygen drops correlating with higher rates of the arrhythmia.

Thyroid problems deserve special mention. An overactive thyroid gland, called hyperthyroidism, revs up the entire metabolism, including the heart, and is a well-established cause of atrial fibrillation. Even subtly elevated thyroid function, not quite high enough to cause obvious symptoms, can push the heart toward fibrillation.

The Lifestyle Connection

Here's where things get interesting from a public health perspective. Many risk factors for atrial fibrillation are things people can actually change.

Obesity stands out as a major modifiable risk. Excess body weight stresses the heart in multiple ways—it raises blood pressure, promotes inflammation, increases the likelihood of sleep apnea, and causes structural changes in the heart itself. Weight loss, conversely, can reduce the burden of atrial fibrillation in people who already have it. This is one of the few arrhythmias where lifestyle modification demonstrably helps.

Alcohol and atrial fibrillation have a complicated relationship. Heavy drinking—what doctors sometimes call binge drinking or, more colorfully, "holiday heart syndrome"—can directly trigger episodes of atrial fibrillation, sometimes within hours of excessive consumption. The mechanism involves alcohol's effects on the heart's electrical system combined with the dehydration and electrolyte disturbances that accompany heavy drinking.

But even moderate alcohol consumption, perhaps surprisingly, appears to increase risk. The effect is small for people who drink less than two drinks daily, but it's real. Long-term alcohol use changes both the structure and electrical properties of the heart, stimulating the sympathetic nervous system, promoting inflammation, raising blood pressure, and depleting potassium and magnesium—all of which favor the development of atrial fibrillation.

Smoking increases the risk of atrial fibrillation by about 40 percent compared to never smoking. Even secondhand smoke exposure elevates risk. Interestingly, Swedish snus—a form of smokeless tobacco that delivers nicotine at doses comparable to cigarettes—doesn't appear to share this association, suggesting that something in tobacco smoke beyond nicotine itself is responsible.

The relationship with exercise reveals an interesting U-shaped curve. Sedentary lifestyle increases risk through its associations with obesity, hypertension, and diabetes. Moderate regular exercise reduces risk—this is one of the protective factors that public health campaigns emphasize. But at the extreme end, long-term endurance exercise at levels far exceeding typical recommendations—think ultramarathon runners, professional cyclists, and elite endurance athletes—modestly increases risk again. The proposed mechanism involves exercise-induced remodeling of the heart combined with changes in the autonomic nervous system.

What about caffeine? Despite widespread belief that coffee triggers heart rhythm problems, the evidence doesn't support this. Caffeine consumption does not appear to increase atrial fibrillation risk—a finding that probably comes as welcome news to the millions who depend on their morning coffee.

Stress, Inflammation, and the Night Shift

Stress hormones, particularly cortisol, appear to play a role in triggering atrial fibrillation. Studies examining various biomarkers of stress, including heat shock proteins—molecules cells produce when under duress—suggest that psychological and physiological stress can tip a vulnerable heart into fibrillation. This aligns with the clinical observation that major life stressors sometimes precede the onset of the arrhythmia.

Chronic inflammation also contributes. People with atrial fibrillation tend to have elevated levels of inflammatory markers in their blood. More compellingly, sophisticated genetic studies using a technique called Mendelian randomization suggest that inflammation doesn't merely accompany atrial fibrillation—it actually causes it. This has implications for prevention, as reducing chronic inflammation through lifestyle changes might help protect against the arrhythmia.

Night shift work has emerged as a possible risk factor, though the evidence is still accumulating. The proposed connection involves disruption of circadian rhythms, the body's internal clock, which influences heart rhythm among countless other physiological processes.

It Runs in Families

Having a parent or sibling with atrial fibrillation increases your own risk by about 40 percent. This familial clustering prompted scientists to search for the genetic variants responsible, and they've found quite a few.

Early genetic studies identified mutations affecting ion channels—the protein structures that control the flow of electrically charged particles like potassium and sodium in and out of heart cells. These ion flows generate the electrical signals that coordinate heartbeat. Mutations that alter channel function can shorten what's called the effective refractory period—essentially the reset time a heart cell needs between electrical activations. Shortened refractory periods make it easier for electrical signals to circle back and re-excite tissue that has just fired, creating the self-perpetuating loops of chaotic activity that characterize fibrillation.

More recent genome-wide association studies, which scan the entire genetic code for variations linked to disease, have identified nearly 100 locations in the genome associated with atrial fibrillation. Many of these involve genes that control heart development and the regulation of cardiac electrical conduction. One particularly important gene, Pitx2c, helps direct the formation of the pulmonary veins during embryonic development—the very structures that so often serve as the launching point for atrial fibrillation.

When Medications Are the Culprit

A variety of medications can trigger atrial fibrillation, adding a layer of complexity for doctors trying to identify why someone developed the arrhythmia. The heart stimulant dobutamine, used in intensive care settings, carries an elevated risk, as does the chemotherapy drug cisplatin. Nonsteroidal anti-inflammatory drugs like ibuprofen—available over the counter and used by millions—are associated with a moderate increase in risk. Various other medications, from corticosteroids to certain antipsychotics to the nausea drug ondansetron, have been linked to atrial fibrillation as well.

Medication-induced atrial fibrillation can occur at any age but is most common in elderly patients, those who already have other risk factors, and people recovering from heart surgery.

Making the Diagnosis

Suspecting atrial fibrillation often begins with a simple physical finding: an irregular pulse. Instead of the steady lub-dub, lub-dub rhythm of a normal heart, a healthcare provider feeling the pulse at the wrist notices an erratic pattern—beats coming in rapid succession, then a pause, then another burst. The rate is often fast, typically above 100 beats per minute.

The confirmatory test is an electrocardiogram, or ECG (sometimes called EKG, from the German elektrokardiogramm). This recording of the heart's electrical activity reveals the characteristic signature of atrial fibrillation: irregularly spaced QRS complexes—the tall spiky waves that represent ventricular contraction—without the normal P waves that should precede them. P waves represent atrial contraction; their absence reflects the fact that the atria aren't contracting in any organized way.

The electrocardiographic diagnosis of atrial fibrillation was first documented in 1909 by the British cardiologist Thomas Lewis, though the clinical recognition of an irregular pulse dates back much further. The French physician Jean-Baptiste de Sénac described irregular heart rhythms in 1749, making atrial fibrillation one of the first cardiac arrhythmias to be identified in medical literature.

Treatment: Control the Rate or Restore the Rhythm?

Two fundamental approaches exist for managing atrial fibrillation, and choosing between them has occupied cardiologists for decades.

Rate control accepts that the heart will remain in atrial fibrillation but uses medications to slow down the ventricular response—preventing the heart from racing even while the atria continue their chaotic quivering. Beta-blockers, calcium channel blockers, and digoxin are commonly used for this purpose. The goal is a resting heart rate somewhere in the normal range, reducing symptoms and preventing the heart from wearing itself out.

Rhythm control attempts to restore and maintain normal sinus rhythm—getting the heart back to its regular, coordinated beating. This can be achieved through medications called antiarrhythmics or through procedures like electrical cardioversion, in which a controlled electric shock is delivered to reset the heart's rhythm, or catheter ablation, the procedure that isolates the pulmonary veins from the rest of the heart.

For years, large clinical trials suggested that rate control and rhythm control produced similar outcomes in terms of survival. However, more recent evidence has shifted opinion somewhat toward rhythm control, particularly when pursued early in the course of the disease, before the atria have undergone extensive electrical remodeling.

Electrical cardioversion deserves special mention as an emergency intervention. When someone with atrial fibrillation is hemodynamically unstable—meaning their blood pressure has dropped dangerously, they're in heart failure, or they're experiencing chest pain from inadequate blood flow to the heart muscle—cardioversion can be lifesaving. The procedure involves delivering a synchronized electrical shock through paddles or pads placed on the chest, briefly stopping all electrical activity in the heart and allowing its natural pacemaker to resume control.

Preventing Stroke: The Blood Thinning Question

Because atrial fibrillation so dramatically increases stroke risk, preventing clot formation becomes a central concern. For most people with atrial fibrillation, doctors recommend anticoagulant medications—blood thinners that make clot formation less likely.

For decades, warfarin was the standard choice. This medication, originally developed as a rat poison before finding medical applications, interferes with the liver's production of clotting factors. It's highly effective but requires careful monitoring—patients need regular blood tests to ensure their clotting time falls within the therapeutic range, and dietary vitamin K intake must remain relatively consistent since vitamin K counteracts warfarin's effects.

Newer medications called direct oral anticoagulants have simplified anticoagulation for many patients. Drugs like apixaban, rivaroxaban, dabigatran, and edoxaban work through different mechanisms than warfarin and don't require the same intensive monitoring. They've become first-line therapy for most patients with non-valvular atrial fibrillation.

But anticoagulants carry their own serious risk: bleeding. The same mechanism that prevents clots from forming in the heart also prevents clots from forming when you need them—after a cut, during surgery, or after trauma. Major bleeding, including bleeding into the brain, is a known complication of anticoagulant therapy. This creates a clinical balancing act: the stroke risk from not anticoagulating must be weighed against the bleeding risk from doing so.

For people at the lowest risk of stroke—generally younger patients without other cardiovascular conditions—the bleeding risk may outweigh the benefit, and anticoagulation may not be necessary. Doctors use scoring systems that incorporate age, sex, history of prior stroke, high blood pressure, diabetes, heart failure, and vascular disease to estimate each patient's stroke risk and guide the anticoagulation decision.

A Growing Epidemic

Atrial fibrillation is becoming more common, and the trend shows no signs of reversing. As of 2020, more than 33 million people worldwide had the condition. In Europe and North America, two to three percent of the adult population is affected. These numbers have been climbing for years, driven by population aging and the increasing prevalence of conditions like obesity, hypertension, and diabetes that predispose people to atrial fibrillation.

The consequences extend beyond the individuals affected. Atrial fibrillation is associated with increased risks of heart failure, dementia, and—most devastatingly—stroke. Managing the condition and its complications consumes substantial healthcare resources. The economic burden is enormous and growing.

Yet there's also reason for cautious optimism. The modifiable nature of many risk factors means that public health interventions targeting obesity, hypertension, physical inactivity, and excessive alcohol consumption could meaningfully reduce the burden of disease. Advances in ablation technology continue to improve outcomes for those who develop atrial fibrillation. And the growing understanding of the genetic architecture underlying the condition may eventually enable more targeted prevention and treatment strategies.

For now, atrial fibrillation remains one of modern cardiology's most common and challenging conditions—a disorder of electrical chaos in an organ that functions, above all else, through exquisite electrical coordination. Understanding it means understanding how the heart's elegant machinery can fail, and how medicine continues to search for ways to restore order to a heart that has lost its rhythm.