Summary
Highlights
Atrial fibrillation (AFib) involves a rapid and chaotic rhythm in the top part of the heart (atria), causing the bottom chambers (ventricles) to beat irregularly and often too fast. This can lead to symptoms like palpitations. AFib is caused by abnormal electrical trigger spots and scar tissue, which become more common with age.
AFib increases the risk of stroke because the chaotic atrial contractions allow blood to pool and form clots, especially in the left atrial appendage. If a clot breaks off and travels to the brain, it causes a stroke. The primary way to prevent this is through blood thinner medications (anticoagulants) like Warfarin, Eliquis, Xarelto, and Pradaxa. For those who cannot take blood thinners, surgical or catheter-based procedures can close off the left atrial appendage.
During AFib, the heart's pumping chambers (ventricles) can beat too fast, causing symptoms and potentially weakening the heart over time. The heart rate is controlled by the AV node, an electrical 'bridge' between the atria and ventricles. Medications called 'bridge slowing medicines' (beta-blockers, calcium channel blockers, digoxin) are used to slow down this bridge, reducing the number of signals reaching the ventricles. In rare cases where medications are ineffective, an AV node ablation can permanently damage the bridge, necessitating a pacemaker.
EKG readings and heart monitors help doctors diagnose AFib and determine if the heart rate is fast or slow. AFib is characterized by an irregular and often rapid pulse. A normal heart rate doesn't always rule out AFib, as the irregularity of the beats is a key indicator. Tools like smartwatches can detect irregularity, often suggesting possible AFib, but an EKG provides a definitive diagnosis.
Patients can have paroxysmal AFib (going in and out of AFib on their own) or persistent AFib (staying in AFib long-term). For persistent AFib, an electrical cardioversion can reset the heart to a normal rhythm, but it doesn't prevent future episodes. A complex situation called Tachy-Brady Syndrome occurs when AFib causes a fast heart rate, but upon returning to normal rhythm, the heart rate becomes dangerously slow, often requiring a pacemaker to manage.
This step focuses on preventing future AFib episodes. AFib triggers are often located near the pulmonary veins in the left atrium, and scarring can also contribute. Lifestyle factors like sleep apnea, obesity, high blood pressure, and alcohol consumption can increase AFib risk. Medications (anti-arrhythmic drugs) can quiet these trigger spots, while catheter ablation procedures aim to permanently eliminate them by creating controlled burns or freezes around the pulmonary veins or in scarred areas.
An AFib ablation involves inserting catheters through leg veins into the heart. A tiny puncture is made between the heart chambers to access the left atrium. A 3D map of the heart is created to identify trigger spots and scar tissue. Radiofrequency, cryoablation (freezing), or pulsed field ablation (PFA) are used to create lesions that block abnormal electrical signals. The procedure is generally safe with small risks, and patients often go home the same day.
If medications and other procedures are ineffective, an AV node ablation can be a last resort. This procedure permanently burns the AV node, preventing any electrical signals from reaching the ventricles. This makes a pacemaker necessary to ensure the heart beats at a steady, controlled rate. This can effectively manage symptoms for patients unresponsive to other treatments.
Patients with AFib often have other fast heart rhythms like atrial flutter (a simpler, large short circuit) or atrial tachycardia (repeated firing of a single trigger spot). These rhythms can be regular or irregular and may also be targeted during ablation procedures or managed with medications, as they are often related to AFib and can sometimes trigger it or result from it.