Ablation of atrial fibrillation

Key points: There is an epidemic of atrial fibrillation and may reduce quality of life, increase risk of stroke, heart failure and even death.  Atrial fibrillation results in adverse atrial remodeling and eventually leads to persistence of atrial fibrillation making it more difficult over time.  Catheter ablation has evolved to be a safe procedure in experienced centers, but we need to do it carefully.

Multiple wavelet hypothesis: According to this hypothesis, atrial fibrillation begins with multiple independent waves spreading to both atria.  The surgical maze procedure was predicated on this model and the theory was that the surgical lesions would compartmentalize the atria into discrete electrical segments and reduce the number of circulating random wave lengths and thereby reduce atrial fibrillation.  However, the results were not as favorable as expected.

Nowadays, it is established that ectopic foci in the pulmonic veins are crucial triggers that initiate atrial fibrillation and that these foci can be ablated. Therefore, the most widely accepted theory today is that atrial fibrillation requires both a trigger and a sustainable substrate.  The triggers consist of rapidly firing foci most commonly located in the pulmonic veins but also in the superior vena cava, posterior wall of the left atrium, the vein and ligament of Marshall, the coronary sinus, as well as the left atrial appendage.  The substrate to maintain atrial fibrillation consists of an abnormal left atrium with heterogeneous fibrosis and conduction delays.  Any disease that increases left atrial pressure and leads to left atrial dilation in remodeling provides a substrate for atrial fibrillation.  Mitral valvular disease causes left atrium dilation and remodeling and also thereby provides the substrate for atrial fibrillation.  When the substrate is there, eradicating the triggers may not always provide the solution of atrial fibrillation.

If the patient should remain in atrial fibrillation, they will get further dilation of the left atrium because of loss of muscle mass, and this causes a further propensity to atrial fibrillation because the substrate becomes more favorable. Hence, it is important to intervene relatively early.

Catheter ablation of atrial fibrillation: The goal here is to prevent atrial fibrillation by eliminating the trigger that initiates it, altering the arrhythmogenic substrate or both.

Pulmonic vein isolation is the most common ablation strategy by creating circumferential lesions around the opening. The nonconducting rim of scar tissue therefore electrically disconnects the pulmonic veins from the atrium.  Linear ablations are used to create lines of ablation at isolated different segments of the left atrium and this is often created on the roof of the left atrium between the right and the left upper pulmonic veins and from the mitral valve to the left inferior pulmonic veins.  The posterior wall of the left atrium superior vena cava and coronary sinus can often have trigger points which can be provoked with the use of Isuprel in the lab and then can be ablated.  Complex fractionated atrial electrograms of areas in the atrium with highly fractionated low potentials, and can also be targeted.

Most ablation operators, isolate the pulmonic veins with and control ablations, then ablate the posterior wall, and extend the ablation towards the septum and inferior to the right pulmonic veins and get good results. If atrial flutter is present also or has been present, then ablation lines in the left and the right atrium can also be helpful.  In repeat ablations, empiric ablation of the left atrial appendage, coronary sinus, is usually recommended.


Indications: Primarily it is to reduce symptoms and improve quality of life.  If the patient has intractable symptoms of palpitations, lightheadedness, dizziness, angina, or congestive heart failure when in atrial fibrillation, then ablation therapy may be helpful.  Further, if they have failed pharmacological trials.  If there are relative contraindications to antiarrhythmic therapies, this patient should also be considered candidates for ablation therapy.  There is no survival benefit status so far.  Following the ablation therapy, anticoagulation therapy should be continued for at least 6 months.  Beyond that, one needs to assess the risk of recurrent atrial fibrillation and the patient’s risk of cardioembolic episodes.  Ablation therapy is not offered with a goal of discontinuing anticoagulation therapy.  Stopping anticoagulation is considered on a case by case basis only.

There are 2 types of energy that are used for ablation: Radiofrequency energy which produces focal thermal ablation, and extreme cold delivered via a balloon catheter which creates circumferential lesions around the pulmonic vein openings. The randomized trials demonstrate that these ablation technologies are equivalent.


Complications of ablation: Minor procedural complications include pericarditis, vascular access site implications, and anesthesia related complications. Major complications include cardiac perforation and tamponade, periprocedural stroke, pulmonic vein stenosis, atrial esophageal fistula, phrenic nerve paralysis, myocardial infarction, and death.  The rate of major complications was 6% and has declined to around 4.5%. In best centers, it is probably less than 2%.


Outcomes: The maintenance rate of sinus rhythm is between 65% and 85% which is certainly better than with drug therapy which is less than 25%.  Catheter ablation reduces symptoms and improves quality of life especially for paroxysmal atrial fibrillation.  It is less effective in persistent atrial fibrillation.


Periprocedural anticoagulation: The risk of thromboembolic episodes is increased during the procedure, immediately after, and several weeks to months after atrial fibrillation ablation.  During procedure, bubbles, catheter manipulations, blood clots can occur, and heparin is used for this.  The damaged endothelium can be a focus of blood clots but this heals rapidly.  It is important to continue anticoagulation uninterrupted throughout the procedure.  Coumadin is usually continued preoperatively and not discontinued for the procedure.  If the patient is taking a NOAC, they are instructed to skip the dose on the day before the ablation and on the morning of the procedure but resume it immediately after the procedure.  Following the procedure, anticoagulation is mandatory for 2 months at least, and then the decision to stop anticoagulation is based on the chadsvasc scores.


Antiarrhythmic drugs: Some patients can experience atrial fibrillation even after the procedure and immediately after the procedure. This is probably inflammation that induces it with autonomic imbalance, and as the scar heals, atrial fibrillation settles down.  A short-term use of an antiarrhythmic may be helpful in these patients.  Any arrhythmias that are clean the first 3 months do not necessarily affect long-term success and this is referred to as the blanking period.  So when atrial fibrillation is seen, consider antiarrhythmic therapy for these patients.  The mechanism of late recurrence of atrial fibrillation is thought to be different from the early recurrence, and may be due to incomplete pulmonic vein isolation, recovery of connections, recovery of ablation lines, and may require a repeat procedure.