Atrial Fibrillation

Atrial fibrillation (AF) is a disorder that results in multiple wavefronts of reentry simultaneously circulating around the atria, giving the appearance of disorganized electrical activity of the atria.  AF can be recognized on the ECG by an irregularly irregular ventricular rhythm with disorganized fibrillatory activity in the baseline.  The incidence of atrial fibrillation increases dramatically with age, affecting 2-3% of patients in their seventies and 10-12% of patients over the age of eighty.  It is also commonly seen in patients with valvular heart disease, ischemic heart disease, cardiomyopathy, and hypertension. Occasionally, atrial fibrillation occurs in the absence of underlying heart disease, and in those cases it is known as “lone” atrial fibrillation.  Atrial fibrillation results in a number of physiologic disturbances.  First, the heart rhythm is often rapid and irregular, which can cause patients to experience palpitations. Also, the heart rate may increase dramatically with only mild physical activity, resulting in exertional dyspnea and exercise intolerance.  Second, shortening of left ventricular filling time caused by the rapid rate combined with the loss of the atrial “kick” results in a decrease in the cardiac output, which may also cause dyspnea and exercise intolerance, as well as lightheadedness, hypotension, and fatigue.  Patients with diastolic dysfunction (non-compliant or “stiff” ventricles) are particularly affected by the compromised LV filling.  Third, the loss of an organized atrial contraction results in stasis of the atrial blood, particularly in the left atrial appendage. This can result in thrombosis and embolization.  Stroke is the major source of morbidity and mortality from atrial fibrillation, and it is believed that 15% of all strokes occur as a result of atrial fibrillation.  The risk factors for stroke in AF include age over 65 (especially over 70), diabetes, left ventricular dysfunction, a history of a prior stroke, and hypertension.

Patients presenting with new onset atrial fibrillation (less than 24 hours) with a rapid ventricular response should be treated initially with AV nodal blocking agents such as beta-blockers, verapamil, or diltiazem.  Spontaneous conversion to sinus rhythm generally occurs in the majority of patients within 24 hours with just rate control. Digoxin does not result in conversion to normal sinus rhythm any more frequently than placebo, and is not particularly useful to control the ventricular response of atrial fibrillation. Once the ventricular rate has been controlled and the patient's symptoms have been relieved, electrical cardioversion or initiation of antiarrhythmic drugs for “chemical” cardioversion may be performed in patients who do not convert spontaneously, as long as the AF has been present for less than 48 hours.  Once the duration of AF exceeds 48 hours, the risk of embolic complications of cardioversion increases significantly. These patients should be anticoagulated with warfarin for a minimum of three weeks, maintaining the INR at 2-3. Patients needing cardioversion urgently can have trans-esophageal echocardiography to rule out a left atrial thrombus, followed by cardioversion if a thombus is not present. Cardioversion, if done correctly, has a 98% success rate and a 0.5% risk of stroke regardless of whether a TEE is performed. The use of antiarrhythmic drugs to maintain normal sinus rhythm after cardioversion is necessary in most patients, as atrial fibrillation is a recurrent disease.  However, the risk of proarrhythmia from these drugs is significant, and the observation by meta-analysis trials of decreased survival in patients treated with antiarrhythmic drugs has made the use of these drugs for the maintenance of normal sinus rhythm controversial. The results of the AFFIRM (Atrial Fibrillation Follow-up Investigation for Rhythm Management) trial suggested that treating minimally symptomatic patients with warfarin and rate-controlling medications such as beta- or calcium-channel blockers is an acceptable alternative to cardioversion and antiarrhythmic drugs, particularly in older patients. In patients treated with cardioversion and antiarrhythmic medications, warfarin should still be continued, because relying on symptoms to detect arrhythmia recurrence  has been found to be unreliable.  With respect to the AFFIRM trial, the only patients who had strokes were those whose INR was subtherapeutic or those whose warfarin was stopped because they were thought to be in stable sinus rhythm.

Patients who are felt to be in chronic or “permanent” atrial fibrillation should be anticoagulated with warfarin indefinitely, as many large studies have demonstrated that this reduces the risk of stroke by nearly 80%.  The only patients who do not require warfarin are those with “lone” atrial fibrillation under the age of sixty-five.  These patients appear to have a very low risk of stroke and can be managed with aspirin alone.  Although the risk of bleeding complications (particularly intracerebral bleed) from warfarin increases dramatically with age over seventy-five years, so does the risk of stroke from atrial fibrillation.  Therefore, each elderly patient’s risk-to-benefit ratio must be assessed individually. Overall, the risk of stroke without warfarin may exceed 10% per year, yet the risk of serious bleeding complications from warfarin therapy is only 1-2% per year.

Nearly all patients with “lone” atrial fibrillation and most patients with paroxysmal atrial fibrillation seem to have discrete “trigger foci” that serve to initiate AF. Most of these foci have been mapped to the pulmonary veins behind the  left atrium. “Focal atrial fibrillation” can be treated with catheter ablation of the focus, but there is a reported risk of pulmonary vein stenosis, not to mention the risk of a trans-septal puncture to gain access to the left atrium. Newer catheter ablation procedures have been developed to “isolate” the pulmonary veins from the rest of the atrial myocardium, thus disconnecting the arrhythmogenic focus from the heart and preventing recurrent AF. Similar to the surgical “maze” procedure developed in the 1980s, these catheter-based ablation procedures can reduce or eliminate AF in up to 80% of patients. Although the technique is still evolving, it remains tedious and time-consuming, and is associated with a 3-4% risk of serious complications, including cardiac puncture, tamponade, systemic embolization, pulmonary vein stenosis, atrio-esophageal fistula, and phrenic nerve damage, and even death.  Many patients have to have repeat procedures because of recurrent atrial fibrillation or flutter. Nevertheless, AF ablation continues to be an exciting and promising treatment for this otherwise frustrating condition.