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 24-48 hours. If the duration of AF exceeds 24-48 hours, the risk of embolic complications of cardioversion increases significantly. These patients should be anticoagulated for a minimum of three weeks. 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.
The "gold standard" of anticoagulation for stroke prevention in atrial fibrillation is warfarin (Coumadin). However, three new anticoagulant medications have been released and have certain advantages over warfarin in patients who do not have severe valvular heart disease. The dose of warfarin has to be adjusted very carefully and is very unpredictable in most patients, so the Prothrombin Time (PT) and International Normalized Ratio (INR) needs to be monitored carefully – at least once a month and sometimes 1-2 times a week in patients who need a dose adjustment or are just starting on this medication. Keeping the INR between 2 and 3 is best to reduce the risk of blood clot formation and stroke while minimizing the risk of bleeding complications. The newer agents do not need to be monitored because they act much more predictably. They are at least as good as warfarin in preventing stroke and are associated with a lower risk of serious bleeding complications.
Patients with atrial fibrillation and increased risk of stroke should be anticoagulated indefinitely, as many large studies have demonstrated that this can reduce the risk of stroke by nearly 80%. The only patients who do not require anticoagulation 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 80 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. There are a number of risk factors for stroke that need to be assessed, including a history of hypertension, diabetes, heart failure, and especially a history of a prior stroke or TIA.
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. 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, 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.