AF increases in frequency with aging, particularly in patients older than 65 years. At least 10% of the population older than 80 years will develop AF. The aging of a significant proportion of the population in the next 15 years will likely result in a significant increase in the number of patents with AF.

Adrenergically triggered AF generally occurs during exercise or in association with caffeine excess. This mechanism probably plays a role in AF associated with acute systemic illness or in the postoperative (noncardiac surgery) state. In the authors’ experience, dietary caffeine is infrequently a consistent trigger for AF and they rarely limit caffeine intake in their patients. Vagally triggered AF is a relatively common form of AF. It is most often associated with sleep (particularly in the setting of obstructive sleep apnea), large meals, or the termination of significant exercise. A common scenario is the development of AF the evening or morning after an afternoon of significant exercise or activity. It may also occur in association with a vasovagal syncopal episode. This form of AF often develops during middle age and is most often paroxysmal and highly symptomatic. It may in fact be that some of what is believed to be vagal AF is really a combination of both enhanced sympathetic and vagal tone, particularly at the end of exercise and postoperatively.

AF is commonly associated with hyperthyroidism, whereas only 1% of cases of new-onset AF are due to hyperthyroidism. It is very difficult to maintain sinus rhythm in the presence of active hyperthyroidism and therefore rate control should be the strategy until a euthyroid state is achieved. β-Blockers are the first choice for rate control and combination therapy with a calcium channel blocker or digoxin may be required. There is some scant evidence
that thromboembolic risk is increased in the presence of hyperthyroidism and therefore many practitioners choose to anticoagulate patients in this circumstance, even in the absence of other clinical risk factors for stroke.

There is a 50% to 60% risk of AF development post cardiovascular surgery. This risk is slightly higher with valvular disease compared with coronary artery bypass graft (CABG). The risk of AF development is greatest in the first week following surgery with a peak at days 2 to 3. It is important to realize that the likelihood of being in sinus rhythm 4 weeks following cardiac surgery is the same regardless of the strategy of rate or rhythm control employed. The authors choose to restore and maintain sinus rhythm in patients who are highly symptomatic in AF or difficult to rate control. Their preferred strategy is to load with amiodarone and continue therapy for a total of 6 weeks following surgery. Alternatives to amiodarone in this population include sotalol and dofetilide. Type 1A drugs are also useful particularly for patients with renal insufficiency.

Prophylactic therapy for AF prevention before cardiac surgery: It is well established that the discontinuation of previously prescribed β-blockers is associated with an increased risk of postoperative AF. It is therefore important to maintain β-blocker therapy through cardiovascular surgery. Amiodarone can be initiated in the week or weeks before electively scheduled cardiac surgery. This strategy will reduce the occurrence postoperative AF.

AF frequently occurs in the immediate period post MAZE or percutaneous AF ablation procedure. AF should be differentiated from atrial tachycardia, which also can occur as an arrhythmic complication of these procedures. In both circumstances, these arrhythmias often subside over a period of weeks. As a result, many practitioners choose to treat their postprocedure patients with an antiarrhythmic drug (AAD) for 4 to 12 weeks after the procedure.

AF is rarely, if ever, a manifestation of acute ischemia or infarction. When it does, it is usually in the setting of CHF with or without mitral regurgitation (MR) and is associated with a poor prognosis. It is common to develop AF with CHF or MR which develops in the setting of infarction. It is not common to develop AF in an uncomplicated MI or as a sole manifestation of ischemia or infarction. The authors do not recommend routine evaluation for coronary
artery disease in patients with new onset AF unless there is other clinical evidence of ischemia.

There are likely multiple forms of familial AF. One phenotype which is easily identified is families with multiple members who develop AF at a young age (younger than 40 years). These patients often have significant atrial electrical dysfunction with sinus node dysfunction.

Binge drinking is commonly associated with AF. Moderate alcohol consumption is probably not a risk for AF; however, excessive alcohol use does seem to predispose to AF.

The term coarse as is often used when atrial activity in lead V₁ appears to be organized and is relatively high amplitude. If the remainder of the leads have low-amplitude fibrillatory waves and the ventricular response is irregularly irregular this rhythm should be characterized as typical AF.

A regular ventricular response during AF, particularly if slow, is indicative of heart block. This is shown in Figure 6-2.

Tachybrady syndrome refers to the presence of rapid and slow rhythms in the same patient (see Fig. 6-3). Most commonly this is AF with a rapid ventricular response and sinus bradycardia. This bradycardia often manifests as a prolonged sinus pause at the time of conversion from AF or flutter to sinus rhythm (Fig. 6-3).

Most patients with new-onset AF have symptoms at the onset of their disease. With time and therapy many patients will report a significant reduction in their symptoms even with persistence of AF. The most commonly reported symptoms include dyspnea, palpitations, fatigue, and chest pain. Frequent urination may also be described as a consequence of atrial stretch-induced release of atrial natriuretic peptide. Patients with diastolic dysfunction, particularly those with hypertrophic cardiomyopathy and aortic stenosis, develop symptoms and hemodynamic compromise due to the loss of the atrial contribution to ventricular filling. Most other patients do not suffer significantly from the loss of atrial filling. Symptoms associated with AF result predominantly from a rapid ventricular response. This is particularly true if tachycardia-induced cardiomyopathy develops. Tachycardia-induced cardiomyopathy is characterized as a global cardiomyopathy which develops as a consequence of a rapid ventricular response. It is also believed that the ventricular irregularity associated with AF can be hemodynamically disadvantageous. Syncope or lightheadedness can also be associated with AF. This is almost always due to a sinus pause at the termination of AF, particularly in those with sinus node dysfunction. AF should be considered a proarrhythmic arrhythmia, particularly in the setting of old MI and CHF. AF can induce ventricular arrhythmias in this patient population.