American College of Cardiology

1. Clinical History and Physical Examination

The initial evaluation of a patient with suspected or proven AF includes characterizing the pattern of the arrhythmia as paroxysmal or persistent, determining its cause, and defining associated cardiac and extracardiac factors (Table 4). A careful history will result in a well-planned, focused workup that serves as an effective guide to therapy ⁽²⁾. The workup of an AF patient can usually take place and therapy can be initiated in 1 outpatient encounter. Delay occurs when the rhythm has not been specifically documented and additional monitoring is necessary.

As emphasized, AF may present with a wide array of symptoms. (See Section VI, Associated Conditions, Clinical Manifestations, and Quality of Life.) Factors contributing to symptoms include the rate and irregularity of the ventricular response and the loss of atrial contribution to ventricular filling. Patients with atrial flutter and a regular pulse, even if rapid, are less often symptomatic than patients with AF ⁽¹⁹²⁾.

Typically, AF occurs in patients with underlying heart disease, usually hypertensive heart disease ^(24,193). (See Section VI, Associated Conditions, Clinical Manifestations, and Quality of Life.) Atherosclerotic heart disease or valvular heart diseases are also common substrates, whereas pulmonary pathology, preexcitation syndromes, and thyroid disease are less frequent causes that should still be sought ⁽¹⁹⁴⁾. Because reports of genetic transmission of AF have been published, the family history is becoming important as well ⁽¹⁷²⁾. The setting in which the physician initially encounters the AF patient may be a clue to its origin. Patients seen in the hospital emergency department tend to have a higher incidence of organic heart disease than those seen in an ambulatory clinic setting, where the incidence of lone AF can be higher than 30% ⁽²¹⁾ (Table 3).

Although various environmental triggers can initiate episodes of AF, this aspect may not emerge from the initial history given spontaneously by the patient and often requires specific inquiry. Commonly mentioned triggers include alcohol, sleep deprivation, and emotional stress, but vagally mediated AF episodes may occur during sleep or after a large meal and are more likely to arise during a period of rest after a period of stress. Stimulants such as caffeine or exercise may also precipitate AF.

Patients with paroxysmal AF may be particularly frightened by the symptoms, and the initial physician encounter must be complete and reassuring. Even when the patient with AF is relatively asymptomatic, the interview should include an effort to characterize the episodes in terms of onset and duration. The clinician should determine whether the onset and termination of palpitations is abrupt or gradual; the former favors AF or another supraventricular tachyarrhythmia, whereas the latter suggests a mechanism other than AF, including sinus tachycardia. As the arrhythmia begins, is the pulse regular or irregular? If it begins as a regular rhythm and then becomes irregular, another atrial arrhythmia should be considered, such as one involving a bypass tract. Are there associated symptoms? Dyspnea may indicate underlying heart disease, whereas angina pectoris points toward CAD. Syncope may be associated with AF, but ventricular arrhythmias should not be overlooked as a possible cause. The patient may relate the onset of AF to environmental factors including food, drink, emotional stress, sleep, or other details. Some of these factors may indicate a provocative vagal component; vagally mediated AF is also suggested when a beta-blocker or digitalis has increased the tendency to AF ⁽¹⁷³⁾. Finally, an effort should be made to quantify the episodes in terms of frequency and duration, because AF episodes tend to become more frequent and more symptomatic over time.

The physical examination may suggest AF on the basis of irregular pulse, irregular jugular venous pulsations, and variation in the loudness of the first heart sound. Examination may also disclose associated valvular heart disease, myocardial abnormalities, or HF. The findings on examination are similar in patients with atrial flutter, except that the rhythm may be regular and rapid venous oscillations may occasionally be visible in the jugular pulse.

2. Investigations

The diagnosis of AF requires ECG documentation by at least single-lead ECG recording during the dysrhythmia, which may be facilitated by review of emergency department records, Holter monitoring, or transtelephonic or telemetric recordings. A portable ECG recording tool may help establish the diagnosis in cases of paroxysmal AF and provide a permanent ECG record of the dysrhythmia. If episodes are frequent, then a 24-hour Holter monitor can be used. If episodes are infrequent, then an event recorder, which allows the patient to transmit the ECG to a recording facility when the arrhythmia occurs, may be more useful.

A chest radiograph may detect enlargement of the cardiac chambers and HF but is valuable mostly for detection of intrinsic pulmonary pathology and evaluation of the pulmonary vasculature. It is less important than echocardiography for the routine evaluation of patients with AF. Two-dimensional transthoracic echocardiography should be acquired during the initial workup of all AF patients to determine LA and LV dimensions and LV wall thickness and function and to exclude occult valvular or pericardial disease or HCM. LV systolic and diastolic performance help guide decisions regarding antiarrhythmic and antithrombotic therapy. Thrombus should be sought in the LA but is seldom detected without TEE ^{(121,127,195)}.

Blood tests are routine but can be abbreviated. It is important that thyroid function, serum electrolytes, and the hemogram be measured at least once ⁽¹⁹⁶⁾.

2. Transesophageal Echocardiography

TEE places high-frequency ultrasound transducers in close proximity to the heart to provide high-quality images of cardiac structure ⁽¹⁹⁸⁾ and function ⁽¹⁹⁹⁾. It is the most sensitive and specific technique to detect sources and potential mechanisms for cardiogenic embolism ⁽²⁰⁰⁾ and has been used in AF to stratify patients in terms of stroke risk and to guide cardioversion. (See Section VIII-G, Preventing Thromboembolism.)

TEE of patients with AF before cardioversion has shown an LA or LAA thrombus in 5% to 15% ^(195,201). Detection of LA/LAA thrombus in the setting of stroke or systemic embolism is convincing evidence of a cardiogenic mechanism ⁽¹³⁴⁾.

Several TEE features have been associated with thromboembolism in patients with nonvalvular AF, including LA/LAA thrombus, LA/LAA spontaneous echo contrast, reduced LAA flow velocity, and aortic atheromatous abnormalities ⁽¹⁵⁶⁾. Although these features are associated with cardiogenic embolism ^(169,202), further prospective investigation is needed to compare these TEE findings with clinical and transthoracic echocardiographic predictors of thromboembolism.

TEE has also been used to exclude LA/LAA thrombus before elective cardioversion ^(203,204). In a multicenter observational study, however, 17 cases of thromboembolism in AF patients were reported after conversion to sinus rhythm even after TEE showed no LA/LAA thrombus ⁽²⁰⁵⁾. All of the strokes occurred relatively soon after cardioversion in patients who did not receive therapeutic anticoagulation. These observations reinforce the need to maintain therapeutic anticoagulation in patients with AF undergoing cardioversion even when no thrombus is identified by TEE. For patients with AF of greater than 48 hours' duration, a TEE-guided strategy and the traditional strategy of anticoagulation for 3 weeks before and 4 weeks after elective cardioversion resulted in similar rates of thromboembolism (less than 1%) during the 8 weeks after randomization ⁽²⁰¹⁾. (See Section VIII-G-3, Conversion to Sinus Rhythm and Thromboembolism.)

3. Electrophysiological Study