Lone Atrial Fibrillation in a Young Man
A 23-year-old man presents to the emergency department (ED) with acute chest discomfort, which started in the morning. He describes the discomfort as more akin to palpitations than to actual pain. The discomfort is midsternal, nonradiating, nonpleuritic, and associated with dyspnea; it is neither exertional nor positional. There is no viral prodrome.
The patient’s history is unremarkable; he does not smoke, drink alcohol, or use illicit drugs. He is a dance instructor and has excellent exercise tolerance. There is no family history of sudden death or cardiac disease.
The patient is alert and oriented but mildly anxious. His temperature is 36.7°C (98.2°F); blood pressure, 129/69 mm Hg; heart rate, 93 beats per minute; and respiration rate, 14 breaths per minute. His pupils are equal, round, and reactive. His neck is free of jugular venous distention, bruits, and rigidity. His heart rate and rhythm are regular, with no murmurs, rubs, or gallops. Point of maximum impulse is normal; extremity pulses are equal. His abdomen is soft, nontender, and nondistended. His skin is warm and dry with normal color. The neurologic examination reveals intact cranial nerves, normal strength and reflexes, and normal coordination and gait.
A chest radiograph is normal. Results of a complete blood cell count, chemistry panel, and thyroid function studies are unremarkable. A urine toxicology screen is negative for alcohol and substances of abuse. The electrolyte level is normal. An ECG shows rate-controlled atrial fibrillation (AF) (Figure). The patient remains hemodynamically stable in the ED and is admitted to a monitored floor.
The workup continues in the telemetry unit. An echocardiogram shows normal heart size and contractility and no intracardiac thrombus. Serial cardiac markers are negative for myocardial infarction. Results of a CT scan of the chest, extremity duplex scans, and D-dimer test are all normal, which rules out a pulmonary embolus as the cause of the arrhythmia. During the first night on the telemetry floor, the patient’s heart rate spontaneously converts to normal sinus rhythm, without rate-controlling medications, antiarrhythmics, anticoagulation, or cardioversion.
DIFFERENTIAL DIAGNOSIS OF AF
Cardiac arrhythmias occur frequently, and it is important to formulate a good differential diagnosis. Hypoxia, ischemia, cardiac irritability, and sympathetic stimulation can all cause or contribute to an electrophysiologic irregularity. Other causes include effects of medications or illicit drugs, electrolyte disturbances, bradycardia, and chamber stretch (from heart failure) (Table). Additional considerations in AF. Bear the following in mind:
- Hypertension may be implicated. Accurate blood pressure readings are crucial, and a review of previous medical records is recommended.
- Coronary artery disease may be a factor. Obtain a careful history of anginal episodes (or equivalents) and associated symptoms.
- A screening thyroid-stimulating hormone (TSH) test is warranted, followed by an appropriate thyroid panel if the TSH level is abnormal.
- Careful evaluation of the ECG for signs of an accessory pathway, such as in Wolff-Parkinson-White syndrome, is important, especially when rate control allows adequate inspection of the ECG.
- Pulmonary embolism must be considered and excluded with the appropriate tests—either a CT scan with contrast of the chest or a ventilation- perfusion scan, followed by duplex ultrasonography of the lower extremities if the scans are inconclusive and suspicion remains high.
Because our patient—once his heart rate had converted to sinus rhythm—showed no signs of an accessory pathway syndrome and no other cause of AF, such as ventricular dysfunction, a diagnosis of lone AF was made.
LONE AF: AN OVERVIEW
The incidence of lone AF is not completely known, but a population based 30-year longitudinal study showed that 2.7% of patients with AF had lone AF.1 The recurrence rate of lone AF is also unclear. In the same study, 21% of patients with lone AF had an isolated episode, 58% had recurrent episodes, and 22% had chronic lone AF. A review of the literature suggests that the incidence and recurrence rate are low, but no further objective descriptors could be found.
In one longitudinal study, there was no difference in survival or in the incidence of stroke in patients with isolated, current, or chronic lone AF, which suggests that, at least in those younger than 60 years, routine anticoagulation with warfarin is not warranted.1 Pharmacologic and surgical correction of AF in this age group is undertaken solely to control symptoms.
However, the risk of chronic AF, heart disease, and stroke is elevated in persons older than 60 years. Antithrombotic therapy may, therefore, be warranted in this age group.2,3
In addition to antiarrhythmic regimens, radiofrequency ablation can be used to eliminate chronic, drug-refractory lone AF by isolating the pulmonary venous region from the remaining atrial region.4 In one trial, radiofrequency ablation successfully eliminated lone AF.4
CAUSES OF LONE AF
Numerous theories have been proposed, and a number of causes may be implicated. One hypothesis is that obstructive sleep apnea (OSA) predisposes to cardiac arrhythmias.5 A case-control study of 59 patients, mostly men, showed no difference in the incidence of OSA by sleep study between normal persons and those with lone AF; however, the latter group reported more symptoms consistent with OSA, such as daytime sleepiness and nightly breathing pauses during sleep. Patients with lone AF had statistically significantly thicker necks. Neck circum- ference was independently related to AF.
Another hypothesis is that gastroesophageal reflux disease (GERD) is a risk factor for AF. In a pilot study in which patients with paroxysmal AF were treated with a proton pump inhibitor, most reported a decrease in their AF symptoms as well as in their GERD symptoms.6
Some researchers have proposed a connection between lone AF and heavy exercise. This theory seems plausible for our patient, a dance instructor in excellent condition. One retrospective study of patients with known lone AF suggested that these patients were more likely than the controls to have engaged in long-term sports practice. Echocardiographic comparison revealed that the patients with lone AF had greater atrial and ventricular dimensions and higher ventricular mass than the controls.7
Another study also showed an association between vigorous exercise and the incidence of lone AF.8 Hypothetical causes include heightened vagal tone, as well as increases in atrial size and ventricular mass. In this study, patients with frequent paroxysmal AF responded well to antiarrhythmic control. A case report that appears to refute the theory of exercise-induced lone AF is that of a middle-aged athlete who terminated his episodes of paroxysmal lone AF by engaging in heavy endurance exercise.9
OUTCOME OF THIS CASE
The patient was hospitalized for 36 hours and remained in sinus rhythm. He was at extremely low risk for a thromboembolic event. Current guidelines do not recommend anticoagulant therapy in this setting— even in patients with recurrent episodes of lone AF.10
Patients with lone AF are best followed closely for 1 to 2 years to ensure that AF does not recur. If chronic AF develops, good control can be achieved with antiarrhythmic therapy. Radiofrequency ablation is an excellent alternative if medication fails to control symptoms.