Case In Point: Lone Atrial Fibrillation in a Young Man

March 2, 2005
Michael D. Smith, MD
Michael D. Smith, MD

Janet Poponick, MD
Janet Poponick, MD

A 23-year-old man presents to theemergency department (ED) withacute chest discomfort, which startedin the morning. He describes the discomfortas more akin to palpitationsthan to actual pain. The discomfortis midsternal, nonradiating, nonpleuritic,and associated with dyspnea; itis neither exertional nor positional.There is no viral prodrome.

A 23-year-old man presents to theemergency department (ED) withacute chest discomfort, which startedin the morning. He describes the discomfortas more akin to palpitationsthan to actual pain. The discomfortis midsternal, nonradiating, nonpleuritic,and associated with dyspnea; itis 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 instructorand has excellent exercise tolerance.There is no family history ofsudden death or cardiac disease.

The patient is alert and orientedbut mildly anxious. His temperatureis 36.7C (98.2F); blood pressure,129/69 mm Hg; heart rate, 93beats per minute; and respirationrate, 14 breaths per minute. His pupilsare equal, round, and reactive.His neck is free of jugular venousdistention, bruits, and rigidity. Hisheart rate and rhythm are regular,with no murmurs, rubs, or gallops.Point of maximum impulse is normal;extremity pulses are equal. Hisabdomen is soft, nontender, andnondistended. His skin is warm anddry with normal color. The neurologicexamination reveals intactcranial nerves, normal strength andreflexes, and normal coordinationand gait.

A chest radiograph is normal.Results of a complete blood cellcount, chemistry panel, and thyroidfunction studies are unremarkable.A urine toxicology screen is negativefor alcohol and substances of abuse.The electrolyte level is normal. AnECG shows rate-controlled atrialfibrillation (AF) (Figure). The patientremains hemodynamically stablein the ED and is admitted to amonitored floor.

The workup continues in thetelemetry unit. An echocardiogramshows normal heart size and contractilityand no intracardiac thrombus.Serial cardiac markers are negativefor myocardial infarction.Results of a CT scan of the chest, extremityduplex scans, and D-dimertest are all normal, which rules outa pulmonary embolus as the causeof the arrhythmia. During the firstnight on the telemetry floor, the patient'sheart rate spontaneously convertsto normal sinus rhythm, withoutrate-controlling medications, antiarrhythmics,anticoagulation, orcardioversion.


Cardiac arrhythmias occur frequently,and it is important to formulatea good differential diagnosis.Hypoxia, ischemia, cardiac irritability,and sympathetic stimulation canall cause or contribute to an electrophysiologicirregularity. Other causesinclude effects of medications orillicit drugs, electrolyte disturbances,bradycardia, and chamber stretch(from heart failure) (Table).Additional considerations inAF. Bear the following in mind:

  • Hypertension may be implicated.Accurate blood pressure readingsare crucial, and a review of previousmedical records is recommended.
  • Coronary artery disease may bea factor. Obtain a careful history ofanginal episodes (or equivalents) andassociated symptoms.
  • A screening thyroid-stimulatinghormone (TSH) test is warranted,followed by an appropriate thyroidpanel if the TSH level is abnormal.
  • Careful evaluation of the ECG forsigns of an accessory pathway, suchas in Wolff-Parkinson-White syndrome,is important, especially whenrate control allows adequate inspectionof the ECG.
  • Pulmonary embolism must beconsidered and excluded with theappropriate tests--either a CT scanwith contrast of the chest or a ventilation-perfusion scan, followed byduplex ultrasonography of the lowerextremities if the scans are inconclusiveand suspicion remains high.

Because our patient--once hisheart rate had converted to sinusrhythm--showed no signs of an accessorypathway syndrome and noother cause of AF, such as ventriculardysfunction, a diagnosis of loneAF was made.


The incidence of lone AF is notcompletely known, but a population based30-year longitudinal studyshowed that 2.7% of patients with AFhad lone AF.1 The recurrence rate of lone AF is also unclear. In the samestudy, 21% of patients with loneAF had an isolated episode, 58% hadrecurrent episodes, and 22% hadchronic lone AF. A review of the literaturesuggests that the incidenceand recurrence rate are low, but nofurther objective descriptors couldbe found.

In one longitudinal study, therewas no difference in survival or inthe incidence of stroke in patientswith isolated, current, or chroniclone AF, which suggests that, at leastin those younger than 60 years, routineanticoagulation with warfarin isnot warranted.1 Pharmacologic andsurgical correction of AF in this agegroup is undertaken solely to controlsymptoms.

However, the risk of chronicAF, heart disease, and stroke is elevatedin persons older than 60 years.Antithrombotic therapy may, therefore,be warranted in this agegroup.2,3

In addition to antiarrhythmicregimens, radiofrequency ablationcan be used to eliminate chronic,drug-refractory lone AF by isolatingthe pulmonary venous region fromthe remaining atrial region.4 Inone trial, radiofrequency ablationsuccessfully eliminated lone AF.4


Numerous theories have beenproposed, and a number of causesmay be implicated. One hypothesisis that obstructive sleep apnea (OSA)predisposes to cardiac arrhythmias.5A case-control study of 59 patients,mostly men, showed no differencein the incidence of OSA by sleepstudy between normal persons andthose with lone AF; however, the lattergroup reported more symptomsconsistent with OSA, such as daytimesleepiness and nightly breathingpauses during sleep. Patientswith lone AF had statistically significantlythicker necks. Neck circum-ference was independently related toAF.

Another hypothesis is that gastroesophagealreflux disease (GERD)is a risk factor for AF. In a pilotstudy in which patients with paroxysmalAF were treated with a protonpump inhibitor, most reported a decreasein their AF symptoms as wellas in their GERD symptoms.6

Some researchers have proposeda connection between loneAF and heavy exercise. This theoryseems plausible for our patient, adance instructor in excellent condition.One retrospective study of patientswith known lone AF suggestedthat these patients were morelikely than the controls to have engagedin long-term sports practice.Echocardiographic comparison revealedthat the patients with loneAF had greater atrial and ventriculardimensions and higher ventricularmass than the controls.7

Another study also showed anassociation between vigorous exerciseand the incidence of lone AF.8Hypothetical causes include heightenedvagal tone, as well as increasesin atrial size and ventricular mass.In this study, patients with frequentparoxysmal AF responded well toantiarrhythmic control. A case reportthat appears to refute the theoryof exercise-induced lone AF isthat of a middle-aged athlete whoterminated his episodes of paroxysmallone AF by engaging in heavyendurance exercise.9


The patient was hospitalized for36 hours and remained in sinus rhythm.He was at extremely low riskfor a thromboembolic event. Currentguidelines do not recommend anticoagulanttherapy in this setting--even in patients with recurrent episodesof lone AF.10

Patients with lone AF are bestfollowed closely for 1 to 2 years to ensure that AF does not recur. Ifchronic AF develops, good controlcan be achieved with antiarrhythmictherapy. Radiofrequency ablation isan excellent alternative if medicationfails to control symptoms.