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Atrial Flutter in a College Football Player

Return to Play or Not?

Dennis Y. Wen, MD; Greg Flaker, MD; Rex L. Sharp, ATC; Patrick A. Smith, MD


In Brief: Atrial flutter is relatively uncommon, especially among athletic populations. The case of a 19-year-old college football player who spontaneously developed atrial flutter illustrates recent advances in treatment, including electrical cardioversion and radiofrequency catheter ablation. Return-to-play decisions center around the risk of recurrence and the degree of symptoms during recurrences. Clinicians should be aware that the most current return-to-play guidelines do not take into consideration the newer treatment techniques that have greatly changed definitive management of atrial flutter.

Atrial flutter is an uncommon supraventricular tachyarrhythmia with an unknown cause. Physical exertion is not considered a precipitating factor, nor is use of beta-agonist medication.1 Recent mapping studies have determined the mechanism to be a reentrant circuit involving the atria.1 We report a case of atrial flutter occurring in a college football player whose treatment included radiofrequency catheter ablation. Considerations for return to play are highlighted.

Case Report

History. A 19-year-old college freshman linebacker reported palpitations to the training staff in early May. Two days earlier, he had been running sprints at the end of a conditioning workout when he suddenly felt fatigued with palpitations, mild chest discomfort, mild shortness of breath, and light-headedness, and he was able to complete the workout. Attributing his symptoms to his allergic rhinitis and asthma, he took some antihistamines and used a nasal steroid spray and an albuterol inhaler. He worked out the next day but still had palpitations and the same associated symptoms.

No personal or family history of cardiac problems was noted. His only medications (listed above) were for allergic rhinitis and asthma. He did not use supplements or illicit drugs, including cocaine. His medical history included shoulder surgery.

Physical exam. When examined, his blood pressure was 96/60 mm Hg, and his pulse varied between 96 and 120 per minute and was regular. He was in no acute distress and had comfortable respirations. No jugular venous distention was noted. His lungs were clear without wheezes. His cardiac exam showed normal heart sounds without murmurs, gallops, or rub. His extremities were well perfused without edema.

Tests and diagnosis. His electrocardiogram (ECG) depicted positive atrial flutter waves at a rate close to 300/min and 2:1 ventricular conduction (figure 1). Laboratory tests, including thyroid, were normal. No toxicology screen was performed. He was admitted to the hospital for further tests and given intravenous esmolol hydrochloride, which did not adequately control his ventricular rate. Because more than 48 hours had passed since the onset of flutter, transesophageal echocardiography (TEE) was performed the following day. The TEE showed normal left ventricular function, with an ejection fraction of 60% to 65%, a normal left atrial size, and no evidence of atrial thrombus.

Treatment. Direct current (DC) cardioversion with 100 J successfully converted his rhythm to normal sinus. He remained stable, and 2 days after cardioversion he underwent radiofrequency catheter ablation. He was discharged the same day with instruction to take a daily aspirin until his next follow-up, because atrial thrombus formation was a concern.

He was allowed to return to running and lifting weights, but was withheld from competition for 3 months. He had no recurrences, did well over the summer, and was cleared to participate in fall preseason drills and competition. He experienced no problems throughout training camp and returned to competition without incident 3-1/2 months after the onset of the flutter. He has remained without recurrence for 18 months.

Flutter and Fibrillation

Atrial flutter, a relatively uncommon tachyarrhythmia, has no known cause. Our patient's symptoms were typical, but the abnormality is more common in older patients and those with cardiac conditions.

The mechanism of atrial flutter appears to be a reentrant circuit involving both the left and right atria, but this is debated. Atrial flutter can occur in two patterns. In the common counterclockwise or typical atrial flutter, the left atrium is activated from low to high, giving rise to the usual negative sawtooth flutter waves seen on ECG in leads II, III, and aVF.

A more uncommon pattern, seen in our patient, is the clockwise or reverse atrial flutter that occurs when the same pathway is used in the opposite direction. The left atrium is activated from high to low, resulting in positive flutter waves on the ECG inferior leads. While the reentrant circuit is mainly in the right atrium and both atria are involved, it appears that the P-wave pattern on the ECG reflects mostly the left atrial activity.

Atrial flutter can be an unstable arrhythmia that results in rapid ventricular responses. It is important to exclude preexcitation (such as in Wolff-Parkinson-White syndrome) or very rapid AV node conduction. Our patient's relatively slow ventricular response (2:1) may have resulted from the increased vagal tone of an athlete. Even when the patient is hemodynamically stable, loss of the atrial contribution to preload can be a problem, especially during exercise.2

Management options. Acute management of atrial flutter and atrial fibrillation is similar. Options for cardioversion include pharmacologic therapy (generally with class IC antiarrhythmics or ibutilide fumarate), electrical DC cardioversion, or overdrive pacing. Since our patient was not hemodynamically unstable, immediate cardioversion was not indicated. Instead, rate control was initiated, which can be done with digoxin, beta-blockers, or calcium-channel blockers.

Our patient's ventricular rate did not respond well to intravenous esmolol. Recent data have indicated a risk of atrial clot formation if the flutter lasts longer than about 48 hours, similar to the situation for atrial fibrillation.1 Therefore, if the duration of flutter exceeds 48 hours, anticoagulation with warfarin sodium for 3 to 4 weeks is indicated before cardioversion, followed by continued anticoagulation. Alternatively, TEE can be done, as in our patient's case, to document lack of an atrial thrombus. Even in this situation, postcardioversion anticoagulation can be instituted since atrial thrombi may still form after the procedure. We prescribed daily aspirin after cardioversion and radiofrequency ablation.

Radiofrequency Ablation

Traditional long-term treatment of atrial flutter involves class IA or IC antiarrhythmics, or amiodarone hydrochloride, none of which is consistently effective. Rate control and chronic anticoagulation are also generally necessary. Mapping studies3,4 that documented atrial flutter as a reentrant tachycardia led to radiofrequency catheter ablation techniques that have revolutionized treatment for atrial flutter. Reports4,5 of radiofrequency ablation of the isthmus between the inferior vena cava-eustachian ridge-coronary ostium and tricuspid valve (figure 2), have documented high success rates of 81% to 100%. Mapping of the arrhythmia to document its dependence on this isthmus prior to ablation would be ideal; however, our patient's arrhythmia could not be induced in the electrophysiology lab. The isthmus was ablated in hopes that his arrhythmia was isthmus dependent. Recurrence is possible if it was not isthmus dependent despite effective ablation.

The exact indications for radiofrequency ablation are not clear. An alternative approach could have been taken for our patient's first episode of atrial flutter, with long-term heart rate-controlling medications following cardioversion, and without ablation. Ablation could still be considered for recurrence. Our patient's lack of structural cardiac disease would presumably make recurrent episodes less likely.

It is also possible that his arrhythmia was an atrial tachycardia and not an isthmus-dependent flutter. Radiofrequency ablation was elected in our patient's case because attempts at heart rate control were not successful and because he was an athlete who very strongly desired an early return to sports. We, therefore, felt that the more aggressive approach with radiofrequency ablation would result in the least risk of the condition to recur.

Return to Play

Atrial flutter in athletes is very rare, and we are aware of very few case reports.2,6 Atrial flutter cannot be considered part of athletic heart syndrome,7 nor is it a known cause of sudden cardiac death. Return-to-play decisions for athletes with atrial flutter can be influenced by a number of considerations.

The first consideration is whether this represents a potentially lethal arrhythmia. Atrial flutter is generally not lethal in the absence of structural cardiac disease or preexcitation syndrome. Although our patient was symptomatic with a 2:1 ventricular response rate, he was not hemodynamically unstable, nor was he at risk of injuring himself or others should the flutter recur during practice or competition.

Another consideration is whether the rhythm is exercise induced. Presumably, atrial flutter is not exercise induced, and therefore we felt that practice and competition would not lead to recurrent episodes. For patients who have recurrent episodes, anticoagulation would be necessary, precluding participation in contact or collision sports. We presumed our patient's atrial flutter was "cured" after radiofrequency ablation—although recurrences are still possible4,5—and, therefore, we did not prescribe anticoagulation or rate-control medications.

Guidelines from the 26th Bethesda Conference on athletes with cardiovascular abnormalities,8 commonly used to determine athletic eligibility, recommend only low-intensity sports for athletes who have atrial flutter, if no structural heart disease is detected and ventricular rate is normal. The recommendations for atrial fibrillation allow immediate full sports participation in the absence of structural heart disease if ventricular rate is normal.8 For atrial flutter, full participation in any sport is allowed if no flutter episodes recur for 3 to 6 months. However, these guidelines were written before the use of radiofrequency catheter ablation, which has markedly changed treatment and prognosis. Recurrences have markedly decreased, and cures can occur. The Bethesda guidelines do not take into account athletes who are potentially cured after ablation procedures. We presumed our patient to be cured by the ablation, but allowed for the possibility of recurrence resulting from either ineffective ablation or a rhythm that was not isthmus dependent. We therefore prohibited full competition for 3 months.


This case demonstrates that very good outcomes are possible for active patients who experience atrial flutter. Physicians who use the Bethesda guidelines should keep in mind that they were written prior to the recent development of ablation techniques. Athletes who make a complete recovery need not be restricted from practice or play. The Bethesda guidelines may need to be revised in the future as more clinician experience is gained with patients who undergo radiofrequency catheter ablation.


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  2. Blair TP, Baker WP: Atrial fibrillation and flutter in athletes. Phys Sportsmed 120215;13(3):57-71
  3. Cosio FG, Lopez-Gil M, Goicolea A, et al: Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71(8):705-709
  4. Kottkamp H, Hindricks G: Catheter ablation of atrial flutter. Thorac Cardiovasc Surg 1999;47(3 suppl):357-361
  5. Kosinski D, Grubb BP, Wolfe DA, et al: Catheter ablation for atrial flutter and fibrillation: an effective alternative to medical therapy. Postgrad Med 192021;103(1):103-110
  6. Panebianco R, Coplan NL: Atrial arrhythmias in athletes. Am Heart J 1994;127(2):471-474
  7. Huston TP, Puffer JC, Rodney WM: The athletic heart syndrome. N Engl J Med 120215;313(1):24-32
  8. Zipes DP, Garson A Jr: 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 6: arrythmias. Med Sci Sports Exec 1994;26(10 suppl):S276-S283

Dr Wen is a family practice physician in the department of family and community medicine, Dr Flaker is a cardiologist in the division of cardiology, and Mr Sharp is head athletic trainer in the department of intercollegiate athletics, all at the University of Missouri-Columbia. Dr Smith is an orthopedic surgeon at the Columbia Orthopedic Group in Columbia, Missouri. Address correspondence to Dennis Y. Wen, MD, Dept of Family and Community Medicine, University of Missouri-Columbia, M245 Medical Sciences Bldg, Columbia, MO 65212; e-mail to [email protected].

Disclosure information: Drs Wen, Flaker, and Smith and Mr Sharp disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.