The Physician and Sportsmedicine
Menubar Home Journal Personal Health Resource Center CME Advertiser Services About Us

Managing Atrial Fibrillation in Active Patients and Athletes

Robert A. Reiss, MD

Internal Medicine Series Editor: Donald M. Christie, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 3 - MARCH 1999


In Brief: Atrial fibrillation in young or middle-aged active patients can often be managed with medication. Evaluation should address associated conditions and predisposing factors such as idiopathic hypertrophic subaortic stenosis, Wolff-Parkinson-White syndrome, congenital heart disease, hyperthyroidism, excess alcohol or other drug use, and exercise-induced catecholamine release. Diagnostic studies may include an ECG, 24-hour Holter or event monitoring, exercise treadmill testing, stress echocardiography, electrophysiologic studies, and laboratory testing. Electrocardioversion provides rapid, predictable treatment, but ablation therapy is sometimes needed.

Atrial fibrillation (AF) is a common supraventricular tachyarrhythmia in the elderly. Its prevalence, estimated to be 2.3% in those over 40, increases to 5.9% in people 65 years and older. Seventy percent of the people who have AF are between 65 and 85 years old (1). Most have hypertension, ischemic heart disease, congestive heart failure (2,3), or other underlying conditions such as mitral valve disease (4), hyperthyroidism (5), and pulmonary disease.

In those under 40, the prevalence of AF is estimated to be less than 0.004% (6), but there is some suggestion that the disorder may be less rare among people who exercise. Paritano and Oriel (7) evaluated 60 asymptomatic, highly trained runners and found one patient who had exercise-induced AF. Coelho et al (8) identified 5 patients who had AF among 19 young athletes (average age, 22) referred for evaluation because of palpitations. Further, paroxysmal AF has also been observed in patients who have otherwise normal hearts after thoracic surgery, acute alcohol intoxication, or exercise (9).

Although competitive athletes and other well-conditioned individuals can tolerate high ventricular rates at rest and during exercise, the need for maximal cardiac output makes persistent AF incompatible with optimal performance. Therefore, it is essential that the evaluation be carried out so as to unmask underlying disorders and that treatment be swift and reliable.

Case Report

A 52-year-old man noticed a rapid, irregular pulse while running. The problem would abate with rest. He noticed decreased endurance but continued to run, and the problem recurred about every third run. He reported no chest pain, shortness of breath, nausea, vomiting, or diaphoresis. He also noted similar episodes at times of high stress.

Although the episodes occurred during exercise, they never limited his activities, which included running 2 to 3 miles two times a week at a 10-minute-mile pace, playing softball once a week, and lifting weights two to three times per week. He also played tennis regularly and was a strong competitor in his age bracket at his tennis club. He did not smoke or use illicit drugs, rarely drank alcohol, and drank no caffeinated beverages. The patient took no medications except for vitamin supplements that included no sympathomimetic substances and were felt to be innocuous.

Physical examination revealed a blood pressure of 110/60 mm Hg and a regular pulse of 50 per minute. The patient was 70 1/2 in. tall and weighed 160 lb. The thyroid gland was not palpable, and the cardiopulmonary exam was normal.

Laboratory results, including a complete blood count, urine analysis, and tests for electrolytes and levels of calcium and thyroid stimulating hormone, were all normal. A resting electrocardiogram (ECG) and pulmonary function tests were also normal.

The patient underwent treadmill exercise testing using the standard Bruce protocol. At 7 minutes 57 seconds into the study, the patient spontaneously converted to AF, with a ventricular rate of 150 beats per minute (figure 1). He noted the change in rhythm but continued to exercise. At 11 minutes 12 seconds, the patient's heart rate reached a maximum of 207 beats per minute, and the test was terminated at the examiner's request. The patient spontaneously converted to sinus rhythm after 13 minutes of recovery.

[Figure 1]

A stress echocardiogram was then performed. At 9 minutes 46 seconds into the study, the patient developed rapid AF. The arrhythmia resolved spontaneously during recovery. No ventricular abnormalities were identified.

Beta blockade was prescribed because the patient's AF was believed to be catecholamine induced, and his symptoms affected his running. He declined beta blockade because he feared decreased exercise tolerance. He continued his running regimen for about a month but felt early onset of fatigue, so he agreed to try propranolol therapy. Six months after his initial presentation, the patient was doing well and was using propranolol only before exercise, as recommended by his cardiologist.

Evaluation

Presenting symptoms. Like most patients who have AF, an athlete or active person who has the condition may or may not have symptoms. If he or she is symptomatic, a history of rapid or irregular heartbeat or decreased exercise tolerance is the most frequent complaint.

Young, active patients are less likely to have symptoms than older patients, who are more affected by the decreased cardiac output (10) and more likely to have underlying coronary artery disease that will become symptomatic in the event of AF with high ventricular rates. In contrast, the well-conditioned person is more likely to be able to tolerate the high ventricular rates of paroxysmal AF than older patients. Middle-aged athletes can perform at high levels in spite of AF (11).

Young, active patients will have significant symptoms if there is an underlying heart disorder such as idiopathic hypertrophic subaortic stenosis (IHSS, also known as hypertrophic obstructive cardiomyopathy) or Wolff-Parkinson-White syndrome (WPW).

In a person who has IHSS, increased outflow obstruction can lead to rapid heart rates, decreased diastolic filling times, and low ventricular end-diastolic volumes. The first diagnostic sign of IHSS is sometimes the rapid onset of hemodynamic instability in an otherwise healthy young person who has AF at a seemingly tolerable ventricular rate (12). Although shortness of breath on exertion and paroxysmal nocturnal dyspnea are common symptoms, effort-related syncope and sudden death are frequently the first indication of IHSS.

In WPW, an accessory pathway prematurely activates the ventricular muscle, altering the resting ECG pattern and sometimes leading to arrhythmias. Patients who have WPW are susceptible to very high ventricular rates that can reach 300 beats per minute and lead to hemodynamic instability. In addition, their rhythms can degenerate into ventricular fibrillation (13).

Risk factors and triggers. As mentioned above, the major risk factors for AF in the elderly are hypertension, ischemic heart disease, and congestive heart failure (2,3). Others include mitral valve disease (4), hyperthyroidism (5), pulmonary disease, and febrile illnesses.

AF in young, active patients is more likely to be a manifestation of congenital heart disease, hyperthyroidism, excess alcohol or other drug use, including caffeine, and exercise-induced catecholamine release. But AF can also be "lone," occurring when no specific predisposing factor can be found.

History. These patients should be questioned about the use of alcohol and over-the-counter preparations that might include sympathomimetic amines, such as pseudoephedrine and ephedrine (14). Beta-agonists, including clenbuterol—a substance banned in some sports because of reputed ergogenic properties—have also been implicated as a cause of AF (15).

The physician should also ask about symptoms or practices that might reveal electrolyte abnormalities, including recent gastrointestinal disease, purging, or surreptitious use of diuretics or laxatives. Although these problems have not been directly implicated as a cause of AF, they can complicate treatment decisions because hypokalemia or hypomagnesemia can increase the risk of digitalis toxicity.

Physical exam. The physical examination, of course, should include a careful evaluation of the heart and a search for signs of pulmonary and thyroid disease.

Diagnostic studies. A simple 12-lead ECG confirms the diagnosis when the patient is fibrillating at the time of presentation. If the patient is in normal sinus rhythm, examination of a rhythm tracing for a delta wave with a short PR interval (figure 2) can lead to the diagnosis of WPW. In symptomatic patients who have WPW, referral to a cardiologist for consideration of electrophysiologic studies is warranted.

[Figure 2]

Diagnosis of paroxysmal AF can be more difficult, but the use of 24-hour Holter or event monitors in patients who have intermittent symptoms can be helpful (16). Exercise treadmill testing can reveal exercise-induced AF and contribute to the assessment of the patient's fitness. An echocardiogram is useful in the diagnosis of structural heart disease, including IHSS and mitral valve stenosis. Stress echocardiography and thallium studies can be helpful in revealing coronary artery disease in older patients.

Laboratory studies should include a complete blood count and measurements of thyroid stimulating hormone, serum electrolytes, calcium, and magnesium. If pulmonary problems are suspected, a chest x-ray and arterial blood gas determinations should be done.

Management

Medication. In patients who are in AF and who are hemodynamically stable, treatment should first be aimed at controlling the ventricular rate. Digoxin, calcium channel blockers, and beta-blockers all control the ventricular rate in AF but are not effective in maintaining sinus rhythm. Digoxin is of less benefit than the other two medications in catecholamine-mediated exercise tachycardia because it primarily increases vagal tone (17). The use of beta-blockers is limited by side effects such as fatigue, lethargy, and lower maximal heart rate, and they are also barred from use in some athletic events, such as riflery (18).

Pharmacologic agents can also be used to convert the patient to sinus rhythm. Pharmalogic cardioversion needs to be done with full ECG monitoring, and anticoagulants must be considered before using drug treatment, just as when considering electrocardioversion (see below). Drugs such as procainamide hydrochloride, quinidine, amiodarone, ibutilide fumarate, and sotalol hydrochloride have been used with variable success. These drugs have been associated with proarrhythmic risks (19) and other side effects. Magnesium has also been suggested as a possible agent for the reversal of AF (20).

Management decisions are more difficult in patients who have paroxysmal AF (PAF). Digoxin was once given to decrease the number of episodes of PAF as well as to avoid rapid rates when such episodes do occur. However, there is now evidence that patients who are treated with digoxin actually have more PAF occurrences and that these events are poorly controlled (21). Side effects limit the usefulness of antiarrhythmics in class 1 (eg, procainamide hydrochloride and quinidine) and class 3 (eg, amiodarone, ibutilide fumarate, and sotalol hydrochloride). Treatment with these drugs should be patient specific and reserved for patients who have repeated episodes of PAF (22).

Electrocardioversion. In competitive athletes, a rapid, predictable treatment to convert the rhythm to sinus is desired, so electrocardioversion is often chosen (23). If an athlete has had AF for less than 48 hours, anticoagulation is not necessary before cardioversion. However, if AF has been present for more than 48 hours or if the date of onset cannot be determined, the patient should be anticoagulated with warfarin sodium for 3 to 6 weeks before attempting cardioversion (24). If the patient is seen shortly after onset, controlling the rate for 24 to 36 hours prior to using cardioversion is recommended because some well-conditioned patients will spontaneously revert to sinus rhythm.

Anticoagulation. Because of the risk of stroke, chronic anticoagulation must be considered in older patients who have hypertension, left ventricular dysfunction, or a history of recurrent AF. However, anticoagulation is not needed in normotensive patients under 60 years old who have normal left ventricular function (25), which includes most competitive athletes. Further, patients who participate in contact sports or other activities that could result in injury are at extreme risk if they undergo anticoagulation treatment.

Ablation. Patients who do not respond to conventional treatment for AF can be considered for ablation therapy, which results in atrioventricular block and the need for permanent pacing (26). Symptomatic patients who have WPW can be successfully treated with ablation therapy, eliminating their arrhythmias without leading to heart block. Surgical treatment of AF has been attempted but is not widely accepted because it has not been proven to be more effective than medical therapy (27).

Athletic activity. The 26th Bethesda Conference task force recommended that athletes be allowed to compete if they have no evidence of structural heart disease and, with or without drug treatment, maintain a ventricular rate comparable to the sinus tachycardia expected during physical activity (28). In addition, patients who have evidence of structural heart disease and AF should be allowed to participate to the extent of the limitations imposed by their disease. The Bethesda recommendations also apply to recreational athletes.

Keeping Patients Active

AF is less common and better tolerated in young athletes and active people than in elderly patients. However, it can be a problem for those whose activities demand a high cardiac output, such as competitive athletes. Fortunately, most cases can be traced to correctable risk factors and controlled by medication or, if persistent, by electrocardioversion. Consequently, athletes and active people can usually recover rapidly and resume athletic participation quickly.

References

  1. Feinberg WM, Blackshear JL, Laupacis A, et al: Prevalence, age distribution, and gender of patients with atrial fibrillation: analysis and implications. Arch Intern Med 1995;155(5):469-473
  2. Kalman JM, Tonkin AM: Atrial fibrillation epidemiology and the risk and prevention of stroke. Pacing Clin Electrophysiol 1992;15(9):1332-1346
  3. Krahn AD, Manfreda J, Tate RB, et al: The natural history of atrial fibrillation: incidence, risk factors, and prognosis in the Manitoba Follow-Up Study. Am J Med 1995;98(5):476-484
  4. Diker E, Aydogdu S, Ozdemir M, et al: Prevalence and predictors of atrial fibrillation in rheumatic valvular heart disease. Am J Cardiol 1996;77(1):96-98
  5. Forfar JC, Miller HC, Toft AD: Occult thyrotoxicosis: a correctable cause of 'idiopathic' atrial fibrillation. Am J Cardiol 1997;44(1):9-12
  6. Hiss RG, Lamb LE: Electrocardiographic findings in 122,043 individuals. Circulation 1962;25:947-961
  7. Paritano JA, Oriel RJ: Prevalence and nature of cardiac arrhythmias in apparently normal well-trained runners. Am Heart J 1982;104(4 pt 2):762-768
  8. Coelho A, Palileo E, Ashley W, et al: Tachyarrhythmias in young athletes. J Am Coll Cardiol 1986;7(1):237-243
  9. Maki T, Toivonen L, Koskinen P, et al: Effect of ethanol drinking, hangover, and exercise on adrenergic activity and heart rate variability in patients with a history of alcohol-induced atrial fibrillation. Am J Cardiol 1998;82(3):317-322
  10. Peters KG, Kienzle MG: Severe cardiomyopathy due to chronic rapidly conducted atrial fibrillation: complete recovery after restoration of sinus rhythm. Am J Med 1988;85(2):242-244
  11. Karjalainen J, Kujala UM, Kaprio J, et al: Lone atrial fibrillation in vigorously exercising middle-aged men: case-control study. BMJ 1998;316(7147):1784-1785
  12. Wigle ED, Rakowski H, Kimball BP, et al: Hypertrophic cardiomyopathy: clinical spectrum and treatment. Circulation 1995; 92(7):1680-1692
  13. Timmermans C, Smeets JL, Rodriguez LM, et al: Aborted sudden death in the Wolff-Parkinson-White syndrome. Am J Cardiol 1995;76(7):492-494
  14. MacMahon JR: Atrial fibrillation and sympathomimetics, letter. J Pediatr 1974;84(4):613
  15. Sporano V, Grasso L, Esposito M, et al: Clenbuterol residues in non-liver containing meat as a cause of collective food poisoning. Vet Hum Toxicol 1998;40(3):141-143
  16. Kinlay S, Leitch JW, Neil A, et al: Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter monitoring in patients with palpitations: a controlled clinical trial. Ann Intern Med 1996;124(1 pt 1):16-20
  17. Falk RH, Leavitt JI: Digoxin for atrial fibrillation: a drug whose time has gone? Ann Intern Med 1991; 4(7):573-575
  18. Catlin DH, Murray TH: Performance-enhancing drugs, fair competition, and Olympic sports. JAMA 1996;276(3):231-237
  19. Falk RH: Proarrhythmia in patients treated for atrial fibrillation or flutter. Ann Intern Med 1992;7(2):141-150
  20. Brodsky MA, Orlov MV, Capparelli EV, et al: Magnesium therapy in new-onset atrial fibrillation. Am J Cardiol 1994;73(16):1227-1229
  21. Rawles JM, Metcalfe MJ, Jennings K: Time of occurrence, duration, and ventricular rate of paroxysmal atrial fibrillation: the effect of digoxin. Br Heart J 1990;63(4):225-227
  22. Reiffel JA: Selecting an antiarrhythmic agent for atrial fibrillation should be a patient-specific, data-driven decision. Am J Cardiol 1998;82(8A):72N-81N
  23. Ricard P, Levy S, Trigano J, et al: Prospective assessment of the minimum energy needed for external electrical cardioversion of atrial fibrillation. Am J Cardiol 1997;79(6):815-816
  24. Laupacis A, Albers G, Dalen J, et al: Antithrombotic therapy in atrial fibrillation. Chest 1995;108(4 suppl):352S-359S
  25. Kopecky SL, Gersh BJ, McGoon MD, et al: The natural history of lone atrial fibrillation: a population-based study over three decades. N Engl J Med 1987;317(11):669-674
  26. Brignole N, Menozzi C, Gianfranchi L, et al: Assessment of atrioventricular junction ablation and DDDR mode-switching pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study. Circulation 1998;98(10):953-960
  27. Cox JL, Schuessler RB. Lappas DG, et al: An 8 H-year clinical experience with surgery for atrial fibrillation. Ann Surg 1996;224(3):267-273
  28. Zipes DP, Garson A Jr: 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities: Task Force 6: arrhythmias. J Am Coll Cardiol 1994;24(4):892-899

Dr Reiss is a clinical associate professor of family and internal medicine at the University of Southern California (USC) School of Medicine and director of Westchester Medical Group Center for Heart and Health in Los Angeles. He is a USC team physician, holds a certificate of added qualifications in sports medicine, and is a fellow of the American College of Physicians and a member of the American College of Sports Medicine. Dr Christie is a board certified internist and holds a certificate of added qualifications in sports medicine. He is director of Northeast Sportsmedicine at St Mary's Regional Medical Center in Lewiston, Maine. Address correspondence to Robert A. Reiss, MD, The Westchester Medical Group Center for Heart and Health, 8540 S Sepulveda Blvd, Suite 118, Los Angeles, CA, 90045; e-mail to [email protected].


RETURN TO MARCH 1999 TABLE OF CONTENTS

HOME  |   JOURNAL  |   PERSONAL HEALTH  |   RESOURCE CENTER  |   CME  |   ADVERTISER SERVICES  |   ABOUT US