Arrhythmias

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Cardiac arrhythmias in athletes range from benign to life threatening. Bradyarrhythmias are more common in athletes than in the general population because of an increase in resting vagal tone as a response to regular strenuous exercise. Common bradyarrhythmias include sinus bradycardia, sinus arrhythmia, first-degree atrioventricular (AV) block, and Wenckebach (or Mobitz I) second-degree AV block (Huston et al., 1985; Link et al., 2001). These bradyarrhythmias are usually asymptomatic and should resolve during exercise by the withdrawal of vagal tone and associated catecholamine influx.

Athletes with symptomatic Wenckebach block, such as presyncope or syncope during exertion, require further evaluation by a cardiologist and often placement of a permanent pacemaker and restriction of activities. Higher degrees of heart block, such as Mobitz II second-degree and complete third-degree AV blocks, are always pathologic in any individual, including athletes (Fig 29-2). Mobitz II and complete heart blocks signify marked disease in the His-Purkinje system and are generally accepted as a class I indication for permanent pacemaker placement, even in the absence of symptoms (Link et al, 2001).

Tachyarrhythmias in the athlete are abnormal and require further evaluation and treatment before participation in strenuous exercise. The treatment of many supraventricular

alternate P wave is blocked.

(From Goldberger E. Treatment of Cardiac Emergencies, 5th ed. Philadelphia, Saunders, 1990.)

alternate P wave is blocked.

(From Goldberger E. Treatment of Cardiac Emergencies, 5th ed. Philadelphia, Saunders, 1990.)

tachyarrhythmias has been greatly advanced by the use of radiofrequency (RF) ablation, which might offer an actual cure and obviate the need for lifelong pharmacologic treatment.

The most common tachyarrhythmia in athletes is atrial fibrillation (AF). Studies have suggested that AF occurs more frequently in athletes than in the general population (Fur-lanello et al., 1998; Huston et al., 1985). This might be a consequence of increased vagal tone and bradycardia in athletes, which allows dispersion of atrial repolarization and results in a higher susceptibility to AF. Radiofrequency ablation is curative in most cases of paroxysmal AF (Link et al., 2001). If pharmacologic treatment is needed, rate control can be accomplished with beta-adrenergic blockers or calcium channel blockers, and anticoagulation should be considered with aspirin or warfarin, depending on the frequency of AF and other risk factors for thromboembolism. Any athlete receiving anticoagulation therapy with warfarin should be restricted from sports involving collision or bodily contact.

Atrioventricular nodal reentrant tachycardia (AVNRT) is characterized by abrupt onset and termination of symptoms, a narrow QRS complex, and no evidence of atrial activity on the ECG during the tachycardia. AVNRT caused by an accessory bypass tract, known as Wolff-Parkinson-White (WPW) syndrome, may be evident on the ECG by the characteristic delta wave (slurred upstroke of QRS complex), short PR interval, and prolonged QRS complex (Fig. 29-3). Athletes with WPW may be at risk of sudden death and should be strongly considered for RF ablation. Radiofrequency ablation for both AVNRT and WPW offers cure rates higher than 95% (Link et al., 2001; Manolis et al., 1994).

Atrial flutter is an unusual arrhythmia in trained athletes and typically results from an underlying cardiomyopathy.

Ventricular tachyarrhythmias in athletes are life threatening and usually the result of structural heart disease such as hypertrophic cardiomyopathy, anomalous coronary artery, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia (ARVD), or atherosclerotic coronary artery disease (CAD). Ventricular arrhythmias and sudden death may also occur in individuals with structurally normal hearts. This may occur from ion channel disorders, such as long QT syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and Brugada syndrome, or from commotio cordis. Long QT syndrome is characterized by a prolonged QTc interval, and Brugada syndrome is suggested by an incomplete right bundle branch block and ST-segment elevation in the precordial leads. Exercise may provoke ventricular arrhythmias because of high catecholamine levels and make ventricular fibrillation more difficult to terminate. Athletes who experience a resuscitated sudden death should undergo an extensive workup and treatment with an implantable cardioverter-defibrillator (Link et al., 2001).

Sudden Cardiac Death

Sudden cardiac death in athletes is a catastrophic event and the leading cause of death in exercising young athletes (Maron et al., 2009) The estimated incidence of sudden cardiac death in high school and college athletes is 1 in 100,000 to 200,000 athletes per year (Maron et al., 2009; van Camp et al., 1995). However, these studies are limited by the lack of a mandatory reporting system for juvenile sudden death and their reliance on electronic databases and media reports to identify cases of sudden death. Thus, current reports likely underestimate the true incidence of sudden cardiac death in athletes.

Figure 29-3 Atrioventricular nodal reentrant tachycardia. Notice the characteristic triad of the Wolff-Parkinson-White (WPW) pattern: wide QRS complexes, short PR intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVF are the result of abnormal ventricular conduction (negative delta waves) rather than an inferior myocardial infarction. This pattern is consistent with a bypass tract inserting into the posterior wall of the left ventricle.

(From Goldberger AL. Clinical Electrocardiography: a Simplified Approach, 7th ed. Philadelphia, Saunders-Elsevier, 2006.)

Figure 29-3 Atrioventricular nodal reentrant tachycardia. Notice the characteristic triad of the Wolff-Parkinson-White (WPW) pattern: wide QRS complexes, short PR intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVF are the result of abnormal ventricular conduction (negative delta waves) rather than an inferior myocardial infarction. This pattern is consistent with a bypass tract inserting into the posterior wall of the left ventricle.

(From Goldberger AL. Clinical Electrocardiography: a Simplified Approach, 7th ed. Philadelphia, Saunders-Elsevier, 2006.)

Box 29-2 Causes of Sudden Cardiac Death in Young Athletes

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