63 Exercise-Induced Atrial Arrhythmias Exercise-Induced Ventricular Arrhythmias Outflow Tract Ventricular Tachycardia Idiopathic Left Ventricular Tachycardia Arrhythmogenic Right Ventricular Dysplasia Catecholaminergic Polymorphic Ventricular Tachycardia Antiarrhythmics and Exercise-Induced Ventricular Arrhythmias Several physiological changes that occur during exercise may precipitate cardiac arrhythmias. Activation of the sympathetic nervous system results in an increase in circulating catecholamines.1 Increased automaticity and enhanced triggered activity may increase the likelihood of arrhythmias. The presence of premature beats during exercise can lead to initiation of reentrant supraventricular and ventricular arrhythmias. Important factors in arrhythmogenicity include electrolyte shifts, baroreceptor activation, myocardial stretch, ischemia, and genetic predisposition. Exercise can increase potassium levels, decrease pH, and raise catecholamines.2 These catecholamines may counterbalance the harmful cardiac effects of hyperkalemia and acidosis and improve action potential characteristics in potassium-depolarized ventricular myocytes.3 In normal myocardial tissue, hyperkalemia decreases the incidence of norepinephrine-induced arrhythmias. However in ischemic or infarcted tissue, hyperkalemia and catecholamines may jointly potentiate arrhythmias. The heart is also at increased risk in the post-exercise period. During this time, plasma potassium is low and adrenergic tone is high. An abnormal regulation of sympathovagal balance and electrolytes in recovery, compounded with ischemia, may increase the susceptibility to arrhythmias.1 Despite the myriad of physiological changes that occur in exercise, in the absence of structural or electrical heart disease sudden death due to arrhythmias is extremely rate. Exercise-induced atrial arrhythmias are less common than ventricular arrhythmias. In the Baltimore Longitudinal Study of Aging, 1383 asymptomatic volunteers aged 20 to 94 years underwent exercise testing.4 Exercise treadmill–induced supraventricular arrhythmia (ETISVA) was noted in 85 subjects (6%). An eightfold increase in the relative risk of developing lone atrial fibrillation (AF) was noted in subjects with exercise-induced ETISVA. In a 5.7-year follow-up, 10% of 85 subjects with ETISVA developed AF or paroxysmal supraventricular tachycardia (SVT). Therefore, ETISVA may be a marker for AF or paroxysmal SVT during follow-up. The relationship between exercise and atrial fibrillation is particularly relevant to athletes. The overall risk for AF is significantly higher in athletes than in controls (odds ratio 5.29, 95% confidence interval [CI] 3.57 to 7.85, P = .0001).5 Endurance sports increase preload, which increases atrial pressure and therefore shortens atrial refractory periods and increases the dispersion of atrial refractoriness. Increased vagal tone in athletes, sympathetic surges during exercise, and fluid and electrolyte changes during exercise may also contribute to the development of atrial arrhythmias.6 Anatomically, athletes may have larger left atrial dimensions and fibrosis secondary to chronic systemic inflammation from excessive endurance exercise.7 In patients with no structural heart disease, treatment is generally targeted at addressing the trigger for the arrhythmia. A reduction in exercise intensity or duration is often highly effective in reducing arrhythmia burden.8 However, many patients, especially competitive athletes, may be unwilling or unable to reduce or refrain from exercise. In these cases, β-blockers, antiarrhythmics, and catheter ablation can be considered. In a study of 5375 patients with known or suspected coronary artery disease (CAD), 24% of patients developed atrial ectopy, 3.4% developed SVT, and 0.8% developed AF upon treadmill testing.9 Exercise treadmill–induced supraventricular arrhythmias were not predictive of any end point. Asymptomatic patients without prior evidence of CAD have been noted to have variable rates of ventricular ectopy. In the Advisory Group for Aerospace Research and Development study of 1640 healthy aviators, the prevalence of PVCs (other than single or occasional) increased with age: 6.6% for ages 20 to 29, 7.6% for ages 30 to 39, and 13.1% for ages 40 to 53.10 The percentages of patients with three or more consecutive PVCs were 0.8% for ages 20 to 29, 1.0% for ages 30 to 39, and 3.5% for ages 40 to 53. In another study of 597 male and 325 female healthy adult volunteers, only 1.1% of the patients had exercise treadmill–induced ventricular arrhythmias (ETIVAs).11 These episodes were typically asymptomatic, short, and limited to 3 to 6 beats, usually near peak exercise. The prognostic significance of ventricular ectopy in asymptomatic healthy individuals remains controversial. In a population of veterans referred for exercise stress testing, the risk of mortality in patients with resting (pre-exercise) PVCs and ETIVA was increased.12 The combination of rest PVCs and ETIVA carries the highest risk.1 These variables were independent predictors of cardiovascular mortality after adjustment for other clinical and exercise test variables, which included exercise-induced ischemia. However it is possible that additional adjustment for left ventricular functional abnormalities or coronary disease burden might have mitigated the association. Regardless, patients found to have arrhythmias during exercise testing should undergo an evaluation of their left ventricular function. Congenital coronary anomalies are implicated in 10% to 20% of all deaths in young athletes.13 The right coronary artery arising from the left coronary sinus is more common than the left coronary artery arising from the anterior sinus, although the latter is a more common cause of sudden death. Of the four types of anomalous left coronary arteries, the interarterial type is the only type that places the patient at increased risk for sudden death. In this variant, the left coronary artery arises from the right cusp and passes anteriorly between the aorta and the right ventricular outflow tract (RVOT). Similarly, an interarterial course of an anomalous right coronary artery that arises from the left cusp would also put patients at risk for sudden cardiac death (SCD). However, the larger territory supplied by the left coronary artery results in increased risk over right coronary artery anomalies. SCD associated with or shortly after vigorous exercise is very unusual after the patient is >35 years of age. Angelini et al report that the incidence of anomalous coronary arteries was 1.07% (right anomalous coronary from the left coronary sinus in 0.92%; left anomalous coronary from the right coronary sinus in 0.15%).14 Davis et al. report a prevalence of 0.17% for anomalous origins of coronary arteries among 2388 children and adolescents.15 Among 1686 coronary anomalies found in 126,595 adult coronary angiograms, Yamanaka and Hobbs reported an incidence of 0.17% for anomalous left coronary arteries and 0.107% for anomalous right coronary arteries.16 The mechanism by which the coronary anomaly causes SCD is hypothesized to be a sudden occlusion of the vessel that may involve damage, thrombosis, or spasm, resulting in severe myocardial ischemia and ventricular tachycardia/fibrillation.17 During exercise, increased dP/dt and stroke volume may result in increased systolic expansion of the proximal aorta and pulmonary artery, which could collapse the proximal anomalous coronary artery. Because exercise results in a greater percentage of time spent in systole, which is when compression occurs, SCD most frequently occurs with or shortly after exercise. Other coronary anomalies may also be implicated in arrhythmias and sudden death. Patients with a single coronary artery that divides into all three major branches are at risk for SCD during athletic activity.18,19 Patients with hypoplasia of portions of the coronary tree or with coronary fistulas, or the small minority of patients with an anomalous left coronary artery arising from the pulmonary artery (ALCAPA) who reached adulthood, would also be at risk for exercise-induced arrhythmias. Outflow tract VT should be considered in patients with a structurally normal heart and a QRS in VT that features a left bundle branch block morphology and an inferior axis. Most outflow tract VTs originate from the RVOT (80%), and the remainder originate from the left ventricular outflow tract (LVOT).20 RVOT VT has a left bundle branch QRS morphology and an inferior axis, with an R/S transition typically in V3 or V4. LVOT VT may also have left bundle branch QRS morphology but with small R waves in V1 and an earlier R/S transition. Lerman and collegues have determined that outflow tract VTs are the product of triggered activity secondary to cyclic adenosine monophosphate–mediated delayed afterdepolarizations. 21 The VT is adrenergically mediated and is sensitive to perturbations that lower intracellular calcium such as adenosine and verapamil. The diagnosis of idiopathic VT is one of exclusion; therefore other causes of left bundle branch block (LBBB) pattern VT should be considered. Clinically, outflow tract VT accounts for the vast majority of idiopathic VTs. The age of presentation is usually 30 to 50 years, and patients usually have a benign clinical course.20 The most common complaint among patients is palpitations (48% to 80%), followed by presyncope or light-headedness (28% to 50%). Syncope is rare (<10%) and SCD is extremely rare. However, some patients may develop cardiomyopathy from incessant repetitive monomorphic VT or from a high burden of ventricular premature complexes (VPCs). Ablation of the focus usually normalizes left ventricular function in a few months. The spectrum of outflow tract VT includes three clinical subtypes.22 Patients may have repetitive monomorphic VPCs, repetitive nonsustained monomorphic VT, or exercise-induced sustained VT. Patients may present with a predominance of one type; however, significant overlap has been noted, and it is believed that the subtypes share the same cellular mechanism. Generally, outflow tract tachycardias are provoked by exercise, and treadmill testing is useful in reproducing the clinical VT. Approximately 70% of patients who present with sustained VT will have VT induced by exercise testing.22 However, in patients who present with monomorphic nonsustained ventricular tachycardia (NSVT) or VPCs on monitoring, exercise testing may induce sustained VT in only 10%. Overall, exercise testing reproduces VT in less than 50% of patients with clinical VT. As a result, exercise testing may not be a reliable indicator of β-blocker or antiarrhythmic efficacy, and ambulatory monitoring would be an appropriate adjunct. Two responses of outflow tract VT to exercise testing have been reported. In the first case, VT occurs during acceleration of the heart rate with exercise. A progression from VPCs to salvos of NSVT to sustained VT may be observed. In contrast, patients with repetitive monomorphic VT may have suppression of their VT during exercise and development of VT during the recovery phase of exercise.23 These responses indicate that a critical window of heart rates is required for VT initiation. This cycle length dependence of ventricular ectopy may also be observed on ambulatory monitoring. 23,24 In general, patients with exercise-induced outflow tract VTs have no structural heart disease. In contrast, patients with post-infarction septal VTs will have a history of coronary disease and myocardial infarction. Bundle branch reentry VT is usually seen in the setting of structural heart disease, most commonly a dilated cardiomyopathy.25 Patients with antidromic atrioventricular reciprocating tachycardia (AVRT) using an atriofascicular bypass tract might also demonstrate an LBBB morphology VT, although the axis is usually leftward.26 The triggered activity of outflow tract VT also differs from the reentry mechanisms of post-infarction VT, bundle branch reentry VT, and antidromic AVRT using an atriofascicular bypass tract. Although they characteristically have exercise-induced VT, patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) will have polymorphic ventricular ectopy and will manifest bidirectional VT. Last, outflow tract morphology VTs may be a manifestation of arrhythmogenic right ventricular dysplasia (ARVD), although the morphology of VT is often varied in ARVD. In addition to exercise, ventricular ectopy, including sustained VT, can be provoked by emotional stress. High levels of sympathetic tone contribute to arrhythmogenicity. This is also illustrated in the circadian variations in episodes of VT, ventricular runs (2 to 4 beats), and VPCs. Hayashi et al. demonstrated that peaks for these ventricular arrhythmias occurred around 7 AM and 6 PM.27 β-Blockers completely eliminated VT episodes and blunted ventricular runs; however rates of single VPCs were similar to those before β-blockade therapy. Approximately 10% of idiopathic VTs originate from the fascicles of the left ventricle. These arrhythmias are referred to as fascicular VT or verapamil-sensitive VT.28 This condition should be considered in the differential diagnosis of right bundle branch block (RBBB) with left anterior fascicular block pattern VT. Less commonly, a left posterior block pattern may be seen (5% to 10%).28 The usual age of presentation is between 15 and 40 years, and patients usually have normal resting electrocardiogram (ECG) and left ventricular function.29
Exercise-Induced Arrhythmias
Exercise-Induced Atrial Arrhythmias
Exercise-Induced Ventricular Arrhythmias
Apparently Healthy Subjects
Coronary Artery Disease
Coronary Anomalies
Outflow Tract Ventricular Tachycardia
Idiopathic Left Ventricular Tachycardia
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