Evaluation of Suspected Right Ventricular Pathology in the Athlete

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Abstract

Rigorous training remodels the heart of elite endurance athletes to produce the phenotype of the “athlete's heart.” This remodeling, which advantages cardiac performance, creates challenges in the diagnosis of cardiac disorders within this population. This is particularly so for right ventricular pathologies because of the limited number of studies documenting the impact of training on right ventricular remodeling. Although arrhythmogenic right ventricular cardiomyopathy is the focus of this review, several other pathologies that may mimic arrhythmogenic right ventricular cardiomyopathy, including right ventricular outflow tract tachycardia, Wolff-Parkinson-White syndrome, Brugada syndrome, pulmonary embolism, cardiac sarcoidosis, myocarditis, and right ventricular infarction, are also included. In particular, the electrocardiographic findings for each condition are highlighted because this is the most informative and easily accessible diagnostic clinical tool.

Section snippets

Cardiovascular adaptation in the highly trained athlete

The phenotypic changes associated with endurance training are well established and include the development of cardiac hypertrophy and dilation with bradyarrhythmias and increased vagal tone.1 These adaptations augment stroke volume and, therefore, the ability to increase cardiac output with exercise above the normal as documented by objective measures of exercise capacity, especially peak oxygen consumption, which increases up to 40% to 50%.2 The magnitude of this beneficial adaptation depends

Arrhythmogenic RV cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy is a desmosomal disease linked to mutations of multiple genes implicated in maintaining the structure of the intercalated discs.13, 14, 15 It is believed that instability of the intercalated disk and the electrical gap junctions between myocytes produces a propensity for ventricular arrhythmias and, therefore, an increased risk of sudden cardiac death. The distinctive clinical features of ARVC relate to its RV manifestation and, hence, the

Diagnosing ARVC in athletes

There is overlap between the electrophysiologic and imaging findings in ARVC and athlete's heart. For a full review of the diagnostic criteria of ARVC, see Table 1.26 Many of the electrical and morphologic findings related to athlete's heart resolve with detraining of sufficient duration.27, 28, 29, 30 There are no published data on the effects of detraining athletes with ARVC, but the belief is that the pathologic changes remain even after detraining is complete.

Repolarization abnormalities on

Right ventricular outflow tract ventricular tachycardia

Right ventricular outflow tract ventricular tachycardia is a relatively common cause of ventricular tachycardia in the young athlete. It is classically described as a ventricular tachycardia with the QRS complex demonstrating a left bundle-branch block and inferior axis.35 Occasionally, however, left bundle-branch block ventricular tachycardia may originate from the left ventricular outflow tract and the aortic sinus of Valsalva. Palpitations, presyncope, and syncope are the usual clinical

Wolff-Parkinson-White

Wolff-Parkinson-White (WPW) is the most common accessory pathway causing arrhythmias in athletes and is present in 0.1% to 0.3% of the general population.38, 39, 40 The ECG appearance of a shortened PR interval and delta waves in an athlete, classically found in WPW, is never the result of physiologic changes alone but requires an accessory pathway. Right-sided accessory pathways can produce a leftward ventricular depolarization vector resulting in amplified R waves in left-sided limb leads (I,

Brugada syndrome

Brugada syndrome is characterized by the findings of right precordial ST-segment elevation, possible conduction delays, and the potential for lethal arrhythmias in a structurally “normal” heart on imaging.45 There is an apparent increase in arrhythmias during periods of sleep or rest, and increased vagal tone may be one of the triggers.46 This is particularly important for athletes because the increased vagal tone from training could theoretically increase susceptibility to arrhythmia. Evidence

Right ventricular sarcoidosis/myocarditis

Chronic inflammatory conditions, whether of infectious (viral cardiomyopathy), genetic (arrhythmogenic cardiomyopathy), or uncertain etiology (sarcoidosis), may present with predominantly RV manifestations. Typically, these can be distinguished from coronary artery disease because the distribution of ECG, arrhythmic, and imaging abnormalities does not conform to a recognized coronary arterial territory. ST-segment or T-wave changes, the morphology of ventricular arrhythmia, and the distribution

Pulmonary embolism with pulmonary hypertension

Athletes may be at risk for deep venous thrombosis from trauma suffered during competition.55, 56 Those competing in triathlons or marathons are particularly susceptible because of the risk of microtrauma and endothelial injury, which may go unnoticed during competition.57 The risk of deep venous thrombosis can further be increased due to dehydration and the accompanying hemoconcentration and travel.58 Virchow triad of risk is completed in those athletes traveling long distances on buses or

Right ventricular myocardial infarction

Premature coronary artery disease and myocardial infarction of any etiology are rare in the young athlete unless associated with an inherited major lipid abnormality such as familial hypercholesterolemia. Furthermore, isolated RV infarction is uncommon at any age and is usually associated with evident inferior infarction of the left ventricle.59, 60 Typically, patients present with severe chest pain, although cardiac arrest due to complete heart block or significant ventricular arrhythmias may

Summary

The cardiovascular adaptation that accompanies endurance training includes RV ECG and imaging changes, which may overlap with clinical features of several inherited (eg, ARVC) and acquired (eg, sarcoidosis) cardiac conditions. The diagnosis of these, however, relies on demonstration of pathologic changes (eg, T-wave inversion, ventricular aneurysms, late enhancement), which, when present in athletes, should be considered as abnormal and not accepted as adaptation to training.

Statement of Conflict of Interest

All authors declare that there are no conflicts of interest.

Acknowledgments

University College London Hospitals/University College London receives a proportion of funding from the Department of Health's National Institute for Health Research Biomedical Research Centres funding scheme.

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