Evaluation of Suspected Right Ventricular Pathology in the Athlete
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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Unraveling the role of high-intensity resistance training on left ventricle proteome: Is there a shift towards maladaptation?
2016, Life SciencesCitation Excerpt :Regular exercise is effective for prevention and treatment of several chronic diseases, and type of training as well as its duration and intensity promotes distinct changes in cardiac tissue. These morphological changes depend on the kind of training, are clinically characterized by modifications in cardiac size and shape due to increased load, and are not always confined to the left ventricle, considering that exercise requires both the left and right ventricle to accept and eject relatively large quantities of blood [1,2]. It is well known that high-intensity resistance training (RT) increases left ventricular wall thickness and cardiomyocyte cell width, with unaltered internal cavity size, resulting on concentric cardiac hypertrophy [2,3].
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Statement of Conflict of Interest: see page 405.