Case Report
Exercise-Induced Right Ventricular Dysplasia/Cardiomyopathy—An Emerging Condition Distinct from Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

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We report a case of a 32-year-old female world champion triathlete who developed exercise induced recurrent ventricular tachycardia (VT). Investigations supported a diagnosis of the newly recognised condition “exercise induced right ventricular dysplasia/cardiomyopathy” (EIRVD/C). The VT could be easily terminated by burst pacing from the RV apex and the athlete has been successfully treated with an internal cardioverter defibrillator (ICD).

Introduction

Larger recurrent sustained exercise induced ventricular tachycardia (VT) in elite ultra-endurance athletes is a rare but serious problem. Recent studies indicate that most serious ventricular arrhythmias (VA) in elite endurance athletes arise from the right ventricle (RV).1 In some the diagnosis may be arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). In others it is postulated that repeated extreme exercise may damage the RV thus providing a substrate for arrhythmias.1, 2, 3 In such cases the term EIRVD/C is applicable.4 Distinction between these two entities (ARVD/C and EIRVD/C) is important. ARVD/C is an inherited disorder characterised by progressive fibrofatty replacement of RV myocardium eventually leading to ventricular arrhythmias and right heart failure.5 The underlying pathophysiology is a genetic abnormality of cell adhesion proteins such as plakoglobulin, desmoplakin, plakophillin-2, and desmoglein-2.5 In patients with ARVD/C exercise may precipitate ventricular arrhythmias and aggravate or accelerate the condition but it is not the fundamental cause of the disorder. On the other hand EIRVD/C is thought to be the cumulative result of repeated bouts of extreme endurance exercise each of which has caused a small amount of damage to the RV.4 We report a case of exercise-precipitated recurrent sustained monomorphic ventricular tachycardia (VT) occurring in a 32-year-old multiple world champion female triathlete without a family history to suggest ARVD/C and in whom investigations support a diagnosis of EIRVD/C rather than ARVD/C.

Section snippets

Case Report

The subject is a former world champion tri-athlete. Over a career of 10 years during which time she averaged 10–15 events per year she won many world class events and for a 4-year-period was rated number one in the world. In 2004 during a swimming training session she became dizzy and aware of palpitations. An ECG showed sustained monomorphic VT with LBBB morphology (Fig. 1b). DC cardioversion was required. She subsequently suffered further similar episodes each related to exercise. A typical

Discussion

The absence of a family history and lack of typical changes on the MRI scan and cardiac biopsy make a diagnosis of ARVD/C unlikely in this case. Furthermore it is improbable that someone with ARVD/C could achieve world status in triathlon over such a long period of time with this diagnosis. We believe it more likely that the athlete suffers from the newly described condition EIRVD/C.

The evidence that extreme endurance athletic activity can cause RV damage and dysfunction eventually leading to

References (6)

  • H. Heidbüchel et al.

    High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification

    Eur Heart J

    (2003)
  • J. Ector et al.

    Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment

    Eur Heart J

    (2007)
  • La Gerche A, Connelly KA, Mooney DJ, MacIsaac AI, Prior DL. Biochemical and functional abnormalities of left and right...
There are more references available in the full text version of this article.

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