Running the risk: extreme right ventricular remodelling in an endurance athlete-a case report

Abstract

Background: Distinguishing physiological cardiac adaptation from pathological remodelling in endurance athletes is challenging. While the athletic heart typically demonstrates balanced biventricular enlargement, extreme exercise may rarely trigger disproportionate right ventricular (RV) changes that challenge diagnostic classification.

Case summary: A 47-year-old male ultra-endurance athlete presented with exertional symptoms 3 months after recovery from a pulmonary embolism (PE). Initial post-PE echocardiography was normal. After resuming extreme training, he developed severe RV dilation (basal diameter 5.7 cm on echocardiography; RV volume index 92 cc/m² on cardiac magnetic resonance imaging) disproportionate to the left ventricle, with preserved systolic function and no late gadolinium enhancement. Cardiopulmonary exercise testing revealed significant chronotropic incompetence with below-expected peak oxygen uptake for his elite training status. Symptoms and ventricular ectopy improved with detraining, but severe RV dilation persisted. Evaluation excluded arrhythmogenic cardiomyopathy and significant pulmonary vascular sequelae.

Discussion: This case illustrates disproportionate RV remodelling precipitated by the resumption of extreme exercise in a susceptible athlete post-PE. The temporal dissociation from the PE and absence of residual clot burden implicate exercise-related haemodynamic stress as the primary driver, challenging the boundary between physiological adaptation and maladaptation. These findings highlight a potential maladaptive response to extreme exercise, possibly potentiated by a prior vascular insult, and underscore the value of integrated functional assessment and monitored detraining in athletes with borderline findings.

Keywords: Athletic heart; Cardiac remodelling; Case report; Exercise-induced cardiomyopathy; Right ventricular dilation.

Figure 1

The electrocardiogram shows normal sinus rhythm with QRS fragmentation in aVL and V1, normal early repolarization patterns, and no epsilon waves.

Figure 2

(Left) Key parameters of the cardiopulmonary exercise testing include maximal effort (peak RER 1.21), reduced chronotropic response (peak heart rate 130 bpm; 70% age-predicted), below-expected aerobic capacity for elite status (peak VO₂ 39.3 mL/kg/min; 115% predicted), preserved stroke volume (O₂ pulse 25 mL/beat; 156% predicted), normal ventilatory efficiency (VE/VCO₂ slope 23.2), and no desaturation (peak SpO₂ 98%); (Right) The nine-panel plot of the cardiopulmonary exercise testing.

Figure 3

The stress electrocardiogram shows marginally increased QRS duration and premature ventricular contractions. Of note, the isolated premature ventricular contractions exhibit a LBBB morphology with inferior axis (infundibular) pattern.

Figure 4

The cardiac magnetic resonance imaging shows: (left) still frame of an axial SSFP cine sequence, demonstrating a dilated right ventricle measuring around 70 mm at the base (volume index of 92 cc/m²) and without focal wall motion abnormalities to suggest arrhythmogenic right ventricular cardiomyopathy; (Right) Late gadolinium enhancement sequence, showing no signs of myocardial fibrosis.

Figure 5

A) The 48-h three-channel Holter monitor shows increased frequency of monomorphic premature ventricular contractions of infundibular origin at elevated heart rates during training. B) Morphology review of the 48-h Holter shows an overall 1% PVC burden without nonsustained ventricular tachycardia. One couplet and zero triplets were noted.