Key result
Moderate exercise raises right ventricular late potentials by ~3% in definitive ACM without inducing exercise PH.
Why the study?
Patients with arrhythmogenic cardiomyopathy (ACM) are advised to perform no more than moderate-intensity exercise, but whether such exercise acutely alters hemodynamic, electrophysiological, or cardiac biomarker profiles was unknown.
Does acute moderate-intensity isometric, resistance, or aerobic exercise induce exercise pulmonary hypertension, troponin T elevation, or changes in right ventricular late potentials in patients with definitive or probable arrhythmogenic cardiomyopathy?
Observational (n=20)
Does acute moderate-intensity isometric, resistance, or aerobic exercise induce exercise pulmonary hypertension, troponin T elevation, or changes in right ventricular late potentials in patients with definitive or probable arrhythmogenic cardiomyopathy?
Although acute moderate-intensity isometric, resistance, and aerobic exercise did not cause exercise pulmonary hypertension in ACM patients, it acutely increased arrhythmogenic substrate (late potentials) in definitive ACM while decreasing it in probable ACM.
Answers are grounded in this paper and cite their sources.
May inform stage-specific exercise assessment in arrhythmogenic cardiomyopathy; hypothesis-generating and should not yet change practice.
Patients with arrhythmogenic cardiomyopathy (ACM) are advised to perform no more than moderate-intensity exercise, but whether such exercise acutely alters hemodynamic, electrophysiological, or cardiac biomarker profiles is unknown. We investigated whether moderate-intensity isometric, resistance, or aerobic exercise induces exercise pulmonary hypertension (exPH, mean pulmonary artery pressure to cardiac output slope >3 mmHg/L/min), troponin T elevation, or changes in late potentials (LP) in definitive or probable ACM. Twenty patients (13 definitive, 7 probable ACM; age 42.2 ± 10.7 years) underwent exercise right heart catheterization during isometric handgrip (HG) and bicep curl (BC) (1 minute each at 70% of maximal voluntary contraction), followed by 2 × 20 minutes of supine cycling (CYC) at the first ventilatory threshold. Central hemodynamics and cardiac biomarkers were measured during each condition, and high-density right ventricular electroanatomical mapping was performed before and after exercise. exPH did not occur in either group (all <3 mmHg/L/min), whereas troponin T rose progressively without group differences (p=0.880). LP within the "arrhythmogenic triangle" decreased in probable (mean change -1.95 ± 1.59%) but increased in definitive ACM (mean change 2.72 ± 2.16%, p<0.001). In conclusion, moderate-intensity HG, BC, and CYC exercise were not associated with exPH in probable or definitive ACM. Despite similar hemodynamic and biomarker responses, post-exercise LP diverged between groups, decreasing in probable but increasing in definitive ACM. This observation warrants validation in larger cohorts with better control for baseline substrate and longitudinal clinical outcomes.
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Wernhart et al. (2026) conducted an observational in Arrhythmogenic cardiomyopathy (ACM) (n=20). Moderate-intensity isometric (handgrip, bicep curl) and aerobic (supine cycling) exercise vs. Probable ACM vs. definitive ACM (and pre- vs. post-exercise) was evaluated on Exercise pulmonary hypertension (mPAP/CO slope >3 mmHg/L/min), troponin T elevation, and changes in right ventricular late potentials (LP) within the arrhythmogenic triangle (p=<0.001). Moderate-intensity exercise did not induce exercise PH (0%), while post-exercise late potentials increased in definitive (+2.72%) vs decreased in probable ACM (-1.95%, p<0.001).
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