title: Vigorous physical activity impairs myocardial function in patients with arrhythmogenic right ventricular cardiomyopathy and in mutation positive family members.
abstract: OBJECTIVE
  Exercise increases risk of ventricular arrhythmia in subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC). We aimed to investigate the impact of exercise on myocardial function in ARVC subjects.
  
  
  RESULTS
  We included 110 subjects (age 42 ± 17 years), 65 ARVC patients and 45 mutation-positive family members. Athletes were defined as subjects with ≥4 h vigorous exercise/week [≥1440 metabolic equivalents (METs × minutes/week)] during a minimum of 6 years. Athlete definition was fulfilled in 37/110 (34%) subjects. We assessed right ventricular (RV) and left ventricular (LV) myocardial function by echocardiography, and by magnetic resonance imaging (MRI). The RV function by RV fractional area change (FAC), RV global longitudinal strain (GLS) by echocardiography, and RV ejection fraction (EF) by MRI was reduced in athletes compared with non-athletes (FAC 34 ± 9% vs. 40 ± 11%, RVGLS -18.3 ± 6.1% vs. -22.0 ± 4.8%, RVEF 32 ± 8% vs. 43 ± 10%, all P < 0.01). LV function by LVEF and LVGLS was reduced in athletes compared with non-athletes (LVEF by echocardiography 50 ± 10% vs. 57 ± 5%, LVEF by MRI 46 ± 6% vs. 53 ± 8%, and LVGLS -16.7 ± 4.2% vs. -19.4 ± 2.9%, all P < 0.01). The METs × minutes/week correlated with reduced RV and LV function by echocardiography and MRI (all P < 0.01). The LVEF by MRI was also reduced in subgroups of athlete index patients (46 ± 7% vs. 54 ± 10%, P = 0.02) and in athlete family members (47 ± 3% vs. 52 ± 6%, P < 0.05).
  
  
  CONCLUSIONS
  Athletes showed reduced biventricular function compared with non-athletes in ARVC patients and in mutation-positive family members. The amount and intensity of exercise activity was associated with impaired LV and RV function. Exercise may aggravate and accelerate myocardial dysfunction in ARVC.
authors.affiliation: Department of Cardiology, Institute for Surgical Research and Centre for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, PO Box 4950 Nydalen, N-0424, Oslo, Norway; University of Oslo, Norway.
authors.forename: Jørg
authors.initials: J
authors.lastname: Saberniak
authors.forename: Nina E
authors.initials: NE
authors.lastname: Hasselberg
authors.forename: Rasmus
authors.initials: R
authors.lastname: Borgquist
authors.forename: Pyotr G
authors.initials: PG
authors.lastname: Platonov
authors.forename: Sebastian I
authors.initials: SI
authors.lastname: Sarvari
authors.forename: Hans-Jørgen
authors.initials: HJ
authors.lastname: Smith
authors.forename: Margareth
authors.initials: M
authors.lastname: Ribe
authors.forename: Anders G
authors.initials: AG
authors.lastname: Holst
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
authors.forename: Kristina H
authors.initials: KH
authors.lastname: Haugaa
mesh_terms: D000971:Antineoplastic Combined Chemotherapy Protocols; D019571:Arrhythmogenic Right Ventricular Dysplasia / Q000000981:diagnostic imaging / Q000235:genetics* / Q000503:physiopathology*; D056352:Athletes; D003430:Cross-Sectional Studies; D004452:Echocardiography; D015444:Exercise / Q000502:physiology*; D005260:Female; D005820:Genetic Testing / Q000379:methods; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009154:Mutation / Q000235:genetics; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*
keywords: Arrhythmogenic cardiomyopathy; Exercise; Heart failure; Myocardial function; Ventricular arrhythmia