title: Right ventricular mechanical dispersion is related to malignant arrhythmias: a study of patients with arrhythmogenic right ventricular cardiomyopathy and subclinical right ventricular dysfunction.
abstract: OBJECTIVE
  We evaluated if right ventricular (RV) mechanical dispersion by strain was related to ventricular arrhythmias (VT/VF) in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and if mechanical dispersion was increased in so far asymptomatic mutation carriers.
  
  
  RESULTS
  We included 69 patients, 42 had symptomatic ARVC and 27 were mutation positive asymptomatic family members. Forty healthy individuals served as controls. Myocardial strain was assessed in 6 RV and 16 left ventricular (LV) segments. Contraction duration (CD) in 6 RV and 16 LV segments were measured as the time from onset R on electrocardiogram to maximum myocardial shortening in each segment. The standard deviation of CD was defined as mechanical dispersion. Mechanical dispersion was more pronounced in ARVC patients with arrhythmias compared with asymptomatic mutation carriers and healthy individuals in RV [52(41,63) vs. 35(23,47) vs. 13(9,19)ms, P < 0.001]. Mechanical dispersion was more pronounced in asymptomatic mutation carriers compared with healthy individuals (P < 0.001). Right ventricular mechanical dispersion predicted VT/VF in a multivariate logistic regression analysis [odds ratio (OR), 1.66 (95% confidence interval (CI) 1.06-2.58), P < 0.03]. Right ventricular and LV function by strain were reduced in symptomatic ARVC patients and correlated significantly (R = 0.81, P < 0.001). Right ventricular and LV strain were reduced in asymptomatic mutation carriers compared with healthy individuals (P < 0.001).
  
  
  CONCLUSIONS
  Right ventricular mechanical dispersion was pronounced in patients with ARVC with VT/VF. Right ventricular mechanical dispersion was present in asymptomatic mutation carriers and may be helpful in risk stratification. Right ventricular and LV function correlated in ARVC patients implying that ARVC is a biventricular disease.
authors.affiliation: Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
authors.forename: Sebastian I
authors.initials: SI
authors.lastname: Sarvari
authors.forename: Kristina H
authors.initials: KH
authors.lastname: Haugaa
authors.forename: Ole-Gunnar
authors.initials: OG
authors.lastname: Anfinsen
authors.forename: Trond P
authors.initials: TP
authors.lastname: Leren
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
authors.forename: Erik
authors.initials: E
authors.lastname: Kongsgaard
authors.forename: Jan P
authors.initials: JP
authors.lastname: Amlie
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
mesh_terms: D000328:Adult; D019571:Arrhythmogenic Right Ventricular Dysplasia / Q000150:complications / Q000235:genetics* / Q000503:physiopathology; D016022:Case-Control Studies; D015716:Electrocardiography, Ambulatory; D005260:Female; D006579:Heterozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D009200:Myocardial Contraction / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D018497:Ventricular Dysfunction, Right / Q000209:etiology*; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000503:physiopathology; D055815:Young Adult