title: Non sustained ventricular tachycardia in hypertrophic cardiomyopathy and new ultrasonic derived parameters.
abstract: BACKGROUND
  The mechanism of sudden death in hypertrophic cardiomyopathy (HCM) is ventricular tachyarrhythmia emanating from myocyte disarray, fibrosis, and inhomogeneity in intramyocardial activation. Tissue synchronization imaging (TSI) allows the measurement of regional delay, while two-dimensional strain can be used to identify myocardial fibrosis. The aim of this study was to assess the relationship between new ultrasonically derived parameters and nonsustained ventricular tachycardia (NSVT) in patients with HCM.
  
  
  METHODS
  Ninety-three patients with HCM (mean age, 36 +/- 16 years) and 30 patients with hypertension with secondary left ventricular (LV) hypertrophy (mean age, 42 +/- 10 years; 65% men) were studied. All underwent standard echocardiographic, TSI, and two-dimensional strain examinations. Patients were followed every 3 months for 2 years. Holter monitoring was performed every 3 months. The primary endpoint was the occurrence of NSVT.
  
  
  RESULTS
  Twenty-four patients (26%) had >or=1 episode of NSVT. Patients with NSVT had a higher value of maximal LV thickness (22 +/- 6 vs 19 +/- 5 mm, P = .04). There were no significant associations between NSVT on Holter monitoring and LV outflow gradient, New York Heart Association class, syncope, and medical therapy. N-terminal pro-brain natriuretic peptide values were significantly (P = .01) higher in patients with NSTV (1034 +/- 1088 vs 561 +/- 593 pg/mL). Patients with HCM and NSVT had (1) similar values on TSI-studied parameters to patients without NSVT, (2) significant reductions in basal and mid septal strain and in basal anterior-septal strain, and (3) more frequently peak systolic strain >or= -10% (P < .0001). In multivariate analysis, the presence of >3 LV segments with longitudinal two-dimensional strain >or= -10% (sensitivity, 81%; specificity, 97.1%; area under the curve, 0.944; P < .0001) was an independent predictor of NSVT.
  
  
  CONCLUSIONS
  Using a simple, inexpensive, easily available, and bedside-usable tool, it was possible to recognize with good sensitivity and specificity patients with HCM at higher risk for NSVT.
authors.affiliation: Second University of Naples, Chair of Cardiology, Naples, Italy. giodisal@yahoo.it
authors.forename: Giovanni
authors.initials: G
authors.lastname: Di Salvo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Pacileo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Limongelli
authors.forename: Luca
authors.initials: L
authors.lastname: Baldini
authors.forename: Alessandra
authors.initials: A
authors.lastname: Rea
authors.forename: Marina
authors.initials: M
authors.lastname: Verrengia
authors.forename: Antonello
authors.initials: A
authors.lastname: D'Andrea
authors.forename: Maria Giovanna
authors.initials: MG
authors.lastname: Russo
authors.forename: Raffaele
authors.initials: R
authors.lastname: Calabrò
mesh_terms: D000328:Adult; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications*; D004452:Echocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors; D012680:Sensitivity and Specificity; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000000981:diagnostic imaging* / Q000209:etiology; D055815:Young Adult