title: Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism.
abstract: BACKGROUND
  "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.
  
  
  RESULTS
  One hundred twenty-two consecutive patients (61 male; 50.9 +/- 15.2 years) with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT) (RVOT = 28%, LVOT = 36%), nonsustained VT (RVOT = 40%, LVOT = 23%), and premature ventricular complexes (RVOT = 32%, LVOT = 41%) (P = 0.32). Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT = 70%, LVOT = 80%; P = 1.00) in both groups.
  
  
  CONCLUSIONS
  Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."
authors.affiliation: Division of Cardiology, Department of Medicine, Cornell University Medical Center, New York, NY 10021, USA.
authors.forename: Sei
authors.initials: S
authors.lastname: Iwai
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Cantillon
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Kim
authors.forename: Steven M
authors.initials: SM
authors.lastname: Markowitz
authors.forename: Suneet
authors.initials: S
authors.lastname: Mittal
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Stein
authors.forename: Bindi K
authors.initials: BK
authors.lastname: Shah
authors.forename: Ravi K
authors.initials: RK
authors.lastname: Yarlagadda
authors.forename: Jim W
authors.initials: JW
authors.lastname: Cheung
authors.forename: Vivian R
authors.initials: VR
authors.lastname: Tan
authors.forename: Bruce B
authors.initials: BB
authors.lastname: Lerman
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000241:Adenosine / Q000008:administration & dosage; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000889:Anti-Arrhythmia Agents; D002648:Child; D004562:Electrocardiography; D019317:Evidence-Based Medicine; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017180:Tachycardia, Ventricular / Q000150:complications / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000209:etiology / Q000503:physiopathology*
chemical_list: D000889:Anti-Arrhythmia Agents; D000241:Adenosine