title: Effects of selective autonomic blockade on T-wave alternans in humans.
abstract: BACKGROUND
  T-wave alternans (TWA) is an important noninvasive measure of ventricular arrhythmia vulnerability. This study tested the hypothesis that the autonomic nervous system influences TWA measurement in high-risk subjects with coronary artery disease.
  
  
  RESULTS
  T-wave alternans was measured in 60 patients with coronary artery disease, left ventricular dysfunction, and inducible sustained ventricular tachycardia during electrophysiological studies. All patients had TWA measured at baseline with atrial pacing at 100 bpm (600 ms), 109 bpm (550 ms), and 120 bpm (500 ms). After a 10-minute recovery period, TWA was measured again after sympathetic blockade (esmolol, n=20), parasympathetic blockade (atropine, n=20), or no intervention (control subjects, n=20). The prevalence of significant TWA was unchanged compared with baseline after atropine infusion and in the control group. In contrast, the amplitude of TWA in the vector magnitude lead was significantly reduced after esmolol infusion (P<0.001), and the number of positive TWA tests was reduced by 50% (70% versus 35%, P<0.05).
  
  
  CONCLUSIONS
  Our findings have important implications for the use of TWA to risk-stratify patients for life-threatening ventricular arrhythmias and provide a new potential mechanism for the reduction in sudden cardiac death conferred by beta-blockers among patients with coronary artery disease and congestive heart failure.
authors.affiliation: Division of Cardiology, Department of Medicine, University of Maryland at Baltimore, 21201, USA. erashba@medicine.umaryland.edu
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Rashba
authors.forename: Michael
authors.initials: M
authors.lastname: Cooklin
authors.forename: Karen
authors.initials: K
authors.lastname: MacMurdy
authors.forename: Neal
authors.initials: N
authors.lastname: Kavesh
authors.forename: Malcolm
authors.initials: M
authors.lastname: Kirk
authors.forename: Samantha
authors.initials: S
authors.lastname: Sarang
authors.forename: Robert W
authors.initials: RW
authors.lastname: Peters
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Shorofsky
authors.forename: Michael R
authors.initials: MR
authors.lastname: Gold
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage; D001285:Atropine / Q000008:administration & dosage; D001341:Autonomic Nervous System / Q000187:drug effects / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D003324:Coronary Artery Disease / Q000150:complications / Q000503:physiopathology*; D004562:Electrocardiography / Q000187:drug effects; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D010276:Parasympatholytics / Q000008:administration & dosage; D011412:Propanolamines / Q000008:administration & dosage; D011446:Prospective Studies; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D013565:Sympatholytics / Q000008:administration & dosage; D017180:Tachycardia, Ventricular / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D010276:Parasympatholytics; D011412:Propanolamines; D013565:Sympatholytics; D001285:Atropine; C036604:esmolol