title: Changes in autonomic activity and ventricular repolarization.
abstract: An increase in sympathetic activity, manifested by shortening of RR intervals (RRi) and changes in RRi variability, precedes and possibly triggers ventricular tachyarrhythmias (VTAs) by altering repolarization. We examined the effects of autonomic activity on the projection of repolarization as detected by body surface potential maps (BSPMs). We recorded 32 lead/192-point BSPMs during passive head-up tilt, tilt + infusion of isoproterenol, rapid atrial pacing, and atrial pacing + infusion of isoproterenol. Changes in QT; recovery time; activation-recovery interval (ARi); T-wave amplitude; and QT, QRST, and ST integrals and their dispersion were analyzed. Autonomic effects on sinus node were inferred from the Fourier transform-derived low and high frequency powers of RRi variability. Patients were divided into those with (SHD) and without structural heart disease (NSHD). Heart rate increased, whereas QT interval and ARi declined with tilt in both groups. RRi variability indices of sympathetic activity increased in NSHD but did not change in SHD. T-wave amplitudes declined in NSHD but did not change in SHD, suggesting altered responsiveness of ventricular repolarization to autonomic stimulation. Tilt and rapid atrial pacing during infusion of isoproterenol resulted in a paradoxical increase in T-wave amplitudes in some patients, similar to that observed before the onset of spontaneous arrhythmias. We conclude that altering autonomic activity by head-up tilt and/or infusion of sympathomimetic agents results in significant changes in the body surface projection of cardiac repolarization, which differ in patients with SHD from those without SHD. Similar paradoxical changes in the T-wave amplitude have been observed before the onset of spontaneous VTA, suggesting that abnormal response of repolarization to autonomic stimulation predisposes to arrhythmogenesis.
authors.affiliation: Cardiac Electrophysiology Program, Cardiovascular Institute, University of Pittsburgh Health System, Pennsylvania 15213-2582, USA.
authors.forename: V
authors.initials: V
authors.lastname: Shusterman
authors.forename: A
authors.initials: A
authors.lastname: Beigel
authors.forename: S I
authors.initials: SI
authors.lastname: Shah
authors.forename: B
authors.initials: B
authors.lastname: Aysin
authors.forename: R
authors.initials: R
authors.lastname: Weiss
authors.forename: V K
authors.initials: VK
authors.lastname: Gottipaty
authors.forename: D
authors.initials: D
authors.lastname: Schwartzman
authors.forename: K P
authors.initials: KP
authors.lastname: Anderson
mesh_terms: D000328:Adult; D000368:Aged; D001341:Autonomic Nervous System / Q000503:physiopathology*; D018780:Body Surface Potential Mapping; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D003327:Coronary Disease / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000294:innervation*; D006333:Heart Failure / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology; D012016:Reference Values; D012815:Signal Processing, Computer-Assisted; D017180:Tachycardia, Ventricular / Q000503:physiopathology*; D018667:Tilt-Table Test