Changes in autonomic activity and ventricular repolarization

An increase in sympathetic activity, manifested by shortening of RR interva ls (RRi) and changes in RRL variability, precedes and possibly triggers ven tricular tachyarrhythmias (VTAs) by altering repolarization. We examined th e effects of autonomic activity on the projection of repolarization as dete cted 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 ef fects on sinus node were inferred from the Fourier transform-derived low an d high frequency powers of RRi variability. Patients were divided into thos e with (SHD) and without structural heart disease (NSHD). Heart rate increa sed, whereas QT interval and ARi declined with tilt in both groups. RRi var iability indices of sympathetic activity increased in NSHD but did not chan ge in SHD. T-wave amplitudes declined in NSHD but did not change in SHD, su ggesting 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, s imilar to that observed before the onset of spontaneous arrhythmias. We con clude that altering autonomic activity by head-up tilt and/or infusion of s ympathomimetic agents results in significant changes in the body surface pr ojection 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 abnorma l response of repolarization to autonomic stimulation predisposes to arrhyt hmogenesis.