Dispersion Of Repolarization Time Research Articles

Attenuation of KATP channel-opener induced shortening of repolarization time by alpha 1-adrenoceptor antagonist during ischemia in canine heart.

The purpose of the study was to determine whether a new KATP channel opener, Y 26763 (Y), can influence the electrophysiological properties in the ischemic myocardium as well as to determine whether the blunting effect of the alpha 1-adrenoceptor antagonist bunazosin (BN) on an ischemia-induced shortening of repolarization time can be related to the KATP channel activity. The anterior descending branch of the left coronary artery was ligated four times for 5 minutes, separated by 15 minutes of reperfusion (stages 1-4) to test the dose-dependent effect of drugs on repolarization. Dogs received either vehicle (n = 9), Y (0.4, 2.0, and 4.0 micrograms/kg at stages 2, 3, and 4, respectively, with 0.4 microgram/kg/min drip infusion at each of stages 2-4, n = 7), BN (0.1 mg at each of stages 2-4, n = 8), or a combination of these two drugs (BN + Y, the same dose of BN and Y in groups BN and Y, respectively, n = 9). Drugs were administered into the left atrium. The monophasic action potential (MAP) and regional electrograms were recorded. The MAP90 and the duration of the slow deflections (DSD) of the regional electrogram were used as markers of repolarization. The Vmax of the MAP and the rapid deflections (DRD) of the regional electrogram were used as markers of conduction. Y augmented an ischemia-induced shortening of MAP90 and DSD in proportion to an increase in the dose given and the plasma concentration (P < .05-.01), especially at the epicardial site. BN and BN + Y blunted the ischemia-related shortening of MAP90 and DSD, causing a reduction in repolarization time dispersion between the ischemic and normal zones. There were no significant changes in the Vmax or DRD in the ischemic zone between periods before and after an increase in each drug dose in the four groups. None of the seven dogs developed ventricular tachycardia (VT)/ventricular fibrillation (VF) in the Y group, whereas two of the eight dogs in the BN group, three of the nine dogs in the BN + Y group, and three of the nine dogs in the control group developed VT/VF. These results suggest that the alpha 1-adrenergic blocker bunazosin blunts the shortening effect of KATP channel activator on repolarization time, and that the KATP channel opener Y may be antiarrhythmic, although the repolarization time dispersion during myocardial ischemia is increased.

Dispersion of the monophasic action potential duration in patients with polymorphic ventricular tachycardia

The mechanism of polymorphic ventricular tachycardia (PMVT) remains unclear. To investigate the electrophysiologic mechanism of PMVT, monophasic action potentials (MAPs) were recorded with a contact electrode technique from right ventricular sites during sinus rhythm and right ventricular pacing. MAPs were obtained from 6 patients with PMVT (PMVT group) and II patients without PMVT (control group). The duration from the onset of the upstroke to 90% repolarization of the MAP (MAPD90) during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was significantly longer in the PMVT group than in the control group (332 ± 60 ms vs 279 ± 33 ms [ P < .005] and 276 ± 32 ms vs 229 ± 23 ms [ P < .0001], respectively). Dispersion of the MAPD90 in sinus rhythm was significantly larger in the PMVT group than in the control group (52.5 ± 34.6 ms vs 26.1 ± 12.0 ms [ P < .005]), and dispersion of the MAPD90 during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was also significantly larger in the PMVT group than in the control group (86.0 ± 44.2 ms vs 37.4 ± 28.6 ms [ P <.005], and 48.8 ± 19.3 ms vs 27.1 ± 7.1 ms [ P < .05], respectively). Dispersion of repolarization time (activation time plus MAPD90) at a pacing cycle length of 600 ms was longer in the PMVT group than in the control group (104.3 ± 38.9 ms vs 49.4 ± 31.2 ms [ P < .05]). These results suggest that the patients with PMVT have a greater regional dispersion of ventricular repolarization time and that the heterogeneity of ventricular repolarization may play an important role in the genesis of PMVT.

The dispersion of repolarization in patients with ventricular tachycardia. A study using simultaneous monophasic action potential recordings from two sites in the right ventricle.

The role of increased dispersion of repolarization in the genesis of torsade de pointes and ventricular fibrillation has been well recognized generally, but not in the genesis of monomorphic ventricular tachycardia (VT). Monophasic action potentials (MAP) were therefore recorded simultaneously from the right ventricular (RV) apex (RVA) and outflow tract (RVOT) during sinus rhythm, RV pacing and programmed extra stimulation (PES) in 24 patients with VT. The activation time (AT), MAP duration at 90% repolarization (MAPd), and repolarization time (RT) were measured and their dispersions, defined as the differences in these parameters between RVA and RVOT, were calculated. During sinus rhythm and RV pacing, the dispersions of AT, MAPd and RT (dispersions) were significantly larger in the 17 patients with a VT induced than in those without. During PES, the dispersions were further augmented in the S2 beats in the seven patients with a sustained VT induced, the maximal dispersion of RT being 85 +/- 22 ms. Both the dispersion of AT and that of MAPd contributed to the dispersion of RT. In both of our two patients with a sustained VT induced during MAP recording, a marked increase in dispersions of RT (140 and 190 ms, respectively) was observed immediately before the initiation of the VT. A link between the dispersions and the inducibility of a monomorphic VT was found in our patients, which suggests that the increased dispersions play an important role in the genesis of a monomorphic VT.