Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation

Abstract

I. Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation. Am J Physiol Heart Circ Physiol 294: H1896-H1905, 2008. First published February 29, 2008 doi:10.1152/ajpheart.00986.2007.-In cardiac arrest due to ventricular fibrillation (VF), moderate hypothermia (MH, 33°C) has been shown to improve defibrillation success compared with normothermia (NR, 37°C) and severe hypothermia (SH, 30°C). The underlying mechanisms remain unclear. We hypothesized that MH might prevent reentrant excitations rotating around functional obstacles (rotors) that are responsible for the genesis of VF. In two-dimensional Langendorff-perfused rabbit hearts prepared by cryoablation (n ϭ 13), action potential signals were recorded by a high-resolution optical mapping system. During basic stimulation (2.5-5.0 Hz), MH and SH caused significant prolongation of action potential duration and significant reduction of conduction velocity. Wavelength was unchanged at MH, whereas it was shortened significantly at SH at higher stimulation frequencies (4.0 -5.0 Hz). The duration of direct current stimulation-induced ventricular tachycardia (VT)/VF was reduced dramatically at MH compared with NR and SH. The spiral wave (SW) excitations documented during VT at NR were by and large organized, whereas those during VT/VF at MH and SH were characterized by disorganization with frequent breakup. Phase maps during VT/VF at MH showed a higher incidence of SW collision (mutual annihilation or exit from the anatomical boundaries), which caused a temporal disappearance of phase singularity points (PS-0), compared with that at NR and SH. There was an inverse relation between PS-0 period in the observation area and VT/VF duration. MH data points were located in a longer PS-0 period and a shorter VT/VF duration zone compared with SH. MH causes a modification of SW dynamics, leading to an increase in the chance of SW collision in favor of self-termination of VT/VF. optical mapping; ventricular fibrillation SUCCESSFUL USE OF THERAPEUTIC hypothermia after cardiac arrest in humans was described in the late 1950s as a procedure to improve the clinical outcomes but then almost abandoned because of uncertain benefits and difficulties with its use (17). It was demonstrated in 2002 by two prospective randomized trials that the induction of therapeutic hypothermia in patients, who had been resuscitated after cardiac arrest due to ventricular fibrillation (VF), increased neurological recovery and reduced mortality (2, 12a). This has led to recent guideline recommendations that all unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-34°C for 12-24 h when the initial rhythm was VF (1). In experiments using swines with induced VF, Boddicker et al. (3) demonstrated that defibrillation success of electrical shocks and resuscitation outcomes were significantly improved under moderate hypothermia (MH, 33°C) compared with normothermia (NR, 3...

Therapeutic Hypothermia (30.DEG.C) Enhances Arrhythmogenic Substrates, Including Spatially Discordant Alternans, and Facilitates Pacing-Induced Ventricular Fibrillation in Isolated Rabbit Hearts

“…28 Using a clinically applicable temperature (30°C), we observed that TH decreased CV, shortened WL, and enhanced APD dispersion and spatial heterogeneity of CT -1 restitution, consistent with the results reported by Harada et al in a 2-dimensional rabbit ventricle at TH (30°C). 12 The only difference was that Harada et al reported that the maximal slope of APDR significantly increased, 12 whereas we found no difference among baseline, TH (30°C) and rewarming.…”

“…10, 11 Harada et al found that in 2-dimensional rabbit ventricular preparations, TH (30°C) enhanced wavebreaks and regeneration of new spiral waves during VF, facilitating the maintenance of ventricular tachycardia (VT) and VF. 12 While using a clinically appropriate temperature of 32-34°C, they demonstrated that the spiral waves of VT/VF frequently collided and dissipated in favor of self-termination of VT/VF, a different effect from that of TH at 30°C. 12 Whether the wavefront characteristics (ie, wavebreaks) of VF in this 2-dimensional model also occur in 3-dimensional intact hearts at TH (30°C) remains unclear.…”

“…12 While using a clinically appropriate temperature of 32-34°C, they demonstrated that the spiral waves of VT/VF frequently collided and dissipated in favor of self-termination of VT/VF, a different effect from that of TH at 30°C. 12 Whether the wavefront characteristics (ie, wavebreaks) of VF in this 2-dimensional model also occur in 3-dimensional intact hearts at TH (30°C) remains unclear. Cardiac alternans, particularly spatially discordant alternans (SDA), is a key arrhythmogenic factor for ventricular tachyarrhythmia.…”

Short-Duration Therapeutic Hypothermia Causes Prompt Connexin43 Gap Junction Remodeling in Isolated Rabbit Hearts

“…4, 26 Other studies investigating the effect of TH on ventricular conduction did not explore GJ remodeling. 5 In this study, we investigated the conduction properties and Cx43 GJ remodeling specifically in the therapeutic range of hypothermia (33°C and 30°C) in non-hibernating rabbit hearts.…”

In vitroarrhythmia generation by mild hypothermia: a pitchfork bifurcation type process

“…And at lower temperature (deeper hypothermia 5.9 • C ± 1.3 • C), local cooling facilitates termination of spiral waves [54]. The latter two studies [54,53] showed the positive effect of hypothermia in macro / organ scale.…”