title: Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation.
abstract: In cardiac arrest due to ventricular fibrillation (VF), moderate hypothermia (MH, 33 degrees C) has been shown to improve defibrillation success compared with normothermia (NR, 37 degrees C) and severe hypothermia (SH, 30 degrees 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 = 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.
authors.affiliation: Dept. of Cardiovascular Research, Research Inst. of Environmental Medicine, Nagoya University,Nagoya, 464-8601, Japan.
authors.forename: Masahide
authors.initials: M
authors.lastname: Harada
authors.forename: Haruo
authors.initials: H
authors.lastname: Honjo
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Yamazaki
authors.forename: Harumichi
authors.initials: H
authors.lastname: Nakagawa
authors.forename: Yuko S
authors.initials: YS
authors.lastname: Ishiguro
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Okuno
authors.forename: Takashi
authors.initials: T
authors.lastname: Ashihara
authors.forename: Ichiro
authors.initials: I
authors.lastname: Sakuma
authors.forename: Kaichiro
authors.initials: K
authors.lastname: Kamiya
authors.forename: Itsuo
authors.initials: I
authors.lastname: Kodama
mesh_terms: D000200:Action Potentials; D000818:Animals; D002304:Cardiac Pacing, Artificial; D003452:Cryosurgery; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D007036:Hypothermia, Induced; D066298:In Vitro Techniques; D008297:Male; D055095:Optics and Photonics; D010477:Perfusion; D011817:Rabbits; D012107:Research Design; D012815:Signal Processing, Computer-Assisted; D017180:Tachycardia, Ventricular / Q000503:physiopathology / Q000517:prevention & control*; D013817:Thermography; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000517:prevention & control*