Abstract P205: Therapeutic Hypothermia Decreases Arrhythmia Substrates During Myocardial Ischemia
Therapeutic hypothermia (TH) is recommended for selected patients with return of spontaneous circulation after cardiac arrest. As the majority of cardiac arrests are secondary to ischemia-induced ventricular arrhythmias (VA), it is important to understand the interaction between hypothermia and ischemia because both have proarrhythmic effects, including enhancement of transmural dispersion of repolarization (DOR) and impairment of conduction. Although hypothermia can be proarrhythmic, VA are rare during TH. Therefore, we hypothesized that mild hypothermia would have beneficial electrophysiological effects in the ischemic heart and be antiarrhythmic. To test this hypothesis, the transmural electrophysiologic effects of ischemia in canine left ventricular wedge preparations cooled to 32°C were compared to normothermic controls. Optical action potentials with high spatial (1 mm), temporal (.5 ms) and voltage (.5mv) resolution from cells spanning the transmural surface were recorded at
normal temperature (n=3, 36°C) or
TH (cooled to 32°C, n=4), both at baseline and during 15 minutes of no-flow ischemia.
Prior to ischemia, conduction velocity (CV) and DOR were similar between groups. At 15 min of ischemia in controls (C), epicardial action potential duration (APD) decreased by 50% resulting in a 223% increase in DOR (both p<.04), while during TH, epicardial APD decreased by only 15% (p=ns), without significant increase in DOR. CV decreased by 54% in C and 37% in TH (both p<.05). Importantly, all control preparations (4/4) exhibited conduction failure into the epicardium, but this was never observed in TH.
Conclusions: Hypothermia attenuates ischemia-induced transmural heterogeneities in repolarization by preserving APD of epicardial cells and prevents ischemia-induced conduction block. These data suggest that therapeutic hypothermia may be antiarrhythmic in this setting and may be beneficial in the treatment of ongoing ischemia both before and after cardiac arrest.