Mild Hypothermia Delays the Evolution of Early LV Dilatation and Late Stone Heart from Untreated Sustained Ventricular Fibrillation

Abstract

Introduction: Mild induced hypothermia is now the recommended treatment for persistently comatose adults after resuscitation from out-of-hospital ventricular fibrillation (VF) cardiac arrest. The cardio-protective benefits of induced mild hypothermia are still unclear. Although induced mild hypothermia is a well-established effective therapy for improving neurological outcomes, its effects on early ventricular dilatation or late stone heart development, secondary to untreated VF, are unknown. Hypothesis: Pre-arrest induced mild hypothermia in sustained VF substantially extends the time interval from commencement of cardiac arrest until the development of stone heart, thereby prolonging the limit of rescusitability. Method: Fourteen female swine (27 ± 1 kg) were used in this study. Animals were randomized to 2 groups, normothermia (n=6) and hypothermia (n=8). Mild hypothermia (32-34 °C) was induced by surrounding the swine body with ice packs for prior to imaging. After achieving a rectal temperature of 32-34 °C, routine CMR images in normal sinus rhythm were obtained. A pacing catheter electrode was placed temporarily into the RV to induce VF with 100Hz alternating current. Before fibrillation, a set of short-axis views were acquired. Data collection started immediately after the initiation of VF, every minute for the first 5 minutes, and every 5 minutes thereafter until the development of stone heart (2/3 reduction in the baseline mean LV volume). Results: Time to stone heart occurred at 52 ± 4 minutes in the hypothermia animals compared to 29 ± 3 minutes in the normothermia animals (P<0.001). During the first 5 minutes of untreated VF, mean LV volume increased by 11% in the hypothermia group compared to 34% increase in the normothermia group (P<0.05). Between 10 and 30 minutes of untreated VF, there were no significant changes in LV volumes in the hypothermia group versus 75% decrease in LV volume in the normothermia group. Conclusion: Stone heart, or severe LV myocardial ischemic contracture, is an irreversible phenomenon and marks the limit of myocardial resuscitability. This study demonstrates that in a closed-chest whole animal model of untreated prolonged VF cardiac arrest, pre-arrest induced mild hypothermia substantially delays the development of stone heart. This adds to our current understanding of the beneficial mechanism of mild hypothermia and suggests that morphologic changes are at least in part responsible for or an important by-product of this practice. Introduction: Mild induced hypothermia is now the recommended treatment for persistently comatose adults after resuscitation from out-of-hospital ventricular fibrillation (VF) cardiac arrest. The cardio-protective benefits of induced mild hypothermia are still unclear. Although induced mild hypothermia is a well-established effective therapy for improving neurological outcomes, its effects on early ventricular dilatation or late stone heart development, secondary to untreated VF, are unknown. Hypothesis: Pre-arrest induced mild hypothermia in sustained VF substantially extends the time interval from commencement of cardiac arrest until the development of stone heart, thereby prolonging the limit of rescusitability. Method: Fourteen female swine (27 ± 1 kg) were used in this study. Animals were randomized to 2 groups, normothermia (n=6) and hypothermia (n=8). Mild hypothermia (32-34 °C) was induced by surrounding the swine body with ice packs for prior to imaging. After achieving a rectal temperature of 32-34 °C, routine CMR images in normal sinus rhythm were obtained. A pacing catheter electrode was placed temporarily into the RV to induce VF with 100Hz alternating current. Before fibrillation, a set of short-axis views were acquired. Data collection started immediately after the initiation of VF, every minute for the first 5 minutes, and every 5 minutes thereafter until the development of stone heart (2/3 reduction in the baseline mean LV volume). Results: Time to stone heart occurred at 52 ± 4 minutes in the hypothermia animals compared to 29 ± 3 minutes in the normothermia animals (P<0.001). During the first 5 minutes of untreated VF, mean LV volume increased by 11% in the hypothermia group compared to 34% increase in the normothermia group (P<0.05). Between 10 and 30 minutes of untreated VF, there were no significant changes in LV volumes in the hypothermia group versus 75% decrease in LV volume in the normothermia group. Conclusion: Stone heart, or severe LV myocardial ischemic contracture, is an irreversible phenomenon and marks the limit of myocardial resuscitability. This study demonstrates that in a closed-chest whole animal model of untreated prolonged VF cardiac arrest, pre-arrest induced mild hypothermia substantially delays the development of stone heart. This adds to our current understanding of the beneficial mechanism of mild hypothermia and suggests that morphologic changes are at least in part responsible for or an important by-product of this practice.