Abstract P46: Hypothermia And Pharmacological Postconditioning After Cardiopulmonary Resuscitation Reduce Myocardial Damage And Dysfunction: Implications Of Inflammation, Apoptosis And Matrix Remodeling
Background: Mild hypothermia following cardiac arrest is neuroprotective, but its effect on myocardial dysfunction that is a critical issue following resuscitation is not clear. This study sought to examine whether hypothermia and the combination of hypothermia and pharmacological postconditioning are cardioprotective in a model of cardiopulmonary resuscitation following acute myocardial ischemia.
Methods: Thirty pigs (28 –34kg) were subjected to cardiac arrest following left anterior descending coronary artery ischemia. After 7 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started according to the current AHA guidelines. After successful return of spontaneous circulation (n=21), coronary perfusion was reestablished after 60 minutes of occlusion, and animals were randomized to either normothermia at 38°C, hypothermia at 33°C or hypothermia at 33°C combined with sevoflurane (each group n=7) for 24 hours. The effects on cardiac damage especially on inflammation, apoptosis, and remodeling were studied using cellular and molecular approaches. Five animals were sham operated.
Results: Animals treated with hypothermia had lower troponin T levels (p<0.01), reduced infarct size (34±7 versus 57±12 %; p<0.05) and improved left ventricular function compared to normothermia (p<0.05). Hypothermia was associated with reduced immune cell infiltration, apoptosis, upregulation of IL-1β, IL-6 mRNA and IL-1β protein expression (p<0.05) as well as decreased matrix metalloproteinase-9 activity in the ischemic myocardium. Sevoflurane conferred additional protective effects although statistic significance was not reached.
Conclusion: Hypothermia reduced myocardial damage and dysfunction after cardiopulmonary resuscitation possible via a reduced rate of apoptosis and pro-inflammatory cytokine expression.