In patients with spontaneous circulation after cardiopulmonary resuscitation, therapeutic hypothermia is defined as the reduction of body temperature to 32-34 ° C within the first 4-6 hours for neuroprotective purposes and to be maintained at this level for 12-24 hours after reaching the target temperature. Therapeutic hypothermia has been practiced since the 1940s. The aim of therapeutic hypothermia is to reduce cerebral edema, convulsive activity, metabolic demand and associated complications by providing low body heat. Therapeutic hypothermia is applied to increase life expectancy and quality of life. In out-of-hospital cardiac arrest, should be performed in comatose patients where initial rhythm is ventricular fibrillation and spontaneous circulation is returned. Herein, we present a 44 years old patient who had an aborted sudden cardiac death due to acute myocardial infarction and performing cardiopulmonary resuscitation for 30 minutes and discharged after 6 days with a successful therapeutic hypothermia. '+st+' -Polderman KH. Induced hypothermia and fever control for prevention and treatment of neurological injuries. Lancet. 2008 Jun 7;371(9628):1955-69. - Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med (2004) 30:2126–2128. - M. Holzer, E. Cerchiari, P. Martens, R. Roine, F. Sterz, P. Eisenburge et al. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002 May 30;346(22):1756. - Gebhardt K, Guyette FX, Doshi AA, Callaway CW, Rittenberger JC,Post Cardiac Arrest Service. Prevalence and effect of fever on outcome following resuscitation from cardiac arrest. Resuscitation. 2013;84:1062. - Arrich J,Holzer M, Havel C, Müllner M, Herkner H. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev 2012; 9:CD004128. -Wright WL, Geocadin RG. Postresuscitative intensive care: Neuroprotective strategies after cardiac arrest. Semin Neurol 2006; 26: 396-402. - John Bailitz, MD, Mark Hansen, MD, Mike Nelson, MD. Therapeutic Hypothermia in the Emergency Department .The Practical Journal of Emergency Phsycians. Emergency Medicine Reports 2009; 30(20):14. - Busto R, Globus MY, Dietrich WD, Martinez E, Valdes I, Ginnberg MD. Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. Stroke 1989;20:904-10. - Hypothermia after Cardiac Arrest Study Group; Holzer M. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346: 549-556. - Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346: 557-563. - Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, et al. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. N Engl J Med 2013; 369:2197. - Bernard S. Hypothermia after cardiac arrest: Ex¬panding the therapeutic scope. Crit Care Med2009;37:S227-33. Copyright (c) 2018 Abdullah Özçelik, Yakup Alsancak, Ahmet Seyfeddin Gürbüz, Abdullah İçli, Ahmet Soylu This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Background: Lipoprotein metabolism, inflammation, and oxidative stress (OS) play interconnected roles in the pathogenesis of acute coronary syndrome (ACS). However, the relationship between oxidative stress biomarkers and coronary artery disease (CAD) complexity, particularly as assessed by the SYNTAX II score, remains incompletely understood. This study aimed to evaluate serum levels of oxidative stress–related biomarkers and to investigate their association with the SYNTAX II score in patients with newly diagnosed ACS. Methods: This was a retrospective, single-center observational study. A total of 60 patients with newly diagnosed ACS who underwent percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) were consecutively enrolled. Serum levels of superoxide dismutase (SOD), advanced oxidation protein products (AOPP), glutathione, catalase, and malondialdehyde (MDA) were measured using ELISA methods. Associations between oxidative stress markers and the SYNTAX II score were analyzed using correlation and regression analyses. Results: Median levels of SOD, AOPP, and glutathione were 261.0 (244.18–324.86) U/L, 23.81 (22.62–25.80) ng/mL, and 6.08 (5.28–11.46) ng/mL, respectively. Mean catalase and MDA levels were 339.07 ± 44.81 pg/mL and 0.66 ± 0.07 mmol/L. The SYNTAX II score was positively correlated with SOD, AOPP, glutathione, catalase, and MDA, as well as with age, female sex, and potassium levels, while it was negatively correlated with hemoglobin, creatinine clearance, and left ventricular ejection fraction (all p < 0.05). Patients with higher SYNTAX II scores demonstrated elevated levels of both oxidant and antioxidant biomarkers. Conclusions: Oxidative stress-related biomarkers were associated with the SYNTAX II score in patients with newly diagnosed ACS.