P1 Efects of thyroid hormones on major cardiovascular risk in acute coronary syndromes A Bayrak 1 , A Bayır 2 , K Uçar Karabulut 3 1 Selçuk University, Meram Faculty of Medicine, Konya, Turkey; 2 Selçuk University, Selçuklu Faculty of Medicine, Emergency Department, Konya, Turkey; 3 Emergency Sercice of Şırnak State Hospital, Şırnak, Turkey Critical Care 2011, 15(Suppl 1):P1 (doi: 10.1186/cc9421) Introduction In this study we aimed to investigate the relationship between thyroid hormone abnormalities and major cardiovascular events and sudden cardiac death at 3 and 6 months after discharge in patients who were admitted to the Emergency Department with acute coronary syndrome. Methods The study group included 110 patients without known thyroid dysfunction who were referred to the Emergency Department with acute coronary syndrome. FT3, FT4 and TSH levels were measured in all patients on admission. Patients were divided into STEMI, NSTEMI and UAP groups. Patient records were checked at 3 and 6 months of discharge in terms of sudden cardiac death and major cardiovascular events. The relationship between thyroid hormone levels and acute cardiac death and major cardiovascular disorders at 3 and 6 months of discharge was evaluated. Results The mean TSH, FT3 and FT4 levels of the study group versus control group were as follows: TSH levels of study group 1.87 ± 1.73 μIU/ ml, FT3 3.2 ± 1.34 pg/ml, FT4 1.45 ± 0.64 ng/dl. Abnormalities in the thyroid function tests were noted in 26 patients (23.6%). Of these seven patients (6.36%) had subclinical hypothyroidism, two patients (1.8%) had euthyroid sick syndrome and 10 patients (9%) had high serum FT4 levels despite normal FT3 and TSH values. Conclusions We noted subclinical hypothyroidism, less frequently euthyroid sick syndrome and hyperthyroidism. No relationship was noted between thyroid hormone levels and sudden cardiac death and major cardiovascular disorders at 3 and 6 months follow-up. However, studies including larger patient groups are needed to clarify if there is a relationship between thyroid hormone levels on admission and sudden death and major cardiovascular events in patients with acute coronary syndrome. References 1. Paulou HN, et al.: Angiology 2002, 53:699-707. 2. Pingitore A, et al.: Am J Med 2005, 118:132-136. P2 Efect of reperfusion therapy on QTd and QTcd in patients with acute STEMI D Ragab, H Elghawaby, M Eldesouky, T Elsayed Cairo University, Cairo, Egypt Critical Care 2011, 15(Suppl 1):P2 (doi: 10.1186/cc9422) Introduction Acute ischemia alters action potentials and afects myocardial repolarization. Dispersion of repolarization is arrhythmogenic. QT dispersion has been suggested to give information about the heterogeneity of myocardial repolarization. Methods Our study included 60 patients presented with acute STEMI, the study populations were divided into two groups: Group I: 30 patients who underwent primary PCI. Group II: 15 patients who received streptokinase. Group III: 15 patients who did not receive reperfusion therapy. QTd and QTcd were measured and compared in the three groups on admission, after 24 hours and after 5 days. Results QTd and QTcd were signiicantly higher in patients with anterior compared with inferior MI (79.16 ± 25.67 ms vs. 62 ± 18.17 ms, P = 0.004 regarding QTd and 91.95 ± 28.76 ms vs. 68.33 ± 23.52 ms, P <0.001 regarding QTcd). After 24 hours, QTd and QTcd were signiicantly lower in group I than groups II and III (34.33 ± 13.56 ms vs. 48 ± 18.2 ms vs. 66 ± 24.43 ms respectively, P <0.05 as regards QTd and 39.33 ± 11.72 ms vs. 56 ± 23.84 ms vs. 74.60 ± 26.7 ms respectively, P <0.05 as regards QTcd). On the 5th day reduction in QTd and QTcd was statistically signiicantly lower in group I than groups II and III (23 ± 9.52 ms vs. 45.33 ± 15.97 ms vs. 58.66 ± 23.25 ms respectively, P <0.05 for QTd and 26 ± 11.63 ms vs. 52.66 ± 21.2 ms vs. 60.66 ± 23.25 ms respectively, P <0.05 for QTcd). QT and QTcd on admission were higher in patients who developed ventricular arrhythmias than patients who did not (90 ± 11.55 ms vs. 70 ± 24.54 ms; P = 0.05 regarding QTd and 110 ± 8.61 ms vs. 80.53 ± 28.78 ms with P = 0.028 regarding QTcd). Patients with early peaking of enzymes had more reduction in QTd and QTcd early after reperfusion (43.2 ± 11.44 vs. 60.5 ± 13.16, P <0.001 regarding QTd and 49.60 ± 15.93 vs. 68.5 ± 17.55, P <0.001 regarding QTcd). Conclusions QTd is higher in patients with acute MI (AMI) who developed ventricular arrhythmias. So QTd and QTcd on admission may be a helpful parameter that can detect patients with AMI who are at risk for development of ventricular arrhythmias. Reperfusion therapy with primary PCI or thrombolytic agents reduces QTd and QTcd in patients with AMI, however; QTd and QTcd are shorter with primary PCI compared with thrombolytic therapy. P3 Biochemical studies of some diagnostic enzymes in myocardial infarction M Samir, H Khaled Nagi, D Ragab, M Refaie Cairo University, Cairo, Egypt Critical Care 2011, 15(Suppl 1):P3 (doi: 10.1186/cc9423) Introduction Myocardial infarction (MI) is a key component of the burden of cardiovascular disease (CVD). The main causal and treatable risk factors for MI include hypertension, hypercholesterolemia or dyslipidemia, diabetes mellitus, and smoking. Acute MI results in cellular necrosis with release of constituent proteins into the circulation. Measurement of speciic enzymes has become an important clinical tool for the diagnosis and management of MI. The aim of this study was to demonstrate the role of arginase and adenosine deaminase (ADA) in patients sufering from MI, and in a group of patients with chronic renal failure (CRF) with cardiovascular diseases (CVD). Methods In this prospective study including 90 consecutive subjects were included the MI group (GI) consisting of 30 patients with mean age = 51.7 admitted to critical care medicine (CCM) in Cairo University © 2010 BioMed Central Ltd 31st International Symposium on Intensive Care and Emergency Medicine Brussels, Belgium, 22-25 March 2011 Published: 1 March 2011 MEETING ABSTRACTS Critical Care 2011, Volume 15 Suppl 1 http://ccforum.com/supplements/15/S1 © 2011 BioMed Central Ltd