Effect of anemia on coagulation and platelet function: a whole blood in vitro study

Abstract

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. Critical Care 2011, 15(Suppl 1):P2 (doi: 10.1186/cc9422) Introduction Acute ischemia alters action potentials and aff ects 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 signifi cantly 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 signifi cantly 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 signifi cantly 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.