title: The effect of reperfusion on plasma tumor necrosis factor alpha and C reactive protein levels in the course of acute myocardial infarction.
abstract: Severe acute response, the synthesis of human acute-phase proteins and the increase of plasma cytokines and adhesion molecules occur in patients in the course of acute myocardial infarction. We examined the plasma tumor necrosis factor alpha (TNF alpha), plasma creatinkinase (CK) and C-reactive protein (C-RP) levels in patients with acute myocardial infarction (AMI) in the course of 96 hours. Venous blood samples were taken at 3-hour intervals during the first 48 hours, and at 6-hour intervals during the next 48 hours. All patients were treated using thrombolytic therapy (streptokinase). Detection of the reperfusion was based on the method of measuring the time to achieve peak serum creatinkinase activity. The study was done on a group of 24 patients. Plasma levels of the parameters were compared between the group of patients with expected reperfusion versus the group of patients in which reperfusion is not suggested. The plasma TNF alpha level was elevated constantly without any significant peak. The mean plasma TNF alpha concentration was 46.8 pg/ml, SD 2.13, vs. normal level 4.35 pg/ml, p < 0.001. The plasma TNF alpha level in the group of patients with reperfused coronary artery showed a significant decrease especially during the 3rd and 4th day (the mean peak plasma TNF alpha concentration was 35.2 pg/ml, SD 15.8, vs. 66.9 pg/ml, SD 38.3 pg/ml, p < 0.005). The plasma C-RP levels were elevated throughout the time of observation in the both groups. The elevation of the plasma C-RP levels was more significant in the group of patients without successful reperfusion (80.6 mg/ml, SD 31.2, the mean plasma C-RP level of the group of the patients with successful reperfusion was 45.7 mg/ml, SD 18.1, p < 0.005). We conclude, that TNF alpha can play a role in the mechanisms of tissue injury. The successful reperfusion of coronary artery leads to significant decrease of plasma TNF alpha and C-RP levels.
authors.affiliation: IInd Dept. of Medicine, Charles University, Faculty of Medicine, Hradec Králové.
authors.forename: R
authors.initials: R
authors.lastname: Pudil
authors.forename: V
authors.initials: V
authors.lastname: Pidrman
authors.forename: J
authors.initials: J
authors.lastname: Krejsek
authors.forename: J
authors.initials: J
authors.lastname: Gregor
authors.forename: M
authors.initials: M
authors.lastname: Tichý
authors.forename: C
authors.initials: C
authors.lastname: Andrýs
authors.forename: M
authors.initials: M
authors.lastname: Drahosová
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D015425:Myocardial Reperfusion; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D005343:Fibrinolytic Agents; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D003402:Creatine Kinase; D013300:Streptokinase