Association of thrombotic and fibrinolytic factors with severity of culprit lesion in patients with acute coronary syndromes without ST elevation.
BACKGROUND
Increased procoagulant activity and/or impaired fibrinolysis contribute to the development and organization of thrombus, subsequently resulting in complete or incomplete obstruction in acute coronary syndromes (ACS). We investigated the relationship between culprit lesion severity and thrombotic and fibrinolytic parameters in patients who had non-ST elevation ACS (NSTE-ACS).


METHODS
This study included 95 consecutive patients with NSTE-ACS. All patients underwent coronary angiography within the first 72 hours depending on the clinical situation. Stenosis >or=50% in the coronary artery was considered significant. NSTE-ACS patients were then divided into two groups: patients with critical stenosis (n = 53) and patients with noncritical stenosis (n = 35). Plasma levels of D-dimer, fibrinogen, thrombin-antithrombin III complex (TAT), and prothrombin fragment 1 + 2 (PF 1 + 2) were measured.


RESULTS
D-dimer (338 +/- 192 vs. 190 +/- 170 microg/dL, P < 0.001), TAT (4.4 +/- 2.0 vs. 1.2 +/- 0.7 ng/mL, P < 0.001), and PF 1 + 2 (1.6 +/- 0.6 vs. 0.7 +/- 0.3 nmol/L) levels were significantly higher in the critical stenosis group as compared to the noncritical stenosis group. However, fibrinogen levels were similar in both groups. The levels of TAT (r = 0.76, P < 0.001) and PF 1 + 2 (r = 0.73, P < 0.001) were correlated with the culprit lesion severity, but D-dimer and fibrinogen levels were not. Thrombolysis in myocardial infarction flow grades were also correlated with TAT (r = -0.42, P < 0.001) and PF 1 + 2 (r = -0.40, P < 0.001).


CONCLUSIONS
The severity of culprit lesion may be associated with plasma D-dimer, TAT, and PF 1 + 2 levels in NSTE-ACS patients. These prothrombotic factors may have a role in the development of significant stenosis in the NSTE-ACS setting.
Turker
Yasin
Y
Cardiology Clinic, Gulkent State Hospital, Department of Cardiology, Suleyman Demirel University Medical School, Isparta, Turkey. dryasinturker@hotmail.com
Dogan
Abdullah
A
Ozaydin
Mehmet
M
Kaya
Selcuk
S
Onal
Suleyman
S
Akkaya
Mehmet
M
Erdogan
Dogan
D
D054058:Acute Coronary Syndrome / Q000097:blood* / Q000503:physiopathology; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D023921:Coronary Stenosis / Q000097:blood*; D004562:Electrocardiography; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis*; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D010446:Peptide Fragments / Q000097:blood*; D010447:Peptide Hydrolases / Q000097:blood*; D011516:Prothrombin; D013927:Thrombosis
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D005340:Fibrinogen; D010447:Peptide Hydrolases