title: [Relation of an increase of von Willebrand factor in the blood, acute myocardial infarction, unstable angina and coronary thrombosis].
abstract: Forty six patients admitted for precordial chest pain were included in this study. The clinical, electrocardiographic, enzymatic and angiographic features allowed retrospective identification of 6 subgroups (nos 1 to 6): all transmural myocardial infarction (Q-MI) (Group 1), Q-MI without intracoronary thrombus (Group 2), Q-MI with intracoronary thrombus (Group 3), acute non-Q wave infarction (non Q-MI) (Group 4), unstable angina (Group 5) and atypical chest pain (Group 6). Several blood clotting factors were studied; von Willebrand factor (VWF), fibrinogen, tissue plasminogen activator (t-PA) and its inhibitor (PAI-1) and factor VII. There was no significant difference in the fibrinogen, t-PA, PAI-1 or factor VII levels between the 6 groups. On the other hand, the VWF was increased in the all transmural myocardial infarction (Q-MI) groups (n. 1). In Group 3 with visible intracoronary thrombus the VWF was high or very high in all patients, attaining three times the normal values. The values were lower in Group 5 (unstable angina) patients in whom no thrombus was observed on coronary angiography. The differences between Group 1 and Groups 4, 5 and 6 were statistically significant (p less than 0.05). The VWF was higher in the Q-MI group with intracoronary thrombus than in the group without thrombus, but the difference was not statistically different. In conclusion, the VWF may be considered to be a marker for thrombus and/or endothelial activation but a larger study population would be required to identify more accurately the subgroups with thrombosis or risk of thrombosis.
authors.affiliation: Service de cardiologie, hôpital de Hautepierre, CHU de Strasbourg.
authors.forename: J M
authors.initials: JM
authors.lastname: Mossard
authors.forename: M L
authors.initials: ML
authors.lastname: Wiesel
authors.forename: J P
authors.initials: JP
authors.lastname: Cazenave
authors.forename: L
authors.initials: L
authors.lastname: Grunebaum
authors.forename: T
authors.initials: T
authors.lastname: Drawin
authors.forename: J R
authors.initials: JR
authors.lastname: Kieny
authors.forename: G
authors.initials: G
authors.lastname: Roul
authors.forename: P
authors.initials: P
authors.lastname: Bareiss
authors.forename: A
authors.initials: A
authors.lastname: Sacrez
mesh_terms: D000328:Adult; D000787:Angina Pectoris / Q000097:blood*; D000789:Angina, Unstable / Q000097:blood*; D003327:Coronary Disease / Q000097:blood*; D003328:Coronary Thrombosis / Q000097:blood*; D003402:Creatine Kinase / Q000097:blood; D005167:Factor VII / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D015849:Plasminogen Inactivators / Q000032:analysis; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D015849:Plasminogen Inactivators; D014841:von Willebrand Factor; D005167:Factor VII; D005340:Fibrinogen; D003402:Creatine Kinase; D010959:Tissue Plasminogen Activator
vernacular_title: Relations entre augmentation du facteur de Willebrand plasmatique, infarctus du myocarde aigu, angor instable et thrombose coronaire.