title: Increased thrombin generation after acute versus chronic coronary disease as assessed by the thrombin generation test.
abstract: Atherosclerosis is the most common pathophysiologic substrate of coronary artery disease (CAD). Whereas plaque progression and arterial remodeling are critical components in chronic CAD, intracoronary thrombosis over plaque disruption is causally related to acute CAD. It was the objective of this study to investigate the differences between prior acute CAD and chronic CAD by a simple global coagulation assay measuring thrombin generation. A cross-sectional study involving 15 healthy controls, 35 patients with chronic stable CAD, and 60 patients after an episode of acute myocardial infarction (AMI) was performed. Thrombin generation was measured between three and 11 months after the initial diagnosis (mean 6 months) by a commercially available fluorogenic assay (Technothrombin TGA). In each patient the lag phase, velocity index and peak thrombin were obtained from the thrombogram profile. Traditional cardiovascular risk factors were recorded, and the inflammatory markers, fibrinogen and hs-C-reactive protein were determined. Compared with stable CAD patients, showing normal thrombograms, those with previous AMI showed earlier lag phase (p < 0.05) and significant increase of both the velocity index (p < 0.001) and peak thrombin (p < 0.05), indicating faster and higher thrombin generation in the AMI group. Differences in thrombin generation between stable and acute CAD patients remained significant (p < 0.001) after adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia). In conclusion, patients with a previous history of acute CAD showed earlier, faster and higher thrombin generation than stable chronic CAD patients. The thrombin generation test may be of clinical value to monitor hypercoagulable/vulnerable blood and/or guide therapy in CAD.
authors.affiliation: Atherosclerosis Research Laboratory, Division of Cardiovascular Sciences, CIMA, University of Navarra, Avda Pio XII 55, Pamplona, Spain.
authors.forename: Josune
authors.initials: J
authors.lastname: Orbe
authors.forename: Maite
authors.initials: M
authors.lastname: Zudaire
authors.forename: Rosario
authors.initials: R
authors.lastname: Serrano
authors.forename: Isabel
authors.initials: I
authors.lastname: Coma-Canella
authors.forename: Sara
authors.initials: S
authors.lastname: Martínez de Sizarrondo
authors.forename: Jose A
authors.initials: JA
authors.lastname: Rodríguez
authors.forename: Jose A
authors.initials: JA
authors.lastname: Páramo
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000209:etiology*; D001777:Blood Coagulation; D001780:Blood Coagulation Tests; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications; D003430:Cross-Sectional Studies; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology*; D012307:Risk Factors; D013917:Thrombin / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D005340:Fibrinogen; D002097:C-Reactive Protein; D013917:Thrombin