Activation products of the haemostatic system in coronary, cerebrovascular and peripheral arterial disease.
To determine the presence of a 'hypercoagulable state' as assessed by indices of thrombin and plasmin generation and of the amount of fibrin that is lysed, in patients with stable coronary, cerebral and peripheral arterial disease a population-based cross-sectional study was performed. From a population-based cohort comprising 7983 men and women aged 55 years and over, we randomly selected 127 subjects with a history of myocardial infarction, 124 with a history of stroke and/or transient ischemic attack, 131 patients with peripheral arterial disease and 263 control subjects in the same age group without arterial disease. Subjects using anticoagulant drugs were not selected. F1+2, TAT, and PAP were not associated with a history of cardiovascular events, nor with peripheral arterial disease. In contrast, positive associations were found for D-Dimer. Mean D-Dimer level was 40 microg/l (95% CI 35, 44) in control subjects; 53 microg/l (47, 61) in those with a history of myocardial infarction and 51 microg/l (45, 58) in those with a history of stroke and or transient ischemic attack. D-Dimer increased gradually with increasing severity of peripheral atherosclerosis; a decrease in ankle/arm systolic blood pressure ratio of 0.1 was associated with an increase in D-Dimer of 3.9 microg/l (p<0.01). This was more pronounced in subjects with higher F1+2, TAT and PAP concentration. In conclusion, the markers of onset of coagulation F1+2, TAT and PAP are not associated with the presence of arterial disease, but increased levels of these markers are necessary for the positive association between D-Dimer and arterial disease.
Julius Center for Patient Oriented Research, University Medical Center, Utrecht, The Netherlands. j.g.vanderbom@jc.azu.nl
J G
JG
van der Bom
M L
ML
Bots
F
F
Haverkate
P
P
Meijer
A
A
Hofman
C
C
Kluft
D E
DE
Grobbee
D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D000933:Antifibrinolytic Agents / Q000009:adverse effects / Q000097:blood*; D000990:Antithrombin III; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000209:etiology; D016022:Case-Control Studies; D002561:Cerebrovascular Disorders / Q000097:blood / Q000209:etiology; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood / Q000209:etiology; D003430:Cross-Sectional Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000209:etiology; D011516:Prothrombin; D014652:Vascular Diseases / Q000097:blood* / Q000209:etiology; D000979:alpha-2-Antiplasmin
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases; D005341:Fibrinolysin