Plasma resistance to activated protein C regulates the activation of coagulation induced by thrombolysis in patients with ischaemic heart disease.
OBJECTIVE
To determine whether there was a relation between plasma resistance to activated protein C and the coagulation activation induced during thrombolysis with 100 mg alteplase in 25 patients with acute ischaemic heart disease.


METHODS
Blood samples were collected before (t = 0 h), during (t = 2.25 h), and after (t = 4 h, t = 12 h, and t = 24 h) thrombolysis to examine the relation between baseline activated protein C resistance ratio and markers of coagulation activation-that is, thrombinantithrombin III-complexes and prothrombin fragment 1 + 2 generated during thrombolysis.


RESULTS
There was a negative correlation between activated protein C resistance ratio and area under the curve of thrombin-antithrombin III-complexes (rs = - 0.60; P < 0.003) and there was a trend to a negative correlation between activated protein C resistance ratio and area under the curve of prothrombin fragment 1 + 2 (rs = - 0.37; P = 0.07). This accorded with the negative correlation between activated protein C resistance ratio and the peak value of thrombin-antithrombin III-complexes (rs = - 0.55; P < 0.005) and between activated protein C resistance ratio and the peak value of prothrombin fragment 1 + 2 (rs = - 0.42; P < 0.04). Components of the protein C/S system or known inhibitors of activated protein C may influence the activated protein C resistance ratio. There were no associations between the activated protein C resistance ratio and protein C, protein C inhibitor, or plasminogen activator inhibitor type-1, whereas there was a trend to a negative correlation between activated protein C resistance ratio and protein S.


CONCLUSIONS
The results indicate that plasma resistance to activated protein C may be one of the main mechanisms regulating the activation of coagulation induced by thrombolysis. This study suggests that it may be possible to single out individuals with a high risk of reocclusion before the start of thrombolytic therapy.
Pedersen
O D
OD
Department of Internal Medicine, Ribe County Hospital, Esbjerg, Denmark.
Gram
J
J
Jespersen
J
J
D000368:Aged; D000990:Antithrombin III / Q000032:analysis; D001780:Blood Coagulation Tests; D005260:Female; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D010447:Peptide Hydrolases / Q000032:analysis; D010960:Plasminogen Activators / Q000627:therapeutic use*; D011486:Protein C / Q000378:metabolism*; D011516:Prothrombin / Q000032:analysis; D018709:Statistics, Nonparametric; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D014914:Whole Blood Coagulation Time
D011486:Protein C; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D011516:Prothrombin; D006493:Heparin; D010447:Peptide Hydrolases; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator