Absence of a prothrombotic state in restenotic patients?
OBJECTIVE
To determine whether, in patients undergoing percutaneous transluminal coronary angioplasty (PTCA), there are prothrombotic markers indicating those with a predisposition to restenosis.


METHODS
Venous blood samples were obtained from patients undergoing PTCA for chronic stable angina. Patients with restenotic lesions, conduit stenoses or occlusive lesions were not included in the study. Samples were assayed for coagulation factors (fibrinopeptide A, antithrombin III, protein C), fibrinolytic factors [tissue-type plasminogen activator (t-PA), alpha 2 antiplasmin, plasminogen activator inhibitor (PAI-1)] and markers of platelet activation (platelet factor 4, beta thromboglobulin).


RESULTS
Of 46 patients who underwent successful PTCA, restenosis, defined as loss in absolute gain of more than 50%, occurred in 16 (35%). The minimal luminal diameter (mean +/- SD) at follow-up in those who had suffered restenosis was 1.07 +/- 0.7 mm compared with 1.73 +/- 0.5 mm in the non-restenotic patients. However, no significant differences in the levels of markers of platelet activation, coagulation factors, or fibrinolytic factors were observed between the two groups. The only significant difference between the groups was a higher platelet count in the restenotic patients [median (interquartile range): 263 (247-278) versus 224 (175-263), P < 0.05].


CONCLUSIONS
Our results suggest that patients who suffer restenosis following PTCA appear to have no clearly detectable pre-existing imbalance in their prothrombotic/antithrombotic status. Although the platelet count was higher in restenotic patients, the levels of markers of platelet activation were no different in the two groups. Thus, it is at present unlikely that simple blood assays before PTCA assessing an individual's 'thrombotic state' can help to predict which of the 30-40% of patients undergoing PTCA will suffer restenosis.
Academic Department of Cardiology, Glenfield Hospital, Leicester, UK.
M J
MJ
Brack
R S
RS
More
S
S
Pringle
A H
AH
Gershlick
D000787:Angina Pectoris / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood*; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000628:therapy*; D005260:Female; D005344:Fibrinopeptide A / Q000032:analysis; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010958:Plasminogen / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010978:Platelet Factor 4 / Q000032:analysis; D011486:Protein C / Q000032:analysis; D012008:Recurrence; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000032:analysis; D001620:beta-Thromboglobulin / Q000032:analysis
D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D000979:alpha-2-Antiplasmin; D001620:beta-Thromboglobulin; D005344:Fibrinopeptide A; D010978:Platelet Factor 4; D000990:Antithrombin III; D010958:Plasminogen; D010959:Tissue Plasminogen Activator