Relevance of hemostasis on restenosis in clinically stable patients undergoing elective PTCA

• Published in: Thrombosis research 2008-01, Vol.122 (2), p.229-236
• Main Authors: Schoebel, F.C, Peters, A.J, Kreis, I, Gradaus, F, Heins, M, Jax, T.W
• Format: Article
• Language: English
• Subjects: Aged; alpha-2-Antiplasmin - metabolism; Angioplasty, Balloon, Coronary - methods; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cardiovascular system; Coronary Angiography - methods; Coronary Artery Disease - pathology; Coronary Restenosis; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Erythrocytes - cytology; Female; Hematology, Oncology and Palliative Medicine; Hemostasis; Humans; Lipid Metabolism; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Plasminogen Activators - antagonists & inhibitors; Stress, Mechanical; Thrombin - chemistry; Thrombin - metabolism; Vasodilator agents. Cerebral vasodilators
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/j.thromres.2007.10.007

Abstract Background Secondary coronary thrombus formation is considered to be co-factor in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Therefore systemic factors indicating a hypercoagulable disease state may be relevant for the process of coronary renarrowing. Even though experimental data suggest that in particular thrombin may be of major relevance for restenosis induced by mechanical injury, only little clinical data has been presented so far. Methods and results In 60 consecutive patients, who had been clinical stable for at least 2 months, and who underwent elective and primarily successful PTCA, follow-up films were evaluated by means of quantitative coronary angiography in respect to a categorical and a continuous definition of restenosis, luminal narrowing > 50% and late luminal loss respectively. Of the chosen laboratory variables prothrombin fragment 1 + 2 (1.3 ± 0.5 vs. 0.9 ± 0.4 mmol/l, p < 0.001) red blood cell aggregation at low shear stress (13.5 ± 2.9 vs. 11.6 ± 2.8 units, p < 0.05), and plasminogen-activator inhibitor (3.7 ± 1.8 vs. 5.3 ± 3.2 U/ml p < 0.05) differentiated between patients with ( n = 18) and without restenosis ( n = 42). Late luminal loss correlated positively with prothrombin fragment 1 + 2 ( r = 0.41, p < 0.001), plasminogen-activator inhibitor ( r = − 0.28, p < 0.05) and plasmin–α2 -antiplasmin complex ( r = 0.39, p < 0.01). Conclusions A hypercoagulable disease state and in particular thrombin generation characterize a high-risk group prone for restenosis in clinically stable oronary arterydisease.