The role of coagulation and inflammation after angioplasty in patients with peripheral arterial disease

被引:16
|
作者
Wahlgren, C. M. [1 ]
Sten-Linder, M.
Egberg, N.
Kalin, B.
Blohme, L.
Swedenborg, J.
机构
[1] Karolinska Univ Hosp, Dept Vasc Surg, S-17176 Stockholm, Sweden
[2] Karolinska Univ Hosp, Dept Clin Chem, S-17176 Stockholm, Sweden
[3] Karolinska Univ Hosp, Dept Thorac Radiol, S-17176 Stockholm, Sweden
关键词
angioplasty; coagulation; CRP; inflammation; PTA;
D O I
10.1007/s00270-005-0159-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose: Restenosis remains a frequent complication after angioplasty in peripheral arterial disease. Inflammation plays a critical role in the vascular response to injury. Effective medical treatment to improve patency after angioplasty is still elusive. The aims of this prospective clinical study were to investigate changes in blood coagulation and inflammatory markers after angioplasty and their significance for restenosis. Methods: Thirty-four patients with peripheral arterial disease underwent angioplasty of the iliac and superficial femoral arteries. Ten patients undergoing diagnostic angiography were included in the study as controls. Plasma levels of tissue factor, prothrombin fragment 1 + 2, D-dimer, P-selectin, C-reactive protein (CRP), and fibrinogen were analyzed before and after angioplasty. Patients were followed up with angiography after 6 months to assess restenosis. Results: CRP was elevated the day after angioplasty (6.6 mg/l, p = 0.0001) and tended to peak after 1 week (11 mg/l, p = 0.09). There was a significant increase of D-dimer and P-selectin 1-4 hr after angioplasty (0.4 mg/l, p = 0.001 and 68 ng/ml, p = 0.05, respectively). None of the biochemical markers was a statistically significant predictor of restenosis. Conclusion: We have observed a much more prolonged inflammatory response than previously noted, but only minor changes in coagulation activity after angioplasty. The biochemical markers, before and after angioplasty, were not related to restenosis. Further studies are needed to delineate the molecular mechanisms behind these observations and their involvement in thrombosis and restenosis. If these pathways are further defined, improved treatment strategies, including antithrombotic treatments and statins, could be tailored to modulate postprocedural inflammation.
引用
收藏
页码:530 / 535
页数:6
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