4.6 Article

Mean platelet volume as marker of restenosis after percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris

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THROMBOSIS RESEARCH
卷 117, 期 4, 页码 371-377

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2005.04.004

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platelet volume; platelet count; platelet activity; angioplasty; restenosis

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Introduction: Several experimental and clinical studies have demonstrated that platelet size and function correlate since large platelets are hemostatically more reactive than platelets of normal size. Since platelets play a crucial role in vascular remodeling after percutaneous transluminal coronary angioplasty (PTCA), we investigated the influence of the mean platelet volume (MPV), a parameter of platelet size, on restenosis after PTCA. Methods: The retrospective study comprised 174 patients who underwent elective PTCA and follow-up angiography within 6 months thereafter. According to the follow-up angiograms, the patients were assigned to group A (restenosis, n = 74) or group B (no restenosis, n=100). Both groups were compared in regard to pre-procedural hematological routine parameters including MPV, platelet count, hematocrit, white blood cell count and fibrinogen. Results: MPV was significantly increased in group A, compared with that in group B (8.75 +/- 0.99 fL vs. 8.04 +/- 0.74 fl, p<0.001). This difference in MPV was evident in patients with stable and unstable angina pectoris. In addition, MPV had an impact on the time-related incidence of angiographic restenosis, as early restenosis was associated with higher pre-procedural, MPV values. Platelet count correlated inversely with MPV (r = -0. 36, p <0.01) and was significantly lower in group A than in group B. The remaining hematological parameters were not different in both groups. Conclusions: The MPV seems to be a marker of coronary restenosis in patients undergoing PTCA. Patients with high pre-procedural MPV values might benefit from an intensified antiplatetet therapy after coronary interventions. (C) 2005 Elsevier Ltd. All rights reserved.

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