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European Heart Journal 1996 17(8):1216-1222;
Copyright © 1996 by the European Society of Cardiology.
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© 1996 The European Society of Cardiology

PTCA: Periprocedural platelet activation Part II of the Duesseldorf PTCA Platelet Study (DPPS)

P. Kolarov*, D. Tschoepe*,, H. K. Nieuwenhuis{dagger}, F. A. Gries*, B. Strauer{ddagger} and H. P. SchultheiB{ddagger}

*Cellular Haemostasis and Clinical Angiology Group, Diabetes Research Institute Duesseldorf, Germany
{ddagger}Department of Cardiology, Pulmonology and Angiology, Heinrich Heine University Duesseldorf, Germany
{dagger}Department of Hematology, University Hospital Utrecht, The Netherlands

revised 23 October 1995; accepted 13 November 1995.

Correspondence. Privatdozent Dr D. Tschcepe, MD, Diabetes Research Institute at the Heinrich Heine University, Cellular Haemostasis and Clinical Angiology Group, Aufm Hennekamp 65, 40225 Duesseldorf, FRG.

Abstract

BACKGROUND: Percutaneous transluminal coronary angio-plasty (PTCA) with its various manipulations could create a dangerous, sudden haemostatic response. This study was performed to investigate PTCA-induced periprocedural changes in platelet activation and its consequences.

METHODS: Twenty-five consecutive patients admitted for elective PTCA were preclassified as having or not having circulating activated platelets. Blood samples were taken for platelet activation marker analysis before, six times during and 2 h after PTCA. Intravascular platelet activation was analysed by flow cytometry to measure activation-dependent surface markers thrombospondin, P-selectin (CD62) and lysosomal GP53 (CD63).

RESULTS: PTCA was associated with a significant reduction of peripheral platelet count. The initiation of the PTCA procedure led to a significant loss of more than 50% of the degranulated, activated platelets. After PTCA, the number of degranulated, activated platelets uniformly increased.

CONCLUSIONS: We conclude that PTCA can induce consumption, particularly of preactivated platelets, and lead to sustained platelet activation after the procedure. This might explain why preactivated patients are at increased risk of suffering periprocedural ischaemic events and why increased thrombogenicity favours acute flow disruption and the progression of coronary stenosis at the lesion site.

Key Words: PTCA • platelet activation • flow cytometry • adhesion molecules


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