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

Kolarov, P; Tschöepe, Diethelm; Hk, Nieuwenhuis; Fa, Gries; Strauer, Bodo E.; Hp, Schultheiss

doi:10.1093/oxfordjournals.eurheartj.a015039

Cited by 37 publications

(19 citation statements)

References 24 publications

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“…The majority of flow cytometric studies that have previously reported platelet activation following PTCA have used local sampling techniques, either from the coronary sinus [23,24] , or directly from the coronary artery [25] . In contrast to our present findings, Kolarov et al [26] , using flow cytometry in peripheral blood, reported both a significant reduction in platelet count and increased platelet activation following PTCA, but sampling was performed much earlier (2 h post PTCA), at a time when platelet behaviour might still be affected by periprocedural anticoagulation. Gawaz et al [27] showed no significant changes in platelet activation in peripheral blood samples from patients undergoing elective PTCA, although changes were observed in patients undergoing PTCA for acute myocardial infarction.…”

Section: Discussioncontrasting

confidence: 99%

Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Knight

Panesar²,

Wilson³

et al. 1998

European Heart Journal

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Section: Discussioncontrasting

confidence: 99%

Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Knight

Panesar²,

Wilson³

et al. 1998

European Heart Journal

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“…Since leukocytes and platelets were obtained from the coronary sinus before and immediately after successful intervention, our findings may reflect a consumption of activated platelets and leukocytes during the procedure at the site of vessel injury. A loss of activated platelets during percutaneous transluminal coronary angioplasty has been reported [11]. It was suggested that circulating preactivated platelets aggregate and immediately respond to the performed manipulations [11].…”

Section: Discussionmentioning

confidence: 99%

“…To analyze platelet adhesion proteins, blood was drawn from the coronary sinus and immediately fixed as described above [11,12]. A single-platelet flow cytometry assay was used to measure platelet activation [10][11][12].…”

Section: Assessment Of Adhesion Proteins On Plateletsmentioning

confidence: 99%

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Leukocyte CD15 Expression and Platelet Activation in the Coronary Sinus after Coronary Intervention

Rauch

Wolff²,

Schultheiss³

et al. 2003

Pathophysiol Haemos Thromb

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Markers associated with coronary restenosis must be identified to develop therapeutic strategies for improving the clinical outcome. We studied whether adhesion proteins on leukocytes and platelets from coronary sinus blood were associated with restenosis after coronary intervention in patients with stable coronary artery disease. Adhesion proteins on platelets and leukocytes were measured by flow cytometry. Pre- and postinterventional leukocyte CD15 expression was significantly higher in patients with restenosis than in those without it. Increased leukocyte CD15 expression during the intervention may contribute to coronary restenosis. Inhibition of leukocyte adhesion may be useful for the prevention of restenosis.

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“…They reported significant platelet activation after PTCA. Kolarov et al [31] studied 25 patients receiving PTCA. For flow cytometry they used CD62p, CD63, and thrombospondin.…”

Section: Discussionmentioning

confidence: 99%

Flow-Cytometric Analysis Comparing Platelet Activation during Percutaneous Transluminal Coronary Angioplasty, Stent Placement and Rotablation

Bau¹,

Beythien²,

Brockmann³

et al. 2001

Transfus Med Hemother

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Background: Acute occlusion and subacute restenosis of the coronary artery remain the limiting factors of the otherwise successful techniques of interventional cardiology. Platelets and especially activated platelet subpopulations play a key role in these sometimes fatal complications. In this study, we used flow cytometry to compare the influences of percutaneous transluminal coronary angioplasty (PTCA, n = 12 patients), stenting (n = 8) and rotablation (n = 10) on platelet antigens and their possible alteration, indicating platelet activation. Material and Methods: Samples for flow cytometry were taken directly from the arterial sheath in free flow before the procedures, directly after the procedures, and 30 min after finishing either PTCA, stenting or rotablation. One aliquot of the sample was immediately fixed and then stabilized. Aliquots were labeled with saturating amounts of antibodies against CD41a (GPIIb-IIIa), CD42b (GPIb-V-IX), CD62p (P-selectin), CD63 (GP53), and antihuman fibrinogen, and measured within 2 h. For flow-cytometric analyses we used a FACScan cytometer. Results: CD41a and CD42b did not show significant alterations in mean channel fluorescence intensity (MCFI) before, directly after, and 30 min after finishing PTCA, stenting, or rotablation (PTCA: CD41a p = 0.8 directly after and p = 0.9 30 min after finishing; CD42b p = 0.5 and p = 0.2; stenting: CD41a p = 0.3 and p = 0.2, CD42b p = 0.5 and p = 0.7; rotablation: CD41a p = 0.2 and p = 0.2; CD42b p = 0.4 and p = 0.1). However, measuring the MCFI of CD62p, CD63, and fibrinogen binding (all p < 0.05), platelet activation could be detected directly after PTCA, stenting, or rotablation. Compared with values obtained directly after the procedures, there were further significant changes 30 min after finishing the procedures in MCFI after PTCA and stenting (CD62p, CD63, fibrinogen binding, all p < 0.05), but not after rotablation (CD62p p = 0.1; CD63 p = 0.9; fibrinogen binding p = 0.5). Conclusions: The results of our study show that all three techniques induce significant platelet activation. Activation differs between the procedures. Detecting platelet activation may help to determine patients at risk for thrombophilic adverse effects.

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

Cited by 37 publications

References 24 publications

Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Increased platelet responsiveness following coronary stenting Heparin as a possible aetiological factor in stent thrombosis

Leukocyte CD15 Expression and Platelet Activation in the Coronary Sinus after Coronary Intervention

Flow-Cytometric Analysis Comparing Platelet Activation during Percutaneous Transluminal Coronary Angioplasty, Stent Placement and Rotablation

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