Increased platelet-derived microparticles in the coronary circulation of percutaneous transluminal coronary angioplasty patients.
Platelet-derived microparticles that are produced during platelet activation are capable of adhesion and aggregation. Endothelial trauma that occurs during percutaneous transluminal coronary angioplasty (PTCA) may support platelet-derived microparticle adhesion and contribute to development of restenosis. We have previously reported an increase in platelet-derived microparticles in peripheral arterial blood with angioplasty. This finding raised concerns regarding the role of platelet-derived microparticles in restenosis, and therefore the aim of this study was to monitor levels in the coronary circulation. The study population consisted of 19 angioplasty patients. Paired coronary artery and sinus samples were obtained following heparinization, following contrast administration, and subsequent to all vessel manipulation. Platelet-derived microparticles were identified with an anti-CD61 (glycoprotein IIIa) fluorescence-conjugated antibody using flow cytometry. There was a significant decrease in arterial platelet-derived microparticles from heparinization to contrast administration (P = 0.001), followed by a significant increase to the end of angioplasty (P = 0.004). However, there was no significant change throughout the venous samples. These results indicate that the higher level of platelet-derived microparticles after angioplasty in arterial blood remained in the coronary circulation. Interestingly, levels of thrombin-antithrombin complexes did not rise during PTCA. This may have implications for the development of coronary restenosis post-PTCA, although this remains to be determined.
School of Life Sciences, Queensland University of Technology, Brisbane, Australia. jcraft@soms.uq.edu.au
Judy A
JA
Craft
Paul P
PP
Masci
Michael S
MS
Roberts
Tim A
TA
Brighton
Paul
P
Garrahy
Stephen
S
Cox
Neville A
NA
Marsh
D015906:Angioplasty, Balloon, Coronary; D000990:Antithrombin III / Q000032:analysis; D001792:Blood Platelets / Q000648:ultrastructure*; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003131:Combined Modality Therapy; D003326:Coronary Circulation; D023903:Coronary Restenosis / Q000209:etiology; D023921:Coronary Stenosis / Q000097:blood* / Q000188:drug therapy / Q000628:therapy; D003331:Coronary Vessels; D005260:Female; D006801:Humans; D039661:Integrin beta3 / Q000032:analysis; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010316:Particle Size; D010447:Peptide Hydrolases / Q000032:analysis; D010973:Platelet Adhesiveness; D010976:Platelet Count; D015607:Stents; D013929:Thromboxane B2 / Q000097:blood
D002317:Cardiovascular Agents; D039661:Integrin beta3; C046193:antithrombin III-protease complex; D013929:Thromboxane B2; D000990:Antithrombin III; D007770:L-Lactate Dehydrogenase; D010447:Peptide Hydrolases