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Haemostasis, Thrombosis and Vascular Biology Unit; University Department of Medicine; City Hospital; Birmingham B18 7QH, England, UK
g.y.h.lip{at}bham.ac.uk
Abstract
BackgroundPlatelet activation and aggregation play a key role in coronary artery disease, with anti-platelet therapies leading to improved clinical outcomes. Limited data exists as to whether peripheral venous blood measurements of platelet physical indices (platelet count, volume and granularity) and soluble markers of platelet activation (eg. P-selectin [sP-sel] and CD 40 ligand [CD40L]) reflect the local (intracardiac) coronary environment. Furthermore, how percutaneous coronary interventions (PCI) affect levels of peripheral/cardiac platelet indices is unclear.
MethodsBlood samples were sequentially acquired from the coronary os, aortic root, coronary sinus and the femoral vein, and where relevant, pre- and post-PCI. Patients undergoing coronary angiography were recruited [n = 87, mean age 59.8 ± 10.8 years; 54 (62%) males], of whom 36 proceeded to PCI. Platelet physical indices and plasma sP-sel and CD40L levels (ELISAs) were measured.
ResultsAt baseline, no intra cardiac vs peripheral differences were noted in sP sel levels, whilst CD40L levels were elevated in the aorta compared to coronary sinus and femoral venous samples. Mean platelet count (MPC) was similar at all 4 sites but within coronary sinus blood, mean volume (MPV) was significantly lower - and mean granularity (MPG) higher - when compared to arterial levels. Though aortic and femoral levels of sP-sel were raised following PCI, trans-cardiac gradients of plasma sP-sel levels were unaffected. PCI was associated with lower CD40L, MPC and MPV levels but a higher granularity of platelets in all sampling sites.
ConclusionsP-sel levels measured peripherally do reflect the cardiac environment, unlike CD40L, MPC, MPV and MPG. PCI leads to further platelet activation (raised sP-sel) despite aggressive anti-platelet therapy use.
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