Influence of platelet count on the expression of platelet collagen receptor glycoprotein VI (GPVI) in patients with acute coronary syndrome.
Platelets play a key role in the development of an acute coronary syndrome (ACS) and contribute to cardiovascular events. Platelet collagen receptor glycoprotein VI (GPVI) contributes significantly to platelet adhesion and thrombus formation in ACS. We consecutively investigated both the platelet count and the platelet surface expression of GPVI in 843 patients with a symptomatic coronary artery disease verified by coronary angiography. Four hundred fourteen patients presented with stable angina pectoris and 429 patients with ACS. Platelet surface expression of GPVI and CD62P was determined by flow cytometry and platelet count with a coulter counter, plasmatic soluble GPVI was measured by ELISA. Platelet GPVI expression in patients with ACS was compared to platelet count. Patients with ACS showed significantly elevated GPVI expression levels in the first and second quartiles of platelet count compared to patients with higher platelet count [mean fluorescence intensity (MFI) +/- standard deviation): 1(st) vs. 4(th): 20.44 +/- 6.1 vs. 18.62 +/- 3.7; p=0.012; 2(nd)vs.3(rd):21.2+/-8.5vs.18.76+/-3.7;P=0.03; 2(nd)vs.4(th): 21.2+/-8.5vs.18.62+/-3.7;P=0.004], which was paralleled in trend for the CD62P expression [MFI: 1(st) vs. 4(th): 11.2 +/- 6.8 vs. 12.3 +/- 9; p=0.057; 2(nd) vs. 3(rd): 16.3 +/- 16 vs.12.7 +/- 5.3; p=0.138; 2(nd) vs. 4(th): 16.3 +/- 16 vs.11 +/- 4.4; p=0.043]. In a subgroup of 48 patients with ACS, determination of soluble GPVI showed similar results [plasma GPVI (ng/ml): 1(st)vs.4(th): 1.6 +/- 0.6 vs. 1.2 +/- 0.4; p=0.046; 1(st) vs. 3(rd): 1.6 +/- 0.6 vs. 1.1 +/- 0.5; p=0.038; 2(nd) vs. 3(rd): 1.9 +/- 0.8 vs. 1.1 +/- 0.5; p=0.04; 2(nd) vs. 4(th): 1.9 +/- 0.8 vs. 1.2 +/- 0.4; p=0.056]. Thus, a lower platelet count comes along with a higher GPVI surface expression and plasma concentration in patients with ACS, which potentially reflects increased activation and enhanced recruitment of platelets to the site of vascular injury.
Bigalke
Boris
B
Medizinische Klinik III, Eberhard Karls Universität Tübingen, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.
Stellos
Konstantinos
K
Stakos
Dimitrios
D
Joos
Thomas
T
Pötz
Oliver
O
Geisler
Tobias
T
Bischofs
Christian
C
Kremmer
Elisabeth
E
Krämer
Björn F
BF
Seizer
Peter
P
May
Andreas E
AE
Lindemann
Stephan
S
Gawaz
Meinrad
M
D054058:Acute Coronary Syndrome / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology / Q000401:mortality; D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology / Q000401:mortality; D015415:Biomarkers / Q000097:blood; D018955:CD36 Antigens / Q000097:blood*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications / Q000000981:diagnostic imaging / Q000401:mortality; D005260:Female; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation; D010976:Platelet Count; D011237:Predictive Value of Tests; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000209:etiology; D013997:Time Factors
D015415:Biomarkers; D018955:CD36 Antigens; D019007:P-Selectin