Platelet collagen receptor glycoprotein VI as a possible novel indicator for the acute coronary syndrome.
BACKGROUND
Platelet collagen receptor glycoprotein VI (GPVI) plays a critical role in acute coronary thrombosis. This prospective study examined the predictive value of GPVI for acute coronary syndromes (ACS) in a large consecutive group of patients with symptomatic coronary artery disease to identify the high-risk cohort with imminent coronary events.


METHODS
We evaluated 1,003 patients with symptomatic coronary artery disease, verified by coronary angiography, and determined the surface expression of GPVI using flow cytometry. In a subgroup of 471 patients, who were treated with aspirin plus clopidogrel for coronary stenting, adenosine disphosphate (20 micromol/L)-induced platelet aggregation was evaluated.


RESULTS
Patients with ACS (n = 485) showed a significantly enhanced GPVI expression compared to patients with stable angina pectoris (SAP; n = 518) (mean fluorescence intensity for ACS 19.8 +/- 5.9; SAP 18.7 +/- 8.5, P = .01). Patients with elevated GPVI levels on admission (GPVI cutoff value > or =18.6 mean fluorescence intensity) had a 1.4-fold relative risk for ACS. Logistic regression analysis showed that an elevated platelet GPVI level may indicate ACS independent of biomarkers of myocardial necrosis including troponin, creatine kinase, and creatine kinase-MB. Patients with increased platelet activation (GPVI expression level > or =18.6) showed significant enhanced residual platelet aggregation despite dual antiplatelet therapy compared to patients with low GPVI levels (P = .028).


CONCLUSIONS
Surface expression of GPVI is enhanced in patients with ACS and indicates an imminent acute coronary event before irreversible myocardial necrosis is evident. High GPVI levels are associated with increased residual platelet aggregation despite antiplatelet therapy. Therefore, GPVI is useful to identify the subgroup of patients with a high risk for coronary stent thrombosis and thromboischemic events.
Bigalke
Boris
B
Medizinische Klinik, Klinik für Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen, Germany.
Geisler
Tobias
T
Stellos
Konstantinos
K
Langer
Harald
H
Daub
Karin
K
Kremmer
Elisabeth
E
Seizer
Peter
P
May
Andreas E
AE
Lindemann
Stephan
S
Gawaz
Meinrad
M
D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis* / Q000401:mortality / Q000628:therapy; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D015331:Cohort Studies; D017023:Coronary Angiography; D003328:Coronary Thrombosis / Q000097:blood / Q000175:diagnosis* / Q000401:mortality / Q000628:therapy; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000502:physiology; D010980:Platelet Membrane Glycoproteins / Q000032:analysis*; D011336:Probability; D011379:Prognosis; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012372:ROC Curve; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D016019:Survival Analysis
D015415:Biomarkers; D010980:Platelet Membrane Glycoproteins; C098341:platelet membrane glycoprotein VI