BACKGROUND: The platelet collagen receptor glycoprotein VI (GPVI) mediates platelet adhesion to subendothelial matrix and thrombus formation in acute coronary syndrome (ACS). This study examined patients with both ACS and stable coronary artery disease (CAD), which presented with atrial fibrillation (AF) and sinus rhythm (SR). METHODS AND RESULTS: We evaluated 992 patients with acute or stable CAD, and determined platelet surface expression of GPVI using flow cytometry. Seventy-eight patients presented with nonvalvular persistent AF. After 1:1 propensity score matching 156 matched cases with 78 pairs were obtained. Patients with AF and ACS showed a significantly decreased GPVI expression compared to patients with ACS and SR, whereas patients with stable angina pectoris (SA) presented with low level activation and no significant difference between SR and AF [mean fluorescence intensity (MFI) for ACS (SR Vs. AF): 20 +/- 6.3 Vs. 17.7 +/- 4.4; P = 0.023; SA (SR Vs. AF): 18.8 +/- 9.4 Vs. 18.1 +/- 6.1; P = 0.649]. In contrast, soluble GPVI was increased in ACS and AF accordingly [plasma GPVI (ng/ml) for ACS (SR Vs. AF): 1.4 +/- 0.8 Vs. 1.9 +/- 1.1; P = 0.038; SA (SR Vs. AF): 0.9 +/- 0.4 Vs. 1.1 +/- 0.5; P = 0.127]. CONCLUSION: Platelet GPVI surface expression is decreased in patients with AF and ACS compared to patients with SR and ACS. Nonvalvular AF is related to indices of chronic platelet activation and might be responsible for a down-regulation of GPVI receptor density on platelets, while soluble GPVI was increased in ACS and AF accordingly.
BACKGROUND: The platelet collagen receptor glycoprotein VI (GPVI) mediates platelet adhesion to subendothelial matrix and thrombus formation in acute coronary syndrome (ACS). This study examined patients with both ACS and stable coronary artery disease (CAD), which presented with atrial fibrillation (AF) and sinus rhythm (SR). METHODS AND RESULTS: We evaluated 992 patients with acute or stable CAD, and determined platelet surface expression of GPVI using flow cytometry. Seventy-eight patients presented with nonvalvular persistent AF. After 1:1 propensity score matching 156 matched cases with 78 pairs were obtained. Patients with AF and ACS showed a significantly decreased GPVI expression compared to patients with ACS and SR, whereas patients with stable angina pectoris (SA) presented with low level activation and no significant difference between SR and AF [mean fluorescence intensity (MFI) for ACS (SR Vs. AF): 20 +/- 6.3 Vs. 17.7 +/- 4.4; P = 0.023; SA (SR Vs. AF): 18.8 +/- 9.4 Vs. 18.1 +/- 6.1; P = 0.649]. In contrast, soluble GPVI was increased in ACS and AF accordingly [plasma GPVI (ng/ml) for ACS (SR Vs. AF): 1.4 +/- 0.8 Vs. 1.9 +/- 1.1; P = 0.038; SA (SR Vs. AF): 0.9 +/- 0.4 Vs. 1.1 +/- 0.5; P = 0.127]. CONCLUSION: Platelet GPVI surface expression is decreased in patients with AF and ACS compared to patients with SR and ACS. Nonvalvular AF is related to indices of chronic platelet activation and might be responsible for a down-regulation of GPVI receptor density on platelets, while soluble GPVI was increased in ACS and AF accordingly.
Authors: Boris Bigalke; Konstantinos Stellos; Tobias Geisler; Stephan Lindemann; Andreas E May; Meinrad Gawaz Journal: Clin Res Cardiol Date: 2010-01-05 Impact factor: 5.460