Glycoprotein VI as a prognostic biomarker for cardiovascular death in patients with symptomatic coronary artery disease (original) (raw)
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Thrombosis Research, 2010
Background: Platelet glycoprotein VI (GPVI) is elevated in patients with acute coronary syndrome (ACS), stroke and associated with acute coronary events. GPVI may be helpful to distinguish an imminent ACS from non-coronary (NC) causes in patients with chest pain who were transferred to chest pain unit, before the myocardial necrosis is evident with classical biomarkers. Methods: Based on the findings of our previous studies, we consecutively examined 1004 patients with chest pain in a prospective study design. ACS was found in 416 (41.4%), stable angina pectoris (SAP) in 233 (23.2%), and NC causes of chest pain (hypertension, musculoskeletal disease, pulmonary embolism, myocarditis, cardiophobia) in 355 patients (35.4%). Platelet surface expression of GPVI was measured by flow cytometry. Results: Patients with ACS showed significantly enhanced GPVI expression levels compared to patients with SAP or NC causes of chest pain (ACSvs.SAP(mean fluorescence intensity (MFI) ± SD):18.9 ± 7.4vs.17.9 ± 9.5; P = 0.028;ACSvs.NC:15.4 ± 6.9;P = 0.002). Elevated GPVI expression was associated with ACS independent of markers of myocardial necrosis like troponin and creatine kinase-MB. Patients with an elevated GPVI expression (MFI ≥ 18.6) had a poorer clinical outcome than patients with baseline GPVI expression in regard to composite cumulative survival that included myocardial infarction, stroke, and cardiovascular death at three months (Log rank;P = 0.025). Discussion: Platelet GPVI surface expression is enhanced in patients at risk for an ACS and is an early marker for imminent acute coronary events in patients with chest pain.
Expression of platelet glycoprotein VI is associated with transient ischemic attack and stroke
European Journal of Neurology, 2010
Background The platelet collagen receptor glycoprotein VI (GPVI) contributes significantly to platelet adhesion and thrombus formation. This study examined the platelet surface expression of GPVI in patients with transient ischemic attack (TIA) and stroke. Methods and results We consecutively evaluated 205 patients, who admitted the stroke unit with symptoms for stroke. Surface expression of the platelet activation markers (GPVI, CD62P, GPIb) was determined by two-color whole blood flow cytometry. Patients with TIA as well as with stroke showed a significantly enhanced GPVI expression on admission compared to patients with non-ischemic (NI) events (TIA (mean fluorescence intensity (MFI) + SD): 20.9±7.1 vs. NI: 16.2±3.9; p=0.002; stroke: 20.4±5.7 vs. NI; p=0.002), whereas CD62P surface expression showed a significant elevation in TIA and merely a trend in stroke (TIA vs. NI: 12.8±4 vs. 10.9±3.6; p=0.048; stroke: 12.6±7.9 vs. NI; p=0.145). Logistic regression analysis revealed that on admission GPVI was associated with stroke independent of conventional laboratory markers such as C-reactive protein, blood glucose, and creatine kinase. Using a receiver operating characteristic (ROC) curve on GPVI, we have determined the cut off value of 18.2 for stroke. The area under the curve was 0.683 (95%CI, 0.585 to 0.757). Thus, patients with enhanced GPVI expression levels (≥18.2) had a 2.4 fold relative risk for stroke. Patients with elevated platelet GPVI expression level had a poorer clinical outcome in cumulative event-free survival for stroke, myocardial infarction, and cerebro-/cardiovascular death at three-month follow-up (Log rank; p=0.045). Conclusion Platelet GPVI surface expression is significantly enhanced in patients with TIA and stroke compared to patients with NI events. Determination of platelet-specific GPVI may be useful as an early biomarker for cerebral ischemia.
Circulation Journal, 2006
latelet activity is crucial to the pathogenesis of atherosclerosis and arterial thrombosis, which are the principal contributors to the development of acute coronary syndrome (ACS) and ischemic stroke. 1-5 Numerous drug trials have shown that antiplatelet agents, such as aspirin, clopidogrel, and glycoprotein (GP) IIb/IIIa receptor inhibitors, provide substantial therapeutic benefit to patients with ACS who are or are not undergoing percutaneous coronary intervention (PCI). 3,4,6,7 A link between high platelet reactivity and 90-day unfavorable clinical outcomes in patients with coronary artery disease undergoing PCI has been reported. 8 Additionally, an association between increased platelet activation and poor long-term outcomes in patients following acute myocardial infarction (AMI) has also been reported. 9 However, the relationship between increased platelet activity and the
Prognostic effect of mean platelet volume in patients with coronary artery disease
Thrombosis and Haemostasis, 2015
SummaryLarge platelets with high haemostatic activity may lead to increased platelet aggregation.. Mean platelet volume (MPV), an indicator of platelet reactivity, may emerge as a prognostic marker in patients with coronary artery disease (CAD). It was the objective of this study to conduct a systematic review and meta-analysis to assess prognostic effects of MPV on cardiovascular events (CVE) in CAD patients. We searched MEDLINE and SCOPUS from inception to January 2, 2014. All studies that reported MPV and the incidence of cardiovascular events in CAD patients were included. Two reviewers independently extracted the data. A random-effects model was applied for pooling the mean difference of MPV between patients with vs without CVE. Among 30 eligible studies, eight studies reported mean difference of MPV between CVE groups, 11 studies reported MPV dichotomous into high vs low MPV groups, and 11 studies reported both. The pooled mean difference was 0.69 fL (95 %CI = 0.36, 1.01), i. ...
Could mean platelet volume be a predictive marker for acute myocardial infarction?
Medical Science Monitor International Medical Journal of Experimental and Clinical Research, 2005
Platelets play an important role in developing intravascular thrombus, the major cause of acute coronary syndromes. We investigated the clinical value of mean platelet volume (MPV) in coronary atherosclerosis and its possibility of being an independent risk factor for acute myocardial infarction (MI). Two hundred patients who underwent coronary angiography were included in the study. Thirty-five patients were randomly selected for each of the four study groups of stable (SAP) and unstable (USAP) angina pectoris and MI with and without ST-segment elevation. Sixty patients with chest pain having normal coronary angiograms were controls. The groups were compared regarding age, sex, smoking, diabetes, hypertension, positive family history, number of diseased vessels, lipid profile, complete blood count, creatine kinase (CK)-MB, Troponin-I, and MPV. MPV was found to be elevated in MI patients compared with controls (p<0.001) and SAP (p<0.05) and patients with two- (p<0.001) and three-vessel (p<0.001) disease. We observed a significant association between MI and higher MPV (> or = 12 fl). High MPV (p<0.001) and WBC (p<0.001) were independent risk factors, among others. CK-MB, Troponin-I, and higher MPV demonstrate MI risk with 87%, 70%, and 87% specificity, respectively, while higher MPV only demonstrates coronary artery disease with 98% specificity. Our study shows high MPV is an independent risk factor for coronary atherosclerosis and MI. Because this is a simple, economic, and practical method, we suggest MPV be considered with other conventional risk factors.
The American Journal of Cardiology, 2011
Larger size platelets have enhanced reactivity. The mean platelet volume (MPV) is a marker of platelet activation and is usually measured as part of blood testing. The aim of the present study was to investigate the utility of the MPV as a biomarker in prognosticating the long-term outcomes after percutaneous coronary intervention (PCI). The baseline MPV values from consecutive patients undergoing PCI were screened. Of the 1,432 patients, the composite primary end point of mortality or myocardial infarction at 1 year occurred in 80 (5.6%). The patients in the highest tertile (MPV >9.1 fL) had an increased frequency of the primary end point compared to those in the mid (8.1 to 9.1 fL) and lowest (<8.1 fL) tertiles (9.0%, 4.5%, and 3.5%, respectively; p <0.01). Logistic regression analysis demonstrated diabetes (odds ratio 2.44, 95% confidence interval 1.48 to 4.00) and highest tertile of MPV (odds ratio 2.42, 95% confidence interval 1.47 to 3.99) as the best predictors of adverse outcomes. In patients with acute coronary syndrome, the preprocedural MPV and troponin levels demonstrated a comparable predictive relation to the primary end point (receiver operator characteristics curve analysis, area under the curve 0.64, p ؍ 0.01; and 0.63, p ؍ 0.01, respectively). In conclusion, an elevated MPV was a strong independent predictor of long-term outcomes after PCI. The preprocedural MPV had prognostic value similar to that of troponin in patients with acute coronary syndrome. These findings could be of importance in the clinical evaluation of patients before PCI and the design of future studies assessing antiplatelet therapies.
American Journal of Therapeutics, 2018
Background: Low response to aspirin, aspirin resistance, and high platelet reactivity on aspirin treatment are similar names for lack of response to block arachidonic acid-induced aggregation with aspirin therapy and have an important role in the evolution of coronary artery disease (CAD) with thromboembolic events. Study Question: Was to evaluate the correlation between cardiovascular risk factors, biomarkers, and low response to aspirin in patients (pts) with CAD. Study Design: Four hundred pts with CAD were divided into 8 groups of study, consistent with the type of CAD and low response to aspirin. Cardiovascular risk factors and biomarkers-including some of high platelet reactivity, endothelial dysfunction, hypercoagulability, and oxidative stresswere evaluated in correlation with low response to aspirin, defined as on treatment aspirin test (ASPItest) .30U by multiple electrode platelet aggregometry. Results: In patients with CAD, low response to aspirin was significantly correlated with age older than 65 years, smoking, presence of diabetes mellitus, body mass index .25, hypertension, previous aspirin treatment, low response to clopidogrel, high mean platelets volume and von Willebrand factor activity, low flow-mediated vasodilation, and total antioxidant status (P , 0.01). In unstable angina patients, low response to aspirin was significantly correlated with male sex (P , 0.03). Incidence of other hypercoagulability biomarkers-S Protein, C Protein, Antithrombin III, and V Factor Leiden resistance to activated protein C-was low and not correlated with low response to aspirin. Conclusions: In CAD, low response to aspirin was significantly correlated with age older than 65 years, smoking, presence of diabetes mellitus, body mass index I .25, hypertension, previous aspirin treatment, and only in unstable angina with male sex. Low response to aspirin was also statistically associated with low response to clopidogrel, high mean platelets volume, high von Willebrand factor activity, low flow-mediated vasodilation, and low total antioxidant status values.