Key result
MA Thrombin correlated with platelet volume indices in NSTEMI patients (MPV r=0.393, P=0.007) and with inflammatory markers in STEMI patients (hs-CRP r=0.499, P<0.001).
Observational (n=206)
Effect estimate: r=0.499
p-value: p=<0.001
Thrombin-induced platelet-fibrin clot strength correlates with platelet volume indices in NSTEMI and with inflammatory markers in STEMI, suggesting distinct mechanisms of platelet aggregation across CAD presentations.
Differential MA Thrombin correlations by ACS type are hypothesis-generating; should not yet change practice.
// Hai-Chen Lv 1, * , Hong-Yi Wu 2, * , Jia-Sheng Yin 2 and Jun-Bo Ge 2 1 Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China 2 Shanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China * These authors have contributed equally to this work Correspondence to: Jun-Bo Ge, email: ge.junbo2@zs-hospital.sh.cn Keywords: coronary artery disease, thrombelastography, inflammatory marker, platelet volume index, platelet activation Received: January 02, 2017 Accepted: April 11, 2017 Published: July 22, 2017 ABSTRACT Platelet aggregation and inflammation are both implicated in coronary artery disease (CAD). Thrombin induced platelet-fibrin clot strength (MA Thrombin ) measured by thrombelastography (TEG) has been proved to be a novel marker of platelet aggregation. The aim of this study was to investigate the correlation of MA Thrombin to platelet volume indices (PVIs) or to inflammatory markers in different types of CAD. 206 patients with different types of CAD were enrolled. MA Thrombin , PVIs, including mean platelet volume (MPV), platelet distribution width (PDW), and platelet-large cell ratio (P-LCR) as well as inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP) and fibrinogen (Fbg) were measured. Multiple linear regression models were used to analyze the association between MA Thrombin , PVIs, and inflammatory markers. MA Thrombin and inflammatory markers both varied with CAD types (P<0.001). MA Thrombin was correlated to PVIs in NSTEMI individuals (MPV, r=0.393, P=0.007; PDW, r=0.334, P=0.023; P-LCR, r=0.382, P=0.008), but had inner-link with inflammatory markers in STEMI cases (hs-CRP, r=0.499, P<0.001; Fbg, r=0.500, P<0.001). These findings may suggest different mechanisms of platelet aggregation in different types of CAD. Moreover, MA Thrombin may be used as a potential parameter to evaluate platelet aggregation and inflammation together.
No takes yet. Share an insight, caveat, or question.
Lv et al. (2017) conducted an observational in coronary artery disease (n=206). Thrombin induced platelet-fibrin clot strength (MA Thrombin) was evaluated on Correlation of MA Thrombin to platelet volume indices or inflammatory markers (r=0.499, p=<0.001). MA Thrombin correlated with platelet volume indices in NSTEMI patients (MPV r=0.393, P=0.007) and with inflammatory markers in STEMI patients (hs-CRP r=0.499, P<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: