Open AccessThrombin induced platelet-fibrin clot strength in relation to platelet volume indices and inflammatory markers in patients with coronary artery disease
Author(s) -
Haichen Lv,
Hongyi Wu,
Jun Yin,
Junbo Ge
Publication year - 2017
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.19450
Subject(s) - mean platelet volume , medicine , platelet , fibrinogen , coronary artery disease , fibrin , inflammation , c reactive protein , platelet activation , cardiology , immunology
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.