Association between Stable Coronary Artery Disease and In Vivo Thrombin Generation

Abstract

Background. Thrombin has been implicated as a key molecule in atherosclerotic progression. Clinical evidence shows that thrombin generation is enhanced in atherosclerosis, but its role as a risk factor for coronary atherosclerotic burden has not been proven in coronary artery disease (CAD) stable patients. Objectives. To evaluate the association between TAT levels and homocysteine levels and the presence of coronary artery disease diagnosed by coronary angiography in patients with stable CAD. Methods and Results. We included 95 stable patients admitted to the Haemodynamics Department, including 63 patients with significant CAD and 32 patients without. We measured the thrombin-antithrombin complex (TAT) and homocysteine concentrations in all the patients. The CAD patients exhibited higher concentrations of TAT (40.76 μg/L versus 20.81 μg/L, p = 0.002) and homocysteine (11.36 μmol/L versus 8.81 μmol/L, p < 0.01) compared to the patients without significant CAD. Specifically, in patients with CAD+ the level of TAT level was associated with the severity of CAD being 36.17 ± 24.48 μg/L in the patients with bivascular obstruction and 42.77 ± 31.81 μg/L in trivascular coronary obstruction, p = 0.002. Conclusions. The level of in vivo thrombin generation, quantified as TAT complexes, is associated with the presence and severity of CAD assessed by coronary angiography in stable CAD patients.

Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease

“…Additionally, thrombin has been shown to augment levels of mRNA that encode monocyte chemoattractant protein 1, a well-characterized chemokine, abundant in human atherosclerotic plaques. 55 In fact, thrombin is a central coagulation protease. It is known to promote numerous pro-atherogenic actions in vitro such as activation of protease-activated receptor 1, endothelial permeability, migration and proliferation of vascular smooth muscle cells, platelet activation, leukocyte adhesion and recruitment, cytokine and chemokine production, vascular calcification, angiogenesis, and apoptosis.…”

Apoliporotein L3 interferes with endothelial tube formation via regulation of ERK1/2, FAK and Akt signaling pathway

“…In this study, we confirmed the expression profile of APOLs in a model of endothelial cells (HMEC-1) in response to TNF-α and IFN-γ. We extended our observations to other inflammatory stimuli involved in cardiovascular diseases: oxLDL and MoxLDL, two pro-atherogenic molecules [29], thrombin a serine protease linking coagulation and inflammation [30], and myeloperoxidase an enzyme released by neutrophils at inflammation sites [29]. We analyzed the functional role of one of the family members in the endothelial phenotype.…”

Factor V Leiden but not the factor II 20210G>A mutation is a risk factor for premature coronary artery disease: a case-control study in Iran

“…This pro-atherogenic effect may be further accelerated when traditional atherogenic risk factors are present. Moreover, the FVL-related hypercoagulability may induce a higher risk of clot formation on the unstable plaque [ [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] ]. However, the interaction analyses rely on a lower number of subjects because of the combination of multiple risk factors, hence, their results should be interpreted with caution.…”