PubMed · 13754532
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A KROTKIEWSKI, E RUZYLLO, A SICINSKIA. 1960. [Atherosclerosis and hyperthyroidism].. https://pubmed.ncbi.nlm.nih.gov/13754532/
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Atherothrombosis, defined as atherosclerotic lesion disruption with superimposed thrombus formation, is the major cause of acute coronary syndromes and cardiovascular deaths. It is the leading cause of morbidity and mortality in the industrialized world. Plaque composition, rather than luminal stenosis, is recognized as the major determinant of this disease. Since tissue factor is found within atheroma and also in the bloodstream of atherosclerotic patients, it likely plays a key role in determining both plaque and blood thrombogenicity. Ongoing clinical and preclinical studies are evaluating the therapeutic possibilities of specific inhibition of the tissue factor pathway. Here, we will review the role of tissue factor in atherothrombosis.
PURPOSE: To compare debris release with primary stent application (self-expanding stent application at stenosis and then balloon dilation through the opened stent) and that with secondary stent application (balloon angioplasty of stenosis and afterward additional stent application) for high-grade internal carotid artery stenosis in human cadaveric specimens. MATERIALS AND METHODS: Fresh human cadaveric internal carotid artery specimens were attached to a tube system. High-grade stenoses (>66%) were selected, randomized for primary or secondary stent application, and then treated, with fluoroscopic guidance, while the system was rinsed in a pulsating flow. Fluid was collected and filtered, and debris particles were examined with a light microscope. Particles were analyzed according to those consecutively caught by 100 x 100-microm and 11 x 11-microm mesh filters. Results were evaluated in relation to stent application. For statistical analyses of group differences, the exact Mann-Whitney U test was used. RESULTS: Thirteen high-grade human cadaveric internal carotid artery stenoses were analyzed. Five specimens were randomly assigned to secondary stent application, and eight were assigned to primary stent application. No significant difference could be demonstrated for debris release with primary or secondary stent application. P values ranged from.051 to.754. CONCLUSION: The reported superiority of primary stent application may not be related to debris reduction.
OBJECTIVE: It has been shown that plasma level of C-reactive protein (CRP) is an independent predictor for acute coronary syndromes and is associated with plaque weakening. However, the underlying mechanisms are not well understood. In this study, we investigated the effect of CRP on the expression of matrix metalloproteinase-1 (MMP-1) that has been implicated in plaque vulnerability by human U937 histiocytes and monocyte-derived macrophages. METHODS AND RESULTS: Enzyme-linked immunosorbent assay of MMP-1 in conditioned medium showed that treatment of U937 cells with 100 microg/mL of CRP for 24 hour led to a 3- to 5-fold increase in MMP-1 secretion. CRP also markedly stimulated MMP-1 release from human monocyte-derived macrophages. In contrast, CRP had no effect on tissue inhibitor of metalloproteinase-1 (TIMP-1) secretion. Northern blot showed that CRP upregulated MMP-1 mRNA expression. Collagenase activity assay showed that CRP increased collagen-degrading activity in cell-conditioned medium. Furthermore, results showed that the stimulation of MMP-1 secretion by CRP was inhibited by anti-CD32, but not by anti-CD64 antibody, and by mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) inhibitor PD98059. Finally, Western blot showed that CRP stimulated phosphorylation of extracellular signal-regulated kinase. CONCLUSIONS: This study demonstrates that CRP stimulates MMP-1 expression by U937 cells through FcgammaRII and extracellular signal-regulated kinase pathway. These findings suggest that CRP may promote matrix degradation and thus contribute to plaque vulnerability.