Abstract
Several reports suggest that fractalkine (FKN) and its cognate receptor, CX3CR1, play a role in atherogenesis. Recent data showed that plasma FKN is elevated in patients with unstable angina pectoris and is more elevated with patients with plaque rapture. We assessed the hypothesis that plasma FKN might be elevated after stentimplantation and related to the plaque-characteristics. First of all we tested the time course of plasma FKN level 30-min., 3-hour, 6-hour and 12-hour after coronary stenting. Their levels are elevated at 30 min. after percutaneous coronary intervention (PCI) and maintained the level until 12-hour after PCI. Then we examined the plasma levels of FKN, IL-8 and IL-6 in fifty consecutive patients before and 12-hour after coronary stenting following in integrated backscatterintravascular ultrasound (IB-IVUS) analysis. The plasma IL-8 did not change 12-hour after stenting. Those of FKN and IL-6, however, were significantly elevated 12-hour after stenting (FKN: from 656 ± 122 pg/mL to 811 ± 177 pg/ mL, p<0.0001, IL-6: from 3.15 ± 3.42 pg/mL to 16.0 ± 15.0 pg/mL, p<0.0001). In IB-IVUS analysis the lipid volume and volume fraction were correlated with post-procedural FKN level (R2=0.29, p<0.0001; R2=0.22, p<0.0001), while they were not related with post-procedural IL-6 level. In conclusion, a local release of FKN and IL-6 occurs shortly after PCI, which is possibly related to plaque rapture and/or endothelial traumatism following stent-implantation. We have further shown that local release of FKN is evoked proportionally to the volume of the lipid-rich plaques which are prone to be ruptured. These suggested that anti-FKN treatment could be of benefit to decrease the amount of lipid-rich plaque.
Highlights
The leukocyte recruitment at all stages of atherosclerotic progression is a crucial feature, besides lipid deposition and vascular smooth muscle cell proliferation [1,2]
Angiography and IVUS measurements shows that target lesions were not long or complicated (Table 2)
Chemokines are inflammatory cytokines characterized by their ability to cause directed migration of leukocytes into inflamed tissue, and raised levels are found in atherosclerosis, both systemically and within the atherosclerotic plaques
Summary
The leukocyte recruitment at all stages of atherosclerotic progression is a crucial feature, besides lipid deposition and vascular smooth muscle cell proliferation [1,2]. The chemokine families are thought to contribute significantly to the pathogenesis of atherosclerosis. Fractakine (FKN) is the unique member of the CX3C chemokine subfamily because of its chemotactic and adhesive properties in the vessel-wall [3,4]. Previous studies have revealed that the rapture of plaques might play a critical role in the acute coronary syndrome (ACS), where the lipid-rich plaques affect the plaque vulnerability [5,6]. The integrated backscatter intravascular ultrasound (IB-IVUS) system, which provides two-dimensional color-coded maps for the tissue characterization of coronary plaques, has been widely used [6,7]. It was revealed that IB-IVUS could differentiate vulnerable plaques and predict acute coronary syndrome (ACS) [6,7,8]
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