Role of cytokines in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty

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Abstract
Background Inflammatory cytokines play an important role in mediating inflammatory/proliferative responses including atherosclerosis. However, their role in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) remains to be clarified. Objective To determine plasma levels of inflammatory cytokines as well as cytokine-generation capacities of monocytes before PTCA and after the follow-up period. Methods Plasma levels of cytokines in 34 consecutive patients before and 3–6 months after PTCA were measured by enzyme-linked immunosorbent assay. We measured the plasma levels of macrophage-colony-stimulating factor (MCSF) and transforming growth factor-β. Cytokine-generation capacities of monocytes were also measured by a whole-blood induction method with lipopolysaccharide. The levels of cytokines measured for assessment of the capacities included those of interleukin-1α, interleukin-1β, interleukin-6, granulocyte-colony-stimulating factor, tumor necrosis factor-α and interferon-γ. Results Plasma levels of MCSF in patients without restenosis (n  = 20) decreased significantly (from 1460 ± 138 μg/ml before PTCA to 1039 ± 125 μg/ml after the follow-up period, P  < 0.01), whereas those in patients with restenosis (n  = 14) increased significantly (from 1107 ± 105 μg/ml before PTCA to 1039 ± 125 μg/ml after the follow-up period, P  < 0.05). We noted a positive correlation between the increase in plasma levels of MCSF and the extent of loss of lumen by restenosis. Cytokine-generation capacities of monocytes for interleukin-1α and interleukin-1β of patients with restenosis significantly increased but those of patients without restenosis did not. Furthermore, plasma levels of C-reactive protein decreased significantly only in patients without restenosis after the follow-up period. Conclusions These results suggest that inflammatory changes mediated by cytokines may be involved in the pathogenesis of restenosis after PTCA.

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