Smoking 10 or more cigarettes daily is associated with a reduced rate of intermediate-term restenosis after lower-limb endovascular interventions.
Smokers typically have elevated levels of carboxyhemoglobin and higher blood concentrations of carbon monoxide (11,12). Carbon monoxide has potent antiinflammatory and antiproliferative capacity, and it inhibits vascular smooth muscle cell proliferation after vascular injury due to balloon dilation (13–16). Furthermore, cigarette smoke extract induces necrosis in proliferating vascular smooth muscle cells (17). Localized proliferationof vascular smooth muscle cells is a key factor in luminal diameter decrease after endovascular treatment (18). On the basis of these findings, we hypothesized that smoking may protect vessels from restenosis after lower-limb endovascular interventions, presumably through the antiproliferative effect of increased carbon monoxide levels.
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