Urinary cysteinyl leukotrienes in one-year follow-up of percutaneous transluminal angioplasty for peripheral arterial occlusive disease

Abstract

Background and aimsTreatment of severe peripheral arterial occlusive disease requires percutaneous revascularization. However, little is known about risk factors or predictors for reocclusion/restenosis. Cysteinyl leukotrienes are highly bioactive lipid mediators of inflammation. Their intravascular production may take place in the atheromatous plaque or result from interaction within activated leukocyte-platelet aggregates. MethodsWe prospectively measured urinary leukotriene E4, the main end-metabolite of cysteinyl leukotrienes in a group of 179 subjects with peripheral artery occlusive disease of the lower extremities. At the enrollment to the study, 22.9% had angioplasty and the remaining had angioplasty with stent implantation. During 12-month follow-up, 29.6% developed reocclusion/restenosis despite a standard pharmacotherapy. We evaluated treatment outcomes at 1, 3, 6 and 12-month follow-up visits, along with urinary leukotriene E4 excretion. ResultsDuring the study period, we observed a linear increase of urinary leukotriene E4 excretion only in subjects whose lower limb ischemia worsened. Moreover, elevated leukotriene E4 in urine was found only in subjects who developed reocclusion/restenosis. This was significant not only as a coincidence at the time of the follow-up visit, but leukotriene E4 elevation preceded clinical manifestation of reocclusion/restenosis. ConclusionsOur results demonstrated that serial measurements of urinary leukotriene E4 allowed to predict failure of angioplasty with/or without stent implantation for peripheral artery occlusive disease. However, to prove causality between cysteinyl leukotrienes overproduction and occlusive lower limb ischemia, a clinical trial with leukotrienes modifying drugs would be required.