First experience with drug-eluting balloons in infrapopliteal arteries: restenosis rate and clinical outcome.

OBJECTIVES: The purpose of this study was to investigate the efficacy of drug-eluting balloons (DEBs) in the treatment of long infrapopliteal lesions with regard to the short-term restenosis rate and midterm clinical result. BACKGROUND: Restenosis rates of long-segment tibial artery disease are very high. Recently, a restenosis rate of 69% at 3 months after standard balloon angioplasty was demonstrated. METHODS: Infrapopliteal angioplasty was performed with a paclitaxel-eluting balloon (In.Pact Amphirion, Medtronic, Minneapolis, Minnesota). Clinical and angiographic follow-up was performed at 3 months to detect binary restenosis, and further clinical assessment was performed over a 12-month period thereafter. RESULTS: In 104 patients, 109 limbs were treated for critical limb ischemia (82.6%) or severe claudication (17.4%). Mean lesion length of the arteries treated was 176 ± 88 mm. Angiography studied in 84 treated arteries at 3 months showed a restenosis in 27.4% (19.1% had restenosis of more than 50%, and 8.3% were totally occluded) and usually occurred focally. Only in 9.5% of all angiographically followed up arteries was the entire treated segment restenosed or reoccluded. During a follow-up period of 378 ± 65 days, 1 patient was lost and 17 died. Of the 91 limbs remaining in the analysis, clinical improvement was present in 83 (91.2%). Complete wound healing occurred in 74.2%, whereas major amputation occurred in 4 patients, resulting in limb salvage of 95.6% for patients with critical limb ischemia. CONCLUSIONS: The early restenosis rate of long-segment infrapopliteal disease is significantly lower after treatment with DEBs compared with historical data using uncoated balloons. Randomized trials are required to show whether this difference will lead to improvement in clinical outcomes.

Angiographic patency and clinical outcome after balloon-angioplasty for extensive infrapopliteal arterial disease.

BACKGROUND AND OBJECTIVE: Restenosis-rate after balloon-angioplasty of long segment tibial arterial disease is largely unknown. We investigated the restenosis-rates angiographically in patients with critical limb ischemia (CLI) due to extensive infrapopliteal lesions. METHODS: Angioplasty for infrapopliteal lesions exclusively ≥80 mm in length was performed using dedicated 80-120 mm long low-profile balloons. Follow-up included angiography at 3 months and clinical assessment at 3 and 15 months. RESULTS: Angioplasty was performed in 77 infrapopliteal arteries of 62 limbs of 58 CLI patients with a Rutherford class 4 in 16 (25.8%) limbs and Rutherford class 5 in 46 limbs (74.2%). Average lesion length was 18.4 cm. Treated arteries were stenosed in 35.1% and occluded in 64.9%. After 3 months, a clinical improvement (marked reduction of ulcer-size or restpain) was seen in 47 (75.8%) limbs, 14 (22.6%) limbs were clinically unchanged and 1 (1.6%) limb showed a clinical deterioration. Angiography at 3 months showed no significant restenosis in 24 of 77 (31.2%) treated arteries, a restenosis ≥50% in 24 (31.2%) arteries and a reocclusion in 29 of 77 (37.6%). At 15 months death rate was 10.5%. After repeat angioplasty in case of restenosis cumulative clinical results at 15 months were minor amputations in 8.1%, no major amputations resulting in a limb-salvage rate of 100% with no patient requiring bypass surgery. CONCLUSIONS: Restenosis-rate after angioplasty of extensive infrapopliteal arterial disease is high and occurs early after treatment. Despite this the clinical results are excellent, especially given the length of the arterial segments diseased.

The pivotal role of scavenger receptor CD36 and phagocyte-derived oxidants in oxidized low density lipoprotein-induced adhesion to endothelial cells.

Adhesion of phagocytes to endothelial cells constitutes a crucial step in atherogenesis. Oxidized low density lipoproteins (LDL) are supposed to facilitate the adhesion process. We investigated the molecular mechanisms by which mildly and extensively hypochlorite-oxidized LDL force adhesion of murine macrophages and human neutrophils to human umbilical venous endothelial cells. After 1h of co-incubation of macrophages, endothelial cells, and lipoproteins adhesion significantly increased to 160+/-13% (S.E.M., n=5) in the presence of mildly oxidized lipoprotein, and 210+/-11% (S.E.M., n=5) in the presence of extensively oxidized lipoprotein. Similar results were obtained with neutrophils. CD36 antibody (FA6-152) significantly reduced adhesion to 102+/-7% (S.E.M., n=5) using mildly oxidized low density lipoprotein and to 179+/-16% (S.E.M., n=5) using extensively oxidized low density lipoprotein. Native high density lipoprotein and to a lesser extent methionine-oxidized high density lipoprotein significantly counteracted the effects of low density lipoprotein. Prior incubation of endothelial cells with modified lipoproteins followed by their removal and subsequent incubation with macrophages or neutrophils resulted in only minor changes of adhesion. This suggests that the direct contact of low density lipoprotein with phagocytes followed by activation of a respiratory burst with release of reactive oxygen species facilitates the adhesion process. Accordingly, the addition of antioxidants (superoxide dismutase and catalase) to the co-incubation medium was followed by a significant decrease in phagocyte adhesion. It is concluded that oxidized low density lipoprotein-induced respiratory burst activation of phagocytes with subsequent release of oxidants constitutes a crucial step in promoting the adhesion of phagocytes to endothelial cells.