Mortality with Paclitaxel-Coated Devices in Peripheral Artery Disease.

BACKGROUND: The results of a recent meta-analysis aroused concern about an increased risk of death associated with the use of paclitaxel-coated angioplasty balloons and stents in lower-limb endovascular interventions for symptomatic peripheral artery disease. METHODS: We conducted an unplanned interim analysis of data from a multicenter, randomized, open-label, registry-based clinical trial. At the time of the analysis, 2289 patients had been randomly assigned to treatment with drug-coated devices (the drug-coated-device group, 1149 patients) or treatment with uncoated devices (the uncoated-device group, 1140 patients). Randomization was stratified according to disease severity on the basis of whether patients had chronic limb-threatening ischemia (1480 patients) or intermittent claudication (809 patients). The single end point for this interim analysis was all-cause mortality. RESULTS: No patients were lost to follow-up. Paclitaxel was used as the coating agent for all the drug-coated devices. During a mean follow-up of 2.49 years, 574 patients died, including 293 patients (25.5%) in the drug-coated-device group and 281 patients (24.6%) in the uncoated-device group (hazard ratio, 1.06; 95% confidence interval, 0.92 to 1.22). At 1 year, all-cause mortality was 10.2% (117 patients) in the drug-coated-device group and 9.9% (113 patients) in the uncoated-device group. During the entire follow-up period, there was no significant difference in the incidence of death between the treatment groups among patients with chronic limb-threatening ischemia (33.4% [249 patients] in the drug-coated-device group and 33.1% [243 patients] in the uncoated-device group) or among those with intermittent claudication (10.9% [44 patients] and 9.4% [38 patients], respectively). CONCLUSIONS: In this randomized trial in which patients with peripheral artery disease received treatment with paclitaxel-coated or uncoated endovascular devices, the results of an unplanned interim analysis of all-cause mortality did not show a difference between the groups in the incidence of death during 1 to 4 years of follow-up. (Funded by the Swedish Research Council and others; ClinicalTrials.gov number, NCT02051088.).

Increased vascular injury reduces the degree of intimal hyperplasia following angioplasty in rabbits.

BACKGROUND/AIMS: Formation of intimal hyperplasia following angioplastic procedures can lead to complications, including restenosis and accelerated atherosclerosis. The vessel wall media is a main source of neointimal cells. However, evidence suggests that there are additional cell sources, such as the adventitia. Here we investigate whether an extensive loss of vascular smooth muscle cells (VSMCs) in the media results in less intimal hyperplasia or if there is compensatory cell recruitment from the adventitia. METHODS: A balloon catheter was pulled through the rabbit carotid artery 4 times (major injury) or 2 times (minor injury). Adventitial cells were labeled with 5-bromo-2-deoxyuridine or PKH26. RESULTS: The major injury, but not the minor injury, resulted in a complete loss of VSMCs in large parts of the media and significant leukocyte infiltration. The major injury resulted in less neointima compared with the minor injury. The thinnest neointima was seen at the most injured parts of the media in the major injury group. Cell-tracking experiments showed that the media, but not the adventitia, served as a source of neointimal cells. CONCLUSION: An augmented angioplastic injury with extensive VSMC loss in rabbits reduced the degree of intimal hyperplasia. No compensatory recruitment of neointimal cells from the adventitia occurred.

Endovascular management of acute bleeding arterioenteric fistulas.

The objective of this study was to review the outcome of endovascular transcatheter repair of emergent arterioenteric fistulas. Cases of abdominal arterioenteric fistulas (defined as a fistula between a major artery and the small intestine or colon, thus not the esophagus or stomach), diagnosed over the 3-year period between December 2002 and December 2005 at our institution, were retrospectively reviewed. Five patients with severe enteric bleeding underwent angiography and endovascular repair. Four presented primary arterioenteric fistulas, and one presented a secondary aortoenteric fistula. All had massive persistent bleeding with hypotension despite volume substitution and transfusion by the time of endovascular management. Outcome after treatment of these patients was investigated for major procedure-related complications, recurrence, reintervention, morbidity, and mortality. Mean follow-up time was 3 months (range, 1-6 months). All massive bleeding was controlled by occlusive balloon catheters. Four fistulas were successfully sealed with stent-grafts, resulting in a technical success rate of 80%. One patient was circulatory stabilized by endovascular management but needed immediate further open surgery. There were no procedure-related major complications. Mean hospital stay after the initial endovascular intervention was 19 days. Rebleeding occurred in four patients (80%) after a free interval of 2 weeks or longer. During the follow-up period three patients needed reintervention. The in-hospital mortality was 20% and the 30-day mortality was 40%. The midterm outcome was poor, due to comorbidities or rebleeding, with a mortality of 80% within 6 months. In conclusion, endovascular repair is an efficient and safe method to stabilize patients with life-threatening bleeding arterioenteric fistulas in the emergent episode. However, in this group of patients with severe comorbidities, the risk of rebleeding is high and further intervention must be considered. Patients with cancer may only need treatment for the acute bleeding episode, and an endovascular approach has the advantage of low morbidity.