Aspirin for Prevention of Cardiovascular Events in a General Population Screened for a Low Ankle Brachial Index: A Randomized Controlled Trial

Abstract

Conclusion:There are no ruptures after open repair for abdominal aortic aneurysm (AAA) and a low rate of rupture after endovascular aneurysm repair (EVAR). Mortality after graft rupture is high. Few ruptures after EVAR are spontaneous, with most having had complications identified during surveillance.Summary: Aneurysm rupture after EVAR is well recognized, and endograft rupture has high mortality (Schlosser FJV, Eur J Vas Endovasc Surg 2009;37:15-22). Graft-related complications after EVAR are frequent. Certain types of endograft complications (endoleak types I and III, stent graft disintegration and migration) increase the risk of aneurysm rupture (Fransen GA, Eur J Vas Endovasc Surg 2003;26:487-93). The authors analyzed the patients in the United Kingdom (UK) EVAR trials to assess the rate and factors associated with rupture after EVAR or open repair of AAA.Up to July 2009, 848 elective EVARS and 594 elective open AAA repairs had been performed in the UK EVAR Trials 1 and 2. Patients were followed-up for complications, reinterventions, and rupture. Incidence of rupture was analyzed with respect to baseline anatomy and subsequent complications in a Cox regression analysis model.No ruptures occurred in patients treated with open repair, but 27 ruptures occurred after EVAR during a mean follow-up of 4.8 years, for a crude rate of 0.7 ruptures/100 person-years (95% CI, 0.5-1.0). Of patients who developed endograft rupture, 67% died Յ30 days of rupture. Five ruptures occurred in the first 30 postoperative days and 22 after that; crude rates of rupture were 7.2 (95% CI, 3.0-17.4) and 0.6/100 person-years (95% CI, 0.4-0.9). Previous complications (endoleak type I, type II with sac expansion, type III, migration or kinking) increased the risk of rupture, with a hazard ratio of 8.83 (95% CI, 3.76-20.76; P Ͻ .0001).Comment: EVAR is a form of management of AAA and not a cure for AAA. As such, patients must be continually monitored for complications associated with potential rupture of an endograft-managed AAA. Patients with rupture fall into roughly three groups. Those who have a rupture in the perioperative EVAR period likely reflect inadequate initial isolation of the aneurysm. A small group of patients rupture with reasonable compliance with recommended surveillance. This suggests complications associated with EVAR that occur after a negative surveillance study can rapidly lead to rupture. Most ruptures, however, occur in patients with an identified problem with their endograft. Sac expansion was documented in 15 of 17 in this group. Rupture after EVAR can be minimized by ensuring that before leaving the hospital, the patients have had technically satisfactory procedures and that sac expansion is evaluated, diagnosed, and aggressively treated.

Efficacy and Safety of Aspirin in Patients With Peripheral Vascular Disease: An Updated Systematic Review and Meta-Analysis of Randomized Controlled Trials

“…For both the primary efficacy and safety outcomes, sensitivity analyses were conducted by excluding the largest trial [10], for low risk of bias trials, for trials explicitly reporting patients with no prior history of an ischemic event (i.e. stroke or MI), and for placebo-controlled trials only.…”

“…A final number of 11 trials reporting outcomes in patients with PDV were included in the analysis [10,[21][22][23][24][25][26][27][28][29][30] (Fig 1).…”

“…Three trials had multiple comparison arms and thus only the aspirin and placebo arms were included [23,25,26]. Three trials were multicenter and reported outcomes exclusively in patients without prior history of an ischemic event (including prior stroke or MI) [10,21,22], and 4 trials included low-dose aspirin ( 325mg per day) [10,21,22,24]. All of the trials included chronic stable PVD patients except one trial [25] that assessed the use of aspirin in setting of acute lower limb ischemia.…”

“…At the individual study level, two trials were considered to have low risk of bias assessed with use of the Cochrane risk of bias tool [10,21]. One trial was considered to have high risk of bias [22], and the remaining trials had unclear risk due to lack of reporting of detailed methods (S4 Table).…”

“…One reason for the disparate results of these meta-analyses is the heterogeneity of patients enrolled in the studies as well as the inclusion of studies with other antiplatelet agents, such as cilostazol or clopidogrel, as comparators. More recently, the Aspirin for Asymptomatic Atherosclerosis (AAA) trial, one of the largest randomized control trials on this topic, also failed to show a statistically significant reduction in vascular events in asymptomatic patients with PVD, adding more to the current debate [10]. Furthermore, the Examining Use of Ticagrelor in Peripheral Artery Disease (EUCLID) trial compared ticagrelor to clopidogrel in symptomatic PVD patients and failed to show any reduction in cardiovascular events with ticagrelor, questioning the general concept of antiplatelet therapy in those patients [11].…”