Author + information
- Marc Bonaca,
- Mark Creager,
- Jeffrey Olin,
- Benjamin Scirica,
- Erin Bohula,
- Sabina Murphy,
- Eugene Braunwald and
- David Morrow
Vorapaxar inhibits protease–activated receptor 1 expressed on platelets and vascular endothelium and reduces ischemic events and revascularization. We investigated whether the reduction in peripheral revascularization with vorapaxar was consistent in patients with polyvascular disease.
TRA2°P–TIMI 50 was a randomized, placebo controlled trial of vorapaxar in 26,449 stable pts with prior MI, PAD, and CVD. We evaluated the rates of subsequent peripheral (limb) revascularization and bleeding with vorapaxar compared with placebo stratified by the number of diseased vascular beds.
Rates of ischemic events (CV death/MI/Stroke) at 3 years increased with the number of symptomatic vascular beds (7.8% one, 14.7% two, 21.7% three). The rate of peripheral revascularization increased with the number of diseased vascular beds (Fig A) and was reduced consistently by vorapaxar (overall HR 0.79, p<0.001, p–interaction = 0.17). Vorapaxar also decreased subsequent limb revascularizations in pts who qualified with MI or stroke and were not known to have PAD at the time of randomization (HR 0.60, 95% CI 0.39–0.91, p=0.017). Bleeding increased with diseased vascular beds (Fig B) and was consistently increased with vorapaxar (p–interaction = 0.49, Fig B)
The rate of peripheral revascularization and bleeding is associated with the number of diseased vascular beds. Vorapaxar reduces peripheral revascularization regardless of known PAD or number of diseased vascular beds.
West, Room 3005
Saturday, March 09, 2013, 8:30 a.m.–8:45 a.m.
Session Title: Vascular Medicine: New Insights in Arterial Disease
Abstract Category: 35. Vascular Medicine: Non Coronary Arterial Disease
Presentation Number: 911–5
- 2013 American College of Cardiology Foundation