Could stent design affect platelet activation? Results of the Platelet Activation in Stenting (PAST) study

Platelet activation induced by coronary artery stenting may be related to stent design. In a prospective, randomized pilot study of 54 elective patients, platelet activation was analyzed before and at 2 hours, 24 hours, 5 days and 30 days post-implantation of either a closed-cell (NIR) or open-cell (TETRA) stent. Platelet activation was less following NIR implantation as indicated by reduced aggregation to 5 μmol adenosine diphosphate at 30 days (32.3 ± 6.1% versus 94.5 ± 18.9%; p = 0.02) and reduced expression of multiple surface markers (log mean fluorescence intensity): at 2 hours, CD 107a (22 ± 13 versus 18 ± 5; p = 0.045); at 24 hours, CD 31 (136 ± 48 versus 110 ± 48; p = 0.04), CD 151 (104 ± 45 versus 91 ± 31; p = 0.048), platelet leukocyte aggregates (95 ± 40 versus 77 ± 24; p = 0.018), and CD 107a (24 ± 12 versus 17 ± 4; p = 0.03); and at 30 days, CD 151 (99 ± 33 versus 81 ± 32; p = 0.03), platelet leukocyte aggregates (84 ± 35 versus 72 ± 31; p = 0.045) and PAC-1 (88 ± 91 versus 72 ± 30; p = 0.025). Ex vivo studies in explanted swine hearts revealed that the NIR stent produced less intimal prolapse and thus a smoother stent-vessel wall interface than the TETRA stent. In this pilot study, platelet activation was greater during the 30 days following implantation of an open-cell versus a closed-cell stent. This finding may be related to superior scaffolding, resulting in a smoother luminal contour after implantation of a closed-cell stent.