BACKGROUND: Rotational atherectomy with the Rotablator catheter has improved percutaneous treatment of certain coronary atherosclerotic lesions, but the "no-reflow" phenomenon remains a serious complication. Because platelet activation by rotablation may contribute to the no-reflow phenomenon, we developed an in vitro system to test the effect of rotablation on platelets in the absence or presence of platelet GP IIb/IIIa receptor blockade with abciximab. METHODS AND RESULTS: Platelet-rich plasma (PRP) was prepared from 28 healthy human volunteers. PRP was divided into 4 samples: (1) no treatment, (2) 6D1 (anti-GP Ib), (3) c7E3 Fab (anti-GP IIb/IIIa+alpha(v)beta3), and (4) c7E3 Fab+6D1. Samples were pumped through a flow chamber containing a 2.5-mm burr rotating at various speeds and then placed in an aggregometer. PRP samples tested in the absence of antibody underwent more rapid and extensive aggregation when rotablated at 150000 and 180000 rpm compared with 0 rpm (P<0.001 at both speeds). Preincubation of platelets with c7E3 Fab decreased the slope of aggregation at each rotablation speed, with 98%, 79%, and 71% reductions at 70000, 150000, and 180000 rpm, respectively (P=0.09 for 70000 and P<0.001 for both 150000 and 180000 rpm). Preincubation of platelets with 6D1 did not decrease the slope of aggregation at any rotablation speed (P>0.5, P=0.99, and P=0.091 for 70000, 150000, and 180000 rpm). Platelet ATP release, a marker of granule release and cell damage, was markedly increased at 180000 rpm (P=0.002 compared with 0 rpm in the control group). Electron microscopy revealed extensive rotablation-induced platelet damage at 150000 and 180000 rpm, and leakage of LDH confirmed platelet lysis at these speeds (P=0.002 and P<0.001 compared with 0 rpm). CONCLUSIONS: High-speed rotablation induces platelet activation of PRP, leading to aggregation; pretreating PRP with abciximab decreases the aggregation. These data suggest that pretreatment of patients with abciximab may decrease rotablation-induced platelet aggregation during rotational atherectomy.
BACKGROUND: Rotational atherectomy with the Rotablator catheter has improved percutaneous treatment of certain coronary atherosclerotic lesions, but the "no-reflow" phenomenon remains a serious complication. Because platelet activation by rotablation may contribute to the no-reflow phenomenon, we developed an in vitro system to test the effect of rotablation on platelets in the absence or presence of platelet GP IIb/IIIa receptor blockade with abciximab. METHODS AND RESULTS: Platelet-rich plasma (PRP) was prepared from 28 healthy human volunteers. PRP was divided into 4 samples: (1) no treatment, (2) 6D1 (anti-GP Ib), (3) c7E3 Fab (anti-GP IIb/IIIa+alpha(v)beta3), and (4) c7E3 Fab+6D1. Samples were pumped through a flow chamber containing a 2.5-mm burr rotating at various speeds and then placed in an aggregometer. PRP samples tested in the absence of antibody underwent more rapid and extensive aggregation when rotablated at 150000 and 180000 rpm compared with 0 rpm (P<0.001 at both speeds). Preincubation of platelets with c7E3 Fab decreased the slope of aggregation at each rotablation speed, with 98%, 79%, and 71% reductions at 70000, 150000, and 180000 rpm, respectively (P=0.09 for 70000 and P<0.001 for both 150000 and 180000 rpm). Preincubation of platelets with 6D1 did not decrease the slope of aggregation at any rotablation speed (P>0.5, P=0.99, and P=0.091 for 70000, 150000, and 180000 rpm). Platelet ATP release, a marker of granule release and cell damage, was markedly increased at 180000 rpm (P=0.002 compared with 0 rpm in the control group). Electron microscopy revealed extensive rotablation-induced platelet damage at 150000 and 180000 rpm, and leakage of LDH confirmed platelet lysis at these speeds (P=0.002 and P<0.001 compared with 0 rpm). CONCLUSIONS: High-speed rotablation induces platelet activation of PRP, leading to aggregation; pretreating PRP with abciximab decreases the aggregation. These data suggest that pretreatment of patients with abciximab may decrease rotablation-induced platelet aggregation during rotational atherectomy.
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