Circulation: Intracoronary STEMI abciximab efficacious in primary PCI
Intracoronary bolus administration of abciximab in primary PCI is superior to standard intravenous treatment with respect to infarct size, extent of microvascular obstruction and perfusion, according to the July 1 issue of Circulation.

Holger Thiele, MD, from the University of Leipzig in Germany, and colleagues randomized the patients undergoing primary PCI to either intracoronary (77 patients) or intravenous (77 patients) bolus abciximab (ReoPro from Eli Lilly) administration with subsequent 12-hour intravenous infusion.

The authors wrote that the primary endpoint was infarct size and extent of microvascular obstruction as assessed by delayed enhancement MR. Secondary endpoints were ST-segment resolution at 90 minutes, thrombolysis in MI (TIMI) flow and perfusion grades after PCI and the occurrence of major adverse cardiac events within 30 days.

The researchers found that the median infarct size was 15.1 percent in the intracoronary versus 23.4 percent in the intravenous group.

Similarly, the investigators found that the extent of microvascular obstruction was significantly smaller in intracoronary compared with intravenous abciximab patients. Myocardial perfusion measured as early ST-segment resolution was significantly improved in intracoronary patients with an absolute ST-segment resolution of 77.8 percent versus 70 percent, the authors wrote.

Thiele and colleagues said the TIMI flow after PCI was not different between treatment groups, but there was a trend toward an improved perfusion grade in the intracoronary group?. They also noted a trend toward a lower major adverse cardiac event rate after intracoronary versus intravenous abciximab application (5.2 vs. 15.6 percent).

The researchers concluded that the “beneficial effects of intracoronary abciximab administration might be explained by the high local doses, which may facilitate the diffusion of the antibody to platelets inside the flow-limiting thrombus, thus resulting in improved dissolution of thrombi and microemboli at the ruptured plaque and further downstream in the microcirculation.”