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Intracoronary STEMI abciximab effective with PCI
8 July 2008
MedWire News: Intracoronary abciximab may improve early measures of infarct size more than standard intravenous treatment among patients with ST-elevation myocardial infarction (STEMI) who undergo primary percutaneous coronary intervention (PCI), an open-label trial indicates.
The findings come from the Randomized Leipzig Immediate PCI Abciximab IV Versus IC in STEMI Trial, in which 154 STEMI patients were assigned to either 0.25 mg/kg bodyweight intracoronary or intravenous abciximab before PCI, followed by a 12-hour intravenous infusion.
Overall, 83% of the intracoronary group and 77% of the intravenous group received bolus administration before PCI.
The primary endpoint was median infarct size and extent of microvascular obstruction assessed by delayed enhancement magnetic resonance imaging a median of 2 days after the index event.
Median infarct size was significantly smaller in the intracoronary than intravenous abciximab group, at 15.1% versus 23.4% of the left ventricle (LV), respectively (p=0.01).
Similarly, the extent of microvascular obstruction was smaller in patients receiving intracoronary rather than intravenous treatment, with early imaging figures, for example, of 1.1% versus 3.4% of the LV, respectively (p=0.01).
The secondary endpoint of ST-segment resolution at 90 minutes was also superior in the intracoronary than intravenous group, at a corresponding 77.8% versus 70.0% (p=0.006).
There was also a trend toward improved myocardial perfusion grades with intracoronary treatment, and a significantly lower combined incidence of death, MI, urgent revascularization, and heart failure compared with intravenous treatment, at 5.2% versus 15.6%, respectively (p=0.06).
"These 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," conclude Holger Thiele (University of Leipzig, Germany) and colleagues in the journal Circulation.
