Intracoronary administration of abciximab acutely increases flow through culprit vessels of patients with acute coronary syndromes undergoing percutaneous coronary intervention.

Acutely Increases Flow Through Culprit Vessels of Patients With Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention To the Editor: We read with interest the article by Wöhrle et al1 reporting the reduction of major coronary events with the intracoronary compared with the intravenous administration of abciximab in patients with acute coronary syndromes undergoing percutaneous coronary interventions. Some cases of rapid reduction of coronary thrombus after intracoronary administration of abciximab have been previously reported. Yet, to date, it has not been determined whether such dethrombosis translates into an improvement of coronary blood flow. To address this issue, we have measured, before and after intracoronary abciximab (0.25 mg · kg ) administration, corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (CTFC) in a cohort of patients with acute coronary syndromes (acute ST-elevation myocardial infarction or IIIB Braunwald class unstable angina) referred to our catheterization laboratory for urgent percutaneous coronary intervention. To enter the analyses, patients had to have angiographic evidence of a culprit lesion with complex morphology defined as evident thrombus or ulceration. Ten patients matched these criteria and constituted the study population (7 males and 3 females, 62 12 years of age). All patients received standard doses of aspirin, heparin, and nitrates at the beginning of the procedure. CTFC was measured, according to Gibson and colleagues,2 in the culprit vessel (5 left anterior descending, 1 circumflex, 3 right coronary arteries, and 1 saphenous vein graft) and in the nonculprit vessel (only in the 6 patients with a target lesion located in the left coronary artery) before and after intracoronary administration of abciximab. Baseline CTFC was 25 16 in culprit vessels and 17 9 in nonculprit ones (P 0.08). CTFC in the culprit vessel significantly decreased from 25 16 before to 16 10 after intracoronary abciximab administration (P 0.024), whereas in the corresponding nonculprit vessel, no evidence of flow modification was observed (17 9 before and 16 11 after). The drop in CTFC was confined to the 6 patients with angiographically evident thrombus (from 35 13 before to 13 10 after abciximab administration, P 0.034). Three of these patients also exhibited an appreciable reduction in the haziness of the thrombotic lesion after intracoronary abciximab. Our angiographic data suggest that in patients with acute coronary syndromes, the reduction of angiographically evident thrombus obtained with intracoronary administration of abciximab translates into an acute improvement of coronary blood flow. This fits with, and extends, the findings of Wöhrle et al,1 who observed a more pronounced clinical benefit with intracoronary administration of abciximab in those patients with unpaired TIMI flow.