Clinical outcomes comparing eptifibatide and abciximab in ST elevation acute myocardial infarction patients undergoing percutaneous coronary interventions.

BACKGROUND: Randomized clinical trials comparing glycoprotein IIb-IIIa inhibitors have largely excluded patients with ST segment elevation myocardial infarction (STEMI). METHODS: We conducted an open-label, sequential comparison of in-hospital and 6-month clinical outcomes in STEMI patients receiving eptifibatide or abciximab as adjunctive therapy during percutaneous coronary intervention (PCI). Registry data were collected and compared for STEMI patients undergoing PCI and receiving eptifibatide or abciximab over a 3.5-year period. Six-month follow-up, using telephone interviews, included major adverse cardiac events and functional status. RESULTS: Baseline characteristics were similar for patients receiving eptifibatide (n = 294) or abciximab (n = 158). No significant differences in hospital clinical outcomes were observed for reinfarction (2 vs. 3% for eptifibatide and abciximab, respectively), repeat revascularization (3 vs. 4%), bleeding complications (8 vs. 12%), congestive heart failure (5 vs. 3%), cerebrovascular accidents (0 vs. 2%), renal failure (2 vs. 3%), and all-cause mortality at discharge (5 vs. 4%). No significant difference was seen between groups in all-cause mortality at 6 months (6.5 vs. 6.4%; hazard ratio 0.976; 95% confidence interval 0.43-2.23; log-rank, p = 0.95). CONCLUSIONS: No significant differences were observed in clinical outcomes between STEMI patients receiving eptifibatide or abciximab in the setting of PCI. Considering the substantially lower cost of eptifibatide, these data suggest that eptifibatide can be substituted for abciximab to lower overall medication costs while maintaining beneficial safety and efficacy effects.

Regional intracoronary analgesia during percutaneous transluminal coronary angioplasty.

The ischemic pain associated with balloon inflation during coronary angioplasty remains a significant source of procedural discomfort and sets a limit on the duration of percutaneous transluminal intravascular interventions. The present study examined whether intracoronary lidocaine reduced the pain of coronary angioplasty. Sixteen patients undergoing elective coronary angioplasty underwent three 90 sec balloon inflations: the first with administration of no intracoronary agent, and the second and third with administration of one or the other of placebo or an equal volume of lidocaine (10-16 mg). Placebo or lidocaine were randomized in administration sequence and were given just before balloon inflation. During the occlusions, pain was scored on an ordinal scale (0 = no pain; 10 = most severe pain). Lidocaine delayed the onset of pain (23 +/- 4 vs. 48 +/- 7 sec, P < 0.005) and reduced its magnitude (at end-inflation: 7.8 +/- 1.3 vs. 3.2 +/- 1.3, P < 0.01). There were no significant hemodynamic or electrophysiologic effects in this group of patients, although atrioventricular conduction was delayed when lidocaine was administered into the epicardial coronary which had the atrioventricular node artery as a branch. Intracoronary analgesia with lidocaine is safe and effective in a select group of patients with normal ventricular function undergoing elective coronary angioplasty.