• Interventional Techniques & Devices
• Cardiology Clinical Trials
• Myocardial Infarction

• Interventional Techniques & Devices
• Cardiology Clinical Trials
• Myocardial Infarction
• Cardiology

The risk of subacute (≤30 days) stent thrombosis (ST) is high after primary percutaneous intervention (PCI) for STEMI. HORIZONS-AMI [The Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction; Dangas GD et al. Circulation. 2011], EUROMAX [European Ambulance Acute Coronary Syndrome (ACS) Angiography Trial; Clemmensen P et al. J Am Coll Cardiol. 2014], and HEAT-PPCI [How Effective Are Antithrombotic Therapies in Primary Percutaneous Coronary Intervention; Shahzad A et al. Lancet. 2014] trials demonstrated an increased risk of acute ST (<24 hours) in patients treated with bivalirudin vs heparin with or without a platelet glycoprotein IIb/IIIa inhibitor (GPI).

George D. Dangas, MD, PhD, Mount Sinai Medical Center, New York, New York, USA, presented the results of a pooled analysis of the international, open-label HORIZONS-AMI and EUROMAX trials. The aim of the analysis was to determine the independent predictors for subacute ST and evaluate mortality after ST according to the antithrombotic therapy used for primary PCI. Patient data from both trials were pooled and analyzed. In both trials, patients were randomized to either bivalirudin or heparin ± GPI.

A total of 5800 patients with STEMI treated with primary PCI was included in the analysis. The baseline and procedural characteristics were similar in the bivalirudin and heparin ± GPI groups. Early ST occurred in 100 patients (1.7%), 20 (20%) of whom died within 30 days. A 1-day landmark analysis of early ST incidence (within 30 days) found an ST event rate of 1.3% in the bivalirudin group vs 0.2% in the heparin ± GPI group during the first 24 hours (P < .0001). There were no statistically significant differences in the incidence of ST after the first 24 hours up to 30 days in those patients treated with bivalirudin (0.9%) when compared with heparin ± GPI (1.2%; P = .271) groups.

A 4-hour landmark analysis demonstrated that the ST event rate was only significantly higher in the bivalirudin group (0.94%) vs the heparin ± GPI group during the first 4 hours (P < .0001). From 4 to 24 hours, the ST event rate was 0.32% in the bivalirudin group vs 0.17% in the heparin ± GPI group (P = .2675).

The 30-day mortality rate for patients with acute ST was 2.8% in the bivalirudin group vs 16.7% in the heparin ± GPI group (P = .14). The 30-day mortality rate for patients with subacute ST was 12.0% in the bivalirudin group vs 44.1% in the heparin ± GPI group (P = .01). The 30-day mortality rate for all early ST was 6.7% with bivalirudin and 40% with heparin ± GPI (P < .0002).

Preprocedural TIMI flow of 0 or 1 predicted acute ST (OR 2.35; 95% CI 1.04 to 5.35; P = .041). Killip Class ≥ II during acute MI predicted subacute ST (OR 3.19; 95% CI 1.70 to 5.60; P < .0003).

The excess risk of ST associated with bivalirudin compared with heparin ± GPI occurred only in the acute phase on day 1 and more specifically during the first 4 hours after primary PCI. The mortality rate associated with subacute ST was higher than with acute ST. Thirty-day mortality after early ST was significantly lower in patients treated with bivalirudin than those treated with heparin ± GPI. These results were consistent for both acute and subacute ST.

• © 2014 MD Conference Express®