PARIS – Antithrombotic therapy with bivalirudin for primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction may have been unfairly tarnished as having a high stent thrombosis rate, according to a large, prospective, observational cohort study.
A new analysis from the Swedish Coronary Angiography and Angioplasty Registry (SCAAR) showed similarly low stent thrombosis rates within 30 days following primary PCI for STEMI regardless of whether the antithrombotic regimen involved bivalirudin (Angiomax), heparin only, or a glycoprotein IIb/IIIa inhibitor, Dr. Per Grimfjard reported at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.
Bruce Jancin/Frontline Medical News
Dr. Per Grimfjard
The SCAAR analysis captured all STEMI patients undergoing primary PCI in Sweden from 2007 through mid-2014. These data reflect real-world interventional practice in Sweden and elsewhere, where bivalirudin is typically administered in a prolonged infusion to protect against early stent thrombosis. In contrast, the randomized trials that linked bivalirudin to high stent thrombosis rates featured protocols in which the drug was stopped immediately after the procedure, noted Dr. Grimfjard, an interventional cardiologist at Uppsala (Sweden) University.
“These are nationwide Swedish numbers, and they are complete. We think the numbers are reassuring in that respect,” he said.
Session chair Dr. Andreas Baumbach said the Swedish data are consistent with his own experience in using bivalirudin in primary PCI for STEMI.
“The headline last year was that bivalirudin has a high stent thrombosis rate. It made the newspapers everywhere. But we never saw that, and we always thought that the difference might be in how we used the drug. There’s a new headline now, that this high stent thrombosis rate is not seen in clinical practice. The practice differs from the randomized trials, and the outcomes differ as well,” observed Dr. Baumbach, professor of interventional cardiology at the University of Bristol (England).
In SCAAR, the 30-day rate of definite, angiographically proven stent thrombosis was 0.84% in 16,860 bivalirudin-treated patients, 0.94% in 3,182 who got heparin only, and 0.83% in 11,216 glycoprotein IIb/IIIa inhibitor recipients. These numeric differences weren’t statistically significant.
All-cause mortality 1 year post-PCI was 9.1% in patients with no stent thrombosis, 16.1% in those who experienced stent thrombosis within 1 day post PCI, and 23.0% in those whose stent thrombosis occurred on days 2-30. Dr. Grimfjard speculated that the explanation for the numerically higher 1-year all-cause mortality rate in patients whose stent thrombosis occurred on days 2-30 as opposed to day 0-1 is probably that they were more likely to have left the hospital when stent thrombosis occurred. That would translate to a longer time to repeat revascularization, hence a larger MI, more heart failure and arrhythmia, and thus a higher long-term risk of death.
Several audience members commented that they weren’t sure what to make of the observational Swedish data because of the looming presence of several potential confounders. For one, clinical practice trends changed considerably during the 7-year time frame of the study, as evidenced by the fact that the use of drug-eluting stents was far more common in bivalirudin-treated patients than in the glycoprotein IIb/IIIa inhibitor group. Also, Swedish cardiologists who put their STEMI patients on bivalirudin were more likely to utilize the more modern radial artery access in performing primary PCI; their practice may have differed from their colleagues’ in other, unrecorded ways as well, it was noted.
Dr. Grimfjard reported having no financial conflicts regarding the study, which was conducted free of commercial support.