Impact of Glycoprotein IIb/IIIa Inhibition in Contemporary Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the National Cardiovascular Data Registry.
OBJECTIVE
This study investigates the effects of glycoprotein IIb/IIIa inhibitors (GPIs) on outcomes after percutaneous coronary intervention (PCI).


BACKGROUND
Ischemic complications are reduced after PCI when a GPI is added to heparin. However, there are limited data on the safety and efficacy in contemporary PCI.


METHODS
We used the National Cardiovascular Data Registry CathPCI Registry data to assess the association between GPI use and PCI outcomes for acute coronary syndrome between July 2009 and September 2011. The primary outcome was all-cause in-hospital mortality. The secondary outcome was major bleeding. To adjust for potential bias, we used multivariable logistic regression, propensity-matched (PM) analysis, and instrumental variable analysis (IVA).


RESULTS
There were 970,865 patients included; 326,283 (33.6%) received a GPI. Unadjusted mortality and major bleeding were more common with a GPI (2.4% vs. 1.4% and 3.7% vs. 1.5%, respectively; p < 0.001 for both). In contrast, GPI use was associated with lower mortality on adjusted analyses; relative risks range from 0.72 (95% confidence interval [CI]: 0.50 to 0.97) with IVA to 0.90 (95% CI: 0.86 to 0.95) with PM. The association of GPI use with bleeding remained in adjusted analyses (multivariable relative risk: 1.93, 95% CI: 1.83 to 2.04; PM relative risk: 1.83, 95% CI: 1.74 to 1.92; and IVA relative risk: 1.53, 95% CI: 1.27 to 2.13). Subgroup analysis revealed enhanced risk reduction with ST-segment elevation myocardial infarction, high predicted mortality, and heparin-based anticoagulation.


CONCLUSIONS
In unselected acute coronary syndrome patients undergoing PCI, GPI use was associated with reduced in-hospital mortality and increased bleeding. In the modern era of PCI, there may still be a role for the judicious use of GPIs.
Saint Luke's Mid America Heart Institute, Kansas City, Missouri; University of Missouri-Kansas City, Kansas City, Missouri. Electronic address: dsafley@saint-lukes.org.
David M
DM
Safley
Department of Biomedical & Health Informatics, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
Lakshmi
L
Venkitachalam
Saint Luke's Mid America Heart Institute, Kansas City, Missouri.
Kevin F
KF
Kennedy
Saint Luke's Mid America Heart Institute, Kansas City, Missouri; University of Missouri-Kansas City, Kansas City, Missouri.
David J
DJ
Cohen
D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis / Q000401:mortality / Q000628:therapy*; D000925:Anticoagulants / Q000627:therapeutic use; D002423:Cause of Death; D016009:Chi-Square Distribution; D006470:Hemorrhage / Q000139:chemically induced; D006493:Heparin / Q000627:therapeutic use; D017052:Hospital Mortality; D006801:Humans; D016014:Linear Models; D016015:Logistic Models; D015999:Multivariate Analysis; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000401:mortality; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors* / Q000378:metabolism; D057216:Propensity Score; D012042:Registries; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014481:United States
D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin
acute coronary syndrome; glycoprotein IIb/IIIa antagonist; myocardial infarction; percutaneous coronary intervention