Related Experiment Video
Updated: Sep 30, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Administration of glycoprotein IIb-IIIa inhibitors in patients with ST-segment elevation myocardial infarction
Paul P Dobesh1, Jennifer B Kasiar
1Division of Pharmacy Practice, St. Louis College of Pharmacy, Missouri 63110, USA.
Abstract:
Patients with ST-segment elevation acute myocardial infarction require immediate reperfusion therapy. Reperfusion therapy can be provided by either pharmacologic or mechanical means. Pharmacologic reperfusion therapy consists of administering fibrinolytics, whereas mechanical reperfusion consists of performing percutaneous intervention, usually with stent placement. Each approach has been shown to decrease mortality, but each has disadvantages in establishing flow in the infarct-related artery. Regardless of the approach, during an acute myocardial infarction, activation and externalization of glycoprotein (GP) IIb-IIIa receptors occur on the surface of platelets. The GP IIb-IIIa inhibitors block the binding of fibrinogen to these platelet receptors. These inhibitors have been investigated in combination with both reperfusion strategies. The goal of adding GP IIb-IIIa inhibitor therapy to either reperfusion approach is to obtain better early, complete, and sustained reperfusion. Subsequently, this should lead to better clinical outcomes for patients with ST-segment elevation acute myocardial infarction. Although no mortality benefit has been seen with the addition of GP IIb-IIIa inhibitor therapy, ischemic complications have been reduced significantly.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Myocarditis III: Medical Management
Acute Coronary Syndrome I: Introduction
Angina IV: Management
Myocarditis IV: Nursing Management
