Glycoprotein IIb/IIIa

This issue could further be addressed by using radial as opposed to femoral access when carrying out pPCI. A trial found that there was a reduced incidence of major bleeding and vascular site complication with a radial approach. Events occurring in 1.4% of those treated with radial approach and 7.2% P<0.0001 of those with femoral access with a reduction in the rate of net adverse clinical events (NACE) defined as “a composite of death, myocardial infarction, stroke, and major bleeding/vascular complications”

hemostasis, platelet aggregation and/or coagulation. 3 Eptifibatide is a cyclic heptapeptide which originated from a protein found in the venom of the southeastern pygmy rattlesnake (Sistrurus miliarus barbouri) and selectively blocks the platelet glycoprotein IIb/IIIa receptor. It belongs to the class of the so called arginin-glycin-aspartat-mimetics and reversibly binds to

with STEMI compared with UFH 3,8. However, bleeding reductions associated with bivalirudin therapy have occurred at the expense of increased rates of acute stent thrombosis 3,4,6,8. These trials have also varied in the proportion of use of glycoprotein IIb/IIIa-inhibitors (GPI) in the UFH arm, ranging from infrequent to moderate to obligatory 3-8. Given the association of GPI therapy with increased bleeding and reduced ischemia, it is nit clear whether observed differences between bivalirudin and

Acute coronary syndrome (ACS) refers to a group of conditions with clinical symptoms similar to acute myocardial ischemia, including pressure-like chest pain associated with nausea and sweating (1). It includes non-ST segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and unstable angina (UA). ACS patients are at increased risk of myocardial infarction and death, therefore, the moderate- to high-risk patients with ACS are treated with early cardiac

antiplatelet agents are efficient in containing ischemic events in relation to PCI, but have been noted to have higher rates of bleeding complications (4-10). Bivalirudin has shown to have a better safety profile when compared with heparin along with glycoprotein IIb/IIIa (GP) administration (11). Bivalirudin for this reason is considered the anticoagulant of choice in patients with ACS. Bivalirudin is a direct thrombin inhibitor (DTI) that is effective against clot-bound thrombin, unlike UFH and LMWHs (12)

In 2014, myocardial infarctions were the second lead cause of death in Northern Ireland, proceeded only by malignant neoplasms. (Department of Finance and Personnel. (2015) They occur as a result of an imbalance between the demand for oxygen and its supply by the coronary arteries. Indeed, MI’s can occur as a result of complications with anemia and heart spasms. However, the main cause of the condition is produced as a result of atheroma. Under normal physiological conditions platelets mediate

platelets, which result in easy bruising and nosebleeds, and was first described in 1918. Glanzmanns disease is a congenital hemorrhagic disorder, meaning it's a bleeding disorder present at birth. Glanzmanns disease results from not having enough glycoprotein, a protein usually found on the surface of blood platelets. Platelets are small blood cells that are the first responders in the case of a cut or injury, they normally clump together to form a plug in the wound and stopped bleeding. Glanzmanns

revascularisation can begin is of the utmost importance with the best results for pPCI coming between 0-2 hours, with faster fibrinolysis (1-2 hours) being as effective if pPCI was delayed beyond 3 hours. Improved pharmacological facilitation of pPCI with glycoprotein IIb/IIIa inhibitors has also led to improved outcome in patients, with some suggesting earlier administration leads to better outcomes, which goes against NICE guidelines and the possibility of pre-hospital fibrinolysis. Whilst further research is done

Is prasugrel as effective as clopidogrel for the patient with acute coronary syndrome? Acute coronary syndrome (ACS) is the most common form of cardiovascular disease.1 In 2006, about 733,000 ACS patients were discharged from hospitals costing the United States $150 billion annually.2 Eighty percent of these cases were either unstable angina (UA) or no ST- elevation myocardial infarction (NSTEMI), and the remaining 20% were ST-elevation myocardial infarction (STEMI). The pathophysiology of ACS

other activated platelets (52,53). The platelet clot formation afterwards undergoes the stabilization phase, wherein the platelets form a close network. Several receptors have been implicated in this process, including the previously mentioned GPIIb/IIIa-receptors as well as CD40 and its ligand (CD40L) (51). The final step in thrombus formation is the activation of the coagulation cascade with the deposition of fibrin to stabilize the thrombus. This process is started by exposure of tissue factor to