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PlasmaThe Non-cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Fibrinogen is a large glycoprotein (340 kDa) that is produced by the liver and has an important role in blood coagulation. Its plasma concentration is 1.5–4 g/L. It has two critical functions in haemostasis. In its soluble form, it acts as a ligand for activated glycoprotein IIb/IIIa receptors on platelets and forms cross-bridges for aggregation. When cleaved by thrombin, fibrinogen is converted to fibrin, which polymerizes into an insoluble form that stabilizes the haemostatic plug and provides a meshwork for clot propagation.
Intravenous anti-platelet therapy—GP IIb/IIIa blockers and cangrelor
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Shraddha Ranjan, Gagandeep Singh Wander
The activation of the GP IIb/IIIa receptor is one of the final steps in platelet activation, building platelet–fibrinogen complexes. Glycoprotein IIb/IIIa inhibitors block the adhesion of fibrinogen to the activated platelet by competing with the von Willebrand factor and fibrinogen, preventing the platelet aggregation and adhesion. Abciximab, tirofiban and eptifibatide are intravenous GP IIb/IIIa inhibitors that are available for use [15].
Emergencies
Published in Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson, Pocket Prescriber Psychiatry, 2019
Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson
Consider (consult local protocol/cardiology on-call if unsure): Glycoprotein IIb/IIIa inhibitor: Especially if not thrombolysed (CI or presentation too late) or PCI planned and still unstable. Use with caution (especially <48 h post-thrombolysis).Rescue PCI: Especially if thrombolysis given and chest pain persists for ≥90 min or non-resolving or worsening (e.g. ≤50% reduction in) ST elevation on ECG.
Antiplatelet therapy for coronary artery disease in 2023: current status and future prospects
Published in Expert Review of Cardiovascular Therapy, 2023
Rishi Chandiramani, Alessandro Spirito, James W. Johnson, Adhya Mehta, Birgit Vogel, Robert T. Faillace, Roxana Mehran
Glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitors are potent inhibitors of platelet aggregation that are administered intravenously. In the past, use of these agents was widespread in patients presenting with ACS; indeed, GPIIb/IIIa inhibitors enable rapid inhibition of platelet aggregation until the full effect of oral antiplatelet agents is achieved. In recent years, however, the development of rapidly acting P2Y12 inhibitors and increased awareness about the high rates and prognostic impact of bleeding after administration of GPIIb/IIIa inhibitors have led to a progressive decrease in the use of these agents. Current guidelines recommend using GPIIb/IIIa inhibitors only as ‘bailout’ strategy in ACS patients with high thrombotic burden with no-reflow phenomenon or thrombotic complications during PCI, or as a bridge before surgery in patients at very high ischemic risk (e.g. coronary stenting <1 month before surgery) [38,39]. Dose of GPIIb/IIIa inhibitors should be adapted based on concomitant anticoagulation treatment and renal function. New compounds not yet available for clinical use [e.g. revacept (a competitive antagonist to platelet glycoprotein VI), conformation-specific GP inhibitors, outside-in signaling GP inhibitors or platelet-targeted CD39 protein derivatives] may have a limited impact on bleeding rates while providing effective platelet inhibition [40,41].
Systemic immune-inflammation index predicts no-reflow phenomenon after primary percutaneous coronary intervention
Published in Acta Cardiologica, 2022
Kerim Esenboğa, Alparslan Kurtul, Yakup Yunus Yamantürk, Türkan Seda Tan, Durmuş Eralp Tutar
Perioperative essential medications followed clinical guidelines [3]. The application of an angiotensin converting enzyme inhibitor or angiotensin II receptor antagonist, beta blockers and statins, and the types and doses were determined by the coronary intensive care cardiologists according to the patient’s condition. The use of glycoprotein IIb/IIIa inhibitors was planned by the operator according to the patient’s clinical condition. The use of other peri-procedural medications such as intracoronary nitroglycerine and adenosine was also left to the discretion of the operator. All echocardiographic measurements were made within 24 h after the procedures, using a GE ViVidE7 ultrasound machine (GE Healthcare, Piscataway, USA) with a 3.5-MHz transducer. Left ventricular ejection fraction (LVEF) was measured using the Simpson method according to the recommendations of the American Society of Echocardiography.
Tackling the gap in platelet inhibition with oral antiplatelet agents in high-risk patients undergoing percutaneous coronary intervention
Published in Expert Review of Cardiovascular Therapy, 2021
Piera Capranzano, Dominick J. Angiolillo
GPIs provide fast and potent antiplatelet effects by competing with von Willebrand factor and fibrinogen for the glycoprotein IIb/IIIa receptor binding to inhibit the final pathway of platelet aggregation. Three types of GPI are approved for clinical use (abciximab, eptifibatide, and tirofiban). Concerns on increased bleeding and no clear evidence of significant additional efficacy, especially in combination with more potent and fast-acting oral P2Y12 inhibitors [66], have led guidelines to restrict GPI use for bail-out circumstances, such as the presence of a large thrombus burden, poor coronary flow after stenting, distal embolization, or thrombotic complications [39, 67]. However, in contemporary practice, the use of GPI as bolus with or without a short (2 hours) infusion has been proposed to achieve high level of platelet inhibition during high-risk PCI while bridging the delayed onset of action of oral P2Y12 inhibitors.