Clinical Review ABC of interventional cardiology

Interventional pharmacotherapy

BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7405.43 (Published 03 July 2003) Cite this as: BMJ 2003;327:43
  1. Roger Philipp, fellow in interventional cardiology,
  2. Ever D Grech, consultant cardiologist, assistant professor
  1. the Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada.
  2. the Health Sciences Centre and St Boniface Hospital, the University of Manitoba, Winnipeg.

    Introduction

    The dramatic increase in the use of percutaneous coronary intervention has been possible because of advances in adjunctive pharmacotherapy, which have greatly improved safety. Percutaneous intervention inevitably causes vessel trauma, with disruption of the endothelium and atheromatous plaque. This activates prothrombotic factors, leading to localised thrombosis; this may impair blood flow, precipitate vessel occlusion, or cause distal embolisation. Coronary stents exacerbate this problem as they are thrombogenic. For these reasons, drug inhibition of thrombus formation during percutaneous coronary intervention is mandatory, although this must be balanced against the risk of bleeding, both systemic and at the access site.

    Action of antiplatelet and antithrombotic agents in inhibiting arterial thrombosis

    Coronary artery thrombosis

    Platelets are central to thrombus formation. Vessel trauma during percutaneous intervention exposes subendothelial collagen and von Willebrand factor, which activate platelet surface receptors and induce the initial steps of platelet activation. Further platelet activation ultimately results in activation of platelet glycoprotein IIb/IIIa receptor—the final common pathway for platelet aggregation.

    View this table:

    Vascular injury and membrane damage also trigger coagulation by exposure of tissue factors. The resulting thrombin formation further activates platelets and converts fibrinogen to fibrin. The final event is the binding of fibrinogen to activated glycoprotein IIb/IIIa receptors to form a platelet aggregate.

    Understanding of these mechanisms has led to the development of potent anticoagulants and antiplatelet inhibitors that can be used for percutaneous coronary intervention. Since the early days of percutaneous transluminal coronary angioplasty, heparin and aspirin have remained a fundamental part of percutaneous coronary intervention treatment. Following the introduction of stents, ticlopidine and more recently clopidogrel have allowed a very low rate of stent thrombosis. More recently, glycoprotein IIb/IIIa receptor antagonists have reduced procedural complications still further and improved the protection of the distal microcirculation, especially in thrombus-containing lesions prevalent in acute coronary syndromes.

    Antithrombotic therapy

    Unfractionated heparin and low molecular weight heparin

    Unfractionated heparin is a heterogeneous mucopolysaccharide that …

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