The problem of persistent platelet activation in acute coronary syndromes and following percutaneous coronary intervention

Clin Cardiol. 2008 Mar;31(3 Suppl 1):I17-20. doi: 10.1002/clc.20363.

Abstract

Platelets play a central role in the atherosclerotic inflammatory response, thrombotic vascular occlusion, microembolization, vasoconstriction, and plaque progression. Persistent platelet activation poses a serious problem among patients with acute coronary syndromes (ACS) and those who have undergone percutaneous coronary intervention (PCI), placing them at risk for ischemic events and subacute stent thrombosis. Patients undergoing PCI are at risk for further ischemic events because of procedure-related platelet activation as well as the inherent persistent platelet hyperreactivity and enhanced thrombin generation associated with ACS. Persistent platelet activation following an acute coronary event and/or PCI supports incorporating antiplatelet strategies into the standard medical management of such patients. In this clinical setting, antiplatelet therapies are capable of improving outcomes. Aspirin, thienopyridines, and glycoprotein IIb/IIIa inhibitors, the 3 major pharmacologic approaches to persistent platelet activation, target various levels of the hemostatic pathways and thrombus formation.

Publication types

  • Review

MeSH terms

  • Acute Coronary Syndrome / blood
  • Acute Coronary Syndrome / therapy*
  • Angioplasty, Balloon, Coronary / adverse effects*
  • Aspirin / therapeutic use
  • Humans
  • Platelet Activation / drug effects*
  • Platelet Aggregation Inhibitors / therapeutic use*
  • Platelet Glycoprotein GPIIb-IIIa Complex / antagonists & inhibitors
  • Pyridines / therapeutic use
  • Thrombosis / blood
  • Thrombosis / etiology
  • Thrombosis / prevention & control*

Substances

  • Platelet Aggregation Inhibitors
  • Platelet Glycoprotein GPIIb-IIIa Complex
  • Pyridines
  • thienopyridine
  • Aspirin