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- Antiplatelet therapy
- drug eluting stents
- surgery-coronary bypass
- coronary intervention
Antiplatelet agents are one of the cornerstones of primary and secondary prevention of stable and unstable coronary artery disease (CAD), and are especially important after percutaneous coronary interventions (PCIs).1 More than two million PCIs are performed annually in western Europe and North America. Currently, over 90% of all PCIs involve the placement of coronary stents, and drug eluting stents are used for a variety of indications. The prevalence of CAD and thereby also of acute coronary syndromes (ACS) is expected to increase dramatically in the next decade due to the progressive ageing of the population.
Stent thromboses are rare but potentially fatal complications after coronary stent implantation.2 Different factors have been identified that independently correlate with the risk for stent thromboses, such as PCI in small vessels or coronary bifurcations and comorbidities like diabetes mellitus or renal failure.2 3 The most important risk factor, however, is premature cessation of dual antiplatelet therapy with aspirin and a thienopyridine.2 The latter has gained in importance considerably in recent years with the use of drug eluting stents, since when increased rates of late stent thromboses (<30 days after implantation) have been reported.
Recent reports suggest that 5% of patients who underwent PCI will also have to undergo non-cardiac or cardiac surgery within the first year after coronary stenting.4 This subset of patients presents cardiologists, surgeons, and anaesthetists with the problem of having to decide between the risk of increased blood loss when continuing the antiplatelet agents in the perioperative period, and the risk of stent thrombosis if the drugs are stopped abruptly and prematurely.
This article aims to balance the individual risks of these patients and to offer a practical approach for daily clinical practice.
Aspirin and clopidogrel: pharmacological mechanisms and indications
Aspirin exerts its antiplatelet effects by irreversibly acetylating serine 529 of cyclooxygenase-1 (COX-1), resulting …
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