One of the first reports of thrombosis of a drug-eluting stent after discontinuation of anti-platelet therapy was by Murphy and Fahy from the Department of Anesthesiology at the University of Kentucky(1). (Patients on clopidogrel status post intracoronary placement of (a) drug-eluting stent(s) are asked to stop taking the drug 7 -10 before surgery to prevent postoperative bleeding). Since then, there has been a myriad of other reports(2) plus the relase of an AHA/ACC/SCAI statement on the prevention of premature discontinuation of clopidogrel and aspirin by internists, surgeons and dentists(3).
Drug-eluting stents were supposed to solve the problem of neo-intimal hyperplasia and in-stent thrombosis seen with bare-metal stents. It has slowly become apparent that the drug-eluting stents may have a problem with arterial healing characterized by fibrin deposition and poorer endothelialization (4).
From Joner M, Finn AV, Farb A, et al. Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk. J Am Coll Cardiol 2006;48:193-202
This translates to a potent thrombogenic surface and the neccesity to take anti-platelet agents till this risk is clinically insignificant. At the moment, some recommendations are for 12 months of dual anti-platelet therapy(3), a far cry from the 6 months initially recommended. And it does not look like there is a real idea of how long this thrombogenic risk is clinically significant.
Since the FDA-approvals of the sirolimus-eluting stent in 2003 and the paclitaxel-eluting one in 2004, a lot of these stents have been placed. Over one million were placed in 2004. (5). With a number of these patients presenting for some surgical procedure or the other in the next few years, the risk of perioperative in-stent thrombosis is a real problem. Why? Because the perioperative period is usually a era of higher thrombogenicity, discontinuation of antiplatelet therapy exposes patients to a higher risk of in-stent thrombosis which can be fatal.
The problem is, there are still lots of surgeons, primary care physicians, dentists, anesthesiologists and even cardiologists who are unaware of this risk. It becomes imperative on all anesthesia caare providers to be vigilant and be the point of last resort for these patients. It is helpful to have institutional guidelines as to how to deal with patients who have stopped taking their clopidogrel and aspirin. Seeing these patients in the pre-op clinic will help prepare them for surgery with the right advice.
If both plavix and aspirin have been stopped, the patient can be given both of them immediately preoperatively – after consulting with the surgeon, of course. The recommendation is to continue at least the aspirin (3). Moreover, recent data shows that the risk of in-stent thrombosis is much greater danger than that of bleeding (6).
References:
1. Murphy JT, Fahy BG. Thrombosis of sirolimus-eluting coronary stent in the postanesthesia care unit. Anesth Analg.101(4):971-3.
2. McFadden EP et al. Late thrombosis in drug-eluting coronary stents after discontinuation of antiplatelet therapy. Lancet. 2004:29;3649444):1519-21.
3. Grines CL et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. J Am Coll Cardiol. 2007 Feb 13;49(6):734-9.
4. Joner M, Finn AV, Farb A, et al. Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk. J Am Coll Cardiol 2006;48:193-202
5. Rosamond W, Flegal K, Friday G, et al. Heart disease and stroke statistics — 2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007;115:e69-e171.
6. Chassot, P. G. et al. Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction. BJA. 99 (3): 316-28 (2007)

