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In reference to what is the optimal perioperative management of antiplatelet therapy?
Author(s) -
Partington Erin,
Woodworth Bradford A.,
Harrigan Mark R.
Publication year - 2016
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1002/lary.25968
Subject(s) - otorhinolaryngology , medicine , head and neck surgery , neurosurgery , general surgery , library science , surgery , computer science
We read the article by Shah and Lalwani titled, “What Is the Optimal Perioperative Management of Antiplatelet Therapy?” with interest. Antiplatelet therapy has become more common in recent years, largely due to the expanding use of stents in the coronary circulation, as well as the carotid arteries, intracranial arteries, and peripheral circulation. As a result, otolaryngologists are undertaking surgical procedures in patients with stents who are on long-term antiplatelet therapy with increasing frequency. Surgeons must balance the risk of bleeding complications due to the presence of antiplatelet agents against the risk of thromboembolic events due to platelet activation by the stent in the absence of antiplatelet therapy. This report purported to summarize the consequences of continuing or interrupting antiplatelet therapy in the perioperative period. Unfortunately, the analysis was incomplete and led the authors to an incorrect conclusion. Specifically, we object to a statement made halfway through the article: “In otolaryngological procedures with low bleeding risk, aspirin continuation may be safe, but until stronger evidence is gathered, the most conservative recommendation is to interrupt aspirin.” First, although the single evidentiary table (Table 1) in the report summarizes the risk of bleeding on single or dual antiplatelet therapy with noncardiac surgery, a similar attempt at systematic analysis of the risk of thromboembolic complications during interruption of antiplatelet therapy, particularly in patients with stents, is absent. In the randomized trial cited in Table I, patients with coronary stents comprised less than 10% of the subjects; the results of this study, therefore, cannot be applied to all patients with stents. Second, this report did not consider patients with carotid, vertebral, or intracranial artery stenosis and/or stents. Anecdotally, we have observed ischemic strokes in two patients with intracranial stents for whom antiplatelet therapy was held for endoscopic sinus procedures. Antiplatelet interruption has been associated with heightened risk of ischemic stroke and intracranial stent thrombosis. Third, the authors convey an overly simplistic view of decision making in this setting. For instance, an array of risk factors for coronary stent thrombosis have been identified, and recently introduced flowdiverting stents for the treatment of intracranial aneurysms have a large metallic surface area and require more prolonged antiplatelet therapy compared to other stents. In summary, we argue that the determination of thromboembolic risk with interruption of antiplatelet agents in patients with stents is complex. The decision to withhold antiplatelet agents for surgery should not be unilateral, and instead should be made jointly with the physician or service that placed the stent.