If you wish to respond to a paper or other item already published in the BJA, please go to the abstract/full text version of that item and click on the link "E-Letters: Submit a response to the article".
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E-letters: Electronic letters published:
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Risk of surgery after coronary stent replacement
- Emmanouil S. Brilakis (8 August 2006)
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Patient and stent characteristics may important for antiplatelet therapy discontinuation
- Ashish Aneja (8 August 2006)
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Re: Unfractionated heparin and coronary artery stenting
- Martin N Vicenzi (13 July 2006)
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Unfractionated heparin and coronary artery stenting
- Howard Dent, Zeljka Lekic (27 June 2006)
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Emmanouil S. Brilakis, Interventional Cardiology University of Texas Southwestern Medical School, Dallas Texas
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We read with great interest the well-written paper by Vicenzi and colleagues, which provides useful information on a very commonly asked but poorly studied question: what is the risk of surgery after coronary stent placement. We would like to ask for some clarifications of the study findings that could help us better interpret the results: 1. The main message of the study is that there was a very high incidence of events after surgery. Many events were considered as the primary outcome of the study, such as cardiac events, bleeding, surgical events, sepsis. Even though all events are important, the main concern and question that most clinicians and especially cardiologists have is how many patients had stent thrombosis in the perioperative period. Stent thrombosis is a highly morbid complication of stent implantation with high mortality. As described by the authors stent thrombosis definitely occurred in the 8 patients who had re-PCI. Did all 5 deaths occur in those patients? How early after surgery did stent thrombosis occur in those 8 patients? Were they receiving dual or single antiplatelet therapy in the perioperative period? Would an alternative interpretation of the study findings be: “The risk of documented stent thrombosis in the study was 8%”, a risk that would be very close to the report by Wilson et al (3.8- 7.1%) and significantly less than the report by Kaluza et al (32%)? 2. A large number of events (22 events) were myocardial cell injury (we assume that those patients did not have other criteria to allow classification as acute myocardial infarction). How large was the enzyme rise in those patients? Did any of them die? Even though no enzyme elevation is desirable, a very small increase in markers of cardiac necrosis may not always be due to myocardial infarction, and may not always be associated with worse clinical outcomes. 3. Even though most events occurred in the early postoperative period, some events occurred late after several months from surgery (median follow-up after surgery was 399 days). How many events occurred >1 month after surgery? Would conclusions change if those events were excluded from the analysis? Patients with coronary artery disease receiving stents often have recurrent events, which may not necessarily be linked to surgery. Stent thrombosis several days after surgery in a patient who was not restarted on aspirin and clopidogrel may be the result of inadequate antiplatelet therapy. Again, we would like to thank the authors for their timely contribution. Conflict of Interest:None declared |
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Ashish Aneja, Physician Cleveland Clinic, Cleveland, OH, USA
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Dear Editor, I read with great interest the research article by Vicenzi et al (1) in the June issue of the BJA. There are several important questions that the authors have not addressed in this important study. While the proportion of drug-eluting stents (DES) in Europe may be 50-60%, almost 90% patients in the US currently receive DES. This obviously poses an important dilemma for physicians and anesthesiologists from the standpoint of preoperative discontinuation of dual antiplatelet therapy. The authors fail to report the exact number of patients in their study with DES and their outcomes in comparison to those with bare metal stents (BMS). While the authors list this as one of their shortcomings, additional effort should have been undertaken to determine stent type and outcomes for different stent types. The authors also seem to have used a suboptimal dose of enoxaparin (at least 1mg/kg/day as opposed to full dose enoxaparin 1mg/kg/twice a day) as a perioperative "bridge" strategy. The smaller dose may have been used because of a perceived elevation in the risk of post-operative hemorrhage. However, perioperative "bridging" therapy with full dose enoxaparin has been shown to be safe and effective in high-risk patients who need "bridging", for e.g., atrial fibrillation and prior stroke, mitral prosthetic cardiac valves etc. The safety and efficacy of a perioperative "bridging" with heparin and related compounds has never been studied in the stent population and requires evaluation in a randomized clinical trial setting. Such a strategy is not likely to be very effective because of the suboptimal effect of heparin and related compounds upon platelet aggregability, which leads to stent thrombosis, a rare yet often lethal complication. A more reasonable and possibly more effective "bridging" strategy (which has never been studied or validated) could be the use of GpIIb/IIIa inhibitors, which specifically target platelets. 1) M. N. Vicenzi, T. Meislitzer, B. Heitzinger, M. Halaj, L. A. Fleisher, and H. Metzler. Coronary artery stenting and non-cardiac surgery—a prospective outcome study Br. J. Anaesth. 2006; 96: 686-693 Conflict of Interest:None declared |
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Martin N Vicenzi Department of Anesthesiology and Intensive Care, Medical University Graz, Austria
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Dent et al relate in their letter to an important topic, namely hypercoagulability with adverse events after discontinuation of unfractionated heparin. In the study "Coronary artery stenting and non- cardiac surgery" (1) we observed the majority of ischemic events clustered around day zero or one after surgery. We think it is reasonable to assume, that above phenomenon contributes to the overall high rate of events - as does postoperative hypercoagulability without prior heparin administration. Certainly neither effect can be proven by above study (1) and remains speculation. Additionally we emphasise that despite more than 80% of the study population took antiplatelet drugs until the day before surgery, the rate of ischemic events was high. More and more evidence is mounting that we desperately need standardized tests to adequately monitor and titrate anticoagulatory and antiplatelet drugs on an individual basis in the perioperative scenario. (1) Coronary artery stenting and non-cardiac surgery;a prospective outcome study. M. N. Vicenzi, T. Meislitzer, B. Heitzinger, M. Halaj, L. A. Fleisher, and H. Metzler. Br. J. Anaesth. 2006; 96: 686-693 Conflict of Interest:None declared |
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Howard Dent Kent & Canterbury Hospital, Zeljka Lekic
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Editor – we read with interest Vicenzi and colleagues’1 paper concerning coronary artery stenting and non-cardiac surgery. We were concerned by the high cardiac complication rate they reported, particularly in patients receiving unfractionated heparin (UFH) as a component of their anticoagulant regime (14 patients out of 16) compared with low molecular weight heparin (LMWH) (32 out of 87). The authors, while noting this association, warn against interpreting this as a significant effect as heparin regime was not subject to randomisation in the study design. We believe, however, that this is further evidence of “heparin rebound” – a period of hypercoagulability following abrupt cessation of an infusion of UFH. This can be associated with ischaemic events when UFH is used in the management of unstable angina2 and myocardial infarction3. This effect has been attributed to an increase in thrombin activity4 and activation of platelets5 during UFH infusion which persist for many hours after cessation of infusion, whilst the protective anticoagulant effects decline rapidly due to the short half life of UFH. Ischaemic events in Theroux and colleagues’ study were clustered around a median time of 9.5 hours after cessation of UFH – was there any temporal relationship between UFH administration and cardiac events in the authors’ study? LMWH which has a longer half life than UFH and does not activate platelets is not associated with an increase in ischaemic events and should, perhaps, be considered the drug of choice in this setting. 1 Vicenzi MN, Meislitzer T, Heitzinger B et al. Coronary artery stenting and non-cardiac surgery – a prospective outcome study. Br J Anaesth 2006;96:686-93 2 Theroux P, Waters D, Lam J et al. Reactivation of unstable angina after the discontinuation of heparin. N Engl J Med 1992;327:141-5 3 Di Tano G, Mazzu A. Early reactivation of ischaemia after abrupt discontinuation of heparin in acute myocardial infarction. Br Heart J 1995;74:131-133 4 Granger CB, Miller JM, Bovill EG et al. Rebound increase in thrombin generation and activity after cessation of intravenous heparin in patients with acute coronary syndromes. Circulation 1995;91:1929-1935 5 Theroux P, Xiao Z. Platelet activation with unfractionated heparin at therapeutic concentrations and comparisons with a low-molecular-weight heparin and with a direct thrombin inhibitor. Circulation 1998;97:251-256 Conflict of Interest:None declared |
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