Unfractionated heparin and coronary artery stenting
*E-mail: howard.dent{at}ekht.nhs.ukEditor—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 the heparin regime was not subject to randomization in the study design. We believe, however, that this is further evidence of ‘heparin rebound’—a period of hypercoagulability after 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 infarction.3 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 because of the short half-life of UFH. Ischaemic events in Theroux and colleagues’ study5 were clustered around a median time of 9.5 h 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.
Kent, UK
Editor—Dent and Lekic relate in their letter to an important topic, namely hypercoagulability with adverse events after discontinuation of unfractionated heparin. In our study1 we observed the majority of ischaemic events clustered around day 0 or 1 after surgery. We think it is reasonable to assume that the above phenomenon contributes to the overall high rate of events—as does postoperative hypercoagulability without earlier heparin administration. Certainly, neither effect can be proven by our study and remains speculation. Additionally, we emphasize that despite >80% of the study population taking antiplatelet drugs until the day before surgery, the rate of ischaemic events was high. More and more evidence is mounting that we need standardized tests to adequately monitor and titrate anticoagulant and antiplatelet drugs on an individual basis in the perioperative scenario.
Graz, Austria
E-mail: Martin.vicenzi{at}meduni-graz.at
References
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[Abstract]
3 Di Tano G and Mazzu A. Early reactivation of ischaemia after abrupt discontinuation of heparin in acute myocardial infarction. Br Heart J 1995; 74:131–3
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; 91:1929–35
5 Theroux P and 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; 97:251–6
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