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Antiplatelet Therapy
with the risk of thrombotic events, especially if the patient has recently normal platelet function. The situation is slightly different according
undergone stent implantation. In the latter case, acute thrombotic to which GPIIb/IIIa inhibitors have been administered. Small molecules
events can occur in the first five days following withdrawal of active (tirofiban and eptifibatide) are rapidly cleared by the renal route, with
treatment leading to catastrophic complications, but the risk may the result that their effects may disappear within four to eight hours
persist for up to one month.
2
after interruption of therapy. However, with abciximab longer
inhibition of platelet function can be anticipated after interruption
Protamine sulphate is a specific inhibitor of unfractionated heparin of treatment.
(UFH), but it has little or no impact on the factor Xa inhibitors. Low-
When active bleeding has been brought under control, anticoagulant
and antiplatelet therapy can be resumed, but not until at least
24 hours have elapsed since the last episode of bleeding. In cases
It is now evident that bleeding has a
of gastrointestinal bleeding linked to peptic ulcer, re-introduction of
antiplatelet therapy, particularly aspirin, needs to be associated with
strong impact on outcome in terms of
proton pump inhibitors.
excess risk of death, myocardial
Conclusion
infarction and stroke.
Until recently, bleeding was considered to be inherent to the
therapeutic approach required to treat ACS patients. However, it is
now evident that bleeding has a strong impact on outcome in terms of
excess risk of death, MI and stroke at 30 days and in the long term.
molecular-weight heparin (LMWH) is only partly inhibited by Blood transfusion may also have a deleterious effect. The exact
protamine sulphate. For fondaparinux recombinant factor VII is the mechanisms by which bleeding and blood transfusion exert their
only possible treatment, but it is particularly costly. deleterious effects are to date only partially elucidated. The
interruption of active therapy and activation of coagulation and
It is impossible to reverse antiplatelet activity, since both aspirin and inflammation in cases of bleeding, the depletion of 2,3DPG and NO in
clopidogrel are irreversible platelet inhibitors. Only the regeneration preserved blood and the stimulation of immunological reactions after
of platelets, whose turnover rate is about 10–20% per day, can transfusion may potentially be explanations. Prevention of bleeding
normalise platelet function. In cases of active bleeding the only has now become equally important as prevention of further ischaemic
possibility is platelet transfusion, although there is no firm evidence or events in patients suffering from ACS. The risk factors for bleeding are
recommendations for the optimal usage or dosage in this context.
23
well-known and should be taken into account in the choice of
appropriate drugs and procedures. In this regard, careful attention
In case of active or acute bleeding occurring under GPIIb/IIIa inhibitor should be paid to use of drugs or drug combinations and dosages that
therapy, the only possibility of returning platelet function to normal is may favour bleeding. Similarly, a radial approach should be favoured
by platelet transfusion. As mentioned above, again there is no firm over a femoral approach if an invasive strategy is required.
evidence of the efficacy of this procedure and no guidelines exist to Furthermore, renal function should be taken into account, as it is a
stipulate optimum levels of platelets to transfuse in order to restore major contributor to bleeding risk. ■
1. Rao SV, Eikelboom JA, Granger CB, et al., Bleeding and blood 9. Granger CB, Goldberg RJ, Dabbous O, et al., Predictors of other strategies for guiding allogeneic red blood cell transfusion,
transfusion issues in patients with non-ST-segment elevation hospital mortality in the global registry of acute coronary events, Cochrane Database Syst Rev, 2002:CD002042.
acute coronary syndromes, Eur Heart J, 2007;28:1193–1204. Arch Intern Med, 2003;163:2345-53. 18. Hebert PC, Wells G, Blajchman MA, et al., A multicenter,
2. Eikelboom JW, Mehta SR, Anand SS, et al., Adverse impact of 10. Nikolsky E, Mehran R, Dangas G, et al., Development and randomized, controlled clinical trial of transfusion requirements in
bleeding on prognosis in patients with acute coronary syndromes, validation of a prognostic risk score for major bleeding in patients critical care. Transfusion Requirements in Critical Care
Circulation, 2006;114:774–82. undergoing percutaneous coronary intervention via the femoral Investigators, Canadian Critical Care Trials Group, N Engl J Med,
3. Rao SV, Jollis JG, Harrington RA, et al., Relationship of blood approach, Eur Heart J, 2007;28:1936–45. 1999;340:409–17.
transfusion and clinical outcomes in patients with acute coronary 11. Subherwal S, Bach RG, Chen AY, et al., Baseline Risk of Major 19. Hebert PC, Yetisir E, Martin C, et al., Is a low transfusion
syndromes, JAMA, 2004;292:1555–62. Bleeding in Non-ST-Segment Elevation Myocardial Infarction: The threshold safe in critically ill patients with cardiovascular
4. Rao SV, O’Grady K, Pieper KS, et al., Impact of bleeding severity CRUSADE Bleeding Score, submiitted. diseases?, Crit Care Med, 2001;29:227–34.
on clinical outcomes among patients with acute coronary 12. Wiviott SD, Braunwald E, McCabe CH, et al., Prasugrel versus 20. Stone GW, Witzenbichler B, Guagliumi G, et al., Bivalirudin
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88 INTERVENTIONAL CARDIOLOGY
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