Stent thrombosis treatment

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Coronary stent thrombosis Microchapters

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Introduction

Definition

Epidemiology and Demographics

Relation to Bare Metal Stents
Relation to Drug Eluting Stents
Relation to Antiplatelet Medications

Pathophysiology

Risk Factors

Relationship to Discontinuation of Antiplatelet Therapy

Treatment

Complications

Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Smita Kohli, M.D.; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Stents are usually placed in the proximal segments of major epicardial vessels, hence in-stent thrombotic occlusion clinically present as severe ischemia or infarction[1].

Treatment

  • Emergent target lesion or target vessel revascularization is the treatment of choice in stent thrombosis to restore vessel patency.
  • Revascularization may be carried out by PCI or in some instances, thrombolytics if PCI is not available [2].
  • If revascularization is not successful, urgent CABG should be considered.

The Underlying Cause of Stent Thrombosis Should Guide Management

The probable cause for stent thrombosis should be evaluated as the treatment varies with etiology.

Modifiable Procedural Related Causes

While the patient is undergoing cardiac catheterization, a careful evaluation should be undertaken to exclude procedure related variables that could be amenable to further treatment such as:

  • Suboptimal stent expansion and poor apposition,
  • Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis[1].

Modifiable Clinical Risk Factors

Likewise, the patient should be questioned thoroughly for the following clinical risk factors for stent thrombosis:

  • Noncompliance with dual antiplatelet therapy,
  • Premature discontinuation of dual antiplatelet therapy

Clopidogrel Resistance: A Clinical Diagnosis of Exclusion

If neither angiographic, procedural nor clinical variables appear to play a role, then clopidogrel resistance should be considered. This diagnosis can of course be confirmed through platelet function testing and genetic testing. If this is the case consideration should be made to switching the patient to prasugrel.[3] The TIMI 38 or TRITON trial demonstrated that newer antiplatelet agents such as prasugrel[4] may be used after weighing the risks of bleeding against benefits of decreased recurrence of stent thrombosis/coronary events. Patients who present with stent thrombosis after completing the recommended duration of treatment with clopidogrel restarting clopidogrel 75 mg daily along with aspirin and continuing for a minimum of one year should be considered.

References

  1. 1.0 1.1 Cutlip DE, Baim DS, Ho KK, Popma JJ, Lansky AJ, Cohen DJ; et al. (2001). "Stent thrombosis in the modern era: a pooled analysis of multicenter coronary stent clinical trials". Circulation. 103 (15): 1967–71. PMID 11306525.
  2. Wenaweser P, Rey C, Eberli FR, Togni M, Tüller D, Locher S, Remondino A, Seiler C, Hess OM, Meier B, Windecker S (2005). "Stent thrombosis following bare-metal stent implantation: success of emergency percutaneous coronary intervention and predictors of adverse outcome". European Heart Journal. 26 (12): 1180–7. doi:10.1093/eurheartj/ehi135. PMID 15728650. Retrieved 2011-05-05. Unknown parameter |month= ignored (help)
  3. Montalescot G, Wiviott SD, Braunwald E, Murphy SA, Gibson CM, McCabe CH, Antman EM (2009). "Prasugrel compared with clopidogrel in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (TRITON-TIMI 38): double-blind, randomised controlled trial". Lancet. 373 (9665): 723–31. doi:10.1016/S0140-6736(09)60441-4. PMID 19249633. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)
  4. Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, Neumann FJ, Ardissino D, De Servi S, Murphy SA, Riesmeyer J, Weerakkody G, Gibson CM, Antman EM (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". The New England Journal of Medicine. 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. PMID 17982182. Retrieved 2010-06-30. Unknown parameter |month= ignored (help)

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