Treatment of coronary stent thrombosis: Difference between revisions
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Varun Kumar (talk | contribs) (New page: {{SI}} {{CMG}} '''Associate Editor-In-Chief:''' Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S. {{EH}} ==Treatment of coronary stent thrombosis== Coronary stent thrombo...) |
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'''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S. | '''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S. | ||
Stents are usually placed in the proximal segments of major epicardial vessels, hence in-stent thrombotic occlusion clinically present as severe [[ischemia]] or [[STEMI|infarction]]<ref name="pmid11306525">{{cite journal| author=Cutlip DE, Baim DS, Ho KK, Popma JJ, Lansky AJ, Cohen DJ et al.| title=Stent thrombosis in the modern era: a pooled analysis of multicenter coronary stent clinical trials. | journal=Circulation | year= 2001 | volume= 103 | issue= 15 | pages= 1967-71 | pmid=11306525 | doi= | pmc= | url= }} </ref>. | |||
The probable cause | ==Management== | ||
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]] <ref name="pmid15728650">{{cite journal |author=Wenaweser P, Rey C, Eberli FR, Togni M, Tüller D, Locher S, Remondino A, Seiler C, Hess OM, Meier B, Windecker S |title=Stent thrombosis following bare-metal stent implantation: success of emergency percutaneous coronary intervention and predictors of adverse outcome |journal=[[European Heart Journal]] |volume=26 |issue=12 |pages=1180–7 |year=2005 |month=June |pmid=15728650 |doi=10.1093/eurheartj/ehi135 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=15728650 |accessdate=2011-05-05}}</ref>. | |||
*If revascularization is not successful, urgent [[CABG]] should be considered. | |||
*The probable cause for stent thrombosis should be evaluated as the treatment varies with etiology. The probable contributing factors are: | |||
**suboptimal stent apposition, | |||
**Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis<ref name="pmid11306525">{{cite journal| author=Cutlip DE, Baim DS, Ho KK, Popma JJ, Lansky AJ, Cohen DJ et al.| title=Stent thrombosis in the modern era: a pooled analysis of multicenter coronary stent clinical trials. | journal=Circulation | year= 2001 | volume= 103 | issue= 15 | pages= 1967-71 | pmid=11306525 | doi= | pmc= | url= }} </ref>. | |||
**premature discontinuation of dual [[antiplatelet]] therapy, | |||
**[[clopidogrel]] resistance. | |||
*If the patient develops stent thrombosis while on [[clopidogrel]], it may suggest that the patient was not responsive to clopidrogrel therapy. TRITON TIMI 38 trial<ref name="pmid19249633">{{cite journal |author=Montalescot G, Wiviott SD, Braunwald E, Murphy SA, Gibson CM, McCabe CH, Antman EM |title=Prasugrel compared with clopidogrel in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (TRITON-TIMI 38): double-blind, randomised controlled trial |journal=[[Lancet]] |volume=373 |issue=9665 |pages=723–31 |year=2009 |month=February |pmid=19249633 |doi=10.1016/S0140-6736(09)60441-4 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(09)60441-4 |issn= |accessdate=2010-06-30}}</ref> demonstrated that newer antiplatelet agents such as [[prasugrel]]<ref name="pmid17982182">{{cite journal |author=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 |title=Prasugrel versus clopidogrel in patients with acute coronary syndromes |journal=[[The New England Journal of Medicine]] |volume=357 |issue=20 |pages=2001–15 |year=2007 |month=November |pmid=17982182 |doi=10.1056/NEJMoa0706482 |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=17982182&promo=ONFLNS19 |issn= |accessdate=2010-06-30}}</ref> 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. | |||
==Sources== | |||
The 2009 ACC/AHA Focused update on the guidelines for STEMI and PCI<ref name="2009 STEMI guidelines">[http://content.onlinejacc.org/cgi/content/full/j.jacc.2009.10.015]</ref> | |||
==References== | ==References== | ||
{{reflist}} | {{reflist|2}} | ||
[[Category: Cardiology]] | [[Category: Cardiology]] | ||
Latest revision as of 15:37, 6 September 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Associate Editor-In-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
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].
Management
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 [2].
- If revascularization is not successful, urgent CABG should be considered.
- The probable cause for stent thrombosis should be evaluated as the treatment varies with etiology. The probable contributing factors are:
- suboptimal stent apposition,
- Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis[1].
- premature discontinuation of dual antiplatelet therapy,
- clopidogrel resistance.
- If the patient develops stent thrombosis while on clopidogrel, it may suggest that the patient was not responsive to clopidrogrel therapy. TRITON TIMI 38 trial[3] 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.
Sources
The 2009 ACC/AHA Focused update on the guidelines for STEMI and PCI[5]
References
- ↑ 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.
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ [1]