Stent thrombosis pathophysiology: Difference between revisions
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Stent thrombosis occurs due to variety of factors inducing thombogenesis. Being an invasive procedure, the trauma from coronary stenting can itself cause platelet activation and thombogenic cascade. There is either creation or an enhancement of a thrombogenic milieu by:
- creating an environment conducive for platelet activation and/or
- creating an environment conducive for instent thrombosis
These processes are facilitated by
- Creating a thrombogenic milieu by
- Slow coronary flow
- local dissection,
- distal untreated critical lesion
- poor out flow
- Persistence of or ceation of substrate for platelet activation
- Exposure of platelet activating factors due to trauma of stenting or ballooning – acutely
- Persistant incomplete endotheliazation (1,6)
- Inadequate platelet inhibition – due to inadeqaue dosing or drug unrespopnsivelness.
- acutely
- subacutely
- long term
- Dosing issues
- with anti thrombotic medicagtions (acutely)
- antiplatelet medications (acutely, subacutly or long term)
- inadequate time for the loading dose to act
- suboptimal/subtherapeutic dosing during the procedure or therafter
- Resistance to antiplatelet medications (2)
- ASA resistance
- Clopidogrel resistance
- Deranaged homeostasis due to disease creating a prothrombotic diathesis
- sepsis
- blood transfusions
- surgery (In one study, following BMS, mortality rate among patients who had non cardiac surgery within two-weeks was 32%, almost exclusively due to ST. (3))
- dehydration
- Other states which may create hypotensive states. (eg. of anectdotal reports of stent thormbosis with defecation syncope)
Mechanisms and pathophysiology of ST in BMS
After BMS implantation, near-complete endothelization has been shown to occur by 3 to 4 months. (4)
This coincides with the reduction of risk of ST. (ref)
Mechanisms and pathophysiology of ST in DES
- Delayed endothelialization of the stented segement serving as a nidus for thrombosis (1,5,7)
- Antineoplastic therapy and delayed endothelialization had been an issue with late ST seen with brachytherapy. (6)
- Coronary brachytherpy use has all but disappeared since the introduction of DES.
- An angioscopic study of stented coronary segments showed that neointimal coverage was complete only in 2 out of 15 patients with sirolimus stents and all of 22 BMS at three to six months. There were thrombi in most of the stented segments which were not seen on angiography which were more common with incomplete neointimal coverage. (1,7) In a study involving serial angioscopy after sirolimus-eluting stent (SES) implantation at 4, 11, and 21.2 ±2.2 months showed that neointimal coverage after sirolimus-eluting stent implantation was incomplete even at that late stage.
- In a post mortem analysis, DES, compared to BMS had delayed endothelial healing. This group was more likely to have ST. (8)
- A post mortem analysis of a patient dying from an unrelated cause but who also had a DES implanted, revealed poor endothelial cell junction formation and micro-thrombi of focal platelet aggregation at 16 months after rapamycin stent implantation. (9)
- Inflammatory response to the stent material serving as a nidus for thrombosis
- Evidence of an inflammatory response was present in nearly 9% of the sirolimus eluting stents (SES) and paclitaxel eluting stents (PES) by the demonstration of late aquired stent malaposition (LASMA) which was more than what was seen with BMS . (10,11)
- Hypersensitivity reaction around the stent material in DES serving as nidus for ST
- Cypher and Taxus DES were shown to provoke chronic eosinophilic infiltration and inflammation of the arterial wall potentially predisposing patients for thrombosis. (12,12,13,14,15,16)
Both red and white thrombi have been demonstrated within sirolimus eluting stents (SES) as a cause of late stent thrombosis. (1)
back to Coronary stent thrombosis main page
References
(1) Masaki Awata, Jun-ichi Kotani et al; Serial Angioscopic Evidence of Incomplete Neointimal Coverage After Sirolimus-Eluting Stent Implantation. Comparison With Bare-Metal Stents Circulation published online Aug 7, 2007
(2) Wenaweser, P, Dorffler-Melly, J, Imboden, K, et al. Stent thrombosis is associated with an impaired response to antiplatelet therapy. J Am Coll Cardiol 2005; 45:1748
(3) Kaluza GL, Joseph J, Lee JR, Raizner ME, Raizner AE. Catastrophic outcomes of non-cardiac surgery soon after coronary stenting. J Am Coll Cardiol 2000;35:1288 –94.
(4) Farb A, Burke AP, Kolodgie FD, Virmani R. Pathological mechanisms of fatal late coronary stent thrombosis in humans. Circulation. 2003;108: 1701–1706.
(5) Edoardo Camenzind, MD; P. Gabriel Steg, MD; William Wijns, MD Stent Thrombosis Late After Implantation of First Generation Drug-Eluting Stents A Cause for Concern Circulation. 2007;115:1440-1455.
(6) Circ 1999 Costa Late coronary occlusion after intra cor brachytherapy.pdf Costa MA, Sabate M, van der Giessen WJ, et al. Late coronary occlusion after intracoronary brachytherapy. Circulation 1999;100: 789–92.
(7)Kotani, J, Awata, M, Nanto, S, et al. Incomplete neointimal coverage of sirolimus-eluting stents: angioscopic findings. J Am Coll Cardiol 2006; 47:2108.
(8) Joner, M, Finn, AV, Farb, A, et al. Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk. J Am Coll Cardiol 2006; 48:193.
(9) Guagliumi G, Farb A, Musumeci G, Valsecchi O, Tespili M, Motta T, Virmani R. Images in cardiovascular medicine: sirolimus-eluting stent implanted in human coronary artery for 16 months: pathological findings. Circulation. 2003;107:1340 –1341.
(10) Leon MB, Abizaid A, Moses JW. Subgroup analysis from the Cypher clinical trials. In: The Cypher Stent: A New Gold Standard in the Treatment of Coronary Artery Disease. New York, NY: Cardiovascular Research Foundation; 2003:54–57.
(11) Tanabe K, Serruys PW, Colombo A et al, for the TAXUS II Study Group. Incomplete stent apposition after implantation of paclitaxel-eluting stents or bare metal stents: insights from the randomized TAXUS II trial. Circulation. 2005;111:900–905.
(12) Virmani R, Guagliumi G, Farb A, et al. Localized hypersensitivity and late coronary thrombosis secondary to a sirolimus-eluting stent: should we be cautious? Circulation 2004;109:701–5.
(13) Nebeker JR, Virmani R, Feldman MD et al, Hypersensitivity cases associated with drug-eluting coronary stents: a review of available cases from the Research on Adverse Drug Events and Reports (RADAR) project. J Am Coll Cardiol. 2006; 47:175–181.
(14) Joner M, Finn AV, Farb A, Mont EK, Kolodgie FD, Ladich E, Kutys R, Skorija K, Gold HK, Virmani R. Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk. J Am Coll Cardiol. 2006;48:193–202.
(15) JACC 2005 Ong LAST Late angiographic ST DES.pdf Ong, AT, McFadden, EP, Regar, E, et al. Late angiographic stent thrombosis (LAST) events with drug-eluting stents. J Am Coll Cardiol 2005; 45:2088.
(16)Grube E, Lansky A, Hauptmann KE, et al. High-dose 7-hexanoyltaxol-eluting stent with polymer sleeves for coronary revascularization: one-year results from the SCORE randomized trial. J Am Coll Cardiol 2004;44:1368 –72.