Predictors of coronary stent thrombosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-in-Chief: Smita Kohli, M.D.; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

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Overview[edit | edit source]

A number of clinical, angiographic, and procedural factors predispose to the occurrence of stent thrombosis. Predictors of stent thrombosis can be classified into anatomic variables, procedure related variables and clinical variables. A new entity which has been recently recognised and is being increasingly studied in relation to stent thrombosis is hyporesponsiveness to antiplatelet agents.

Procedure related variables: Procedure related variables include stent underexpansion, margin dissections, incomplete wall apposition, residual inflow and outflow disease, overlapping stent, polymer materials and use of self expanding or coil stents^[1].

Anatomic variables: Lesion-specific factors that increase the likelihood of stent thrombosis include a residual dissection at the margin of the stent, impaired flow into or out of the stent, small stent diameters (<3 mm), long stent lengths, and treatment of an acute myocardial infarction^[1].

Clinical variables: Clinical variables include acute myocardial infarction, clopidogrel noncompliance and discontinuation, hyporesponsiveness to antiplatelet agents, higher baseline platelet count, diabetes mellitus, renal failure, congestive heart failure, prior radiation brachytherapy^[1][2].

In addition to these, stent implantation for off-label indication of both DES and BMS(such as restenotic lesions, bypass graft lesions, left main coronary artery disease, as well as ostial, bifurcated, and totally occluded lesions) has been associated with higher rates of ischemic complications, including stent thrombosis, as compared with standard indications^[3][4]. In a case control study of 145 patients with stent thrombosis by Rinaldi et al^[1], presence of angiographic thrombus prior to stenting, greater total stent length, higher baseline platelet count, acute MI indication, the use of a self expanding or coil stent, and GpIIb-IIIa exposure were identified as the strongest predictors of stent thrombosis.

In another study by Marroquin et al^[5] to compare the outcomes in bare-metal versus drug-elting stents for off-label indications showed that one year after intervention, there were no significant differences in the adjusted risk of death or myocardial infarction in patients with drug eluting stents as compared with those with bare metal stents. These findings implicate that the poorer outcome observed after stenting for off-label indications are related to patient and lesion characteristics but not to the stent itself. Therefore, large randomized clinical trial are needed to further study the use of DES for off label versus standard indications.

Risk factors for early and late stent thrombosis[edit | edit source]

1. Premature discontinuation of antiplatelets/clopidogrel^[6][2][7]
2. Abscence/dysfunction of CYP2C19 allele which is required for the conversion of clopidogrel to its active metabolite.^[8]
3. Improper opposition of the stent or undersized stent^[6][9]
4. Length of the stent- greater the length, higher the risk^[10]
5. Malignancy^[6]
6. Cocaine use^[11][12]
7. Small caliber of the vessels^[10]
8. Slow intra coronary flow post PCI^[13]
9. Bifurcation lesion^[2]
10. Inadequate periprocedural anticoagulation^[14]
11. Low ejection fraction (<30%)^[13][2][6]
12. Nonionic contrast media^[15]
13. Prior brachytherapy
14. Small stent area on intracoronary ultrasound^[16]
15. Residual plaque/thrombus/dissection after stent placement^[17][13][10]
16. CAD ≥50% proximal of culprit lesion^[6]
17. Chronic kidney disease^[2][18]
18. Diabetes mellitus^[19][2]
19. Black race^[20]
20. Elevated C-reactive protein levels^[21]
21. Hypersensitivity to stents^[22]
22. Young age^[19]
23. Paclitaxel-eluting stent implantation^[19]
24. Multivessel disease^[23]
25. Acute coronary syndrome at presentation^[24]

Risk factors for very late stent thrombosis[edit | edit source]

1. Ongoing vessel inflammation^[25]
2. Delayed neointimal coverage which is usually seen with DES when compared to BMS^[26][25]

References[edit | edit source]