Stent thrombosis is the call I least want at night, because it arrives as an occluded artery in a patient I, or a colleague, stented days or years ago. Below are the six rules I follow when it presents, in the order I apply them on the table. This is operator reasoning anchored to trials and registries, not a guideline summary.

Most of these patients arrive as STEMI. The reflex is to treat the angiogram. My job is to treat the cause, because the cause usually decides whether the stent occludes again.

Rule 1: Classify the stent thrombosis before I touch the wire

I use the Academic Research Consortium language because it forces precision. Definite stent thrombosis needs angiographic or pathological confirmation; probable and possible are clinical inferences. ARC-2 kept this framework and refined it for complex lesions and scaffolds.

Timing tells me where to look

• Acute: within 24 hours of implantation.
• Subacute: 24 hours to 30 days.
• Late: 30 days to 1 year.
• Very late: beyond 1 year.

Early events point me to the procedure and to platelet inhibition. Very late events point me to healing failure and neoatherosclerosis. Before the case starts, I pull the index report: stent size, post-dilatation balloon and pressure, any imaging, and what antiplatelet therapy the patient actually took.

The adherence question comes first

In the Dutch Stent Thrombosis Registry, 437 of 21,009 stented patients (2.1%) had definite stent thrombosis. Absence of clopidogrel in the first 30 days carried a hazard ratio of 36.5 (95% CI 8.0 to 167.8). Undersizing, dissection and TIMI flow below 3 were also independent predictors.

PARIS refined this. Among 5,018 patients, DAPT disruption from non-compliance or bleeding raised MACE risk (adjusted HR 1.50, 95% CI 1.14 to 1.97; p=0.004). Within 7 days of disruption the HR was 7.04 (3.31 to 14.95). Physician-guided discontinuation did not raise risk. So I ask directly, and I ask the family.

Rule 2: Open the artery with a balloon, not a reflex stent

I load heparin, wire the vessel and restore flow with a small, then appropriately sized balloon. Thrombus inside a stent is usually fresh, platelet-rich and sitting on a mechanical defect I have not yet seen.

Aspiration only when thrombus burden demands it

Routine aspiration failed in native-vessel STEMI. TASTE randomised 7,244 patients: 30-day mortality was 2.8% versus 3.0% (HR 0.94, 95% CI 0.72 to 1.22; P=0.63), and stent thrombosis 0.2% versus 0.5% (HR 0.47, 0.20 to 1.02; P=0.06). TOTAL randomised 10,732; the primary outcome was 6.9% versus 7.0% (HR 0.99, 0.85 to 1.15).

TOTAL also showed more 30-day stroke with thrombectomy (0.7% versus 0.3%; HR 2.06, 1.13 to 3.75; P=0.02). Neither trial enrolled patients with a thrombosed stent specifically. I aspirate when a large residual thrombus persists after balloon reperfusion, with the guide deeply engaged and back-bleeding confirmed.

Why I resist a new stent

In the Dutch registry of 431 first definite events, implanting an additional stent during the emergency PCI was associated with worse outcome. ESTROFA identified additional stenting as an independent predictor of mortality. A second layer over an unexplained failure often buries the cause.

Rule 3: Image every stent thrombosis to find the mechanism

Once TIMI 3 flow is back, I image. OCT gives me strut-level detail after thrombus is cleared; IVUS is my choice when thrombus burden or an ostial position makes flushing unreliable. Angiography alone cannot tell underexpansion from malapposition.

PESTO analysed 120 patients by OCT and found a morphological abnormality in 97%. For acute and subacute stent thrombosis, malapposition (48%) and underexpansion (26%) dominated. Late and very late cases were driven by malapposition (31%) and neoatherosclerosis (28%).

PRESTIGE imaged 231 patients. Underexpansion, defined as a stent expansion index below 0.8, was present in 44.4%. Uncovered struts were the dominant finding in acute cases (66.7%); in subacute cases, uncovered struts (61.7%) and underexpansion (25.5%). In very late cases, neoatherosclerosis (31.3%) led.

Rule 4: Correct the cause, not the angiogram

• Underexpansion: a non-compliant balloon sized to the imaging reference, at high pressure, repeated until the expansion target is met. Calcium behind the stent may need intravascular lithotripsy.
• Malapposition: a larger NC balloon at moderate pressure to seat the struts.
• Edge dissection or geographic miss: this is where a new stent belongs, landing in healthy tissue.
• Residual inflow or outflow disease: treat it; an unstented stenosis next to a stent is a thrombosis substrate.

For a structured approach to optimisation at the aorto-ostium, see my post on ostial left main cath-lab decisions.

Rule 5: Escalate platelet inhibition on the table and after

Switch clopidogrel to a potent P2Y12 inhibitor

Unless bleeding risk forbids it, I load prasugrel 60 mg or ticagrelor 180 mg on the table. In the TRITON-TIMI 38 stented cohort (12,844 patients), prasugrel reduced stent thrombosis from 2.35% to 1.13% (HR 0.48, p<0.0001). In PLATO, ticagrelor reduced definite stent thrombosis from 1.93% to 1.37% (HR 0.67, 95% CI 0.50 to 0.90; P=0.0091).

Platelet function and genotype as context, not a reflex

Among clopidogrel-treated TRITON patients, CYP2C19 reduced-function carriers had stent thrombosis in 2.6% versus 0.8% (HR 3.09, 95% CI 1.19 to 8.00; P=0.02). In ADAPT-DES, high on-treatment reactivity on clopidogrel by VerifyNow predicted stent thrombosis (adjusted HR 2.49, 1.43 to 4.31).

GRAVITAS showed that doubling clopidogrel for high PRU did not help: 2.3% versus 2.3% (HR 1.01, 0.58 to 1.76; P=0.97). After a thrombotic event, a PRU or genotype result explains the failure; it rarely changes my decision to switch.

GP IIb/IIIa or cangrelor when thrombus or no-reflow persists

With heavy residual thrombus or slow flow, I add a GP IIb/IIIa inhibitor, often intracoronary. If the patient is P2Y12-naive or oral absorption is doubtful, cangrelor covers the gap. CHAMPION PHOENIX randomised 11,145 patients: stent thrombosis fell from 1.4% to 0.8% (OR 0.62, 0.43 to 0.90; P=0.01).

Anticoagulation during the PCI

I use ACT-guided unfractionated heparin. In HORIZONS-AMI, bivalirudin alone increased acute stent thrombosis within 24 hours compared with heparin plus GP IIb/IIIa, without a significant excess by 30 days. If I use bivalirudin, I continue the infusion after the procedure.

Rule 6: Plan DAPT and prevention after stent thrombosis

The prognosis is poor. In the Dutch registry of 431 first definite events, cardiac death or recurrent definite stent thrombosis reached 18.0% at 30 days and 23.6% at 1 year. ESTROFA reported 16% mortality and 4.6% recurrence at 1 year.

I know of no randomised trial of switching or DAPT duration specifically after stent thrombosis. I keep a potent P2Y12 inhibitor with aspirin and extend DAPT beyond the first year when BARC bleeding risk allows, a position several reviewers share. Every decision is documented for the next operator.

Adherence is the modifiable variable. I explain in plain words why stopping a tablet can close the artery, and I tell every dentist and surgeon to call my team before interrupting therapy. More worked examples are on my interesting cases page.

For structured learning, the Cardiology Learning Center and the courses at Cardiology Course cover intravascular imaging and antithrombotic strategy.

My stent thrombosis checklist

1. Classify by ARC certainty and timing; pull the index procedure report.
2. Ask the patient and family exactly when DAPT stopped and why.
3. Give heparin, wire, and restore flow with a balloon first.
4. Aspirate only for large residual thrombus, never routinely.
5. Image with OCT or IVUS before deciding on any new stent.
6. Correct underexpansion and malapposition with high-pressure NC post-dilatation.
7. Stent only edge dissection, geographic miss or residual disease.
8. Switch clopidogrel to prasugrel or ticagrelor; use GP IIb/IIIa or cangrelor for heavy thrombus.
9. Use PRU and genotype to explain failure, not to delay escalation.
10. Extend DAPT when bleeding risk allows, and educate on adherence.

References

1. Cutlip DE, et al. ARC end point definitions. Circulation 2007;115:2344-51. doi:10.1161/CIRCULATIONAHA.106.685313
2. Garcia-Garcia HM, et al. ARC-2 consensus document. Circulation 2018;137:2635-50. doi:10.1161/CIRCULATIONAHA.117.029289
3. Tyczynski P, et al. Early stent thrombosis: aetiology, treatment, and prognosis. Postepy Kardiol Interwencyjnej 2014;10:221-5. doi:10.5114/pwki.2014.46761
4. van Werkum JW, et al. Dutch Stent Thrombosis Registry predictors. J Am Coll Cardiol 2009;53:1399-409. doi:10.1016/j.jacc.2008.12.055
5. van Werkum JW, et al. Long-term outcome in 431 cases. Circulation 2009;119:828-34. doi:10.1161/CIRCULATIONAHA.108.799403
6. Mehran R, et al. PARIS registry. Lancet 2013;382:1714-22. doi:10.1016/S0140-6736(13)61720-1
7. Frobert O, et al. TASTE. N Engl J Med 2013;369:1587-97. doi:10.1056/NEJMoa1308789
8. Jolly SS, et al. TOTAL. N Engl J Med 2015;372:1389-98. doi:10.1056/NEJMoa1415098
9. de la Torre-Hernandez JM, et al. ESTROFA. J Am Coll Cardiol 2008;51:986-90. doi:10.1016/j.jacc.2007.10.057
10. Souteyrand G, et al. PESTO registry. Eur Heart J 2016;37:1208-16. doi:10.1093/eurheartj/ehv711
11. Adriaenssens T, et al. PRESTIGE consortium. Circulation 2017;136:1007-21. doi:10.1161/CIRCULATIONAHA.117.026788
12. Wiviott SD, et al. TRITON-TIMI 38 stent analysis. Lancet 2008;371:1353-63. doi:10.1016/S0140-6736(08)60422-5
13. Steg PG, et al. PLATO stent analysis. Circulation 2013;128:1055-65. doi:10.1161/CIRCULATIONAHA.113.002589
14. Mega JL, et al. CYP2C19 and clopidogrel. N Engl J Med 2009;360:354-62. doi:10.1056/NEJMoa0809171
15. Stone GW, et al. ADAPT-DES. Lancet 2013;382:614-23. doi:10.1016/S0140-6736(13)61170-8
16. Price MJ, et al. GRAVITAS. JAMA 2011;305:1097-105. doi:10.1001/jama.2011.290
17. Bhatt DL, et al. CHAMPION PHOENIX. N Engl J Med 2013;368:1303-13. doi:10.1056/NEJMoa1300815
18. Stone GW, et al. HORIZONS-AMI. N Engl J Med 2008;358:2218-30. doi:10.1056/NEJMoa0708191

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