Stent thrombosis is uncommon and catastrophic. It presents as ST elevation infarction in a patient who has recently had a stent, mortality is in the region of one in five, and the cause is almost always identifiable in retrospect. Knowing the categories is what makes it identifiable in advance.
On this page
Classification by timing
- Acute: within 24 hours of implantation
- Subacute: 24 hours to 30 days
- Late: 30 days to one year
- Very late: beyond one year
Acute and subacute together are often grouped as early. The timing is not a filing convenience — each window has a characteristically different cause, and the cause determines what you do about it.
Classification by certainty
The Academic Research Consortium definitions: definite requires angiographic or pathological confirmation with an acute coronary syndrome; probable covers unexplained death within thirty days, or target-vessel infarction without angiographic confirmation; possible covers unexplained death beyond thirty days. These matter in trial reporting and appear routinely in examinations.
Why it happens, window by window
Early — mechanical, almost always. Stent under-expansion is the commonest single cause and the most preventable. Then edge dissection left untreated, geographic miss, residual thrombus at the time of implantation, malapposition, and a small vessel or long stented segment. Add inadequate or interrupted antiplatelet therapy, and clopidogrel non-response in patients with reduced-function CYP2C19 alleles.
Late and very late — biological. Delayed endothelialisation, particularly with first-generation drug-eluting stents; neoatherosclerosis within the stent; hypersensitivity to the polymer; late acquired malapposition following positive remodelling; and stent fracture. Premature cessation of antiplatelet therapy — often for a procedure that could have waited — remains a leading precipitant across every window.
How it differs from restenosis
They are commonly confused and are not alike. Stent thrombosis is an abrupt thrombotic occlusion presenting as acute infarction, most often within the first month. Restenosis is progressive neointimal hyperplasia presenting as recurrent stable angina or a positive functional test, typically at six to twelve months. One is an emergency; the other is an outpatient problem. A patient who describes gradually returning exertional angina nine months after a stent has restenosis until proven otherwise.
Immediate management
- Treat as STEMI. Immediate primary PCI is the answer; thrombolysis is markedly less effective against a thrombosed stent.
- Loading doses of aspirin and a potent P2Y12 inhibitor — prasugrel or ticagrelor rather than clopidogrel — with parenteral anticoagulation.
- Aspiration or mechanical thrombectomy where the thrombus burden is heavy, alongside a glycoprotein IIb/IIIa inhibitor if needed.
- Intravascular imaging, always. IVUS or OCT identifies under-expansion, malapposition, edge dissection or neoatherosclerosis, and is what stops the same event happening twice.
- Aggressive high-pressure post-dilatation to correct under-expansion. Additional stent layers should be avoided unless there is a specific indication.
- Reassess the antiplatelet regimen — adherence, absorption, drug interaction, and platelet function or genotype testing where recurrent.
Step four is the one most often skipped under time pressure, and it is the one that changes the next twelve months.
Prevention
Optimal deployment with imaging guidance in complex lesions; adequate post-dilatation; contemporary thin-strut drug-eluting stents; a potent P2Y12 inhibitor after acute coronary syndrome; a documented, dated antiplatelet plan in the discharge summary; and an explicit conversation with the patient about never stopping treatment on the advice of a clinician who does not know a stent is present. Where surgery is unavoidable during the mandatory period, delay it if the operation can wait, and bridge in discussion with the implanting operator if it cannot.
Related reading: DAPT duration after PCI, no-reflow during PCI, the interventional and acute care reading list, and the fifty emergency cases.
