DAPT Duration After PCI: Decisions at the Bedside
A 71-year-old woman attends your clinic with a discharge summary in a language you do not read, a stent card she cannot find, and a surgeon who wants to repair an incarcerated hernia next week. She had “a heart procedure” about five months ago and takes two tablets that she describes by colour. Deciding how long her dual antiplatelet therapy should continue, and whether it can safely be interrupted, is one of the commonest and least standardised decisions in international practice, and it is usually made without the implanting operator on the phone. This reference works through it as a sequence of bedside choices rather than as a summary of guideline tables.
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Framing the question properly
The old question was how many months of treatment a stent requires. The modern question is different: how do the ischaemic and bleeding hazards for this individual cross over in time, and which drug should be carrying the load once they do. Ischaemic risk after intervention is front-loaded and decays over the first months, while bleeding risk is broadly constant and accumulates with exposure. Most of the trial programme of the past decade has been an attempt to find the crossing point, and the practical answer has shifted away from uniform durations towards shorter combined therapy followed by a single potent agent.
The decision points
1. Establish what was implanted, where, and when
Before any duration decision, reconstruct the index procedure. You need the date, the vessel or vessels, the number and length of stents, whether the left main or a bifurcation was treated, and whether the indication was an acute coronary syndrome or stable disease. Where records are unobtainable, a plain fluoroscopic look or the operator’s institution email will often yield more than the patient’s recollection. Treat an undocumented procedure as complex until proven otherwise.
2. Separate acute from chronic coronary syndrome, because the default differs
An acute presentation carries a higher residual thrombotic hazard than elective intervention for stable disease, and current guidance favours a longer default combined course after acute coronary syndrome than after elective stenting, alongside a preference for a potent P2Y12 inhibitor in the acute setting where bleeding risk permits. Elective intervention in a patient with low complexity anatomy can generally be managed with a shorter combined course.
3. Score the bleeding risk formally, not impressionistically
Clinicians consistently underestimate bleeding risk in older patients and overestimate it in patients who simply look frail. Use PRECISE-DAPT at the point of discharge or review, and apply the high bleeding risk criteria set out by the Academic Research Consortium, which capture the features that actually drive events: anaemia, chronic kidney disease, prior spontaneous bleeding, active malignancy, planned surgery and long-term steroid or anti-inflammatory use. In patients who also require anticoagulation, HAS-BLED adds a structured view of the modifiable elements. Grade any bleeding that does occur with the BARC scale so that the next clinician inherits a comparable number.
4. Score the ischaemic side with equal seriousness
Complexity matters more than any single comorbidity. Three or more stents, three or more lesions treated, total stent length beyond about sixty millimetres, bifurcation stenting with two stents, left main intervention, chronic total occlusion recanalisation and last remaining patent vessel all shift the balance towards longer therapy. Diabetes, chronic kidney disease, prior stent thrombosis and recurrent events do the same. The anatomical complexity language of the SYNTAX and EXCEL programmes is useful here, even though those trials addressed revascularisation strategy rather than antiplatelet duration.
5. Choose the agent before you choose the duration
Clopidogrel remains the default in stable disease and in patients with meaningful bleeding vulnerability, with the caveat of variable metabolism. Ticagrelor and prasugrel deliver more consistent and more potent inhibition after acute coronary syndrome; prasugrel is avoided after stroke or transient ischaemic attack and used cautiously in low body weight and advanced age, while ticagrelor requires twice-daily dosing and carries dyspnoea as a recognised nuisance effect that drives discontinuation if not anticipated and explained.
6. Decide between shortening, standard and extending
Three strategies now coexist. Abbreviated combined therapy followed by monotherapy with the P2Y12 agent was the approach tested in TWILIGHT and, in a bleeding-vulnerable population, in MASTER DAPT; both support dropping aspirin early rather than dropping the potent agent. Standard duration remains reasonable for the average patient with an acute presentation and no bleeding flags. Extension beyond a year is for the patient with recurrent events, diffuse disease and low bleeding risk, and is a decision to review annually rather than to set and forget. De-escalation from a potent agent to clopidogrel after the first months is a further legitimate option in patients who tolerate the combination poorly.
7. Handle concurrent anticoagulation as its own problem
When atrial fibrillation or a mechanical valve coexists with recent stenting, the direction of travel is clear: keep triple therapy short, then continue an oral anticoagulant with a single antiplatelet agent, usually clopidogrel. The AUGUSTUS and PIONEER AF-PCI programmes established the shape of that strategy, and the practical consequence is that aspirin is the component that leaves first in most patients. Anticoagulant dose reduction to a level not validated for stroke prevention is a common and serious error in this group.
8. Plan interruptions before they are demanded
Elective surgery should be deferred past the highest-risk window wherever possible. When it cannot be, negotiate the specific procedure rather than the abstract principle: many endoscopic, dental, ophthalmic and superficial procedures proceed safely on continued therapy. Where interruption is genuinely required, stop for the shortest interval, keep aspirin running where the surgeon will accept it, and book the restart date into the operation note. Bridging with parenteral agents is reserved for the small group at genuinely prohibitive thrombotic risk. Wider perioperative and shared-care context is set out in our cardiology handbook for physicians.
When to escalate, transfer or call for help
- Contact the implanting service before any interruption within the first six months, and before de-escalating in a patient with left main or complex bifurcation stenting. Reference material on why those substrates behave differently is collected in our advanced PCI techniques volume and the interventional cardiology collection.
- Escalate urgently if chest pain recurs after any reduction in therapy. Treat it as stent failure until angiography or a convincing alternative says otherwise; the acute pathway is set out in the acute coronary syndromes reference.
- Involve haematology or gastroenterology for recurrent BARC type 2 bleeding rather than serially shortening therapy on your own. Proton pump inhibition, iron replacement and source treatment often preserve the regimen.
- Seek specialist input for the patient who needs anticoagulation, has had a stent thrombosis, and bleeds. That combination has no clean answer and should not be resolved by a single clinician in a corridor.
What to document
- Index procedure date, indication, vessels, number and total length of stents, and any complexity features.
- The bleeding score used, its value, and the individual high bleeding risk criteria met.
- The agent chosen with the reason, particularly when a potent agent is avoided or a de-escalation is made.
- The planned stop date, written as a date rather than a duration, and who is responsible for reviewing it.
- Any interruption: the reason, the interval, and the confirmed restart.
- The conversation with the patient about not stopping treatment on the advice of a non-cardiac clinician without contact.
Bench card
| Clinical situation | Direction of travel | Practical note |
|---|---|---|
| Elective stenting, simple anatomy, low bleeding risk | Shorter combined therapy, then monotherapy | Clopidogrel usually sufficient |
| Acute coronary syndrome, low bleeding risk | Longer default with a potent agent | Review complexity before shortening |
| High bleeding risk by ARC criteria | Abbreviated combined therapy | Drop aspirin, retain the P2Y12 agent |
| Complex or multivessel intervention | Favour longer therapy | Stent length and bifurcation technique drive this |
| Atrial fibrillation with recent stenting | Short triple, then anticoagulant plus clopidogrel | Never reduce the anticoagulant below the stroke prevention dose |
| Prior stent thrombosis | Prolonged therapy with a potent agent | Abbreviated strategies do not apply |
| Surgery required within six months | Defer if possible; negotiate if not | Write the restart date in the operation note |
Three recurring errors worth naming: treating duration as a property of the stent rather than of the patient, stopping the potent agent and keeping aspirin when the modern evidence points the other way, and allowing a non-cardiac clinician to discontinue therapy without a documented conversation. Broader risk-factor management alongside these decisions sits in the prevention and lifestyle reference hub. A guideline-structured account of the same subject is available as this explanation of DAPT duration after PCI.
Questions from the floor
The patient has been on treatment for eleven months with no problems. Do I simply stop at twelve?
Not automatically. Twelve months is a convention derived from trial design, not a biological boundary. Review complexity, residual disease and bleeding history, and make an explicit decision either to stop, to continue a single agent indefinitely, or to extend the combination.
Which single antiplatelet agent should continue long term?
The field has moved away from assuming aspirin. In patients who have completed a combined course after stenting, continuing the P2Y12 inhibitor alone is increasingly favoured, particularly where bleeding risk is a concern, and is supported by the monotherapy arms of the abbreviated-therapy trials.
Is platelet function or genotype testing worth doing?
Routine testing has not shown consistent outcome benefit, but selective genotyping has a place after an event on clopidogrel, in complex left main intervention, and where a potent agent is being avoided for cost reasons and you want to know whether that decision is safe.
How do I handle a patient who cannot afford a potent agent?
State the compromise openly in the notes, use clopidogrel with a lower threshold for genotyping if available, extend rather than shorten the combined course in complex anatomy, and address adherence support directly. An interrupted potent agent is worse than a continuous weaker one.
No-Reflow During PCI: A Bedside Reference for Operators
The stent is deployed, the angiographic result looks acceptable, and then the contrast column stops moving. The patient becomes bradycardic, complains that the pain is worse than before, and the ST segments that were coming down start to climb again. In a large tertiary centre this is a moment for a second operator and a shelf full of intracoronary agents. In much of international practice it happens with one operator, one scrub nurse, whatever vasodilators the pharmacy stocked last quarter, and no surgical cover. This reference is organised around the choices that have to be made in those next fifteen minutes, in the order they arise.
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Naming the problem accurately
Impaired antegrade filling despite a patent, unobstructed epicardial vessel is a microvascular diagnosis made by exclusion at the table. Grade it the same way every time: TIMI flow for the epicardial column, corrected TIMI frame count when the difference between grades 2 and 3 is arguable, and myocardial blush grade for tissue-level perfusion. Blush is the parameter most often omitted and the one that correlates best with infarct size, so make it a habit rather than an afterthought. Where physiology is available, an index of microcirculatory resistance measured after the case gives you a number that predicts subsequent left ventricular remodelling independently of how satisfying the final run looked.
The distinction between transient slow flow and established no-reflow is largely a distinction of duration. Both start with the same four processes: distal embolisation of atherothrombotic debris, microvascular spasm, reperfusion injury with oedema and capillary compression, and a platelet-leukocyte inflammatory response that scaffolds microthrombi. The last of these is what converts a recoverable problem into a fixed one, which is why hesitation is expensive.
The decision points
1. Spend sixty seconds excluding the mimics
Before any drug goes down the guide, rule out the conditions that look identical and need the opposite treatment. Wire position in a false lumen or an unrecognised dissection is the dangerous one: advance a microcatheter and inject selectively, or take an intravascular image. Epicardial spasm responds to intracoronary nitroglycerin and should be tested first. Stent underexpansion and edge dissection are mechanical problems requiring mechanical answers, and imaging settles the question faster than argument. Air embolism is unmistakable once seen and is treated with forceful saline flushing and high-flow oxygen. Residual proximal thrombus and an occluded side branch are excluded with a second projection.
2. Treat perfusion pressure as a drug
Microvascular flow is driven by the gradient between aortic diastolic pressure and left ventricular end-diastolic pressure. Allowing a mean arterial pressure of 55 mmHg to persist while you inject vasodilators is self-defeating. Restore volume, start norepinephrine early rather than late, treat bradycardia and atrioventricular block with atropine and a temporary wire, and load volume with inotropic support in right ventricular infarction. In frank cardiogenic shock, mechanical circulatory support belongs in the conversation before the third dose of anything. Haemodynamic restoration is therapy here, not supportive care.
3. Get the drug to the distal bed, not into the guide catheter
This is the single most consequential technical decision in the whole sequence, and it is the one most often skipped under pressure. Comparative work on delivery route has shown substantially better restoration of epicardial flow and tissue blush when agents are delivered distally through a microcatheter, an over-the-wire balloon or an aspiration catheter, compared with injection into the guide, with the choice of agent mattering considerably less than the route. If you take one habit away from this page, make it the reflex of parking a microcatheter distally before you inject.
4. Climb the pharmacological ladder deliberately
Start with an intracoronary vasodilator delivered distally and repeat it freely. Adenosine is the traditional first agent and has the advantage of a half-life measured in seconds, though the accumulated randomised evidence for it is weaker than its popularity suggests, with calcium channel blockade and diluted epinephrine performing better in pooled analyses of final flow and ST-segment resolution. Where the mechanism is clearly embolic or thrombotic and bleeding risk permits, a glycoprotein IIb/IIIa inhibitor is a reasonable second line. Diluted intracoronary epinephrine is the rational refractory choice in the normotensive or hypotensive patient, where further vasodilatation would be unsafe. Nicorandil, where stocked, and rapid saline boluses through a distally positioned aspiration catheter are useful adjuncts.
5. Reassess with numbers, not impressions
Repeat the frame count and the blush grade after each intervention. Visual estimation drifts towards optimism at exactly the moment optimism is dangerous. Check ST-segment resolution at sixty to ninety minutes; failure to resolve identifies a patient who needs closer surveillance regardless of the final angiographic appearance. The relationship between microvascular integrity and later ventricular function is covered in more depth in our coronary physiology in practice reference.
6. Know when to stop and when not to stent
Deploying a stent into an unperfused bed converts a recoverable problem into a permanent one. If flow remains absent with a heavy thrombus burden after wiring and gentle preparation, deferring stenting for 24 to 48 hours under potent antithrombotic therapy is a legitimate strategy; DEFER-STEMI reduced angiographic no-reflow markedly, although the larger DANAMI-3-DEFER programme did not translate that into a clinical endpoint benefit. Reserve the tactic for the genuinely high thrombus burden case rather than adopting it routinely.
7. Prevent the next one before you start
Anticipation outperforms rescue. Screen every case across patient factors (late presentation, hyperglycaemia on admission, renal impairment, anaemia, shock), lesion factors (large thrombus burden, absent antegrade flow before wiring, long lipid-rich lesions, degenerated vein grafts) and procedural factors (multiple long stents, aggressive high-pressure work, prolonged thrombus manipulation). Grade thrombus burden only after the wire has crossed, since pre-wire grading systematically misleads. High-dose statin loading before intervention, adequate antiplatelet loading, prophylactic distal vasodilatation before stenting, and undersized balloon preparation at a conservative balloon-to-artery ratio all reduce the odds. These pre-case habits are set out procedurally in our primary angioplasty golden hour protocol.
When to escalate, transfer or call for help
- Call the second operator immediately if flow has not recovered after two rounds of distally delivered vasodilator, or if you are considering intravascular imaging while the patient is unstable.
- Escalate to mechanical support when hypotension persists despite vasopressors in a large anterior territory. Support restores the perfusion gradient the microcirculation needs and buys time for the vasodilators to work.
- Place a temporary pacing wire, or at minimum draw up atropine, before giving adenosine or verapamil into a dominant right coronary artery.
- Arrange transfer to a centre with circulatory support and surgical cover if refractory no-reflow coexists with shock, mechanical complication or recurrent ventricular arrhythmia. Reference material for stabilising these patients during transfer is collected in the acute cardiac care worldwide protocols and the interventional and acute care reference hub.
What to document
- TIMI flow before wiring, after wiring, and at the end of the case, with corrected frame counts where the grade is borderline.
- Myocardial blush grade at the end of the case. Its absence from a report is conspicuous.
- Thrombus grade assessed after wire crossing.
- Every agent given, with dose, dilution and the route of delivery stated explicitly as guide or distal.
- Haemodynamic interventions, including pacing, vasopressors and any mechanical support.
- ST-segment resolution at 60 to 90 minutes, and the index of microcirculatory resistance if measured.
- The follow-up imaging plan, since these patients warrant an early assessment of ventricular function.
Bench card
| Agent | Typical intracoronary dose | Watch for |
|---|---|---|
| Adenosine | 50 to 200 micrograms, repeated freely | Transient block, asystole, bronchospasm; avoid in conduction disease |
| Verapamil | 100 to 250 micrograms, repeatable | Largest fall in rate and pressure; avoid in shock or block |
| Nicardipine | 50 to 200 micrograms, repeatable | No nodal effect, useful when already bradycardic |
| Sodium nitroprusside | 50 to 200 micrograms | Dose-related hypotension; avoid in severe aortic stenosis |
| Diluted epinephrine | 50 to 200 micrograms | Tachyarrhythmia; reserve for the hypotensive refractory case |
| Nitroglycerin | 100 to 300 micrograms | Epicardial dilator, used to exclude spasm rather than to treat the microcirculation |
Order of operations to keep taped inside the cupboard door: exclude mimics, fix the pressure, park a microcatheter distally, vasodilate and repeat, escalate to glycoprotein blockade or epinephrine, reassess with frame count and blush, decide about deferring the stent. Wider procedural context sits in the cath lab reference collection and the volume on catheterisation laboratory complications. A more didactic treatment of the same territory is available as this no-reflow and slow flow management guide.
Questions from the floor
Is aspiration thrombectomy justified when flow is lost?
Routine use during primary intervention is not supported, but bailout aspiration for a large residual thrombus remains a defensible operator decision. Its more useful role in this setting is often as a delivery conduit for distal drug administration.
Which agent should a small laboratory stock if it can only stock two?
A calcium channel blocker without strong nodal effect and a preparation of epinephrine suitable for dilution will cover most scenarios, including the hypotensive patient in whom further vasodilatation is unsafe. Adenosine is convenient but should not be the only option available.
Does no-reflow at the table always mean a worse outcome?
It is consistently associated with larger infarcts, more adverse remodelling and higher mortality, but the association is graded. A patient whose flow and blush recover fully during the case sits in a different risk category from one who leaves the laboratory with persistent microvascular obstruction, which is precisely why objective grading before and after matters.
Should these patients have cardiac magnetic resonance imaging?
Where available, it quantifies microvascular obstruction and intramyocardial haemorrhage and refines prognosis, particularly when ventricular function is borderline. In settings without access, an early echocardiogram with strain assessment is a reasonable substitute for follow-up planning.
Acute Stent Thrombosis: A Bedside Reference for Clinicians
It is a Sunday evening. A 58-year-old man who had two drug-eluting stents placed in his left anterior descending artery eleven days ago arrives in your emergency department with crushing pain that began forty minutes ago, cold peripheries and 4 mm of ST elevation in V2 to V4. The nearest catheterisation laboratory is ninety minutes away by road and the interventional team is not yet contactable. This is the situation most doctors in international practice actually face when stent thrombosis walks through the door: no on-site angiography, incomplete records from the index procedure, and a patient who is deteriorating while you assemble the picture. What follows is a decision-led reference for those first two hours, and for the paperwork that has to follow.
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Recognising the event under pressure
Stent thrombosis behaves differently from de novo plaque rupture. The occlusion is abrupt and total, there is no collateral conditioning, and the clinical presentation is skewed towards large-territory ST elevation, malignant arrhythmia and out-of-hospital arrest. Mortality at thirty days after a confirmed event is high enough that this diagnosis should sit at the top of your differential in any patient with recent coronary intervention and new severe chest pain, even when the pain has atypical features. Contemporary platforms have pushed the event rate well under one per cent of procedures, which paradoxically makes the diagnosis easier to miss.
Two things narrow the field quickly. First, an ECG that localises to the previously treated territory. Second, a timeline: the interval between the index procedure and the symptom onset tells you more about mechanism than any single investigation available to you at that moment.
The decision points
1. Confirm the territory before you commit
Compare the current tracing with the post-procedure ECG if you can obtain it, including from the patient’s phone photographs, which are often easier to retrieve than hospital records. New ST elevation in the stented distribution, or new regional wall motion abnormality on a bedside study, converts suspicion into a working diagnosis. A completely normal ECG ten minutes into severe pain should make you consider aortic dissection, oesophageal rupture and pulmonary embolism before you commit a patient to potent antithrombotic loading.
2. Place the event in its timing band, then infer the mechanism
Events within the first twenty-four hours are overwhelmingly mechanical: underexpansion, edge dissection, geographic miss, or a stent margin landing in residual disease. Events between one day and one month usually combine a mechanical substrate with an antiplatelet problem. Beyond a year, the dominant substrates are neoatherosclerosis inside the stent, acquired late malapposition and persistently uncovered struts. This inference matters even before angiography, because it tells you how hard to push on the drug history and how strongly to argue for intravascular imaging when you refer.
3. Take a forensic antiplatelet history
Ask when the last dose of each agent was taken, not whether the patient is compliant. Look specifically for interruption before dental or endoscopic procedures, a pharmacy substitution, vomiting after dosing, and recent opiate administration, which delays oral absorption enough to matter in the first hours. In patients on clopidogrel, a poor-metaboliser CYP2C19 genotype remains a real contributor where potent agents were avoided for cost or bleeding reasons. Record the answers verbatim; they will shape the discharge regimen more than anything else you do tonight.
4. Load, anticoagulate, and start the clock towards a catheterisation laboratory
Emergency angiography with a view to intervention is the treatment. Everything you give before transfer is a bridge. Current guidance favours a potent oral P2Y12 inhibitor over clopidogrel in this setting, given parenterally or intravenously where formulations allow, alongside full anticoagulation and aspirin if the patient is not already loaded. Where a cannulated intravenous P2Y12 agent is available, it removes the absorption uncertainty entirely. Glycoprotein IIb/IIIa inhibition is a reasonable bridging decision in a haemodynamically compromised patient with a very high thrombus burden and no bleeding contraindication, and should be discussed with the receiving operator rather than started unilaterally.
5. Be honest about fibrinolysis
Lytic therapy performs poorly against platelet-rich thrombus organised on a metallic scaffold, and it does nothing about the mechanical substrate underneath. If transfer will genuinely exceed the window and the patient is deteriorating, fibrinolysis is defensible as a rescue manoeuvre, but plan for it to be a partial success at best and continue to push for angiography. Say so explicitly when you refer.
6. Insist that the mechanism is found, not just the vessel opened
Restoring flow without identifying why the stent occluded invites a repeat event. Intravascular imaging with either ultrasound or optical coherence tomography changes management in a substantial proportion of these cases, identifying underexpansion, unrecognised dissection at the stent margin, protruding tissue or neoatherosclerotic rupture. When you refer, ask for imaging by name. Optimisation of an underexpanded segment with high-pressure non-compliant balloon dilatation is frequently a better answer than adding another layer of metal, and readers who work alongside interventional colleagues will find the technical detail set out in our advanced PCI techniques reference and in the case-based catheterisation laboratory complications volume.
7. Decide the long-term antithrombotic strategy before discharge
A patient who has thrombosed a stent while on treatment has declared a phenotype. Escalation to a potent P2Y12 inhibitor, prolonged rather than abbreviated dual therapy, and reassessment of any concurrent anticoagulation indication are the usual conclusions. Where an oral anticoagulant is also required, the balance struck in the AUGUSTUS and PIONEER AF-PCI programmes still frames the discussion: short triple therapy, then a dual regimen, with the P2Y12 agent retained. Weigh this against a formal bleeding assessment using PRECISE-DAPT or HAS-BLED rather than an impression, and grade any subsequent bleeding with the BARC scale so that later decisions rest on a common language.
When to escalate, transfer or call for help
- Immediately, in parallel with resuscitation: cardiogenic shock, sustained ventricular arrhythmia, or arrest with return of circulation. These patients need a laboratory with mechanical circulatory support, not the nearest laboratory.
- Within the primary intervention window: any confirmed or strongly suspected event with ongoing ST elevation. Aim for a door-in to door-out interval under thirty minutes and hand over the index procedure details with the patient.
- Urgently but not emergently: recurrent rest angina without ST elevation after recent stenting. Subacute events can present with a stuttering pattern before occluding; these patients should not wait for an outpatient appointment.
- For a second opinion: any patient in whom you are considering interrupting antiplatelet therapy for surgery within six months of stenting. That conversation belongs with the implanting operator, and our interventional cardiology reference collection is a reasonable starting point for the discussion.
What to document
The record you write becomes the only reliable account of the event once the patient moves institutions, which in international practice is likely. Capture the following.
- Certainty category using the Academic Research Consortium framework: definite when thrombus is confirmed angiographically or at autopsy, probable when there is unexplained death within the first month or an infarction in the stented territory without angiographic confirmation, possible for unexplained death thereafter. Write the term, not a paraphrase.
- Timing band in days from the index procedure, with the index procedure date stated.
- Index procedure detail: vessel, stent platform, nominal diameter and length, post-dilatation pressures, and whether intravascular imaging was used.
- Antiplatelet timeline: agents, doses, last dose taken, any interruption and its reason.
- What you gave and when, including loading doses, anticoagulant, and the time reperfusion therapy was initiated.
- Bleeding events graded on the BARC scale, and the bleeding risk score used at discharge.
Bench card
| Interval since stenting | Label | Dominant mechanism | What to ask for at angiography |
|---|---|---|---|
| Under 24 hours | Acute | Underexpansion, edge dissection, geographic miss | Imaging first, then high-pressure optimisation |
| 1 to 30 days | Subacute | Mechanical substrate plus inadequate platelet inhibition | Imaging plus review of the P2Y12 agent |
| 31 days to 1 year | Late | Delayed healing, uncovered struts, malapposition | Strut coverage assessment where optical imaging is available |
| Beyond 1 year | Very late | Neoatherosclerosis, acquired malapposition, therapy cessation | Plaque characterisation and adherence review |
Three quick correctables to run through at the bedside: absorption (vomiting, opiates, recent surgery), agent (clopidogrel in a likely poor metaboliser), adherence (cost, supply, an interruption nobody documented). For structured revision across the wider acute coronary field, see the cardiology reference library, the acute coronary syndromes handbook and the cath lab reference collection. The original examination-oriented treatment of this topic remains available as acute stent thrombosis board revision notes.
Questions from the floor
Can I exclude stent thrombosis if troponin is only mildly elevated at presentation?
No. Very early in an occlusive event the biomarker has not yet risen, and a reassuring first troponin in a patient with recent stenting and ongoing pain is a trap. Treat the ECG and the clinical picture; repeat the biomarker only to characterise the event afterwards.
The patient stopped their P2Y12 inhibitor two days ago for a dental extraction. Does that change management?
It changes the explanation, not the acute pathway. Reload, anticoagulate and refer as you would otherwise. It should, however, prompt a written plan for future procedural interruptions and a note to the dentist and the primary physician.
Is thrombus aspiration expected in these cases?
Routine aspiration in primary intervention fell out of favour after the large randomised trials, but selective use in a heavily thrombotic occluded stent remains a legitimate operator decision. It is not a substitute for finding the underlying mechanical problem.
How long should dual antiplatelet therapy continue after a confirmed event?
Longer than the standard course, and with a potent agent unless bleeding risk forbids it. Abbreviated strategies of the kind tested in TWILIGHT and MASTER DAPT were designed for bleeding-vulnerable patients without a thrombotic event, and do not transfer to a patient who has already occluded a stent.
