Deep dive #1 · 29 October 2026

Stroke

For health professionals World Stroke Day

An untreated large-vessel stroke burns 1.9 million neurons a minute, so this is written to be read quickly. The numbers, the trials behind them, and where the evidence still has holes.

At a glance

Burden (GBD 2021): 11.9 million new strokes, 93.8 million survivors, 7.3 million deaths (10.7% of all deaths), 160.5 million DALYs. Third leading cause of death.
Lifetime risk: about 1 in 4 adults over 25.
Inequity: 87% of stroke deaths and 89% of DALYs fall in low- and lower-middle-income countries. 53% of incident strokes are in people under 70.
Preventable: about 84% of the burden is attributable to 23 modifiable risk factors (GBD). INTERSTROKE: 10 factors explain 90.7% of population attributable risk.
Treatable: thrombectomy for large-vessel occlusion has an NNT of 2.6 for one-step mRS improvement. Yet only about 13% of patients in the Australian registry received thrombolysis in 2024.

Biggest take-home: systolic blood pressure. It accounts for 56.8% of stroke DALYs worldwide, more than any other factor, before and after the first stroke.

Definition

Classic WHO (time-based): rapidly developing focal (or global) neurological deficit lasting more than 24 hours or causing death, with no apparent non-vascular cause.
AHA/ASA 2013 (tissue-based): CNS infarction is brain, spinal cord or retinal cell death from ischaemia, shown on imaging or pathology. Symptoms of 24 hours or more stand in only when imaging is unavailable or negative.
Ischaemic stroke: symptomatic CNS infarction. Silent infarct: imaging-proven infarct without attributable symptoms. It raises later stroke risk 2 to 4 times.
Intracerebral haemorrhage (ICH): non-traumatic bleeding into brain parenchyma or ventricles. Cerebral microbleeds count as abnormal at any size.
Subarachnoid haemorrhage (SAH): bleeding into the subarachnoid space, mostly from a ruptured aneurysm.
TIA: transient focal brain, spinal cord or retinal ischaemia without acute infarction. A DWI-positive "TIA" is a stroke, however brief the symptoms.
Cerebral venous thrombosis with infarction or haemorrhage also counts as stroke under the AHA/ASA definition.

Pathophysiology

Ischaemic cascade

Falling CBF leads to ATP depletion, then Na⁺/K⁺-ATPase failure and anoxic depolarisation.
Glutamate release causes NMDA-mediated Ca²⁺ influx (excitotoxicity), mitochondrial failure and free radicals.
Cytotoxic oedema comes first. MMP-9-driven blood–brain barrier breakdown then causes vasogenic oedema and haemorrhagic transformation risk.
Microglia and neutrophils drive inflammation, and apoptosis continues for days.
Reperfusion can still fail at microvascular level ("no-reflow"), one rationale for adjunctive neuroprotection.

Core, penumbra and collaterals

Core: irreversibly injured. Penumbra: electrically silent but viable, and salvageable if reperfused.
Leptomeningeal collaterals set how fast the core grows. With good collaterals ("slow progressors") penumbra survives for hours, which is the biology behind the 6–24 hour EVT windows (DAWN, DEFUSE 3).
Perfusion imaging (CTP or MRI) estimates core and penumbra and selects patients beyond fixed time windows.

Time is brain (Saver 2006)

Per minute of untreated large-vessel ischaemia: 1.9 million neurons, 14 billion synapses and 12 km of myelinated fibres lost.
Per hour: 120 million neurons.
Thrombolysis benefit falls steeply with time (see treatment).

Ischaemic mechanisms (TOAST)

Large-artery atherosclerosis: artery-to-artery embolism, in-situ thrombosis, branch occlusion, hypoperfusion. Extracranial carotid disease is commoner in European-ancestry populations. Intracranial atherosclerosis is commoner in Asian, African and Hispanic populations.
Cardioembolism: AF, recent MI or LV thrombus, valve disease, endocarditis, cardiomyopathy.
Small-vessel occlusion: lipohyalinosis or microatheroma of penetrating arteries, causing lacunar infarcts. Part of cerebral small vessel disease.
Other determined: dissection (a leading cause in the young), vasculitis, RCVS, moyamoya, sickle cell, CADASIL, cancer-related hypercoagulability.
Undetermined: cryptogenic, ESUS, or two or more competing causes.

Haemorrhagic mechanisms

Hypertensive arteriopathy: deep ICH (basal ganglia, thalamus, pons, cerebellum).
Cerebral amyloid angiopathy: lobar ICH in older adults, with lobar microbleeds and cortical superficial siderosis.
Other causes: anticoagulants, AVM, cavernoma, tumour, venous thrombosis, sympathomimetic drugs.
Secondary injury: early haematoma expansion, perihaematomal oedema, thrombin and iron toxicity, and intraventricular extension causing hydrocephalus.
SAH: aneurysm rupture, then early brain injury and delayed cerebral ischaemia.

Epidemiology

Global (GBD 2021, WSO Fact Sheet 2025)

Incidence 11.9 million; age-standardised 142 per 100,000.
Prevalence 93.8 million.
Deaths 7.3 million: second among non-communicable causes, third overall after ischaemic heart disease and COVID-19.
DALYs 160.5 million, the fourth commonest cause.
Subtypes (incidence): ischaemic 65.3%, ICH 28.8%, SAH 5.8%. ICH produces about half of all stroke DALYs despite being under a third of cases.
Income split: ICH is 31.1% of strokes in LMICs vs 17.8% in high-income countries.
Trends 1990–2021 (counts): incident strokes +70%, prevalent +86%, deaths +44%, DALYs +32%.
Age-standardised rates have fallen, but the fall in incidence stalled from 2015. Rates are rising in people under 70, in South-East Asia, East Asia and Oceania, and in low-SDI countries.
Age and sex: 53% of incident strokes are in people under 70, and 15% in those aged 15–49. Men have 53% of incident strokes.
Cost: over US$890 billion a year (0.66% of global GDP), projected to nearly double by 2050.

Australia

45,785 strokes in 2023 (34,793 first-ever), about one every 11 minutes. Projected to reach about 72,000 a year by 2050.
About half a million survivors.
9,147 stroke deaths in 2024; cerebrovascular disease was the 4th leading cause of death (ABS).
Age-standardised stroke death rate fell 76% between 1980 and 2019 (104 to 25 per 100,000).
Aboriginal and Torres Strait Islander people: stroke death and hospitalisation rates 1.5 times non-Indigenous rates.
Lifetime cost of 2023's strokes: $15.7 billion.

Causes and risk factors

Non-modifiable: age, family history, ancestry (intracranial atherosclerosis and ICH are commoner in Asian populations), sex.
Ischaemic: hypertension, AF, diabetes, raised ApoB/LDL, smoking, carotid or intracranial atherosclerosis, obesity, inactivity, CKD, sleep apnoea. In the young: dissection, PFO, migraine with aura, drugs, thrombophilia.
ICH: hypertension (more strongly linked to ICH than to ischaemic stroke in INTERSTROKE), CAA, anticoagulation, heavy alcohol, sympathomimetics.
SAH: smoking, hypertension, heavy alcohol, family history, ADPKD.
Women: pregnancy and postpartum, hypertensive disorders of pregnancy, oral oestrogen, migraine with aura.
INTERSTROKE: smoking, diabetes, ApoB/ApoA1 and cardiac causes were more strongly linked to ischaemic stroke than to ICH.

Preventable factors

INTERSTROKE (32 countries, 13,447 cases, Lancet 2016)

Ten factors explain 90.7% of population attributable risk (PAR), similar in men and women and in younger and older patients.
PAR by factor: hypertension 47.9%, physical inactivity 35.8%, ApoB/ApoA1 26.8%, poor diet 23.2%, waist-to-hip ratio 18.6%, smoking 12.4%, cardiac causes 9.1%, alcohol 5.8%, diabetes 3.9%. Psychosocial stress was also significant.

GBD 2021 attributable DALYs

High SBP 56.8%
Ambient particulate matter 16.6%
Smoking 13.7%
High LDL 13.1%
Household air pollution 11.2%
High sodium 10.6%
High fasting glucose 10.3%
Kidney dysfunction 9.3%
By cluster: metabolic 68.8%, environmental 36.7%, behavioural 35.2%.
Fastest rising, 1990–2021: high BMI +88%, high ambient temperature +72%, high fasting glucose +32%, sugar-sweetened beverages +23%.
Falling: smoking −13%, low vegetable intake −30%.
Heat caused almost 2 million stroke DALYs in 2021, so climate is now a stroke risk factor.

Diagnosis essentials

Pre-hospital: FAST recognition and an LVO screen. AHA/ASA 2026 advises taking suspected LVO direct to the nearest thrombectomy-capable centre where access is reasonable.
Imaging: non-contrast CT within 25 minutes of arrival (AHA/ASA 2026), then CTA arch-to-vertex, with CTP or MRI for extended windows or unclear cases. Don't delay thrombolysis for CTA or CTP.
ASPECTS on plain CT can select EVT candidates where perfusion imaging is unavailable.
NIHSS (0–42) grades severity. Low scores can hide disabling deficits (aphasia, hemianopia, gait ataxia).
Mimics: hypoglycaemia, seizure or Todd's paresis, migraine aura, functional disorder, sepsis unmasking an old deficit, tumour, subdural haematoma.
Chameleons: posterior circulation stroke presenting as isolated vertigo. Use HINTS and a low threshold for MRI.
Work-up: ECG and prolonged rhythm monitoring (longer monitoring finds more AF), echo (bubble study in the young), carotid and intracranial imaging, lipids, HbA1c. Screen for vasculitis, thrombophilia or dissection when indicated.
TIA: NICE NG128 advises against using ABCD2 or other scores to triage. Assess suspected TIA within 24 hours.
Where AI fits: automated LVO alerts, core and penumbra maps and ASPECTS scoring speed triage and transfer. Evidence of better patient outcomes is mostly observational, and medium or distal occlusions are easily missed. It supports a clinician's read but doesn't replace one.

Current treatment

IV thrombolysis

Within 4.5 hours: tenecteplase 0.25 mg/kg (max 25 mg) single bolus, or alteplase 0.9 mg/kg (max 90 mg). Both are endorsed by AHA/ASA 2026 and the Stroke Foundation.
Time-dependence (Emberson 2014, 6,756 patients, alteplase): odds of a good outcome were 1.75 at 3 hours or less, 1.26 at 3–4.5 hours, and 1.15 (non-significant) beyond 4.5 hours.
Cost in bleeding (same analysis): fatal parenchymal haemorrhage 2.7% vs 0.4%.
Tenecteplase vs alteplase: AcT (n=1,600): mRS 0–1 36.9% vs 34.8% (non-inferior), sICH 3.4% vs 3.2%, mortality 15.3% vs 15.4%. ATTEST-2 (n=1,858) and TRACE-2 were also non-inferior. Tenecteplase is easier: one bolus and no infusion during transfer.
Extended windows: the Stroke Foundation allows alteplase up to 9 hours with perfusion mismatch. AHA/ASA 2026 allows thrombolysis up to 24 hours in selected imaging-selected patients.
TRACE-III (tenecteplase at 4.5–24 hours for LVO with no EVT access): mRS 0–1 33.0% vs 24.2%, sICH 3.0% vs 0.8%. TIMELESS (tenecteplase before EVT at 4.5–24 hours) was neutral.

Endovascular thrombectomy (EVT)

HERMES (5 RCTs, n=1,287): mRS 0–2 46.0% vs 26.5% (NNT about 5 for independence; 2.6 for one-step mRS shift). No excess mortality or sICH.
Late window: DAWN mRS 0–2 49% vs 13%. DEFUSE 3 45% vs 17%, with mortality 14% vs 26%.
Large core: MAGNA pooled RESCUE-Japan LIMIT, SELECT2 and ANGEL-ASPECT (n=1,009): mRS 0–2 23% vs 9%, mRS 0–3 41% vs 24%, sICH 1.8% vs 1.6%, mortality 27% vs 28%. Benefit extended up to an estimated core of about 150 mL. TENSION and LASTE also support EVT.
AHA/ASA 2026 recommends EVT for ASPECTS 3–5 up to 24 hours (age under 80, NIHSS 6 or more, no significant mass effect).
Basilar occlusion: mRS 0–3 46% vs 23% in ATTENTION (mortality 37% vs 55%) and 46% vs 24% in BAOCHE.
Blood pressure after successful EVT: ENCHANTED2/MT target below 120 mmHg worsened function (OR 1.37). AHA/ASA 2026 lists intensive lowering below 140 mmHg after recanalisation as harmful.

Systems and stroke unit care

Mobile stroke units: BEST-MSU (n=1,047) utility-weighted mRS 0.726 vs 0.657. 33% vs 3% were thrombolysed within 60 minutes of onset. AHA/ASA 2026 gives class 1 where available.
Stroke units (Cochrane): death OR 0.81, death or dependency OR 0.79 vs general wards. The benefit lasts to 5 years.
QASC (Australia): nurse-led fever, sugar and swallowing protocols cut 90-day death or dependency from 58% to 42% (NNT 6.4).
AVERT (Australia): very early, high-dose mobilisation within 24 hours was worse: mRS 0–2 46% vs 50%, OR 0.73.

Intracerebral haemorrhage

INTERACT3 bundle (n=7,036): SBP below 140 within 1 hour, glucose control, temperature 37.5 °C or less, and warfarin reversal to INR below 1.5 within 1.5 hours. Ordinal mRS OR 0.86 (0.76–0.97).
Reversal: warfarin: 4-factor PCC plus vitamin K. Dabigatran: idarucizumab.
Factor Xa inhibitors, ANNEXA-I: andexanet improved haemostatic efficacy (67.0% vs 53.1%) but increased thrombotic events (10.3% vs 5.6%), including ischaemic stroke 6.5% vs 1.5%, with no mortality difference.
Surgery, ENRICH: minimally invasive evacuation within 24 hours of 30–80 mL ICH improved 180-day utility-weighted mRS (0.458 vs 0.374). Benefit was confined to lobar haematomas.

Secondary prevention

Short DAPT (minor stroke or high-risk TIA):
- CHANCE: 8.2% vs 11.7%, HR 0.68, no bleeding excess.
- POINT: 5.0% vs 6.5%, HR 0.75; major haemorrhage 0.9% vs 0.4%. Benefit was concentrated in the first 21 days (3.6% vs 5.6%).
- INSPIRES (start within 72 hours, atherosclerotic): 7.3% vs 9.2%, NNT about 53. Bleeding 0.9% vs 0.4%.
- CHANCE-2: in CYP2C19 loss-of-function carriers, ticagrelor plus aspirin gave 6.0% vs 7.6% with clopidogrel plus aspirin.
- Standard approach: 21 days of DAPT, then a single antiplatelet.
AF: a DOAC, started early.
- ELAN (n=2,013): 30-day composite 2.9% early vs 4.1% later.
- OPTIMAS (n=3,648): 3.3% in both arms (non-inferior).
- CATALYST (pooled TIMING, ELAN, OPTIMAS and START, n=5,411): 2.12% vs 3.02% at 30 days, OR 0.70, with no excess sICH.
ESUS: DOACs failed in NAVIGATE ESUS, RE-SPECT ESUS and ARCADIA (atrial cardiopathy; 4.4% recurrence in both arms). Look for AF; don't empirically anticoagulate.
Lipids:
- SPARCL (atorvastatin 80 mg): stroke 11.2% vs 13.1%, HR 0.84, NNT 46 over 5 years. More haemorrhagic strokes (55 vs 33).
- TST (LDL target below 1.8 mmol/L): 8.5% vs 10.9%, HR 0.78.
- Stroke Foundation and AHA target: LDL below 1.8 mmol/L (70 mg/dL), adding ezetimibe and then a PCSK9 inhibitor if needed.
Blood pressure: target below 130/80 for most (AHA/ASA 2021).
PFO: individual-patient meta-analysis (6 RCTs, n=3,740): HR 0.41; annual stroke 0.47% vs 1.09%. By PASCAL category, "probable" HR 0.10 but "unlikely" HR 1.14. The Stroke Foundation recommends closure under 60 when the PFO is the likely cause.
Symptomatic carotid stenosis 70–99%: NASCET showed 2-year ipsilateral stroke 26% with medical treatment vs 9% with endarterectomy (ARR 17%, NNT about 6). Operate early.
Asymptomatic carotid stenosis, CREST-2: stenting plus intensive medical treatment 2.8% vs 6.0%. Endarterectomy 3.7% vs 5.3% (not significant).

Rehabilitation

Early, task-specific, high-repetition therapy delivered by a stroke-unit team.
Progressive resistance training for weakness is a strong Stroke Foundation recommendation.
Avoid very early high-dose mobilisation (AVERT).
Screen for mood, cognition, fatigue, dysphagia and secondary prevention adherence.

Emerging treatments and trials

Factor XI(a) inhibitors

OCEANIC-STROKE (asundexian 50 mg with antiplatelets, n=12,237, NEJM 2026): ischaemic stroke 6.2% vs 8.4%, HR 0.74, NNT 53 at 1 year. ISTH major bleeding 1.9% vs 1.7% (not significant).
Asundexian is not yet approved anywhere; it has FDA Fast Track status. OCEANIC-AF was stopped early because asundexian was less effective than apixaban.
LIBREXIA-STROKE (milvexian) and LIBREXIA-AF are ongoing and expected to report in 2027. LIBREXIA-ACS stopped for futility (MACE HR 1.05).

Neuroprotection

Nerinetide: ESCAPE-NA1 was neutral overall (RR 1.04), but in the no-alteplase subgroup mRS 0–2 was 59.3% vs 49.6%. Plasmin generated by alteplase is thought to cleave the peptide.
ESCAPE-NEXT and FRONTIER were both neutral. A pooled analysis suggests benefit within 3 hours with reperfusion; ACT-42 is underway.
ApTOLL (TLR4 antagonist): the phase 1b/2a APRIL trial (n=151, with EVT) gave encouraging safety and mortality signals. Phase 2b/3 is planned.

Medium and distal vessel occlusion (EVT)

ESCAPE-MeVO (n=530): mRS 0–1 41.6% vs 43.1%; mortality 13.3% vs 8.4%; sICH 5.4% vs 2.2%.
DISTAL (n=543): common OR 0.90; sICH 5.9% vs 2.6%.
DISCOUNT was stopped early. Treat medium and distal occlusions outside trials only selectively.

Anti-inflammatory

Colchicine: CONVINCE (n=3,154) HR 0.84 (0.68–1.05), missing its primary endpoint, with a per-protocol signal.
CHANCE-3 (n=8,343): 6.3% vs 6.5%, HR 0.98.

Oedema

IV glibenclamide, CHARM (n=535, large hemispheric infarction): primary endpoint neutral, with subgroup signals (lesion volume under 125 mL).
CHARM was stopped early for business reasons.

Recovery

Vagus nerve stimulation paired with rehab, VNS-REHAB (n=108, chronic stroke): Fugl-Meyer upper limb score improved 5.0 vs 2.4 points.
Stem cells: TREASURE (MultiStem, n=206) was neutral (excellent outcome 11.5% vs 9.8%). MASTERS-2 is ongoing.

Gaps and open questions

Labelled hypotheses, not recommendations.

Hypothesis: small vessel disease is under-treated. Lacunes, white matter disease and much vascular dementia share one pathology with no proven disease-modifying drug. Endothelial and blood–brain-barrier targets deserve definitive trials.
Hypothesis: ICH needs its own drugs. ICH causes about half of global stroke DALYs, and close to a third of strokes in LMICs. Yet beyond the INTERACT3 bundle and lobar surgery, no drug has improved outcome. Haemostasis in non-anticoagulated ICH and CAA-specific therapy remain open.
Hypothesis: "ESUS" is several diseases. Three neutral DOAC trials suggest a mixed group (non-stenotic plaque, occult cancer, atrial cardiopathy without AF). Mechanism-stratified trials using imaging and biomarkers are the logical next step.
Hypothesis: neuroprotection failed on timing, not biology. Most agents were tested without reliable reperfusion. The nerinetide no-alteplase and early-window signals argue for testing agents given with or before EVT, including in the ambulance.
Hypothesis: anti-inflammatory therapy works in a subset. CONVINCE's per-protocol signal and coronary colchicine data suggest benefit may be confined to atherosclerotic or high-inflammation phenotypes. This is untested prospectively.
Hypothesis: AF after ICH has an untested best option. The choice between DOAC, left atrial appendage occlusion or nothing rests on small or ongoing trials.
Excluded populations: the very old, people with pre-stroke disability, pregnancy, and patients from LMICs, where ICH is a bigger share, are under-represented. So are Indigenous populations, despite 1.5 times higher Australian stroke mortality.
Implementation gap (Australia):
- About 13% thrombolysed (AuSCR 2024).
- Median door-to-needle 67 minutes; only 11 of 62 hospitals met the 60-minute target.
- 72% admitted to a stroke unit, but only 48% got 90% or more of their care there (Audit 2023).
- Regional patients were 76% less likely to reach a stroke unit.
- Rural access to EVT, not new drugs, may be the biggest unclaimed gain.
Hypothesis: prevention needs population levers. High BMI, glucose, heat and air pollution are rising contributors. Population sodium reduction, polypills and clean-air policy probably have larger effects than any new drug, but trials of stroke outcomes are scarce.
Hypothesis: post-stroke fatigue and depression are neglected. Fatigue affects about half of survivors and has no proven treatment. Depression treatment is under-tested as a target for functional recovery.

Prognosis and quality of life

Short term (AuSCR 2024): about 1 in 5 patients died. At 3–6 months about a third had moderate to severe disability, and about half reported anxiety, depression or problems with usual activities.
ICH: early mortality 30–40%, the deadliest stroke type.
Recurrence after first stroke (Mohan 2011): 3.1% at 30 days, 11.1% at 1 year, 26.4% at 5 years, 39.2% at 10 years. Modern secondary prevention probably lowers this; WSO cites 10–16% at 1 year.
Depression: 31% at any time point (61 studies, 25,488 people).
Fatigue: 48% (35 studies).
Cognition: cognitive impairment without dementia is common in the first year. Screen routinely.
Return to work (among those employed before): 55.7% at 1 year, 67.4% at 2 years.
Change over time: Australian age-standardised stroke death rate down 76% (1980–2019); event rates down 25% (2001–2018). Globally, age-standardised rates are falling but total burden is rising with population growth and ageing.

Guidelines

Key trials

NASCET (1991): endarterectomy for symptomatic 70–99% stenosis, ARR 17% at 2 years.
SPARCL (2006): atorvastatin 80 mg, stroke HR 0.84.
QASC (2011): fever, sugar and swallow protocols, NNT 6.4.
CHANCE (2013): 21-day DAPT, stroke 8.2% vs 11.7%.
Emberson IPD (2014): alteplase benefit falls with time; none beyond 4.5 hours.
AVERT (2015): very early mobilisation was harmful.
HERMES (2016): EVT, mRS 0–2 46% vs 26.5%.
INTERSTROKE (2016): 10 factors, PAR 90.7%.
DAWN and DEFUSE 3 (2018): EVT to 24 hours with imaging selection.
POINT (2018): DAPT benefit concentrated in the first 21 days.
TST (2020): LDL below 1.8 mmol/L, HR 0.78.
ESCAPE-NA1 (2020): nerinetide neutral overall.
CHANCE-2 (2021): ticagrelor in CYP2C19 loss-of-function carriers, HR 0.77.
PFO IPD (2021): closure HR 0.41, driven by PASCAL "probable" and "possible".
VNS-REHAB (2021): Fugl-Meyer upper limb +5.0 vs +2.4.
AcT (2022): tenecteplase non-inferior to alteplase.
ATTENTION and BAOCHE (2022): EVT for basilar occlusion, mRS 0–3 46% vs 23–24%.
ENCHANTED2/MT (2022): SBP below 120 after EVT was harmful.
SELECT2, ANGEL-ASPECT, RESCUE-Japan LIMIT (2022–23): EVT for large core.
ELAN (2023): early DOAC after AF stroke is safe.
INSPIRES (2023): DAPT up to 72 hours, 7.3% vs 9.2%.
INTERACT3 (2023): ICH care bundle, OR 0.86.
ARCADIA (2024): apixaban no better than aspirin in atrial cardiopathy.
ANNEXA-I (2024): andexanet improves haemostasis but more thrombosis.
CONVINCE and CHANCE-3 (2024): colchicine neutral.
ENRICH (2024): minimally invasive surgery for lobar ICH helps.
OPTIMAS (2024): early DOAC non-inferior.
TRACE-III (2024): tenecteplase at 4.5–24 hours without EVT, mRS 0–1 33% vs 24%.
ATTEST-2 (2024): tenecteplase non-inferior.
ESCAPE-MeVO and DISTAL (2025): EVT for medium and distal occlusion, no benefit.
CREST-2 (2025): stenting beat medical treatment for asymptomatic stenosis; endarterectomy did not.
OCEANIC-STROKE (2026): asundexian HR 0.74, no bleeding excess.

Sources

Information only. Doses, time windows and eligibility vary by jurisdiction and product information. Check local protocols and the current guideline before treating.

Reviewed 29 October 2026. General education for health professionals; not a substitute for local protocols.

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