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Stroke Recognition and Prevention

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Top Contributors - Stacy Schiurring  

Introduction

Stroke consistently ranks among the leading causes of death and disability worldwide; its exact position varies between data sources and shifts over time. The most recent World Stroke Organization figures rank it second for death and third for death and disability combined. Each year, nearly 12 million people have a first stroke, around 94 million people are living as stroke survivors, and one in four adults over 25 will have a stroke in their lifetime..[1]

Most strokes occur in older adults, and incidence rises steeply with age. However, ischaemic stroke in adults under 55 rose significantly between 2002 and 2018, even as rates fell in older groups.[2] Stroke in younger adults is often under-recognised, with symptoms attributed to migraine, anxiety or vestibular disorders.

Rehabilitation professionals see people at risk of stroke in every setting, from outpatient and community care to sports and occupational health. Because they see patients regularly, they are well placed to notice new or transient neurological changes, and prompt escalation can determine whether a patient reaches time-critical treatment. This Physiopedia page summarises how to recognise an acute stroke or transient ischaemic attack (TIA), and how to reduce the risk of a first or recurrent stroke.

Stroke Recognition

Rapid recognition directly affects outcome. In a typical large vessel ischaemic stroke, an estimated 1.9 million neurons are lost every minute that blood flow is not restored.[3]

FAST and BE-FAST

FAST (Face, Arm, Speech, Time) has been the standard public recognition tool since the late 1990s. It is simple and memorable but misses some strokes, particularly posterior circulation strokes presenting with dizziness, visual disturbance or imbalance.

BE-FAST adds Balance and Eyes, and in a retrospective cohort reduced the proportion of strokes missed from 14.1% to 4.4%.[4] This gain in sensitivity costs specificity: in the only prospective prehospital comparison, BE-FAST had 91% sensitivity and 53% specificity, compared with 76% and 68% for FAST, although the differences were not statistically significant.[5] More items may also be harder for the public to remember.[6] FAST remains the basis of many national public campaigns.

What to look for Quick check
Balance Sudden loss of balance, coordination or walking ability Observe gait and sitting balance; note sudden onset
Eyes Sudden blurred or double vision, visual field loss, loss of vision in one or both eyes Ask about vision; check visual fields
Face Unilateral facial droop Ask the person to smile
Arms Unilateral weakness or drift (may include the leg) Raise both arms with eyes closed; watch for drift
Speech Slurred speech, word-finding difficulty or impaired comprehension Ask the person to repeat a simple sentence
Time Note time of onset or time last seen well Call emergency services immediately

Sudden painless vision loss from central retinal artery occlusion is a stroke equivalent and needs emergency referral.[7]

Public Awareness Campaigns Worldwide

In a World Stroke Organization survey of 46 countries, 71% of organisations used a message other than FAST or BE-FAST, often a local adaptation including the national emergency number.[8] Stroke 1-2-0 in China, for example, links FAST signs to the emergency number 120,[9] and school programmes such as FAST Heroes teach children to pass the message to their families.[10] Clinicians should know the message their community uses.

Other Recognition Tools

Clinicians will encounter other tools depending on their setting:

Transient Ischaemic Attack

A TIA is a medical emergency even when symptoms have fully resolved, as stroke risk is highest in the first few days afterwards.[14] NICE recommends immediate referral for specialist assessment within 24 hours.[15]

No screening tool is recommended, so recognition relies on the history. A TIA is more likely when symptoms are sudden, focal and "negative" (a loss of function such as weakness, numbness, vision or speech). Gradually spreading "positive" symptoms (new abnormal sensations or movements), such as tingling, flashing lights or jerking, suggest mimics such as migraine aura or seizure, but should not delay referral.[16] Patients may describe a TIA casually, for example an arm that felt strange for a few minutes, so keep a low threshold for escalation.

Stroke Mimics and Chameleons

Mimics look like stroke but have another cause, such as hypoglycaemia, seizure, migraine with aura, sepsis or functional disorders.[17]

Chameleons are strokes that present atypically and are misdiagnosed, for example as vertigo, confusion or a peripheral nerve problem.[18][19] Posterior circulation strokes and strokes in younger adults are common chameleons.

When onset is sudden, treat the presentation as a possible stroke until proven otherwise.

Prevention: The Best Treatment

Stroke prevention reduces the likelihood of stroke by identifying and managing the factors that raise a person's risk. It is divided into two stages:

  • Primary prevention aims to prevent a first stroke, across the whole population.
  • Secondary prevention aims to prevent recurrence after a stroke or TIA, targeting the mechanism of the first event more intensively.

Both depend on understanding which risk factors can be changed and which cannot. The following sections cover these risk factors and primary prevention, then the additional strategies used in secondary prevention.

Non-Modifiable Risk Factors

Non-modifiable risk factors increase stroke risk but cannot be changed, (eg. age, sex, and genetics). They help identify people in whom modifiable risk factors should be addressed most assertively.[20]

Non-modifiable Risk Factors Key evidence
Age The strongest non-modifiable risk factor; risk rises with each decade[20]
Sex Women have a higher lifetime risk than men, partly due to longer life expectancy and sex-specific factors[20]
Ethnicity People of African, Hispanic and South Asian descent have disproportionately higher stroke rates, reflecting both biological and social factors[20]
Family history and genetics
  • Shared environment and inherited conditions contribute
  • Examples include CADASIL (a hereditary small vessel disease causing recurrent strokes and cognitive decline from midlife), sickle cell disease and inherited clotting disorders[20]
Prior stroke or TIA
  • One of the most important predictors of future stroke
  • The cumulative risk of recurrence is around 11% at one year and 26% at five years[21]

Modifiable Risk Factors

Modifiable risk factors re behaviours and health conditions that can be reduced or controlled through lifestyle change, medication or both, and addressing them is the foundation of primary prevention. The 2024 AHA/ASA Guideline for the Primary Prevention of Stroke aligns with Life's Essential 8, a framework of four lifestyle behaviours and four health factors.

Modifiable Risk Factors Key evidence and targets
Diet
Physical activity
  • At least 150 minutes of moderate or 75 minutes of vigorous activity weekly; shorter bouts count
  • Reducing prolonged sedentary time is also recommended[20]
Tobacco and nicotine
  • Includes cigarettes, e-cigarettes and smokeless products; second-hand smoke also raises risk
  • Screen at every encounter; pharmacotherapy plus behavioural support is most effective[20]
Sleep
  • Both short and long sleep increase risk
  • 7 to 9 hours is optimal[18]
Weight
  • Waist circumference predicts risk better than BMI. Common thresholds are 102 cm (men) and 88 cm (women), with lower thresholds for some ethnic groups, such as South Asian populations[22]
  • A 5 to 10% weight loss improves blood pressure, glucose and lipids[20]
Cholesterol
  • Elevated LDL cholesterol drives atherosclerotic stroke
  • Statins are first-line, with additional agents if targets are not met[20]
Blood glucose
  • Diabetes raises risk in a graded way; prediabetes is a window for prevention
  • GLP-1 receptor agonists are recommended for people with diabetes and high cardiovascular risk[20]
Blood pressure
  • Hypertension is the most important modifiable risk factor, with no threshold below which risk disappears
  • Target is below 130/80 mmHg for adults at higher risk; most people need two or more medications[20]

Risk Factors Beyond Life's Essential 8

  • Atrial fibrillation (AF): increases ischaemic stroke risk around fivefold and causes more severe strokes.[23] Many cases are undiagnosed, so opportunistic pulse palpation is a simple screening step.
  • Alcohol: heavy intake increases risk of both ischaemic and haemorrhagic stroke.[24]
  • Psychosocial stress and depression: independently associated with stroke in the INTERSTROKE study.[24]
  • Air pollution: a leading contributor to global stroke burden, particularly in low- and middle-income countries.[25]

Social Determinants and Special Populations

Social Determinants of Health

Social determinants of health Social determinants of health are the non-medical conditions in which people are born, grow, live, work and age, and the wider systems that shape them.[26] Income, education, housing, food security, access to healthcare and discrimination shape stroke risk and recovery, and whether a person can act on prevention advice. Adapt advice accordingly, for example a home-based programme when transport is a barrier, or affordable dietary swaps when fresh produce is inaccessible.

Special Populations

Some groups have a distinct or under-recognised stroke risk profile.

Population Key risk considerations Clinical implications
Women
  • Hypertensive disorders of pregnancy, pre-eclampsia, gestational diabetes and preterm birth signal vascular risk decades later.
  • Migraine with aura is an independent risk factor, compounded by smoking and combined hormonal contraception.
  • Early menopause, premature ovarian insufficiency and endometriosis also increase risk.[20]
  • Include pregnancy and reproductive history in assessment.
  • Flag combined hormonal contraception in women over 35 or with smoking, hypertension or migraine with aura.
Younger adults
  • Traditional risk factors remain the most common contributors but are often under-screened.[27]
  • Cervical artery dissection, patent foramen ovale (PFO), inherited clotting disorders, and cocaine or amphetamine use are more common causes. Evidence on cannabis is mixed.[28][29]
  • A higher proportion of strokes are cryptogenic.
  • Screen for traditional risk factors regardless of age and ask about substance use.
  • Explain that a cryptogenic diagnosis reflects the limits of current tests, not an incomplete workup.
People with pre-existing disabilities
  • Spinal cord injury is associated with nearly three times the risk of stroke.[30]
  • Cerebral palsy is associated with more than double the risk, and nearly five times the risk under 50.[31]
  • Evidence for multiple sclerosis is conflicting.[32][33]
  • Reduced activity, altered metabolism, medication effects and barriers to preventive care all contribute.
  • New vascular symptoms can be mistaken for the existing condition, so keep a low threshold for referral.
  • Use adapted exercise, such as seated exercise, arm ergometry, aquatic therapy or FES (functional electrical stimulation) cycling.

Secondary Prevention

Secondary prevention reduces the risk of a further stroke after stroke or TIA. It builds on primary prevention but pursues targets more intensively and is tailored to the mechanism of the first event.[34] About one in four strokes is recurrent.[35] et recurrence is largely preventable, and falling five-year recurrence rates may partly reflect better secondary prevention.[21]

Stroke Mechanisms

The TOAST classification, developed in 1993 for the Trial of Org 10172 in Acute Stroke Treatment, is the most widely used system for classifying ischaemic stroke by mechanism. It assigns each stroke to one of five subtypes using clinical features and investigations such as brain and vascular imaging, cardiac assessment and blood tests, and does not apply to haemorrhagic stroke.[39] Knowing the subtype helps the therapist understand the patient's medication and ongoing risk.[36]

TOAST Classification Subtypes Mechanism Main prevention approach
Cardioembolic
  • Clot forms in the heart, most often due to atrial fibrillation, then travels to the brain
  • Strokes are often severe and may affect several territories
  • Anticoagulation
Large artery atherosclerosis
  • Plaque in the carotid, vertebral or large intracranial arteries narrows the vessel or releases emboli
  • Preceding TIAs in the same territory are common
  • Antiplatelets
  • Intensive lipid lowering
  • Carotid revascularisation where indicated
Small vessel disease
  • Chronic hypertension damages small penetrating arteries, causing lacunar infarcts
  • Cumulative damage is linked to vascular cognitive impairment
  • Blood pressure control
  • Antiplatelets
Other determined cause For example arterial dissection, thrombophilia or vasculitis Specific to the cause
Undetermined
  • Includes two or more possible causes, an incomplete evaluation, or no cause found despite full investigation (cryptogenic stroke)
  • Cryptogenic stroke includes embolic stroke of undetermined source, where patent foramen ovale is sometimes implicated
  • Antiplatelets
  • PFO closure in selected patients

Risk Factor Targets

Risk factor targets are the values for blood pressure, cholesterol and blood glucose the medical team aims to maintain after stroke or TIA. Because the person has already had a vascular event, targets are pursued more intensively.[34]

  • Blood pressure is generally targeted below 130/80 mmHg.[34]
  • For ischaemic stroke with atherosclerosis, AHA/ASA and UK and Ireland guidelines target LDL cholesterol below 1.8 mmol/L (70 mg/dL).[34][35]
  • For people with diabetes, glycaemic targets are individualised in line with diabetes guidance.[34]
  • Targets differ between countries, so clinicians should follow local guidance.

A progressive, well-documented exercise programme is a secondary prevention intervention in its own right.

Antithrombotic Therapy

Antithrombotic medications are used for cardioembolic stroke, and direct oral anticoagulants have largely replaced warfarin for atrial fibrillation. Antiplatelets are used for non-cardioembolic stroke; after a minor stroke or high-risk TIA, patients often take dual antiplatelet therapy for 21 to 90 days before stepping down to a single agent, and bleeding risk is higher during this phase.[34]

Contact sports, high fall-risk activities and vigorous manual therapy are not automatically excluded but need thoughtful discussion, with fall prevention a consistent priority.

Recognising Problems with Antithrombotic Therapy

Antithrombotic therapy balances clotting risk against bleeding risk. Either can change on a stable prescription, for example after missed doses, a new interacting medication, or declining kidney function, which slows clearance of many anticoagulants.[37]

Signs of a possible new stroke or TIA: any new BE-FAST symptom, even if brief. Do not attribute it to fatigue or the existing stroke; treat it as a suspected stroke and activate emergency services.

Signs of excessive bleeding: minor bruising is expected, but these red flags need immediate medical attention::[38]

  • sudden severe headache, reduced consciousness or new neurological signs
  • any head injury in a person taking an anticoagulant, even if minor, or a major fall[39]
  • large or rapidly expanding bruises
  • bleeding that does not stop with pressure
  • dizziness, collapse or other signs of haemodynamic compromise

Role of the Rehabilitation Professional

Rehabilitation professionals see patients often and over long periods, so they can contribute at every stage of prevention.

Screening: use BE-FAST quickly, ask about brief or transient symptoms, palpate the pulse for irregularity suggesting atrial fibrillation, and use STOP-Bang when sleep apnoea is suspected. Refer any new neurological symptom promptly, even if resolved.

Monitoring: check blood pressure before and after exercise to detect poorly controlled hypertension or overtreatment. Know whether a patient has diabetes and recognise hypoglycaemia. Report unexplained symmetrical proximal muscle pain or weakness in patients taking statins for medical review; many such symptoms also occur on placebo, so patients should not stop the statin themselves.[40] Watch for bleeding during antithrombotic therapy, particularly dual antiplatelet therapy.

Exercise and education: an individualised, progressive aerobic and strengthening programme is both rehabilitation and prevention. Linking prevention to the patient's own goals, such as walking to the shops or playing with grandchildren, and adapting advice to their circumstances supports long-term adherence.

Resources

Practice Guidelines:

Optional Additional Reading:

References

  1. ↑ Feigin VL, Brainin M, Norrving B, Martins SO, Pandian J, Lindsay P, F Grupper M, Rautalin I. World stroke organization: global stroke fact sheet 2025. International Journal of Stroke. 2025 Feb;20(2):132-44.
  2. ↑ Li L, Scott CA, Rothwell PM. Association of younger vs older ages with changes in incidence of stroke and other vascular events, 2002-2018. Jama. 2022 Aug 9;328(6):563-74.
  3. ↑ Saver JL. Time is brain—quantified. Stroke. 2006 Jan 1;37(1):263-6.
  4. ↑ Aroor S, Singh R, Goldstein LB. BE-FAST (balance, eyes, face, arm, speech, time) reducing the proportion of strokes missed using the FAST mnemonic. Stroke. 2017 Feb;48(2):479-81.
  5. ↑ Pickham D, Valdez A, Demeestere J, Lemmens R, Diaz L, Hopper S, de la Cuesta K, Rackover F, Miller K, Lansberg MG. Prognostic value of BEFAST vs. FAST to identify stroke in a prehospital setting. Prehospital Emergency Care. 2019 Mar 4;23(2):195-200.
  6. ↑ Darkhabani MZ, Homa‐Bonell JK, Thoreson L, Bobholz JA, Spaulding D, Engebose M. BE FAST versus FAST: a randomized pilot trial comparing retention of stroke symptoms between 2 mnemonics. Journal of the American Heart Association. 2024 Oct 1;13(19):e035696.
  7. ↑ Mac Grory B, Schrag M, Biousse V, Furie KL, Gerhard-Herman M, Lavin PJ, Sobrin L, Tjoumakaris SI, Weyand CM, Yaghi S, American Heart Association Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; and Council on Peripheral Vascular Disease. Management of central retinal artery occlusion: a scientific statement from the American Heart Association. Stroke. 2021 Jun;52(6):e282-94.
  8. ↑ Singh H, Belson S, Beauchamp JE, Nelson ML. Examining stroke symptom messages implemented globally: a need for contextually relevant stroke symptom messaging. Journal of Nursing Scholarship. 2026 Jan;58(1):e70059.
  9. ↑ Zhao J, Ji Q, Ji X, Liu R. Updating “Stroke 1‐2‐0” by Extending Recognition to Posterior‐Circulation Stroke and Reinforcing Rapid Action in China. CNS Neuroscience & Therapeutics. 2026 Jan 27;32(1):e70764.
  10. ↑ Tsakpounidou K, van der Merwe J, Klinke ME, Webb C, Ouriques Martins SC, Proios H. FAST heroes: results of cross-country implementation of a global school-based stroke education campaign. Frontiers in Public Health. 2022 Apr 18;10:849023.
  11. ↑ Nor AM, Davis J, Sen B, Shipsey D, Louw SJ, Dyker AG, Davis M, Ford GA. The Recognition of Stroke in the Emergency Room (ROSIER) scale: development and validation of a stroke recognition instrument. The Lancet Neurology. 2005 Nov 1;4(11):727-34.
  12. ↑ Pérez de la Ossa N, Carrera D, Gorchs M, Querol M, Millán M, Gomis M, Dorado L, López-Cancio E, Hernández-Pérez M, Chicharro V, Escalada X. Design and validation of a prehospital stroke scale to predict large arterial occlusion: the rapid arterial occlusion evaluation scale. Stroke. 2014 Jan;45(1):87-91.
  13. ↑ Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov 1;40(11):3504-10.
  14. ↑ Giles MF, Rothwell PM. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. The Lancet Neurology. 2007 Dec 1;6(12):1063-72.
  15. ↑ NG128 NI. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management. Guideline (NG128). 2019 May.
  16. ↑ Nadarajan V, Perry RJ, Johnson J, Werring DJ. Transient ischaemic attacks: mimics and chameleons. Practical neurology. 2014 Feb;14(1):23-31.
  17. ↑ Fernandes PM, Whiteley WN, Hart SR, Al-Shahi Salman R. Strokes: mimics and chameleons. Practical neurology. 2013 Feb;13(1):21-8.
  18. ↑ 18.0 18.1 Lloyd-Jones DM, Allen NB, Anderson CA, Black T, Brewer LC, Foraker RE, Grandner MA, Lavretsky H, Perak AM, Sharma G, Rosamond W. Life’s essential 8: updating and enhancing the American Heart Association’s construct of cardiovascular health: a presidential advisory from the American Heart Association. Circulation. 2022 Aug 2;146(5):e18-43.
  19. ↑ 19.0 19.1 Rauber F, da Costa Louzada ML, Chang K, Huybrechts I, Gunter MJ, Monteiro CA, Vamos EP, Levy RB. Implications of food ultra-processing on cardiovascular risk considering plant origin foods: an analysis of the UK Biobank cohort. The Lancet Regional Health–Europe. 2024 Aug 1;43.
  20. ↑ 20.00 20.01 20.02 20.03 20.04 20.05 20.06 20.07 20.08 20.09 20.10 20.11 20.12 Bushnell C, Kernan WN, Sharrief AZ, et al. 2024 Guideline for the Primary Prevention of Stroke: a guideline from the American Heart Association/American Stroke Association. Stroke. 2024;55(12):e344-e424.
  21. ↑ 21.0 21.1 Mohan KM, Wolfe CD, Rudd AG, Heuschmann PU, Kolominsky-Rabas PL, Grieve AP. Risk and cumulative risk of stroke recurrence: a systematic review and meta-analysis. Stroke. 2011 May;42(5):1489-94.
  22. ↑ Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith Jr SC. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; American heart association; world heart federation; international atherosclerosis society; and international association for the study of obesity. Circulation. 2009 Oct 20;120(16):1640-5.
  23. ↑ Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. stroke. 1991 Aug;22(8):983-8.
  24. ↑ 24.0 24.1 O'Donnell MJ, Chin SL, Rangarajan S, Xavier D, Liu L, Zhang H, Rao-Melacini P, Zhang X, Pais P, Agapay S, Lopez-Jaramillo P. Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): a case-control study. The lancet. 2016 Aug 20;388(10046):761-75.
  25. ↑ GBD 2021 Stroke Risk Factor Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2021. Lancet Neurol. 2024;23(10):973-1003.
  26. ↑ World Health Organization. Social determinants of health. Geneva: WHO. Available from:https://www.who.int/health-topics/social-determinants-of-health#tab=tab_1 (last accessed: 30 September 2026).
  27. ↑ Ekker MS, Verhoeven JI, Schellekens MM, Boot EM, Van Alebeek ME, Brouwers PJ, Arntz RM, Van Dijk GW, Gons RA, Van Uden IW, Den Heijer T. Risk factors and causes of ischemic stroke in 1322 young adults. Stroke. 2023 Feb;54(2):439-47.
  28. ↑ Dutta T, Ryan KA, Thompson O, Lopez H, Fecteau N, Sparks MJ, Chaturvedi S, Cronin C, Mehndiratta P, Nunez Gonzalez JR, Phipps M. Marijuana use and the risk of early ischemic stroke: the stroke prevention in young adults study. Stroke. 2021 Oct;52(10):3184-90.
  29. ↑ Liu D, Yang L, Liu P, Wang Y, Gao L. Impact of cannabis abuse on the occurrence of stroke in young people: a systematic review and meta-analysis. Frontiers in Neurology. 2024 Oct 22;15:1426023.
  30. ↑ Wu JC, Chen YC, Liu L, Chen TJ, Huang WC, Cheng H, Tung-Ping S. Increased risk of stroke after spinal cord injury: a nationwide 4-year follow-up cohort study. Neurology. 2012 Apr 3;78(14):1051-7.
  31. ↑ Wu CW, Huang SW, Lin JW, Liou TH, Chou LC, Lin HW. Risk of stroke among patients with cerebral palsy: a population‐based cohort study. Developmental Medicine & Child Neurology. 2017 Jan;59(1):52-6.
  32. ↑ Tseng CH, Huang WS, Lin CL, Chang YJ. Increased risk of ischaemic stroke among patients with multiple sclerosis. European journal of neurology. 2015 Mar;22(3):500-6.
  33. ↑ Yahav A, Ryan D, Golan D, Weinstein G, Arbel A, Barnett-Griness O, Auriel E, Saliba W. Association between multiple sclerosis and the risk of stroke: A population-based retrospective cohort study. Multiple Sclerosis and Related Disorders. 2025 Sep 1:106715.
  34. ↑ 34.0 34.1 34.2 34.3 34.4 34.5 Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, Kamel H, Kernan WN, Kittner SJ, Leira EC, Lennon O. 2021 guideline for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline from the American Heart Association/American Stroke Association. Stroke. 2021 Jul;52(7):e364-467.
  35. ↑ 35.0 35.1 Party IS. National clinical guideline for stroke for the UK and Ireland. London: Intercollegiate Stroke Working Party. 2023 May 4.
  36. ↑ Adams Jr HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh 3rd EE. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. stroke. 1993 Jan;24(1):35-41.
  37. ↑ Steffel J, Collins R, Antz M, Cornu P, Desteghe L, Haeusler KG, Oldgren J, Reinecke H, Roldan-Schilling V, Rowell N, Sinnaeve P. 2021 European Heart Rhythm Association practical guide on the use of non-vitamin K antagonist oral anticoagulants in patients with atrial fibrillation. Ep Europace. 2021 Oct 1;23(10):1612-76.
  38. ↑ Kumbhani DJ, Cannon CP, Beavers CJ, Bhatt DL, Cuker A, Gluckman TJ, Marine JE, Mehran R, Messe SR, Patel NS, Peterson BE. 2020 ACC expert consensus decision pathway for anticoagulant and antiplatelet therapy in patients with atrial fibrillation or venous thromboembolism undergoing percutaneous coronary intervention or with atherosclerotic cardiovascular disease: a report of the American College of Cardiology Solution Set Oversight Committee. Journal of the American College of Cardiology. 2021 Feb 9;77(5):629-58.
  39. ↑ National Institute for Health and Care Excellence. Head injury: assessment and early management (NG232). London: NICE; 2023.
  40. ↑ Howard JP, Wood FA, Finegold JA, Nowbar AN, Thompson DM, Arnold AD, Rajkumar CA, Connolly S, Cegla J, Stride C, Sever P. Side effect patterns in a crossover trial of statin, placebo, and no treatment. Journal of the American College of Cardiology. 2021 Sep 21;78(12):1210-22.
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