Ischemic Stroke & Transient Ischemic Attack 4

Question 1

What are lacunar strokes?

Answer 1

These infarcts are less than 1.5 cm in diameter and are caused by the occlusion of a single small penetrating artery that supplies one of the deep structures in the brain, such as the internal capsule, basal ganglia, corona radiata, thalamus, and brainstem.

Question 2

What is the percentage of lacunar strokes?

Answer 2

15-30% of strokes

Question 3

Pathogenesis of lacunar strokes

Answer 3

These small artery infarcts occur from long-standing hypertension or diabetes, with associated lipohyalinosis or microatheroma leading to narrowing to the point of occlusion through thrombosis

Τα κενοχωριώδη μπορεί επίσης να οφείλονται σε κολπική μαρμαρυγή!!

33ο Πανελλήνιο

Question 4

Which conditions is cerebral small disease associated with

Answer 4

Icreased risk of
1) clinical ischemic and hemorrhagic stroke
2) silent infarcts
3) cognitive decline and dementia

Question 5

Modifiable risk factors for cerebral small vessel disease

Answer 5

hypertension
obstructive sleep apnea
diabetes mellitus
hyperlipidemia
tobacco use

Question 6

Common and uncommon forms of cerebrovascular small vessel disease

Answer 6

Question 7

Radiographic phenotypes of small vessel disease

Answer 7

(1) recent small subcortical infarct
(2) white matter hyperintensity
(3) lacune of presumed vascular origin
(4) widened perivascular spaces
(5) cerebral microbleed
(6) brain atrophy

Question 8

Most common site of lacunar infarcts in descending order

Answer 8

putamen, caudate, thalamus, pons, internal capsule, and
subcortical white matter

Question 9

Typical presentations of CAA

Answer 9

1) neurologic findings attributable to acute hemorrhage
2) transient neurologic episodes
3) cognitive impairment or dementia

Question 10

Boston criteria for cerebral amyloid angiopathy

Answer 10

https://radiopaedia.org/articles/boston-criteria-20-for-cerebral-amyloid-angiopathy?lang=us

Question 11

Radiographic findings in CAA

Answer 11

1) cortical hemorrhage
2) cerebral microbleeds
3) superficial siderosis
4) convexal subarachnoid hemorrhage (SAH)
5) silent infarcts
6) white matter hyperintensities
7) MRI-visible perivascular spaces in the centrum semiovale

Question 12

Lobes affected by symptomatic intracranial hemorrhage in CAA in descending order

Answer 12

occipital lobes,
followed by the
frontal, temporal, and parietal
lobes

Question 13

Diagnostic Characteristics of Cerebral Amyloid Angiopathy–Related Transient Focal Neurologic Episodes

Answer 13

Question 14

Which complication is associated with CAA TFNEs

Answer 14

Patients presenting with CAA-associated TFNEs are at high risk for subsequent lobar ICH and death, particularly with TFNEs characterized by motor symptoms and when antithrombotics are utilized

Question 15

Criteria for the diagnosis of cerebral amyloid angiopathy-related inflammation (CAA-ri)

Answer 15

Question 16

CADASIL clinical features

Answer 16

• migraine with aura (often in the third decade of life)
• recurrent subcortical ischemic events (often in the fifth decade of life - present as lacunar syndromes)
• mood disturbances (apathy, major depression, pseudobulbar affect, and bipolar disorder)
• progressive cognitive impairment
• acute confusional episodes

Question 17

CADASIL cause

Answer 17

CADASIL is caused by mutations in the NOTCH3 gene, which maps to the short arm of chromosome 19.

Question 18

Radiographic findings in CADASIL

Answer 18

• subcortical white matter hyperintensities typically involving the external capsule and temporal poles
• clinically apparent and silent lacunar infarcts
• cerebral microbleeds typically located in subcortical regions

Question 19

Does the absence of family history exclude CADASIL?

Answer 19

As CADASIL inheritance is autosomal dominant, significant family history also supports the diagnosis, but given the possibility of variable presentation within families and the possibility of sporadic mutation, the absence of family history does not exclude CADASIL as a potential diagnosis

Question 20

CADASIL diagnosis

Answer 20

The diagnosis of CADASIL is established by genetic analysis with documentation of a typical NOTCH3 pathogenic variant, or by skin biopsy showing granular osmiophilic material (GOM) within small blood vessels.
Skin biopsy is indicated if genetic testing is negative.

Question 21

In which way is CARASIL different from CADASIL

CARASIL etiology

Answer 21

It differs from CADASIL in that it is characterized by spondylosis deformans and alopecia

homozygous mutation in the high-temperature requirement A serine peptidase 1 (HTRA1) gene

Question 22

Suggestions and Considerations for Investigations in Patients With Silent Brain Infarction
AHA/ASA 2017

Answer 22

1) assessment of common vascular risk factors, including hypertension, diabetes mellitus, hyperlipidemia, smoking, and physical inactivity, as well as active screening for AF by pulse assessment followed by ECG as indicated.

2) For patients with an embolic appearing pattern of infarction, that is, single or multiple cortical infarcts or large, nonlacunar subcortical infarcts, prolonged rhythm monitoring for AF might be considered.

3) The role of echocardiography to identify cardiac sources for embolism has not been defined but could be considered when there is an embolic-appearing pattern of silent brain infarction.

4) Noninvasive carotid imaging may be considered to determine the presence or absence of carotid stenosis in patients with silent brain infarction in the carotid perfusion territory because these patients appear to have an intermediate risk for subsequent brain infarction (between the risk for recently symptomatic [<6 month] and asymptomatic carotid artery stenosis) and therefore could be candidates for carotid intervention, depending on the perioperative risk and patient preferences.

5) Routine genetic testing for monogenic causes of cerebral
small vessel disease is not warranted because they are rare.
Genetic testing should be considered only when lacunes are
present in a young patient with extensive WMHs in the absence of sufficient conventional vascular risk factors.
The presence of migraine, cognitive impairment, and a positive family history are additional features of CADASIL, the commonest monogenic disorder that causes cerebral small vessel disease.

Question 23

Suggestions and Considerations for Investigations in Patients With WMHs of Presumed Vascular Origin

AHA/ASA 2017

Answer 23

In patients with excessive WMHs for age, including patients
with beginning confluent or confluent WMHs (periventricular
or subcortical Fazekas score of 2 or 3), we suggest

1) assessment of common vascular risk factors, including
hypertension, diabetes mellitus, hyperlipidemia, smoking,
and physical inactivity.

2) We also suggest active screening for AF by pulse assessment followed by an ECG as indicated.
Investigations for proximal sources of embolism, including carotid imaging and echocardiography, are probably not needed.

3) Routine genetic testing is not indicated and should be reserved for exceptional cases in which the patient is relatively young, other features of CADASIL or other monogenic disorders are present, the WMH is large and confluent, and the burden of WMH is not well accounted for by conventional vascular risk factors.

Question 24

Suggestions and Considerations for Investigations in
Patients With Silent CMBs

AHA/ASA 2017

Answer 24

1) Assesment of common risk factors for ICH, particularly hypertension

2) CT angiography, CT venography, contrast-enhanced
CT, contrast-enhanced MRI, MR angiography, and MR venography can be useful to evaluate large (ie, >1.0 cm in diameter) silent hemorrhages for underlying structural lesions, including vascular malformations and tumors, when there is clinical or radiological suspicion.

3) For silent hemorrhages or microbleeds not attributable to secondary causes such as vascular malformations, the modified Boston criteria are probably useful to classify the likelihood of underlying CAA pathology.

Question 25

Symptoms suggestive of carotid transient ischemic attacks

Answer 25

1) transient ipsilateral monocular blindness (amaurosis fugax)
2) contralateral body weakness or clumsiness
3) contralateral body sensory loss or paresthesias
4) aphasia with dominant hemisphere involvement
5) various degrees of contralateral homonymous visual field detects
6) dysarthria (not in isolation)

(Bradley)

Question 26

Symptoms suggestive of vertebrobasilar transient ischemic attacks

Answer 26

Usually bilateral weakness or clumsiness but may be unilateral or shifting
Bilateral, shifting or crossed (ipsilateral face and contralateral body) sensory loss or paresthesias
Bilateral or contralateral homonymous visual fields defects or binocular vision loss
Two or more of the following symptoms: vertigo, diplopia, dysphagia, dysarthria, and ataxia

Question 27

When to question the diagnosis of TIA

Answer 27

1) incomplete resolution of neurological dysfunction
2) march of symptoms from one part of the body to another

Question 28

Characteristics of amaurosis fugax

Answer 28

Sudden onset of transient monocular visual loss
Attacks are spontaneous and unrelated to positional changes
Vision loss is brief (usually 1-5 minutes) and painless
After an episode the vision is usually fully restored although some patients may have permanent vision loss

Question 29

Lacunar stroke syndromes

Answer 29

A) Pure motor hemiparesis

i) Internal capsule or corona radiata –> Middle cerebral artery
ii) Pons –> Basilar artery penetrator

B) Pure sensory
Thalamus –> Posterior cerebral artery

C) Sensorimotor
Thalamus, internal capsule –>
Middle and posterior cerebral penetrators

D) Ataxic hemiparesis

i) Pons –> Basilar artery
ii) Internal capsule –> Middle cerebral artery

E) Dysarthria—clumsy hand
Internal capsule –> Middle cerebral artery

Question 30

Monogenic cerebral small vessel diseases

Answer 30

1) CADASIL
2) CARASIL
3) PADMAL (pontine autosomal dominant microangiopathy and leukoencephalopathy)
4) Fabry disease
5) MELAS
6) type IV collagen–related diseases (COL4A1/COL4A2 mutations)

Question 31

Sickle cell disease stroke manifestations

Answer 31

1) Ischemic stroke
2) Hemorrhagic stroke
3) Moya-moya vasculopathy

Question 32

Antiphospholipid syndrome: clinical presentation and laboratory testing

Answer 32

Clinical suspicion for antiphospholipid syndrome should be raised in either of the following settings

Thrombotic events – One or more otherwise unexplained venous or arterial thrombotic events or thromboemboli, especially in young patients.

Adverse pregnancy outcomes – One or more specific adverse pregnancy outcomes, including multiple embryonic losses <10 weeks gestation, fetal death after 10 weeks gestation, or premature birth due to severe preeclampsia or placental insufficiency.

We generally perform initial testing around the time of a clinical event, followed by confirmatory testing ≥12 weeks later.
We test for three aPL

*Anticardiolipin antibodies (aCL); immunoglobulin G (IgG) and IgM, by enzyme-linked immunosorbent assay (ELISA)

*Anti-beta2GPI – Anti-beta2 glycoprotein I (anti-beta2GPI) antibodies; IgG and IgM, by ELISA

*Lupus anticoagulant (LA), using a functional clotting assay

Question 33

Moya - moya disease management

Answer 33

In patients with moyamoya disease and a history of ischemic stroke or TIA, surgical revascularization with direct or indirect
extracranial-intracranial bypass can be beneficial for the prevention of ischemic stroke or TIA

Question 34

Percentage of cryptogenic stroke

Answer 34

20-40% of strokes

Question 35

Uncommon causes of ischemic stroke

Answer 35

Question 36

Patients with ischemic stroke or TIA of unknown source despite thorough diagnostic evaluation and no other thrombotic history
who are found to have prothrombin 20210A mutation, activated protein C resistance, elevated factor VIII levels, or deficiencies of
protein C, protein S, or antithrombin III management

Answer 36

Antiplatelet therapy is reasonable to reduce the risk of recurrent stroke or TIA

Question 37

Patients with ischemic stroke or TIA
1) who meet the criteria for the antiphospholipid syndrome
2) who have an isolated antiphospholipid antibody but do not fulfill the criteria for antiphospholipid syndrome

management

Answer 37

1) It is reasonable to anticoagulate with warfarin to reduce the risk of recurrent stroke or TIA

2) antiplatelet therapy alone is recommended to reduce the risk of recurrent stroke

Question 38

Patients with ischemic stroke or TIA in the setting of AF and cancer management

Answer 38

It is reasonable to consider anticoagulation with DOACs in preference to warfarin for stroke prevention

Question 39

Patients with sickle cell disease and prior ischemic stroke or TIA management

Answer 39

1. chronic blood transfusion(s) to reduce hemoglobin S to
   <30% of total hemoglobin is recommended for the prevention of recurrent ischemic stroke.
2. In patients for whom transfusion therapy is not available or practical, treatment with hydroxyurea is reasonable for the prevention of recurrent ischemic stroke

Question 40

patients with ischemic stroke or TIA and symptoms attributed to giant cell arteritis management

Answer 40

1. immediate initiation of oral high-dose glucocorticoids is recommended to reduce recurrent stroke risk.
2. In patients with ischemic stroke or TIA and diagnosis of giant cell arteritis, methotrexate or tocilizumab therapy adjunctive to steroids is reasonable to lower the risk of recurrent stroke

Question 41

Patients with ischemic stroke or TIA and diagnosis of primary CNS angiitis

Answer 41

Induction therapy with glucocorticoids and/or immunosuppressants followed by long-term maintenance therapy with steroid-sparing immunosuppressants is reasonable to lower the risk of stroke recurrence

Question 42

Recommendation on tenecteplase on acute ischemic stroke
ESO 2023

Answer 42

1) For patients with acute ischaemic stroke of <4.5 hrs
duration who are eligible for intravenous thrombolysis,
tenecteplase 0.25 mg/kg can be used as a safe and effective
alternative to alteplase 0.9 mg/kg.
Quality of evidence: Moderate
Strength of recommendation: Strong

2) For patients with acute ischaemic stroke of <4.5hr duration
with prehospital management with a mobile stroke unit
who are eligible for intravenous thrombolysis, we suggest
tenecteplase 0.25 mg/kg over alteplase 0.90 mg/kg to
increase the rate of early reperfusion and to shorten the
time from imaging to treatment initiation.
Quality of evidence: Low
Strength of recommendation: Weak

3) For patients with large vessel occlusion acute ischaemic
stroke of <4.5 hr duration who are eligible for intravenous
thrombolysis, we recommend tenecteplase 0.25 mg/kg over
alteplase 0.9 mg/kg. Intravenous thrombolysis should not
delay mechanical thrombectomy.
Quality of evidence: Moderate
Strength of recommendation: Strong

** Expert consensus statement
All MWG members suggest favouring tenecteplase 0.25 mg/
kg over alteplase 0.9 mg/kg for patients with acute ischaemic stroke of <4.5 hrs duration in light of safety and efficacy
data and because tenecteplase can be administered with a single bolus rather than a 1-hr infusion.
Voting: 9/9 members

** Expert consensus statement
All MWG members suggest that tenecteplase 0.25 mg/kg could be a reasonable alternative to alteplase 0.9 mg/kg for patients with acute ischaemic stroke on awakening from sleep or acute ischemic stroke of unknown onset and who are eligible for intravenous thrombolysis after selection with advanced imaging (FLAIR-DWI mismatch or perfusion mismatch as outlined in the 2021 ESO Guidelines on IVT).
Voting: 9/9 members

Question 43

Acute stroke management in pregnant women
ESO 2022

Answer 43

Evidence-based Recommendation
Available data do not allow a specific recommendation on IVT
in pregnant women with acute ischaemic stroke.

** Expert consensus statement
A majority of members suggests that pregnant women with acute disabling ischaemic stroke, who otherwise meet eligibility criteria, can be treated with IVT after appropriately assessing the benefit/risk profile on an individual basis.

Evidence-based Recommendation
Available data do not allow a specific recommendation on MT
in women with acute ischaemic stroke during pregnancy.

** Expert Consensus Statement
All members suggest that pregnant women with acute ischaemic stroke and large vessel occlusion, who otherwise
meet eligibility criteria, can be treated with MT after appropriate assessment of the benefit/risk profile on an individual basis.
A majority of members suggests that in pregnant women
with acute ischaemic stroke related to large vessel occlusion,
and if MT is available, MT alone should be preferred over IVT
or bridging therapy (IVT + MT).

Question 44

Acute stroke in postpartum women management

Answer 44

Evidence-based Recommendation
Available data do not allow a specific recommendation on IVT
in postpartum women with acute ischaemic stroke.

** Expert Consensus Statement
All members suggest that postpartum women with disabling ischaemic stroke, occurring at least 10 days after delivery, who otherwise meet eligibility criteria, can be treated with IVT with alteplase after appropriate assessment of the benefit/ risk profile on an individual basis.

Evidence-based Recommendation
Available data do not allow a specific recommendation on MT in women with acute ischaemic stroke during the postpartum period (defined as ≥ 10 days < 3 months).

** Expert Consensus Statement
Although there are no currently available data waiting for evidence from clinical studies, it is reasonably plausible that postpartum women with acute ischaemic stroke, who otherwise meet eligibility criteria, might benefit from MT after appropriate assessment of the benefit/risk profile on an individual basis.
Furthermore, a majority of members suggests that, based on the time of stroke onset from delivery, if the risk of bleeding is deemed high, and if MT is available, it is reasonably plausible to prefer MT alone over IVT or bridging therapy (IVT + MT) on an individual basis.

Question 45

Management of acute stroke and extracranial and intracranial dissection
ESO 2022

Answer 45

Evidence-based recommendation
In patients with symptomatic EAD with acute ischemic stroke within 4.5 hours of onset, we suggest using IVT with alteplase, if the standard inclusion / exclusion criteria are met.
Quality of evidence: Low
Strength of recommendation: Weak for an intervention

In patients with symptomatic IAD with acute ischemic stroke within 4.5 hours of onset, there is insufficient data to provide a recommendation.
Quality of evidence: Very low
Strength of recommendation: -

** Expert consensus statement
In patients with an acute ischemic stroke suspected to be caused by IAD, all but one expert suggest that IVT should be considered, after ruling out standard contra-indications, including subtle signs of subarachnoid bleeding on brain imaging

Question 46

Guideline on screening for subclinical atrial fibrillation after stroke or transient ischaemic attack of undetermined origin
ESO 2022

Answer 46

In adult patients with ischaemic stroke or TIA of undetermined
origin:

• we recommend a prolonged cardiac monitoring instead of standard 24 h monitoring to increase the detection of subclinical AF.
• we suggest the use of additional outpatient monitoring compared with in-hospital cardiac rhythm monitoring alone to increase the detection of subclinical AF.
• we suggest the use of implantable devices for cardiac monitoring instead of non-implantable devices to increase the detection of subclinical AF.

Question 47

Causes of spontaneous aortic dissections

Answer 47

1) Marfan syndrome
2) familial thoracic aortic aneurysm or dissection
3) bicuspid aortic valve
4) Loeys-Dietz aneurysm syndrome
5) vascular Ehlers-Danlos syndrome

Question 48

Ascending aortic dissection and stroke: management

Answer 48

Given the high mortality (approximately 60%) of medically treated patients with ascending aortic dissection, emergent surgical repair is generally performed on patients with ascending aortic dissection with or without cerebral ischemia

Question 49

Ποσοστό επανακαναλοποίησης απόφραξης μεγάλου αγγείου μετά από
1) ενδοφλέβια θρομβόλυση
2) μηχανική θρομβεκτομή

Answer 49

1)10%
2) Ως και 95%

ΑΕΕ 2023

Question 50

Μηχανική θρομβεκτομή βασικής (προς το παρόν εκτός κατευθυντήριων οδηγιών)
Ευρήματα από μελέτες (VERITAS)

Answer 50

• 2.5 x higher likelihood of achieving a good outcome (mRS 0-3)
• 2 x higher likelihood of achieving higher independence (mRS 0-2) at 90 days
• Despite increase in sICH mechanical thrombectomy was associated with a significant reduction in mortality (by 44%)

ΑΕΕ 2023

Question 51

Μηχανική θρομβεκτομή σε ασθενείς με εκτεταμένο όγκο εμφράκτου (ASPECTS <6) (προς το παρόν εκτός κατευθυντήριων οδηγιών)
Ευρήματα από μελέτες (LASTE)

Answer 51

• Υπεροχή MT στη βελτίωση της έκβασης στους 3 μήνες
• Μείωση θνησιμότητας
• Μείωση του όγκου του εμφράκτου
• Χωρίς διαφορά στην αποτελεσματικότητα εάν το ASPECTS ήταν 0-2 ή 3-5
• Χωρίς στατιστικά σημαντική αύξηση αιμορραγιών

ΑΕΕ 2023

Question 52

Πλεονεκτήματα tenecteplase από alteplase ως επιλογή πριν από MT

Answer 52

• Δίνεται bolus
• Έχει μεγαλύτερο χρόνο ημιζωής
• Έχει μεγαλύτερη ειδικότητα για το ινώδες
• Μπορεί να συσχετισθεί με λιγότερες συστηματικές και ενδοκράνιες αιμορραγίες
• Πιο χαμηλό PAM-I inhibition (καλύτερη αποτελεσματικότητα)
• Έχει πιο απλό τρόπο χορήγησης (χρειάζεται μία φλέβα, δεν χρειάζεται αντλία)

Μοναδικό μειονέκτημα:
Εάν έχουμε επιπλοκή δεν μπορούμε να διακόψουμε τη χορήγηση

ΑΕΕ 2023

Question 53

Ο συνδυασμός θρομβόλυσης - θρομβεκτομής

Answer 53

Αυξάνει την πιθανότητα επιτυχούς επανακαναλοποίησης (μαλακώνει τον θρόμβο)
Δεν σχετίζεται με αυξημένη θνητότητα
Δεν σχετίζεται με αύξηση συμπτωματικής ενδοκράνιας αιμορραγίας
Σχετίζεται με αύξηση ασυμπτωματικών ενδοκράνιων αιμορραγιών

ΑΕΕ 2023

Question 54

Αντιμετώπιση επιπλοκών ενδοφλέβιας θρομβόλυσης

Answer 54

Ενδοκράνια αιμορραγία:
2-7 % (τενεκτεπλάση 2%)
κρυοκαθίζημα (διορθώνει το ινοδωγόνο)
αν δεν υπάρχει στο νοσοκομείο, μπορούμε να χορηγήσουμε τρανεξαμικό οξύ ή αμινοκαπροϊκό
διόρθωση ΑΠ: συστολική 140 εντός του πρώτου 2ώρου

Συστηματική αιμορραγία: 2%

Στοματογλωσσικό αγγειοοίδημα:
2%
Συμβαίνει κατά την ώρα της θρομβόλυσης ή σύντομα μετά τη θρομβόλυση
Στην αρχή ετερόπλευρα αντίθετα από τη μεριά του ισχαιμικού
Σχείζεται με προηγούμενη λήψη α-ΜΕΑ και ισχαιμικά έμφρακτα που εντοπίζονται στη νήσο
Η1/ Η2 ανταγωνιστές ισταμίνης - αν δεν περνά κορτιζόνη - αν δεν περνά αδρεναλίνη - πιθανή διασωλήνωση

Question 55

Θεραπευτική αντιμετώπιση αγγειοοιδήματος μετά από θρομβόλυση

Answer 55

Question 56

Χρόνος έναρξης αντιπηκτικού μετά από ΙΑΕΕ σε ασθενή με ΚΜ

Answer 56

• ΤΙΑ: κατευθείαν
• Μικρού μεγέθους (lacunes <1.5cm): 4η μέρα
• Μεσαίου μεγέθους (κατανομής <1/3 μεγάλης αρτηρίας πχ μέση εγκεφαλική): 7η μέρα
• Μεγάλου μεγέθους (κατανομής >1/3 μεγάλης εγκεφαλικής: 14η μέρα

**
Σε ασθενείς με αιμορραγική μετατροπή: 12η μέρα

ΙΑΕΕ 2023

Question 57

ALESSA score

Answer 57

διαστρωμάτωση κινδύνου για το πότε πλεονεκτεί η αντιπηκτική αγωγή στην ισχαιμία σε σχέση με την αιμορραγία σε ασθενείς με ΚΜ
Παράμετροι:
- Ηλικία
- διάμετρος εγκεφαλικού
- διάμετρος αριστερού κόλπου

3-4 υψηλό score - πρέπει να γίνει έναρξη αντιπηκτικών

Question 58

Παράγοντες κινδύνου που σχετίζονται με αυξημένη πιθανότητα αιμορραγίας σε ασθενείς που λαμβάνουν αντιπηκτικά

Answer 58

Τροποποιήσιμοι
- Αρτηριακή υπέρταση
- Συγχορήγηση αντιαιμοπεταλιακών
- Συγχορήγηση ΜΣΑΦ
- Κατάχρηση αλκοόλ

Δυνητικά τροποποιήσιμοι
- Αναιμία
- Επηρεασμένη νεφρική λειτουργία
- Επηρεασμένη ηπατική λειτουργία
- Μειωμένος αριθμός ή λειτουργικότητα αιμοπεταλίων

Question 59

Επιλογή αντιπηκτικού

Answer 59

A) Σε νεφρική ανεπάρκεια (<30 ml/min)
αποφεύγουμε το dabigatran (το 80% απεκκρίνεται μέσω των νεφρών)
Προτιμάται rivaroxaban (15mg x1) ή apixaban (2.5 x2) σε μειωμένη δόση ++

B) Εάν ο ασθενής πάθει εγκεφαλικό υπό αντιπηκτικό
Έλεγχος εάν υποθεραπεύονται
Εάν λάμβαναν την αγωγή όπως πρέπει, έλεγχος για άλλη αιτία εγκεφαλικού (δεν αλλάζουμε αντιπηκτικό!)

Γ) Εάν ο ασθενής έχει ρινογαστρικό σωλήνα
Μόνη επιλογή rivaroxaban!

Δ) Σε υπέρβαρους ασθενείς (>40 BMI)
Αποφεύγουμε το dabigatran για 2 λόγους:
Σε έναν υπέρβαρο ασθενή λόγω της χαμηλής βιοδιαθεσιμότητας το φάρμακο χάνεται
Σε έναν υπέρβαρο ασθενή η νεφρική λειτουργία είναι αυξημένη και έτσι αυξάνεται η απέκκριση του φαρμάκου (80% νεφρική απέκκριση)

Ε) Σε ελλιποβαρείς ασθενείς
Μείωση δόσης σε dabigatran
Μείωση της δόσης σε apixaban (εάν ηλικία >80 ή Cr >1.5)
Δεν αλλάζουμε τη δόση στο rivaroxaban

Στ) Σε ηλικιωμένους ασθενείς (>80 έτη)
Μείωση δόσης σε dabigatran (110mg x2 - ίσως από >75)
++ Μείωση δόσης σε apixaban (εάν συνυπάρχει βάρος <60Kg ή Cr >1.5)
Δεν αλλάζουμε τη δόση στο rivaroxaban

Ζ) Σε ασθενείς με κακοήθεια
Προτιμούνται DOACs από κουμαρινικά αντιπηκτικά

Η) Σε ασθενείς με βαλβιδοπάθεια και ΚΜ
Υπερτερούν τα κουμαρινικά αντιπηκτικά εκτός
από τις βιοπροσθετικές που το rivaroxaban είναι ισοδύναμο

Θ) Αν υπάρχει θρόμβος αριστερής κοιλίας
Τα κουμαρινικά αντιπηκτικά υπερτερούν έναντι των DOACs