Ischemic Stroke & Transient Ischemic Attack 4 Flashcards
What are lacunar strokes?
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.
What is the percentage of lacunar strokes?
15-30% of strokes
Pathogenesis of lacunar strokes
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
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33ο Πανελλήνιο
Which conditions is cerebral small disease associated with
Icreased risk of
1) clinical ischemic and hemorrhagic stroke
2) silent infarcts
3) cognitive decline and dementia
Modifiable risk factors for cerebral small vessel disease
hypertension
obstructive sleep apnea
diabetes mellitus
hyperlipidemia
tobacco use
Common and uncommon forms of cerebrovascular small vessel disease
Radiographic phenotypes of small vessel disease
(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
Most common site of lacunar infarcts in descending order
putamen, caudate, thalamus, pons, internal capsule, and
subcortical white matter
Typical presentations of CAA
1) neurologic findings attributable to acute hemorrhage
2) transient neurologic episodes
3) cognitive impairment or dementia
Boston criteria for cerebral amyloid angiopathy
https://radiopaedia.org/articles/boston-criteria-20-for-cerebral-amyloid-angiopathy?lang=us
Radiographic findings in CAA
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
Lobes affected by symptomatic intracranial hemorrhage in CAA in descending order
occipital lobes,
followed by the
frontal, temporal, and parietal
lobes
Diagnostic Characteristics of Cerebral Amyloid Angiopathy–Related Transient Focal Neurologic Episodes
Which complication is associated with CAA TFNEs
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
Criteria for the diagnosis of cerebral amyloid angiopathy-related inflammation (CAA-ri)
CADASIL clinical features
- 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
CADASIL cause
CADASIL is caused by mutations in the NOTCH3 gene, which maps to the short arm of chromosome 19.
Radiographic findings in CADASIL
- 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
Does the absence of family history exclude CADASIL?
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
CADASIL diagnosis
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.
In which way is CARASIL different from CADASIL
CARASIL etiology
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
Suggestions and Considerations for Investigations in Patients With Silent Brain Infarction
AHA/ASA 2017
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.
Suggestions and Considerations for Investigations in Patients With WMHs of Presumed Vascular Origin
AHA/ASA 2017
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.
Suggestions and Considerations for Investigations in
Patients With Silent CMBs
AHA/ASA 2017
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.
Symptoms suggestive of carotid transient ischemic attacks
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)
Symptoms suggestive of vertebrobasilar transient ischemic attacks
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
When to question the diagnosis of TIA
1) incomplete resolution of neurological dysfunction
2) march of symptoms from one part of the body to another
Characteristics of amaurosis fugax
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
Lacunar stroke syndromes
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
Monogenic cerebral small vessel diseases
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)
Sickle cell disease stroke manifestations
1) Ischemic stroke
2) Hemorrhagic stroke
3) Moya-moya vasculopathy
Antiphospholipid syndrome: clinical presentation and laboratory testing
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
Moya - moya disease management
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
Percentage of cryptogenic stroke
20-40% of strokes
Uncommon causes of ischemic stroke
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
Antiplatelet therapy is reasonable to reduce the risk of recurrent stroke or TIA
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
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
Patients with ischemic stroke or TIA in the setting of AF and cancer management
It is reasonable to consider anticoagulation with DOACs in preference to warfarin for stroke prevention
Patients with sickle cell disease and prior ischemic stroke or TIA management
- chronic blood transfusion(s) to reduce hemoglobin S to
<30% of total hemoglobin is recommended for the prevention of recurrent ischemic stroke. - In patients for whom transfusion therapy is not available or practical, treatment with hydroxyurea is reasonable for the prevention of recurrent ischemic stroke
patients with ischemic stroke or TIA and symptoms attributed to giant cell arteritis management
- immediate initiation of oral high-dose glucocorticoids is recommended to reduce recurrent stroke risk.
- 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
Patients with ischemic stroke or TIA and diagnosis of primary CNS angiitis
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
Recommendation on tenecteplase on acute ischemic stroke
ESO 2023
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
Acute stroke management in pregnant women
ESO 2022
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).
Acute stroke in postpartum women management
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.
Management of acute stroke and extracranial and intracranial dissection
ESO 2022
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
Guideline on screening for subclinical atrial fibrillation after stroke or transient ischaemic attack of undetermined origin
ESO 2022
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.
Causes of spontaneous aortic dissections
1) Marfan syndrome
2) familial thoracic aortic aneurysm or dissection
3) bicuspid aortic valve
4) Loeys-Dietz aneurysm syndrome
5) vascular Ehlers-Danlos syndrome
Ascending aortic dissection and stroke: management
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
Ποσοστό επανακαναλοποίησης απόφραξης μεγάλου αγγείου μετά από
1) ενδοφλέβια θρομβόλυση
2) μηχανική θρομβεκτομή
1)10%
2) Ως και 95%
ΑΕΕ 2023
Μηχανική θρομβεκτομή βασικής (προς το παρόν εκτός κατευθυντήριων οδηγιών)
Ευρήματα από μελέτες (VERITAS)
- 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
Μηχανική θρομβεκτομή σε ασθενείς με εκτεταμένο όγκο εμφράκτου (ASPECTS <6) (προς το παρόν εκτός κατευθυντήριων οδηγιών)
Ευρήματα από μελέτες (LASTE)
- 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
Πλεονεκτήματα tenecteplase από alteplase ως επιλογή πριν από MT
- 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
Ο συνδυασμός θρομβόλυσης - θρομβεκτομής
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
Αντιμετώπιση επιπλοκών ενδοφλέβιας θρομβόλυσης
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
Θεραπευτική αντιμετώπιση αγγειοοιδήματος μετά από θρομβόλυση
Χρόνος έναρξης αντιπηκτικού μετά από ΙΑΕΕ σε ασθενή με ΚΜ
- 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
ALESSA score
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
Παράγοντες κινδύνου που σχετίζονται με αυξημένη πιθανότητα αιμορραγίας σε ασθενείς που λαμβάνουν αντιπηκτικά
Τροποποιήσιμοι
- Αρτηριακή υπέρταση
- Συγχορήγηση αντιαιμοπεταλιακών
- Συγχορήγηση ΜΣΑΦ
- Κατάχρηση αλκοόλ
Δυνητικά τροποποιήσιμοι
- Αναιμία
- Επηρεασμένη νεφρική λειτουργία
- Επηρεασμένη ηπατική λειτουργία
- Μειωμένος αριθμός ή λειτουργικότητα αιμοπεταλίων
Επιλογή αντιπηκτικού
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
