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Ischemic Stroke
Ischemic stroke is sudden neurologic deficits that result
from focal cerebral ischemia associated with permanent brain infarction (eg,
positive results on diffusion-weighted MRI). Common causes are (from most to
least common) atherothrombotic occlusion of large arteries; cerebral embolism
(embolic infarction); nonthrombotic occlusion of small, deep cerebral arteries
(lacunar infarction); and proximal arterial stenosis with hypotension that
decreases cerebral blood flow in arterial watershed zones (hemodynamic stroke).
Diagnosis is clinical, but CT or MRI is done to exclude hemorrhage and confirm
the presence and extent of stroke. Thrombolytic therapy may be useful acutely
in certain patients. Depending on the cause of stroke, carotid endarterectomy
or stenting, antiplatelet drugs, or warfarin may help reduce risk of
subsequent strokes.
Etiology of Ischemic Stroke
The following are the modifiable risk factors that
contribute the most to increased risk of ischemic stroke:
- Hypertension
- Cigarette
smoking
- Dyslipidemia
- Diabetes
- Insulin resistance
( 1)
- Abdominal
obesity
- Excess
alcohol consumption
- Lack
of physical activity
- High-risk
diet (eg, high in saturated fats, trans fats, and calories)
- Psychosocial
stress (eg, depression)
- Heart
disorders (particularly disorders that predispose to emboli, such as acute
myocardial infarction, infective endocarditis, and atrial
fibrillation)
- Use of
certain drugs (eg, cocaine, amphetamines)
- Hypercoagulability
- Vasculitis
- Use of
exogenous estrogen
Unmodifiable risk factors include the following:
- Prior
stroke
- Sex
- Race/ethnicity
- Older
age
- Family
history of stroke
The most common causes of ischemic stroke can be classified
as
- Cryptogenic
(ie, no clear cardioembolic, lacunar, or atherosclerotic source; the most
common classification)
- Cardioembolism
- Lacunar
infarcts
- Large-vessel
atherosclerosis (the 4th most common cause)
Large-vessel atherosclerosis
Large-vessel atherosclerosis can affect intracranial or
extracranial arteries.
Atheromas, particularly if ulcerated, predispose to thrombi.
Atheromas can occur in any major cerebral artery and are common at areas of
turbulent flow, particularly at the carotid bifurcation. Partial or complete
thrombotic occlusion occurs most often at the main trunk of the middle cerebral
artery and its branches but is also common in the large arteries at the base of
the brain, in deep perforating arteries, and in small cortical branches. The
basilar artery and the segment of the internal carotid artery between the
cavernous sinus and supraclinoid process are often occluded.
Cardioembolism
Emboli may lodge anywhere in the cerebral arterial tree.
Emboli may originate as cardiac thrombi, especially in the
following conditions:
- Atrial
fibrillation
- Rheumatic
heart disease (usually mitral stenosis)
- Post–myocardial
infarction
- Vegetations
on heart valves in bacterial or marantic endocarditis
- Prosthetic
heart valves
- Mechanical
circulatory assist devices (eg, left ventricular assist device, or LVAD
[ 2])
Other sources include clots that form after open-heart
surgery and atheromas in neck arteries or in the aortic arch. Rarely, emboli
consist of fat (from fractured long bones), air (in decompression sickness),
or venous clots that pass from the right to the left side of the heart through
a patent foramen ovale with shunt (paradoxical emboli). Emboli may dislodge
spontaneously or after invasive cardiovascular procedures (eg,
catheterization). Rarely, thrombosis of the subclavian artery results in
embolic stroke in the vertebral artery or its branches.
Lacunar infarcts
Ischemic stroke can also result from lacunar infarcts. These
small (≤ 1.5 cm) infarcts result from nonatherothrombotic obstruction of
small, perforating arteries that supply deep cortical structures; the usual
cause is lipohyalinosis (degeneration of the media of small arteries and
replacement by lipids and collagen). Whether emboli cause lacunar infarcts is
controversial.
Lacunar infarcts tend to occur in older patients with
diabetes or poorly controlled hypertension.
Other causes
Less common causes of stroke include vascular inflammation
secondary to disorders such as acute or chronic meningitis, vasculitic
disorders, and syphilis; dissection of intracranial arteries or the aorta;
hypercoagulability disorders (eg, antiphospholipid syndrome,
hyperhomocysteinemia); hyperviscosity disorders (eg, polycythemia,
thrombocytosis, hemoglobinopathies, plasma cell disorders); and rare disorders
(eg, fibromuscular dysplasia, moyamoya disease, Binswanger disease).
In children, sickle cell disease is a common cause
of ischemic stroke.
Any factor that impairs systemic perfusion (eg, carbon
monoxide toxicity, severe anemia or hypoxia, polycythemia, hypotension)
increases risk of all types of ischemic strokes. A stroke may occur along the
borders between territories of arteries (watershed areas); in such areas, blood
supply is normally low, particularly if patients have hypotension and/or if
major cerebral arteries are stenotic.
Less commonly, ischemic stroke results from vasospasm (eg,
during migraine, after subarachnoid hemorrhage, after use of sympathomimetic
drugs such as cocaine or amphetamines) or venous sinus thrombosis (eg, during
intracranial infection, postoperatively, peripartum, secondary to a
hypercoagulability disorder).
Etiology references
- 1. Kernan
WN, Viscoli CM, Furie KL, et al: Pioglitazone after ischemic
stroke or transient ischemic attack. N Engl J Med 374
(14):1321–1331, 2016. doi: 10.1056/NEJMoa1506930.
- 2. Morgan
JA, Brewer RJ, Nemeh HW, et al: Stroke while on long-term left ventricular
assist device support: incidence, outcome, and
predictors. ASAIO J 60 (3):284–289, 2014. doi:
10.1097/MAT.0000000000000074.
Pathophysiology of Ischemic Stroke
Inadequate blood flow in a single brain artery can often be
compensated for by an efficient collateral system, particularly between the
carotid and vertebral arteries via anastomoses at the circle of Willis and, to
a lesser extent, between major arteries supplying the cerebral hemispheres.
However, normal variations in the circle of Willis and in the caliber of
various collateral vessels, atherosclerosis, and other acquired arterial
lesions can interfere with collateral flow, increasing the chance that blockage
of one artery will cause brain ischemia.
Some neurons die when perfusion is < 5% of
normal for > 5 minutes; however, the extent of damage depends on
the severity of ischemia. If it is mild, damage proceeds slowly; thus, even if
perfusion is 40% of normal, 3 to 6 hours may elapse before brain tissue is
completely lost. However, if severe ischemia persists > 15 to 30 minutes,
all of the affected tissue dies (infarction). Damage occurs more rapidly during
hyperthermia and more slowly during hypothermia. If tissues are ischemic but
not yet irreversibly damaged, promptly restoring blood flow may reduce or
reverse injury. For example, intervention may be able to salvage the moderately
ischemic areas (penumbras) that often surround areas of severe ischemia; penumbras
exist because of collateral flow.
Mechanisms of ischemic injury include
- Edema
- Microvascular
thrombosis
- Programmed
cell death (apoptosis)
- Infarction
with cell necrosis
Inflammatory mediators (eg, interleukin-1B, tumor necrosis
factor-alpha) contribute to edema and microvascular thrombosis. Edema, if
severe or extensive, can increase intracranial pressure.
Many factors may contribute to necrotic cell death; they
include loss of adenosine triphosphate (ATP) stores, loss of ionic
homeostasis (including intracellular calcium accumulation), lipid peroxidative
damage to cell membranes by free radicals (an iron-mediated process),
excitatory neurotoxins (eg, glutamate), and intracellular acidosis due to
accumulation of lactate.
Symptoms and Signs of Ischemic Stroke
Symptoms and signs of ischemic stroke depend on the part of
brain affected. Patterns of neurologic deficits often suggest the affected
artery (see table Selected Stroke Syndromes), but correlation is often
inexact.
Selected Stroke Syndromes
Deficits may become maximal within several minutes of onset,
typically in embolic stroke. Less often, deficits evolve slowly, usually over
24 to 48 hours (called evolving stroke or stroke in evolution), typically in
atherothrombotic stroke.
In most evolving strokes, unilateral neurologic dysfunction
(often beginning in one arm, then spreading ipsilaterally) extends without
causing headache, pain, or fever. Progression is usually stepwise, interrupted
by periods of stability.
A stroke is considered submaximal when after it is complete,
there is residual function in the affected area, suggesting viable tissue at
risk of damage.
Embolic strokes often occur during the day; headache may
precede neurologic deficits. Thrombi tend to occur during the night and thus are
first noticed on awakening.
Lacunar infarcts may produce one of the classic lacunar
syndromes (eg, pure motor hemiparesis, pure sensory hemianesthesia, ataxic
hemiparesis, dysarthria–clumsy hand syndrome); signs of cortical dysfunction
(eg, aphasia) are absent. Multiple lacunar infarcts may result in multi-infarct
dementia.
A seizure may occur at stroke onset, more often with embolic
than thrombotic stroke. Seizures may also occur months to years later; late
seizures result from scarring or hemosiderin deposition at the site of
ischemia.
Deterioration during the first 48 to 72 hours after onset of
symptoms, particularly progressively impaired consciousness, results more often
from cerebral edema than from extension of the infarct. Unless the infarct is
large or extensive, function commonly improves within the first few days; further
improvement occurs gradually for up to 1 year.
Diagnosis of Ischemic Stroke
- Primarily
clinical evaluation
- Neuroimaging
and bedside glucose testing
- Evaluation
to identify the cause
Diagnosis of ischemic stroke is suggested by sudden
neurologic deficits referable to a specific arterial territory. Ischemic stroke
must be distinguished from other causes of similar focal deficits (sometimes
called stroke mimics), such as
- Hypoglycemia
- Postictal
[Todd] paralysis (a transient neurologic deficit, usually weakness, of the
limb contralateral to the seizure focus)
- Hemorrhagic
stroke
- Rarely, migraine
Headache, coma or stupor, and vomiting are more likely with
hemorrhagic stroke.
Evaluation of ischemic stroke requires assessment of the
brain parenchyma, vascular system (including the heart and large arteries), and
blood.
Differentiating clinically between the types of stroke is
imprecise; however, some clues based on symptom progression, time of onset, and
type of deficit can help.
Although diagnosis is clinical, neuroimaging and bedside
glucose testing are mandatory.
Distinction between lacunar, embolic, and thrombotic stroke
based on history, examination, and neuroimaging is not always reliable, so
tests to identify common or treatable causes and risk factors for all of these
types of strokes are routinely done. Patients should be evaluated for the
following categories of causes and risk factors:
- Cardiac
(eg, atrial fibrillation, potential structural sources of emboli)
- Vascular
(eg, critical arterial stenosis)
- Blood
(eg, hypercoagulability)
A cause cannot be identified for some strokes (cryptogenic
strokes).
Brain assessment
Neuroimaging with CT or MRI is done first to exclude
intracerebral hemorrhage, subdural or epidural hematoma, and a rapidly growing,
bleeding, or suddenly symptomatic tumor. CT evidence of even a large anterior
circulation ischemic stroke may be subtle during the first few hours; changes
may include effacement of sulci or the insular cortical ribbon, loss of the
gray-white junction between cortex and white matter, and a dense middle
cerebral artery sign. Within 6 to 12 hours of ischemia, medium-sized to large
infarcts start to become visible as hypodensities; small infarcts (eg, lacunar
infarcts) may be visible only with MRI.
Diffusion-weighted MRI (highly sensitive for early ischemia)
can be done immediately after initial CT neuroimaging.
Cardiac causes
For cardiac causes, testing typically includes ECG,
telemetry or Holter monitoring, serum troponin, and transthoracic or
transesophageal echocardiography.
Vascular causes
For vascular causes, testing may include magnetic resonance
angiography (MRA), CT angiography (CTA), carotid and transcranial duplex
ultrasonography, and conventional angiography. The choice and sequence of
testing is individualized, based on clinical findings. MRA, CTA, and carotid
ultrasonography all show the anterior circulation; however, MRA and CTA provide
better images of the posterior circulation than carotid ultrasonography. MRA is
generally preferred to CTA if patients can remain still during MRA (to avoid
motion artifact). Usually, CTA or MRA should be done urgently but should not
delay IV tPA if it is indicated.
Effects of Thrombectomy After Stroke (Arteriogram)
IMAGE COURTESY OF JI Y. CHONG, MD.
Blood-related causes
For blood-related causes (eg, thrombotic disorders), blood
tests are done to assess their contribution and that of other causes. Routine
testing typically includes complete blood count (CBC), platelet count,
prothrombin time/partial thromboplastin time (PT/PTT), fasting blood glucose,
and lipid profile.
Depending on which causes are clinically suspected,
additional tests may include measurement of homocysteine, testing for
thrombotic disorders (antiphospholipid antibodies, protein S, protein C,
antithrombin III, factor V Leiden), testing for rheumatic disorders (eg,
antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate),
syphilis serologic testing, hemoglobin electrophoresis, and a urine drug screen
for cocaine and amphetamines.
Prognosis for Ischemic Stroke
Stroke severity and progression are often assessed using
standardized measures such as the National Institutes of Health (NIH) Stroke
Scale (see table The National Institutes of Health Stroke Scale); the
score on this scale correlates with extent of functional impairment and
prognosis. During the first days, progression and outcome can be difficult to
predict. Older age, impaired consciousness, aphasia, and brain stem signs
suggest a poor prognosis. Early improvement and younger age suggest a favorable
prognosis.
About 50% of patients with moderate or severe hemiplegia and
most with milder deficits have a clear sensorium and eventually can take care
of their basic needs and walk adequately. Complete neurologic recovery occurs
in about 10%. Use of the affected limb is usually limited, and most deficits
that remain after 12 months are permanent. Patients who have had a stroke are
at high risk of subsequent strokes
Treatment of Ischemic Stroke
- General
stroke treatments
- Acute
antihypertensive therapy only in certain circumstances
- Antiplatelet
therapy
- For
acute treatment, sometimes reperfusion with recombinant tissue plasminogen
activator (IV or thrombolysis-in-situ), and/or mechanical thrombectomy
- Sometimes
anticoagulation
- Long-term
control of risk factors
- Sometimes
carotid endarterectomy or stenting
Acute stroke treatment
Guidelines for early management of stroke are available from
the American Heart Association and American Stroke Association. Patients
with acute ischemic strokes are usually hospitalized.
Supportive measures such as the following may be needed
during initial evaluation and stabilization.
- Airway
support and ventilatory assistance if decreased consciousness or bulbar
dysfunction compromises the airway
- Supplemental
oxygen only if needed to maintain oxygen saturation > 94%
- Correction
of hyperthermia (temperature > 38° C) by using an antipyretic drug and
identifying and treating the cause of hypothermia
- Treatment
of hypoglycemia (blood glucose < 60 mg/dL)
- Treatment
of hyperglycemia (a reasonable option) to lower blood glucose to 140 to
180 mg/dL while closely monitoring for hypoglycemia
Perfusion of an ischemic brain area may require a high blood
pressure (BP) because autoregulation is lost; thus, BP should not be decreased
except in the following cases:
- There
are signs of other end-organ damage (eg, aortic dissection, acute
myocardial infarction, pulmonary edema, hypertensive encephalopathy,
retinal hemorrhages, acute renal failure).
- Use
of recombinant tissue plasminogen activator (tPA) and/or mechanical
thrombectomy is likely.
If BP is ≥ 220 mm Hg systolic or ≥ 120 mm Hg diastolic on 2
successive readings 15 minutes apart, lowering BP by 15% in the 24 hours after
stroke onset is reasonable.
For patients who are eligible for acute reperfusion therapy
except that BP is > 185/110 mm Hg, BP can be treated to decrease BP to below
> 185/110 mm Hg0 t with one of the following:
- Labetalol 10
to 20 mg IV bolus over 1 to 2 minutes (may repeat 1 time)
- Nicardipine 5
mg/hour IV infusion initially (dose is increased by 2.5 mg/hour every 5 to
15 minutes to a maximum of 15 mg/hour)
- Clevidipine 1
to 2 mg/hour IV infusion (titrate by doubling the dose every 2 to 5
minutes until desired BP is reached to a maximum of 21 mg/hour)
Patients with presumed thrombi or emboli may be treated with
one or a combination of the following:
- tPA,
thrombolysis-in-situ, and/or mechanical thrombectomy
- Antiplatelet
drugs
- Anticoagulants
Most patients are not candidates for thrombolytic therapy;
they should be given an antiplatelet drug (usually aspirin 325 mg
orally) when they are admitted to the hospital. Contraindications to
antiplatelet drugs include aspirin-induced or nonsteroidal
anti-inflammatory drug (NSAID)-induced asthma or urticaria, other
hypersensitivity to aspirin or to tartrazine, acute gastrointestinal
bleeding, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and use of warfarin.
Recombinant tPA (alteplase) can be used for
patients with acute ischemic stroke up to 3 hours after symptom onset if they
have no contraindications to tPA (see table Exclusion Criteria for Use of
Tissue Plasminogen Activator in Stroke). Some experts recommend using tPA up to
4.5 hours after symptom onset (see Expansion of the Time Window for
Treatment of Acute Ischemic Stroke With Intravenous Tissue Plasminogen
Activator); however, between 3 hours and 4.5 hours after symptom onset,
additional exclusion criteria apply (see table Exclusion Criteria for Use
of Tissue Plasminogen Activator in Stroke).
Although tPA can cause fatal or other symptomatic brain
hemorrhage, patients treated with tPA strictly according to protocols still
have a higher likelihood of functional neurologic recovery. Only physicians
experienced in stroke management should use tPA to treat patients with acute
stroke; inexperienced physicians are more likely to violate protocols,
resulting in more brain hemorrhages and deaths. When tPA is given incorrectly
(eg, when given despite the presence of exclusion criteria), risk of hemorrhage
due to tPA is high mainly for patients who have had stroke; risk of brain
hemorrhage is very low (about 0.5%; 95% confidence interval of 0 to 2.0%
[ 1]) for patients who have had a stroke mimic. If experienced physicians
are not available on site, consultation with an expert at a stroke center
(including video evaluation of the patient [telemedicine]), if possible, may
enable these physicians to use tPA. Because most poor outcomes result from
failure to strictly adhere to the protocol, a checklist of inclusion and
exclusion criteria should be used.
tPA must be given within 4.5 hours of symptom onset—a
difficult requirement. Because the precise time of symptom onset may not be
known, clinicians must start timing from the moment the patient was last
observed to be well.
Before treatment with tPA, the following are required:
- Brain
hemorrhage must be excluded by CT
- Systolic
BP must be < 185 mm Hg
- Diastolic
BP must be < 110 mm Hg
- Blood
glucose must be > 50 mg/dL
Antihypertensive drugs (IV nicardipine, IV labetalol,
IV clevidipine) may be given as above. Blood pressure should be kept <
180/105 mm Hg for at least 24 hours after treatment with tPA.
Dose of tPA is 0.9 mg/kg IV (maximum dose 90 mg); 10% is
given by rapid IV injection over 1 minute, and the remainder by constant
infusion over 60 minutes. Vital signs are closely monitored for 24 hours after
treatment. Any bleeding complications are aggressively managed. Anticoagulants
and antiplatelet drugs are not used within 24 hours of treatment with tPA.
TABLE
Exclusion Criteria for Use of Tissue Plasminogen Activator
in Stroke
Thrombolysis-in-situ (angiographically directed
intra-arterial thrombolysis) of a thrombus or embolus can sometimes be used for
major strokes if symptoms began < 6 hours ago, particularly for
strokes that are due to large occlusions in the middle cerebral artery and
cannot be treated with IV recombinant tPA. Clots in the basilar artery may be
intra-arterially lysed up to 12 hours after stroke onset, sometimes even later
depending on the clinical circumstances. This treatment, although standard of
care in some large stroke centers, is often unavailable in other hospitals.
Mechanical thrombectomy (angiographically
directed intra-arterial removal of a thrombus or embolus by a stent retriever
device) is standard of care in large stroke centers for patients with recent
large-vessel occlusion in the anterior circulation. It should not be used
instead of IV recombinant tPA within 4.5 hours of onset of symptoms in eligible
patients with acute ischemic stroke. Devices used to remove thrombi are being
improved, and recent models reestablish perfusion in 90 to 100% of patients.
Mechanical thrombectomy can be used to treat patients who
have had a severe stroke and have an NIH stroke score ≥ 6. However, recent
trials have shown benefit in patients with NIH stroke scores of ≥ 2 ( 3)
or even any NIH stroke score ( 4), and thus thrombectomy (or thrombolysis)
is indicated.
Mechanical thrombectomy had previously been restricted to
patients within 6 hours of symptom onset in patients with internal carotid
artery or middle cerebral artery occlusion. However, at comprehensive stroke
centers, clinical and/or imaging findings that suggest a substantial amount of
tissue at risk for infarction (penumbra) may justify later treatment. For
example, the volume of infarcted tissue and at-risk underperfused tissue (the
ischemic penumbra) can be identified using CT perfusion or MR perfusion
imaging. A sizeable mismatch between the infarct volume identified by
diffusion-weighted and perfusion-weighted imaging suggests substantial penumbra
that is still potentially salvageable. In the DEFUSE 3 trial, benefit was
evident up to 16 hours after symptom onset in patients with a small infarct and
a larger penumbra, both based on imaging criteria ( 5). In the DAWN trial,
benefit was evident up to 24 hours after symptom onset in patients with a large
mismatch between infarct volume based on imaging and severity of the clinical
deficit based on clinical criteria ( 6); this finding suggests that
salvageable penumbra is present.
Oral antiplatelet drugs are used in acute stroke
treatment. The following may be used:
- Aspirin 100
to 325 mg within 48 hours of stroke onset
- Dual
antiplatelet therapy: Aspirin plus clopidogrel (eg,
300 to 600 mg orally once, then 75 mg orally once a day) within 24 hours
of stroke onset for patients at high risk of a transient ischemic attack
(TIA, ABCD2 score ≥ 4) or minor stroke
Aspirin given within 48 hours reduces the risk of early
recurrent stroke and death ( 7).
The ABCD2 score is calculated by adding the following
- A
(age): ≥ 60 = 1
- B
(blood pressure): Systolic blood pressure ≥ 140 and/or diastolic blood
pressure > 90 = 1
- C
(clinical features): Weakness = 2, speech disturbance without weakness = 1
- D
(TIA duration): ≥ 60 min = 2, 10 to 59 min = 1, < 10 minutes = 0
- D2
(diabetes) = 1
Risk of stroke within 2 days based on the ABCD2 score is
about
- For
a score of 6 to 7: 8%
- For
a score of 4 to 5: 4%
- For
a score of 0 to 3: 1%
If patients have had a TIA or minor stroke, clopidogrel plus aspirin given
within 24 hours of symptom onset and continued for 21 days appears more
effective than aspirin alone for reducing risk of stroke in the first
90 days and does not increase risk of hemorrhage ( 8). However, prolonged
(eg, > 3 months) use of clopidogrel plus aspirin is
avoided because it has no advantage over aspirin alone in long-term
secondary stroke prevention and results in more bleeding complications.
Anticoagulation with heparin or low
molecular weight heparin is used for stroke caused by cerebral venous
thrombosis and sometimes for stroke caused by cervical artery dissection.
Anticoagulation can also be used in patients at high risk of recurrent cardiac
emboli (eg, those with cardiac thrombi or mechanical valves).
Usually, anticoagulation is avoided in the acute stage
because risk of hemorrhage (hemorrhagic transformation) is higher, especially
with large infarcts.
Long-term stroke treatment
Supportive care is continued during
convalescence:
- Controlling
hyperglycemia and fever can limit brain damage after stroke, leading to
better functional outcomes.
- Screening
for dysphagia before patients begin eating, drinking, or receiving oral
drugs can help identify patients at increased risk of aspiration; it
should be done by a speech-language pathologist or other trained health
care practitioner.
- Enteral
nutrition if needed should be started within 7 days of admission after an
acute stoke.
- Intermittent
pneumatic compression (IPC) for deep venous thrombosis prophylaxis is
recommended for immobile stroke patients without contraindications.
- Low
molecular weight heparin may be given to immobile stroke
patients without contraindications.
- Measures
to prevent pressure ulcers are started early.
Long-term management also focuses on prevention of recurrent
stroke (secondary prevention). Modifiable risk factors (eg, hypertension,
diabetes, smoking, alcoholism, dyslipidemia, obesity) are treated. Reducing
systolic BP may be more effective when the target BP is < 120 mm Hg rather
than the typical level (< 140 mm Hg).
Extracranial carotid endarterectomy or stenting is
indicated for patients with recent nondisabling, submaximal stroke attributed
to an ipsilateral carotid obstruction of 70 to 99% of the arterial lumen or to
an ulcerated plaque if life expectancy is at least 5 years. In other
symptomatic patients (eg, patients with TIAs), endarterectomy or stenting with
antiplatelet therapy is indicated for carotid obstruction of ≥ 60%
with or without ulceration if life expectancy is at least 5 years. These
procedures should be done by surgeons and interventionists who have a
successful record with the procedure (ie, morbidity and mortality rate of < 3%)
in the hospital where it will be done. If carotid stenosis is asymptomatic,
endarterectomy or stenting is beneficial only when done by very experienced
surgeons or interventionists, and that benefit is likely to be small. For many
patients, carotid stenting with an emboli-protection device (a type of filter)
is preferred to endarterectomy, particularly if patients are < 70 years and
have a high surgical risk. Carotid endarterectomy and stenting are equally
effective for stroke prevention. In the periprocedural period, myocardial infarction
is more likely after endarterectomy, and recurrent stroke is more likely after
stenting.
Extracranial vertebral angioplasty and/or stenting can
be used in certain patients with recurrent symptoms of vertebrobasilar ischemia
despite optimal medical treatment and a vertebral artery obstruction of 50 to
99%.
Intracranial major artery angioplasty and/or stenting is
considered investigational for patients with recurrent stroke or TIA symptoms
despite optimal medical treatment and a 50 to 99% obstruction of a major
intracranial artery.
Endovascular closure of a patent foramen ovale does
not appear to be more effective for preventing strokes than medical management,
but studies are ongoing.
Oral antiplatelet drugs are used to prevent
subsequent noncardioembolic (atherothrombotic, lacunar, cryptogenic) strokes
(secondary prevention). The following may be used:
- Aspirin 81
or 325 mg once a day
- Clopidogrel 75
mg once a day
- The
combination product aspirin 25 mg/extended-release dipyridamole 200
mg 2 times a day
In patients taking warfarin, antiplatelet drugs
additively increase risk of bleeding and are thus usually avoided;
however, aspirin is occasionally used simultaneously with warfarin in
certain high-risk patients. Clopidogrel is indicated for patients who
are allergic to aspirin. If ischemic stroke recurs or if a coronary artery
stent becomes blocked while patients are taking clopidogrel, clinicians
should suspect impaired metabolism of clopidogrel (ineffective
conversion of clopidogrel to its active form because cytochrome P-450
2C19 [CYP2C19] activity is reduced); a test to determine CYP2C19 status (eg,
genetic testing for CYP450 polymorphisms) is recommended. If impaired
metabolism is confirmed, aspirin or the combination product aspirin/extended-release dipyridamole is
a reasonable alternative.
Clopidogrel plus aspirin, if started during acute
treatment, is given for only a short time (eg, < 3 months) because it has no
advantage over aspirin alone in long-term secondary stroke prevention
and results in more bleeding complications. Clopidogrel plus aspirin before
and for ≥ 30 days after stenting is indicated, usually for ≤ 6 months; if
patients cannot tolerate clopidogrel, ticlopidine 250 mg 2 times
a day can be substituted.
Oral anticoagulants are indicated for secondary
prevention of cardioembolic strokes (as well as primary prevention).
Adjusted-dose warfarin (a vitamin K antagonist) with a target
international normalized ratio (INR) of 2 to 3 is used for certain patients
with nonvalvular or valvular atrial fibrillation. A target INR of 2.5 to 3.5 is
used if patients have a mechanical prosthetic cardiac valve. Efficacious
alternatives to warfarin for patients with nonvalvular atrial
fibrillation include the following new anticoagulants:
- Dabigatran
(a direct thrombin inhibitor) 150 mg 2 times a day in patients without
severe renal failure (creatinine clearance < 15 mL/minute) and/or liver
failure (elevated INR)
- Apixaban (a
direct factor Xa inhibitor) 5 mg 2 times a day in patients ≥ 80 years, in
patients with serum creatinine ≥ 1.5 mg/dL and creatinine clearance ≥ 25
mL/minute, or as an alternative to aspirin in patients who
cannot take warfarin
- Rivaroxaban (a
direct factor Xa inhibitor) 20 mg once a day for patients without severe
renal failure (creatinine clearance < 15 mL/minute)
The main advantage of these new anticoagulants is ease of
use (eg, no need to check anticoagulation level with a blood test after the
initial dose or to use a parenteral anticoagulant such as unfractionated heparin given
by continuous infusion when transitioning from parenteral to oral
anticoagulants). Their main disadvantage is lack of an antidote to reverse
anticoagulation in case a hemorrhagic complication occurs; the exception is
dabigatran, for which idarucizumab is an antidote ( 9). Efficacy
and safety of combining any of these new anticoagulants with an antiplatelet
drug have not been established.
Statins are used to prevent recurrent strokes;
lipid levels must be decreased by substantial amounts. Atorvastatin 80
mg once a day is recommended for patients with evidence of atherosclerotic
stroke and LDL (low-density lipoprotein) cholesterol ≥ 100 mg/dL. A reasonable
LDL cholesterol target is a 50% reduction or a level of < 70 mg/dL. Other
statins (eg, simvastatin, pravastatin) may be also used.
- CORONA VIRUS
- MONKEY POX
- VAGINAL DRYNESS
- FIBROID
- INFERTILITY
- OVULATION CYCLE
- OVARIAN CANCER
- VAGINAL BACTERIA
- MALE INFERTILITY
- BEST DAYS OF CONCIEVING
- MUCUS AFTER OVULATION
- FOODS FOR ERECTILE FUNCTIONS
- PREGNANCY ANEMIA
- DO AND DONT DURING PREGNANCY
- ERECTILE DYSFUNCTION
- U.T.I IN PREGNANCY
- STROKE RISK
- EAT THIS NOT THAT
- HOOKWORMS INFECTION
- OMEGA 3 BENEFITS
- FASTING
- WEIGHT LOSS TIPS
- vitiligo
- ABORTION
- DENGUE VIRUS
- EBORA VIRUS
- FEVER
- URINARY TRACT INFECTION
- HOSPITAL INFECTIONS
- WEST NILE VIRUS
- YELLOW FEVER
- EYE DISEASE
- ZIKA VIRUS
- STRESS
- IRON DEFFICIENCE
- INSOMNIA (SLEEPING PROBLEMS)
- HEART PROBLEMS
- COMPONENTS OF BLOOD
- BLOOD DISORDER
- LABORATORY TEST OF BLOOD DISORDER
- BONE MARROW EXAMINATION
- BLOOD ANEMIA
- ANIMAL BITES
- EYE BURN
- CHOCKING
- HEAT STROKE
- SMOKE EFFECTS
- SNAKE BITE
- MALARIA VACCINE
- BEST WAY TO SLEEP A CHILD
- CHILD FEVER REDUCING
- ELEPHANTIASIS
- WOMEN BEARDS
- DATES
- PAPAYA FRUITS
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