Transcript Stroke

Dec 8th, 2014
Lama Al-Khoury, MD
Clinical Assistant Professor
Neurology
UCI Medical Center
Stroke Epidemiology
 Incidence of stroke in USA is 795,000/ year in
the United States of America
 Incidence of Non-fatal strokes is 15
million/year in the world
 Stroke: 4rd killer in USA (used to be third)
2nd killer in world
 Secondary disability is present in one third of
stroke survivors
Stroke
Stroke is Acute brain injury caused by:
 Ischemic stroke: Reduced blood supply to a
region of the brain resulting in brain ischemic
and neuronal death (87%)
 Hemorrhagic stroke: Primary brain
hemorrhage resulting in compression of
normal brain tissue (13%)
Anterior and Posterior Cerebral Arterial
Circulation
 Internal carotid arteries and their
branches: supply the anterior circulation
 Vertebral arteries and the basilar artery
(and their branches): supply the posterior
cerebral circulation
Mechanism of Ischemic Stroke and
Transient Ischemic Attacks
 Atherosclerotic cerebrovascular disease (20%):
1.
2.
Extracranial carotid or vertebral artery disease
Intracranial cerbrovascular disease
 Penetrating small arterial disease (25%)
 Cardiogenic source (33%):
1.
2.
3.
4.
5.
Atrial fibrillation & other arrythmias
Myocardial infarction
Valvular disease
Ventricular thrombi
Aortic plaque
 Unusual causes (<5%): dissection, migraine, illicit
drugs, vasculitis, venous strokes, hypercoagulability,…
 Cryptogenic source (no mechanism identified)
Transient Ischemic attack (TIA)
 Definition: duration of transient neurologic symptoms
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lasting less than 1 hour
Transient reduction of blood flow to a region in brain in
the absence of evidence of infarction on brain imaging
Mechanisms for TIA similar as for ischemic stroke
Reconstitution of flow to the hypoperfused region hence
the resolution of symptoms
Significance of TIAs is increased risk of stroke after a TIA
specifically early on after a TIA
Prompt evaluation of mechanism and appropriate
treatment
Transient Ischemic Stroke
 ABCD2 score
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Age ≥ 60 years: score 1
HTN (≥140/90): score 1
Diabetes mellitus: score 1
TIA duration: 10-59 min (score 1); ≥60min (score2)
Clinical: Hemiparesis with or without speech deficit (score
2); speech impairment without hemiparesis (score 1)
 Higher ABCD2 scores are associated with greater risk
of stroke during the 2, 7, 30, and 90 days
 Definite admission for ABCD2 score of ≥4
 Caution to work the TIA patients urgently to address
underlying source and treat appropriately
Ischemic Stroke
Signs and Symptoms of Stroke
Acute Onset of Neurologic Symptoms
and Signs of Central Nervous System
Nature
Acute Onset of Any of the Below
Symptoms
 Hemiparesis or quadriparesis ( latter in basilar occlusion)
 Facial weakness
 Aphasia
 Dysarthria
 Limb/truncal/gait ataxia +/- nausea & vomiting
 Vertigo, tinnitus, hearing deficit (posterior circ.)
 Impairment of vision in homonymous visual field defectAdopted from
 Monocular impairment of vision (amaurosis fugax)
AHA
 Diplopia
 Impairment or loss of consciousness or confusion
 Hemineglect (visual or sensory)
 Headache (non-specific symptom)
 New onset seizure (3-4%) or acute new movement abnormality
Differential Diagnosis
 Space occupying lesion
(tumor, infection/
abscess, Epidural,
Subdural Hematomas)
 Subarachnoid
hemorrhage
 Seizures
 Hypoglycemia
 Migraine
 Syncope
 Labyrinthine disorders
NIH Stroke Scale
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Designed for acute stroke trials.
Quick (5-10 min) & reproducible.
Requires speech/language cards & safety pin.
Quantifies clinical stroke deficit:
o < 4 = mild stroke
o
> 15 = poor prognosis if no treatment
o
> 22 =  risk for ICH
NIH Stroke Scale
“Traditional” order of items”
1a.
1b.
1c.
2.
3.
4.
5a.
5b.
LOC
LOC questions
LOC commands
Best gaze
Visual fields
Facial palsy
Right arm motor
Left arm motor
6a.
6b.
7.
8.
9.
10.
11.
Right leg motor
Left leg motor
Limb ataxia
Sensory
Best language
Dysarthria
Extinction/
inattention
Evaluation &Treatment
Initial Evaluation and Management
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Urgent transport to the nearest stroke
receiving hospital via 911 syste
Notification of the destination ED
Alert ED of the need for urgent CT
Code Stroke
Initial Evaluation
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Cardiac monitoring, pulse-ox, ECG
Stat CT brain
c-xray
CBC, Platelet, PT, PTT
Accucheck & blood glucose, serum
electrolytes
Cardiac markers, ABG’s
Blood alcohol level, Toxicology screen,
Pregnancy test
Initial Evaluation and Rx
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IV line: IVF bolus/hydration
2nd IV line in anticipation of IV t-PA
Non contrast CT: rule out hemorrhage
Usually later but may need stat: Carotid U/S,
Echocardiogram, MRI and MR-a, CT-a brain and
cerebral vessels
CT Brain
CT Patterns
MRI Brain
Acute Therapy
 NINDS Stroke Study group: randomized placebo
controlled clinical trial (N Engl J Med 1995)
 Intravenous recombinant tissue Plasminogen
Activator (IV t-PA) given within 3 hour of
symptoms onset in acute ischemic strokes
 N=624 patients (IV t-PA or placebo):dose
0.9mg/kg, 10% IV bolus, then the remainder is IV
drip over 1 hour
NINDS Stroke Study
 Patients in the t-PA arm were at least 30% more
likely to have minimal or no disability at 3 months
 Symptomatic Intracranial Hemorrhage was 6.4%
in the t-PA group versus 0.6% in the placebo arm
 Mortality at 3 months was not statistically
different between t-PA and placebo
 The benefit of IV t-PA was sustained at one year
follow up
 The earlier the treatment the better the outcome
IV t-PA treatment
 IV t-PA was FDA approved for acute ischemic
stroke Rx based on the NINDS study group
 Inclusion and Exclusion criteria
ECASS III Trial
 ECASS 3: N Eng J Med sept 2008
 This study showed persistent benefit of IV t-PA up
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to 4.5 hours from onset in acute ischemic stroke
Excluded patients>80 years of age
Excluded patients with severe deficit NIHSS>25
Excluded patients who have combination of
previous stroke and diabetes
Excluded patients who were on anticoagulation
regardless of the INR
Intravenous t-PA
 Standard FDA approved therapy for acute
stroke Rx
 Window of treatment has been prolonged
after ECASSIII to 4.5 hours
 Not all patients are eligible for the 3 to 4.5
hour window
Inclusion Criteria for IV t-PA
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Ischemic Stroke clinically
Persistent neurologic deficit beyond an
isolated sensory deficit / ataxia
CT brain: No Blood
Initiation of Rx within 3 hours
Exclusion Criteria
Onset to treatment >3 hr
(NINDS)
 Rapid improvement
 Blood on CT
 Oral anticoagulant &
PT>15 sec, INR>1.7
 Heparin (last 48 hr) &
increased PTT
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Platelet<100,000
SBP>185 or DBP>110
Aggressive treatment of
b.p.
Stroke or head trauma (3
months)
Major surgery (2 wks)
Cont’d Exclusion Criteria
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Prior ICH
GI tract/ Urinary
bleed (14 d)
Seizure at onset
Signs & Sx’s of SAH
Non-compressible
site of arterial
puncture (7d)
Additional Exclusions for the 3 to 4.5
Hour
 Age≥80 years
 Any use of anticoagulant regardless of the
PT/PTT
 NIHSS≥25
 Coexistent history of stroke and diabetes
mellitus
Management Post Thrombolysis
Admit to ICU
 BP monitoring (Q 15 m x2 h, Q 30 m x6 h, Q 1 h
x16 h)
 Treat SBP≥185 and DBP≥110
 No anticoagulants, no anti-platelet for 1st 24 hr
post t-PA
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Cont’d Management of Patients
Post-thrombolysis
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Worsening of neurologic state---CT brain
ICH---Neurosurgery consult
Possible surgical intervention
Preferably: no foley or NG for 2 hr > t-PA
(t1/2-t-PA = 8-12 min)
Acute Interventional Treatment
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Intraarterial thrombolysis or mechanical thrombectomy
Successful recanalization has been shown
Clinical benefit?
PROACT II: intra-arterial pro-Urokinase was positive
3 interventional studies published in 2013 were negative
for benefit from endovascular Rx
 Implementation of stent retrieval devices (superior in
recanalization)
 MR CLEAN (Multicenter Randomized Clinical trial of Endovascular
treatment for Acute ischemic stroke in the Netherlands) : positive
trial
 SWIFT PRIME halted enrollment pending review of data
Endovascular Rx
 At the time being and in the United States the only
FDA approved acute treatment for stroke is IV t-PA
 Mechanical thrombectomy: (currently)
 Add on-Rx to the standard FDA approved stroke
Rx IV t-PA in cerebral infarction with proximal
large arterial occlusion within 8 hours from onset
 Or as alternative Rx in patients who do not qualify
for IV t-PA
 For basilar artery occlusion the window is prolonged
to up to 24 hours for concern of locked in syndrome
Poor Outcome Predictors in Ischemic
Stroke
 Age
 Elevated blood sugar
 Initial NIHSS score which is a measure of the
patient’s initial deficit
 Cerebral infarction changes on CT brain
Is Stroke Preventable??
Prevention
 Primary prevention
 Secondary prevention
Primary Prevention
 Primary prevention starts at the level of the
physician playing the role of the primary care
and occasionally at the level of the
cardiologist and the stroke neurologist
 Key is identification of underlying risk factors
and modification and treatment of modifiable
risk factors
Primary Prevention Elements
 Establishing good medical history and family
history
 Identifying the patient’s vascular risks including
medical illnesses, habits such as smoking and
substance use and genetic predisposition through
review of significant family history for
cardiovascular risk factors and stroke
 Exam elements which are key: pulse (rate and
establishing how regular), blood pressure, carotid
auscultation (bruits), cardiac auscultation
(murmurs and abnormal rhythm), symmetry and
detection of pulses, diabetic peripheral changes
Identification of Risk Factors
for Stroke
 Non-modifiable risk factors
 Modifiable risk factors
Modifiable Risk Factors
Non-modifiable Risk Factors
 Age: the risk of stroke doubles with every
decade after the age of 55 years
 Sex: lifetime risk in Male>Female but risk in
F>M after age of 80 years
 Race and ethnicity:
 Stroke incidence and subtypes: higher in African
Americans and Hispanics >Caucasians
 Stroke related mortality is higher in African
American population
 Asian population has an increased risk of
hemorrhagic stroke subtype compared to
Caucasians
Non-modifiable Risk Factors
Genetic Factors
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Family history: inherited susceptibility, inherited predisposition to risk
factors, similar culture and lifestyle
 Hyperhomocysteinemia: C677T allele (one or more) of the
methylenetetrahydrofolate reductase gene (MTHF)
 Inherited coagulopathies:
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FV Leiden mutations, prothrombin gene mutation
PC, PS deficiencies
Anticardiolipin antibodies/LA are genetic in 10% cases
Others
CADASIL: Cerebral autosomal dominant arterof iopathy with subcortical
infarcts and leukoencephalopathy: NOTCH 3 gene mutation on
chromosome 19
 Others: Marfan and NF I and II, Fibromuscular dysplasia (FMD), EhlersDanlos syndrome IV, polycystic kidney disease
 Novel genes identified which may have specific associations with large
artery stroke
Well Documented Modifiable Risk
Factors
 Hypertension
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Smoking
Diabetes Mellitus
Carotid disease
Cardiac disease: Atrial Fibrillation, Myocardial
infarction secondary to coronary artery disease
 Dyslipidemia or hyperlipidemia (high cholesterol,
high LDL, low HDL)
 Migraine with aura in women
 Obstructive sleep apnea
Less-Documented Potentially Modifiable
Risk Factors
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Obesity
Lack of exercise
Poor diet
Alcohol abuse
Hyperhomocysteinemia
 Illicit drug abuse
 Hypercoagulopathy
 Sickle cell disease
 Estrogen/HR
hormonal therapy
 Inflammation
 Infection
Hypertension
Hypertension (HTN)
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Prevalence in USA is 29%- Improved control of HTN over the years 50%
A patient who is normotensive at 55 years of age has a 90% life time risk
of developing hypertension
More than 2/3 of patients ≥ 65 yrs of age have hypertension
Major risk factor for ischemic and hemorrhagic strokes
Throughout usual range of blood pressure (BP) including the normal BP
ranges, the higher the blood pressure the greater the risk of stroke
HTN is undertreated
It ‘s prevalence is increasing partly due to increased prevalence of
patients who are overweight and obese
One of the most important modifiable risk factors for stroke
Hypertension increases stroke risk due to the following:
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It worsens atherosclerosis
It predisposes to small vessel disease
It accelerates heart disease
Antihypertensive Agents
 Multiple clinical trials have established that treatment of BP
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with antihypertensive medications reduces risk of stroke
Several meta-analyses evaluated and compared specific
antihypertensive agents
One meta-analysis: Thiazide diuretics, ACEI and Ca channel
blockers each reduced risk of stroke compared to placebo
Another meta-analysis: showed diuretics superior to ACEI
Subgroup analysis in one trial: benefit if diuretic is more
prominent among African Americans
A meta-analysis of 13 trials in patients with hypertension:
ACEI and ARBs reduced significantly stroke risk
Recent evidence that calcium channel blockers are better in
reducing variability in blood pressure that betablockers
Hypertension Evaluation and Treatment
Current Guidelines
 Regular blood pressure screening
 Behavioral life style modifications should be
recommended to hypertensive patients:
 management of obesity/ weight loss,
 diet: low salt, encourage vegetables. Reduce red meat
(AHA, DASH, Mediterranean diets)
 Encouragement of exercise
 Treatment with antihypertensive agents to
achieve BP< 140/90 mm Hg
 Intraindividual variability of blood pressure may
cause additional risk
Degree of Blood Pressure Reduction
 Current AHA guidelines in chronic
hypertension < 140/90 mm Hg
 Most trials did not test a goal of less intensive
therapy being less than140/90
 One meta-analysis compared clinical trials
with more intensive BP reduction with those
of less intensive reduction and found a 23%
reduced risk of stroke in more intensive
therapy
Cigarette Smoking
 Cigarette smoking doubles the risk of ischemic
stroke
 It also increases subarachnoid hemorrhage by 2-4
folds
 Inconsistent data for parenchymal intracerebral
hemorrhage
 Inconsistent data with second hand smoking
 Contributes to increased risk of stroke by:
 Increased thrombus generation in atherosclerotic
arteries
 Increased atherosclerosis
Cessation of
Smoking
Diabetes Mellitus
 Close to 11% of US population are estimated
to have diabetes mellitus
 Studies have shown that diabetes mellitus
increases the risk of stroke 1.8 - 6 fold
 This increase in stroke risk is related to
increased risk of atherosclerosis & increased
pro-atherogenic risk factors in diabetic
patients
Interventions to Reduce Stroke in
Diabetes Mellitus?
Steno-2 Study
 Patients with DMII and persistent
microalbuminuria
 Intervention with intensive therapy with
behavioral risk factor modification and statin,
ACEI, ARB, or antiplatelet as appropriate
versus conventional Rx
 Intensive therapy was associated with
significant reduction in each of death,
cardiovascular events and stroke endpoints
Diabetes Mellitus: Glycemic control?
 North Manhattan Study: subjects who had
diabetes and fasting blood glucose (FBG)> 126
mg/dl had 2.7 fold increase in stroke risk versus
no increase in risk if FBG<126 mg/dl
 3 clinical trials: ACCORD, ADVANCE, and a trial
which enrolled US veterans
 Failure to demonstrate reduction in stroke in the
group of intensive glycemic control
 ACCORD: halted earlier due to increased all-cause
mortality in the intensive-glycemic control group
Diabetes mellitus: Glycemic Control
 Use standard guidelines for glycemic control
 Avoid lowering of HbA1c<6.5 in patients with
cardiovascular disease or the presence of
vascular risk factors
Hypertension Control in DM
New AHA guidelines
 Evidence from studies and meta-analyses to
suggest that more aggressive bp control in DM
lowers further risk of stroke
 There is an increased risk of adverse events
with more aggressive antihypertensive Rx
Diabetes Mellitus and Lipid Altering Rx
 Clinical evidence of the benefit of statins in
stroke risk reduction in diabetic patients
 No supportive evidence for fibrates in stroke
prevention in diabetic patients
Use of Aspirin in Primary Prevention of
Stroke in Diabetes Mellitus
 No statistically significant benefit from aspirin
in prevention of stroke in diabetes mellitus
has been found
 Use in patients with established carotid
disease or coronary artery disease
Lipids
 Modest association of elevated total
cholesterol or LDL with increased risk of
ischemic stroke
 Association between low HDL and increased
risk of ischemic stroke
 Relationship between low total cholesterol as
well as LDL-C and a higher risk of
hemorrhagic stroke
?? Role of Triglycerides
No consistent association between triglycerides
and risk of stroke
Statins (HMG-CoA Reductase Inhibitors)
 Statins: 3-hydroxy-3methylglutaryl coenzyme A reductase
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inhibitors
Statins lower LDL cholesterol by 30-50%
Treatment with statins reduces the risk of stroke in patients
with or at high risk for atherosclerosis
Meta-analysis of 26 trials: statins reduced risk of all strokes
by 21%
Risk of all strokes was reduced by 15.6% for each 10%
reduction of LDL-C
Statins reduce progression and promote regression of
atherosclerotic plaque
Beneficial effect on carotid intima media thickness (IMT)
mostly with higher intense Rx with statins
Lipid Lowering in Patients with CHD
 National Cholesterol Education Program (NCEP)
 NCEP recommends LDL lowering as primary
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target
Lifestyle modification
Decrease saturated fat, trans fat and cholesterol
intake
weight reduction
Exercise
PMH of CHD and CHD risk equivalents (DM and
symptomatic carotid artery disease): aim at LDL
at least ≤ 100 and preferably ≤70
ACC/AHA Guidelines for the Treatment of
Blood Cholesterol in Primary Prevention
 Recommendations based on the 10 year risk
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for cardiovascular disease
Shifts away from specific cholesterol goals
Estimated risk dictates intensity of statin Rx:
high risk mandates high intensity statin Rx
Atorvastatin 10 mg is moderate intensity
statin Rx and 40 t0 80 mg is high intensity
10 year Risk calculator
Statins in Secondary Prevention of
Stroke
 Statin therapy with intense lipid lowering
effect is recommended to reduce stroke risk
in the population of ischemic stroke and TIA
patients (SPARCL)
 Target LDL-C<70 mg/dl or 50% lowering of
baseline LDL
 May use other agents if patient can not take
statins (Niacin, Gemfibrozil)
 No established benefit in stroke reduction
Carotid Endarterectomy
 Indicated with proven benefit in severe
symptomatic extracranial carotid artery
disease
 Symptomatic = clinical or radiologic evidence
of stroke in the distribution of that carotid
artery
 Stenting is an alternative in patients who are
not eligible for CEA
Asymptomatic Carotid Disease
Asymptomatic Carotid Artery Disease
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Increased risk of stroke with carotid artery stenosis
Asymptomatic Carotid Artery Study (ACAS)
Asymptomatic Carotid Surgery Trial (ACST)
Number needed to treat to prevent 1 stroke patient
was 40
 The low benefit may not justify the risks of carotid
revascularization: individualize patients and assess
risk factors
 The annual rate of stroke associated with
asymptomatic carotid stenosis has significantly
declined with intensive medical management ≤1%
(Statins and antiplatelet Rx)
May consider carotid revascularization in severe
asymptomatic carotid artery stenosis but with
perioperative and surgical risk <3 %
Cardioembolic sources of Stroke
 Cardiac arrhythmias with increased risk of cardiac
clots and cardioembolism: atrial fibrillation
 Coronary artery disease, myocardial infarction/
ischemic cardiomyopathy
 Valvular heart disease (septic embolism or
thromboembolism)
 Aortic arch atheroma
 Paradoxical embolism: presence of right to left
shunt such as a PFO in the presence of a venous
thrombus
Atrial Fibrillation
 Both persistent and paroxysmal atrial
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fibrillation are potent predictors of first as
well as recurrent stroke
Atrial fib >2 million Americans
Increases with age
Atrial fibrillation patients with prior strokes
and TIAs have the highest risk of recurrent
stroke
Other risk factors: age, HTN, CHF, diabetes
mellitus
CHADS2
 Age ≥ 75 years (1)
 HTN (1)
 DM (1)
 CHF (1)
 Ischemic stroke or TIA (2)
------------------------------------------------------- Total score: ------ (maximum is 6)
Antithrombotic Rx in Atrial Fibrillation
 Anticoagulation: CHADS2 >1
 Antiplatelet Rx for CHADS=0
 CHADS2=1 either anticoagulation or antiplatelet
 ASA plus clopidogrel maybe used in patients who
have contraindication to anticoagulation
 If there is Stroke/TIA with atrial fibrillation then
anticoagulation is the recommendation
 Patient has to be cleared for the absence of fall
risk
Oral Anticoagulants
 Warfarin (valvular and non-valvular A.Fib.)
 Apixaban((approved for non-valvular A.Fib.)
 Rivaroxaban(approved for non-valvular A.Fib.)
 Dabigatran (approved for non-valvular A.Fib.)
Carotid Disease
 No role for CEA in carotid occlusion
 No benefit from EC/IC bypass in carotid
occlusion
 SAMPRIS: In intracranial cerebral artery
stenosis, best medical management is
superior to angioplasty and stenting
Migraine with Aura
 An independent risk factor for stroke in women
 It is still unknown if migraine preventive therapy
will reduce the risk of stroke
 A woman who has migraines with aura, who
smokes tobacco and who is on oral contraceptive
pills has a 7-9 fold increase in the risk of stroke
 Cessation of smoking and consideration of
avoiding OCPs in patients with migraines with
aura
Obstructive Sleep Apnea (OSA)
 Increases risk of stroke and cardiovascular
disease
 Screening for symptoms of OSA and
appropriate referrral to sleep center for
evaluation and treatment when appropriate
Hormonal Replacement Therapy and
Oral Contraceptive Pills
 Some increased risk of ischemic stroke
 May avoid or stop using if additional risk
factors for stroke
 Stop/avoid use if patient is a smoker and esp.
if it is a woman who has migraines with aura
Substance Use
 Alcohol beyond 2 drinks/day for men and beyond
1 drink /day for women increases the risk of
stroke
 Illicit drug use increases the risk of intracerebral
hemorrhage (ICH) and ischemic strokes esp. with
Cocaine and Amphetamines/ derivatives
 Substance use increases the risk of development
of poorly controlled BP and its complications
 Cessation should be recommended however with
the help of detox and rehab programs
Antiplatelet Therapy in Primary Stroke
Prevention: No Benefit
 No benefit in primary prevention
 Consider in diabetic patient with high risk
factors and carotid artery disease
 May have some benefit in women ≥ 65 years
old (AHA / AHS guidelines)
 Recent FDA warning about use of aspirin in
primary prevention due to increased
hemorrhagic risks which are not offset by any
significant benefit
Summary
 Goal should be primary prevention in stroke
 Role of the primary care and sometimes the
neurologist and cardiologist in assessing risk
factors for stroke
 Intervention with education about life style
modification and treatment of risk factors for
stroke
Summary
 Family history: identify people who have
higher risk and counseling those patients
 Genetic counseling for rare genetic disorders
 Non-invasive imaging/ screening for patients
with specific disorders: screen for cerebral
artery aneurysms in patients with ≥ 2 first
degree members with SAH/cerebral
aneurysms, EDS IV, polycystic kidney disease
Summary:
 Physical activity is recommended:
 Moderate to vigorous intensity aerobic
 Suggested ≥ 40 min/ time, 3-4 days /wk 2013
AHA/ACC guidelines
 Weight reduction for BMI≥ 25
 Dietary restriction of salt and increased
potassium in diet (HTN conrtol)
 DASH, AHA, Mediterranean diets
Summary: Primary Prevention
 Cessation of smoking esp. in women who
have migraines with aura and who are on
OCPs
 Cessation of illicit drugs
 Cessation of alcohol or limitation to ≤1
drink/day for women and ≤2 drinks/day for
men
Summary: Primary Prevention
 Control of BP<140/90 mm Hg
 Control of blood sugar but avoid intensive
glycemic control
 Use of statins in diabetic patients maybe
protective and particularly if high risk factors
 Maximize medical management with statins and
antiplatelets in carotid artery disease
 Anticoagulation is reserved for atrial fibrillation
and cardiac thrombi or potent hypercoagulable
states (latter in secondary prevention)
Summary: Primary Prevention
 Use of ACE Inhibitors and or an angiotensin II
receptor blocker (ARB) in diabetes mellitus
 No documented benefit for aspirin in primary
prevention of stroke (may consider patients
with high risk factors) with the exception of
some possible benefit for women>65 years
old
Lama Al-Khoury, MD
Clinical Assistant Professor
UCI Medical Center
Stroke Center
T:(714)456-7637
Fax: (714)456-2333