cerebrovascular disease: a discussion of strokes and tia’s accompanied by an explanation of...
TRANSCRIPT
Cerebrovascular Disease:A Discussion of Strokes and TIA’s
Accompanied by an explanation of current use of IMT and Carotid Ultrasound
Reviewed by Bill Rooney MDVP/Medical DirectorSCOR Global Life USA Reinsurance Company
Nebraska Home Office Life Underwriters Association Meeting
1
Overview
Stroke Facts Mortality numbers Definitions Anatomy review Types of strokes Diagnosis Primary and secondary treatment Another look at Mortality numbers CIMT, Carotid US, and Silent strokes
2
“You only live once, but if you do it right, once is enough”Mae West
I have inserted some
life-related quotes at the
bottom of some of the
slides These are intended to
be interesting as well as thought
provoking
And oh, by the way, all of the
authors suffered strokes at some
point in their lifetime
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Cases to Consider
2 cases arrive for underwriter review. Which has the worst mortality risk based upon the limited information provided?
3
Case #265 y/o female with no known neurological complaints—past or present• Hx. of hypertension and hyperlipidemia. BMI 30• MRI of the brain shows 2 small lacunar infarcts—age unknown• US of the carotids is WNL• ECG is WNL• CIMT is WNL
Case #166 y/o female with a hx. of a “TIA-like” event 4 years ago with no subsequent symptoms. Hx. of hypertension and hyperlipidemia. BMI 30• MRI of the brain WNL• US of the carotids is WNL• ECG is WNL• CIMT at 90th percentile for age
Cases described above are not actual cases but instead have been created to illustrate points made during this presentation.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
ECG Puzzler 4
795,000 Americans
suffer s
trokes each
year
.
6,400,000 stroke
survivors
134,000 deaths each year
1 out of every 19 deaths
4th leading cause of death for Americans
Strokes are
frequently
recurrent.
In fact nearly one of
four CVA’s occur in
people who have
had a previous
stroke
34% of people
hospitalized for stroke
in 2009 were under 65
years of age.
STROKES____
Facts to know Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Rosamond W et al. Circulation 2007;115:e69-e171Copyright © American Heart Association
Prevalence of stroke by age and sex 5
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Stroke Facts
1. 1998-2008:
Annual stroke death rate fell 35%. Actual number of deaths fell 19%.
6Nebraska Home Office Life Underwriters
Meeting Presentation 9/2014
Temporal trends in age-adjusted death rates for the top 10 causes of death in the United States from 1931 to 2008.
Towfighi A , and Saver J L Stroke 2011;42:2351-2355
2nd most common cause of death world wide
In 2008 CVA dropped from the 3rd most common cause of death in the US to the 4th.
7
In just this time frame here (1998-2008): – Annual stroke death rate fell 35%. – Actual number of deaths fell 19%.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Similar downward trend noted in the European Union.
Kunst A E et al. Stroke 2011;42:2126-2130Copyright © American Heart Association
Point #1The stroke mortality rate in the Western countries is declining.
• Decreased incidence• Decreased case-fatality
rate
Mortality rate from Stroke
Point #2The projected total number of US deaths from strokes is not expected to decline through 2030 however because of the aging population
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Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Definitions
1. TIA • Classic Definition: Rapidly developing clinical signs of focal or global
disturbance of cerebral function lasting fewer than 24 hours, with no apparent non-vascular cause.
• June 2009 AHA/ASA scientific statement definition: A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction
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2. CVA • An infarction of the central nervous system tissue
Definition and Evaluation of Transient Ischemic Attack. A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke Council; Easton, Donald J et al. Stroke. 2009:40:2276-2293
"You have enemies? Good. That means you’ve stood up for something, sometime in your life.“
Winston Churchill
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Consequences of the definition change
1. Anticipate a drop in annual incidence of TIA’s by 33%
2. Increase in diagnosis of CVA’s by 7%.
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3. There has been a change in the enrollment of members into studies• Potential change in treatment guidelines in the future• Mortality statistics impact
4. Comparison of old statistics to newer and future statistics won’t be apples to apples
5. Potential improvement in CVA morbidity and mortality results from earlier treatment. Decreased “wait and see” approach.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Consequences of definition change---Consider 3 diagnosis outcomes
TIA No longer is this the poor prognostic event that it was 90 day risk of stroke with residual symptoms is <1%
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Image-positive transient event– 90 day risk of stroke with residual symptoms is ~14%– ~15 x the chance of having a stroke with residual symptoms in
the next 7 days as compared to those with a stroke that already have residual neurological symptoms
Ischemic stroke with residual neurological symptoms
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Annual risk for future stroke after an initial TIA or ischemic stroke
Annual risk is estimated at ~3-4%1
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Great progress has occurred in preventing recurrent stroke2.1960’s 8.71%1970’s 6.1%1980’s 5.41%1990’s 4.04%
1. Kernan, Walter et al. Guidelines for the prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline for Healthcare Professionals From the AHA/AS. Stroke. 2014; Accessed 5/5/20142 Hong KS, Yegiaian S, Lee M, Lee J, Saver JL. Declining stroke and vascularevent recurrence rates in secondary prevention trials over the past 50 yearsand consequences for current trial design. Circulation. 2011;123:2111–2119.
Prevention aided by: Antiplatelet therapy/anticoagulation Atrial fibrillation treatments Hypertensive and hyperlipidemia treatments Arterial obstruction treatments
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
CVA’s are caused by anything that can cause vascular compromise
Heart Atrial fibrillation/rhythm disturbances VSD/PFO/Endocarditis
Large Blood Vessels Thrombus
Atherosclerosis Takayasu arteritis Giant cell arteritis Fibromuscular dysplasia
Emboli Dissection
Marfan’s syndrome and other similar conditions Intracranial Blood Vessels
Thrombus Same as large blood vessels but also includes Moya-Moya
Emboli Dissection Rupture of the Blood vessel and bleeding
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Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Vascular Compromise Blood itself
Bleeding Tendencies Complication of anticoagulation medications Hemophilia
Clotting Tendencies Protein C or S deficiency Prothrombin gene mutation Factor V Leiden Antithrombin III deficiency Hyperhomocysteinemia Antiphospholipid syndrome Essential thrombocytosis Sickle cell anemia Polycythemia Vera
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“Today was tomorrow yesterday so don`t inhale.”Mel Blanc
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
What type of vascular problem is occurring is important
Inflammation Atherosclerosis LipohyalinosisAneurysmal
dilationArterial
dissection
Thrombosis Embolus
Rupture of a vessel in the subarachnoid
space or intracerebral tissue
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Two Major Types of Stroke
Ischemia Thrombosis (local obstruction of an artery) Embolism (Debris or blood clot traveling from elsewhere and
lodging in an artery causing obstruction) Systemic hypo-perfusion (general medical condition with lack of
blood supply reaching the brain
Hemorrhage Subarachnoid hemorrhage (bleeding into the CSF within the
subarachnoid space around the brain) Intra-cerebral hemorrhage (bleeding directly into the brain
tissue)
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“Death solves all problems, No man, no problem”
Joseph StalinNebraska Home Office Life Underwriters
Meeting Presentation 9/2014
What type of vascular problem is occurring is important
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Inflammation Atherosclerosis LipohyalinosisAneurysmal
dilationArterial
dissection
Thrombosis Embolus
Rupture of a vessel in the subarachnoid
space or intracerebral tissue
80% of strokes are ischemic
20% of strokes are
hemorrhagic
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
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Smell
Hearing
Speech
Fingers
Arm
Hip
Hand
Language
Vision
Balance
Coordination
Brain cells have different functions in different locations
Frontal LobePersonality
Memory
Reasoning
Temporal LobeSpeech
Memory
Hearing
Parietal LobeLanguage
Sensation
Telling right from left
Occipital LobeVision
CerebellumBalance
Fine motor control
Coordination
Brain StemBreathing
Swallowing
Blood Pressure
Where the vascular compromise occurs is important
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Anatomy of the cerebrovascular system 19
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
20The vascular “tree”
The size of the emboli impacts the size of the infarction
Strokes from atrial fibrillation are typically associated with more brain tissue involved when compared to carotid artery disease-induced strokes.Presumably due to larger emboli.
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http://www.stroke.org/site/PageServer?pagename=brochures
Subarachnoid Hermorrhage
Blood vessel ruptures and blood leaks in between the brain and the skull
Intracerebral Hermorrhage
Blood vessel ruptures and bleeds directly into the brain tissue
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
TIA—Making the diagnosis 22
Neurological Symptoms---A helpful chart
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
TIA—Making the diagnosis 23
Not all neurological symptoms are vascular in etiology
Several important points here:
There are several potential etiologies for transient neurological events
If vascular compromise is of concern there ideally will be results of a typical diagnostic work-up for underwriter review to assess mortality risk
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
CVA—Making the diagnosis
Brain imaging with CT or MRI is indicated in all patients with a suspected TIA or minor non-disabling stroke as soon as possible.
The 2013 AHA/ASA guidelines suggest:
Imaging techniques and quality of the exams has evolved To some extent the type of imaging performed is based upon the availability of testing
devices and expertise of staff Many feel that the Diffusion Weighted Imaging (DWI) MRI is more sensitive than CT
for the early detection of acute ischemia. CT’s are frequently more accessible and are frequently used—especially first tests.
CT’s are also especially good at detecting the presence of hemorrhage.
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http://stroke.ahajournals.org/
Imaging within 24 hours of symptom onset MRI and specifically Diffusion-Weighted Imaging MRI as the preferred modality Noninvasive imaging (MRA, CTA of the cervico-cephalic vessels) to be part of the
evaluation of suspected TIA’s or non-disabling strokes
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
CVA—Making the diagnosis
Cardiac evaluation is important when TIA or CVA is suspected. Testing frequently performed include: ECG Echocardiogram Cardiac monitoring
Other tests are performed as needed Blood cultures Sed rate CBC PT/PTT
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“My formula for living is quite simple. I get up in the morning and I go to bed at night. In between, I occupy
myself as best I can”Cary Grant
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Making the diagnosis of a CVA 26
http://www.medscape.com/viewarticle/452843
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Dissection 28
http://uvahealth.com/services/vascular-center/treatment/arterial-dissections http://www.ajnr.org/content/24/10/2052/F1.expansion.html
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Primary treatment of an acute ischemic CVA or TIA 29
Acute Ischemic strokes:
– Thrombolytic therapy with intravenous alteplase (tPA—recombinant tissue-type plasminogen activator)
• Early treatment important• Many exclusions• Unfortunately, in the US only about 8% of all ischemic
stroke victims present to the ER within 3 hours and also meet the eligibility criteria for tPA.
Vertebral artery or Carotid artery dissecting aneurysms
– Thrombolytic therapy is not contraindicated and the effectiveness and safety is comparable to ischemic strokes from other causes
– Extension of the aortic dissection is a potential complication of the thrombolysis however.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Primary treatment of an acute bleed 30
Subarachnoid hemorrhage– Aneurysmal (~80%)
• Surgical management usually neededSurgical clippingEndovascular therapy with coil system
– Non-aneurysmal (~20%)• AVM
Surgical clippingEndovascular therapy
• Intracranial artery dissectionSurgical clippingEndovascular therapy
• Perimesencephalic non-aneurysmal subarachnoid hemorrhageSubtype identified in 1985Findings of localized blood on CT, normal angiography, and a relatively benign courseLong term mortality is significantly better than aneurysmal SAH approaching normal controls.
Intra-cerebral bleeding– Reversal of anticoagulation– Monitoring of intracranial pressure– Seizure prophylaxis – Surgery for cerebellar decompression and possibly supratentorial ICH (controversial)
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Secondary Treatment of the acute ischemic CVA or TIA
Antiplatelet therapy initiation within 24 hours of stroke and continued for 90 days
BP management—Goal of therapy is BP of <140/90 mm Hg.
Lipid lowering therapy (Statins) for those with elevated LDL >100 mg/dl.
Prophylaxis for DVT and PE important for those at risk
DM management (Diabetics have twice the typical risk for CVA). Unfortunately studies have not provided conclusive evidence that tight control decreases macro-vascular disease similar to the benefit in micro-vascular disease. The AHA/ASA still supports good control of blood sugars however.
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• Smoking cessation
• Heavy ETOH consumption should be avoided but light to moderate consumption (no more than 2 per day
for men and 1 drink per day for women) is reasonable
• Physical exercise—30 min of moderate-intensity for 30 min or more 1-3 times per week
Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack. A guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Stroke. 2011; 42:227-276
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Secondary Treatment of the acute ischemic CVA or TIA—Slide 2 33
Atrial Fibrillation (paroxysmal or permanent):• Anticoagulation with a vitamin K antagonist,
apixaban, dabigatran, or rivaroxaban are indicated
• ASA alone for those who can’t tolerate a vitamin K antagonist
Cardiomyopathy with EF <35%:• Warfarin, ASA, Clopidogrel, or the combo of ASA
and dipyridamole may be considered. It is unclear which is more advantageous.
Acute MI and left ventricular thrombus• Oral anticoagulation recommended for at least 3
months
Prosthetic heart valves• Oral anticoagulation recommended• ASA is recommended to be added to the oral
anticoagulation for those with an ischemic event while on anticoagulation
Non-cardioembolic ischemic strokes or TIA’s • Antiplatelet therapy
Arterial Dissection• Antithrombotic treatment with either antiplatelet or anticoagulant
therapy for 3-6 months• Endovascular stenting should be considered for recurrent ischemic
events despite medical treatment• Surgical treatment should be considered for those failing stenting.
PFO (Patent Foramen Ovale)• Antiplatelet therapy is recommended for those not
obtaining anticoagulation.• Data doesn’t support closure for those with PFO and
TIA/cryptogenic ischemic stroke if no evidence of DVT
• Consider surgical closure with a trans-catheter device for those with PFO and DVT.
Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack. A guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Stroke. 2011; 42:227-276
Secondary Treatment of the acute ischemic CVA or TIA
Symptomatic recent (within last 6 months) extracranial carotid disease: 70-99% stenosis of ipsilateral side: Carotid endarterectomy recommended
When morbidity and mortality risk is <6% 50-69% stenosis: Carotid endarterectomy to be considered
When morbidity and mortality risk is <6% and Dependent on pt specific factors (age, sex, comorbid conditions)
<50% stenosis No indication for endarterectomy or stenting
Carotid angioplasty and stenting is an alternative in some settings > 70% stenosis by noninvasive testing
Especially those difficult to assess surgically such as radiation induced stenosis or restenosis after endarterectomy > 50% stenosis by angiography
Optimal medical therapy including antiplatelet therapy, statins, etc.
Extracranial vertebrobasilar disease: Optimal medical therapy Consider surgery when medical therapy has failed.
Intracranial atherosclerosis 50-99% stenosis:
ASA recommended (in preference to warfarin) Angioplasty and/or stent placement usefulness is unknown and considered E/I for those 70-99% stenotic. It is not
recommended for those <70% stenotic. Bypass surgery is not recommended
34
Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack. A guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Furie, Karen et al. Stroke. 2011; 42:227-276
“There is nothing so strong or safe in an emergency of life as the simple truth”
Charles Dickens
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Mortality implications of TIA’s and CVA’s
CVA CVA’s have a high peri-stroke period mortality rate Complications clearly are determined by
Location of the strokeHow much brain tissue is involved
95% of patients have at least one medical complication1
24% of patients have at least one serious, life threatening complication1
Direct effects of the stroke cause death in the first few days. Medical complications account for the mortality thereafter
In the first year the most common cause of death is2:First week: Cerebrovascular disease2-4 weeks: PE2-3 months: Pneumonia>3 months Cardiac disease
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1Randomized trial of Tirilizad Mesylate in Acute Stroke (RANTTAS)2Risk of myocardial infarction and vascular disease after transient ischemic stroke and ischemic stroke: a systematic review and meta-analysis. Touze E et al. Stroke. 2005:36 (12):2748
TIA• TIA without images being positive 90 day stroke risk <1%• Transient event that is image positive 90 day stroke risk 14%
Cardiac complications of a stroke
Cardiac complications are not just the association of atherosclerosis Stroke is a coronary artery disease risk equivalent
Those with a stroke with no known coronary disease have a similar risk of MI as those with established coronary disease
Takotsubo cardiomyopathy is one condition that can occur Extreme catecholamine release is postulated to cause this Causes an acute cardiomyopathy Interestingly it typically involves the apical and mid sections of the heart
ECG abnormalities present in 92% of patients with an acute stroke Classic large and upright T waves can occur Prolonged QT intervals are common Cardiac arrhythmias
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Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Included those with hx. of heart disease
Did not include those with hx. of heart disease
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Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
4 QUESTIONS 38
1. What percentage of stroke victims die within 1 month of their first stroke?
2. What percentage of stroke victims die within 5, 10 and 15 years?
3. Does age matter?
4. Does type of stroke matter?
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Proportion of patients dead 1 year after first stroke.
Go A S et al. Circulation 2013;127:e6-e245
Copyright © American Heart Association
39
45-64 y/o
>64 y/o
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Proportion of patients dead within 5 years after first stroke.
Writing Group Members et al. Circulation 2012;125:e2-e220
Copyright © American Heart Association
Compared to the general population nonfatal stroke is associated with a:
5 fold increase for death between 1 month and 1 year.2 fold increase for death at 5 years
40
45-64 y/o
>64 y/o
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Figure 1. Short-term survival probability for patients aged 65 years at first nonfatal stroke by subtype (Cox regression).
Copyright © American Heart Association
Estimated cumulative risk for death:28 days 28%1 year 41%5 years 60%
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SAH Subarachnoid Hemorrhage
However, risk of death did vary based upon type of stroke
CI Cerebral Infarct
PICH 1o Intracerebral Bleed
IDS Ill Defined Stroke
Brønnum-Hansen H et al. Stroke 2001;32:2131-2136
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Figure 2. Long-term survival probability for patients aged 65 years at first nonfatal stroke by subtype (Cox regression).
Brønnum-Hansen H et al. Stroke 2001;32:2131-2136
Copyright © American Heart Association
http://www.theuniversityhospital.com/stroke/stats.htm
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SAH Subarachnoid HemorrhageCI Cerebral InfarctPICH 1o Intracerebral BleedIDS Ill Defined Stroke
Estimated cumulative risk for death:5 years 60%10 years 76%15 years 86%
SAH Subarachnoid Hemorrhage
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
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Vascular event (with 95% CI)
Mortality
Stroke
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Individual PrognosisAge
Infarct Location
Interventions done after the CVA
Complications
Comorbid conditions
The Mortality Risk Evaluation Needs to be Individualized
Adherence to therapeutic plan
Stroke Severity
Stroke Mechanism
Clinical Findings
44Nebraska Home Office Life Underwriters
Meeting Presentation 9/2014
Imaging results frequently encountered by the underwriting staff
3 tests, frequently seen, that I want to discuss in more depth are:
CIMT testing
Carotid Duplex Ultrasound testing
MRI or CT scan which shows the presence of a previous infarct—incidental finding
45
“If you want to stay young-looking, pick your parents very carefully”Dick Clark
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Carotid artery intima-media thickness (CIMT) 46
http://www.sonosite.com/apps-n-softwares/sonocalc-imt
http://www.prweb.com/releases/2011/5/prweb8502142.htm
http://www.preventionhealthscreenings.com/services_imt.html
http://www.diabetesresearchclinicalpractice.com/article /S0168-8227(05)00410-9/abstract
• CIMT measures the thickness of 2 layers (intima and media) of the carotid artery walls
• Thought by some to be an even earlier indicator of atherosclerosis than Coronary artery calcium measurements since thickening precedes a plaque
• Carotid artery methods are being refined so it is important to know exactly where the artery is being measured (Carotid bulb, common carotid, or internal carotid), near or far walls or both.
Carotid artery intima-media thickness (CIMT)
Conflicting evidence whether this test has independent predictive power as compared to usual CV risk factors
American Heart Association Position Statement (dated 3/7/12) even suggested this test not be mandated by health insurers as the predictive power hasn’t been established. (Of note however is that they also did not support EBCT measurements whereas there is some evidence this test is helpful, at least in intermediate risk individuals, independently of other tests).
In the Multi-Ethnic Study of Atherosclerosis (MESA) which had 6698 subjects aged 45-89 years CIMT was a modestly better predictor of stroke than EBCT but was not as good as EBCT for CV disease prediction
47
Abnormal (“high risk”) frequently defined as media thickness above the 75th percentile.
Meta-analysis has shown that serial measurements are not useful for predicting progression.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Evaluation of the Carotid arteries
Carotid duplex ultrasound frequently performed: 81-98% sensitive 82-89% specific Less precise for stenosis of <50% Less precise for stenosis of 100% Frequently used with MRA or CTA for confirmation of stenosis of >50% or for
100% stenosis.
Complete Obstruction: No surgical treatment has been proven to be of benefit. Combo of US and MRA very good at detecting this CTA is also extremely good at detecting this Gold standard is angiography
49
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Asymptomatic extracranial carotid artery diseaseThe 2011 AHA/ASA Guidelines Medical therapy and lifestyle changes should be instituted Population screening for asymptomatic carotid artery stenosis is not
recommended Benefit in women is very controversial Prophylactic CEA performed with <3% morbidity and mortality should be
considered when: Minimum of 60% occlusion by angiography or >/= 70% occlusion on doppler
>80% occlusion on CTA or MRA for those with US showing 50% to 69% stenosis
The number to treat (NTT) to prevent 1 stroke over 3 years is 33 Carotid artery stenting can be considered but the advantage over medical
therapy is not well established
50
Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack. A guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Furie, Karen et al. Stroke. 2011; 42:227-276
Bonus Quote: “I like to drive with my knees. Otherwise, how can I put on my lipstick and
talk on the phone”Sharon Stone
“If you act like you know what you are doing, you can do anything you want – except neurosurgery”
Sharon Stone
51
http://www.health.harvard.edu/newsletters/Harvard_Womens_Health_Watch/2012/June/could-a-silent-stroke-erode-your-memory
Evaluated in the Rotterdam Scan study2
• Published in 2003 • 1077 elderly people
followed for over 4 years.• Silent brain infarcts
increased the chance of a subsequent major CVA by 5 times.
• Those with >1 silent infarct were at the highest risk for a subsequent major CVA.
• The presence of silent infarcts significantly increased the risk of dementia
A not so uncommon incidental finding
Evaluated in the Cardiovascular Health Study1
• Published in 2002 • 5888 people >/= 65 y/o
with normal MRI followed by repeat MRI in 5 years.
• 17.7% had 1 or more infarct
• Only 11% had experienced a documented TIA or CVA .
• Those with + MRI scans showed > decline in Mini-Mental exam test results
1. Incidence, manifestations, and predictors of brain infarcts defined by serial cranial magnetic resonance imaging in the elderly: The Cardiovascular Health Study. Longstreth WT et al Stroke. 2002;33(10):2376.
2. Silent brain infarcts and white matter lesions increase stroke risk in the general population: the Rotterdam Scan Study.Vermeer SE, et al, Rotterdam Scan Study Stroke. 2003;34(5):1126
Silent StrokesNot such good outcomes when found
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Zhu Y et al. Stroke 2011;42:1140-1145
Copyright © American Heart Association
More examples of silent CVA’s
Axial T2-weighted Axial T1-weighted FLAIR Axial Proton Density
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Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Summary
CVA rates in the US are declining. However, based upon population demographics the total number/year is anticipated to continue to rise
Definition changes regarding TIA and CVA will impact mortality numbers
There are several types of strokes and multiple etiologies. Regardless of the type there are significant adverse long term mortality concerns
Diagnosis of TIA’s and CVA’s can be accomplished with several types of imaging. A diffusion weighted MRI probably is one of the best methods. Quick evaluation is important
Primary and secondary treatment depends on the etiology of the stroke but does impact mortality
CIMT testing might demonstrate future potential value in underwriting but as an independent cardiac or cerebrovascular disease indicator there are currently conflicting results
Carotid US results and the presence of CVA’s found incidentally do help with underwriting
53
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
Cases to Consider
2 cases arrive for underwriter review. Which has the worst mortality risk based upon the limited information provided?
54
Case #265 y/o female with no known neurological complaints—past or present• Hx. of hypertension and hyperlipidemia. BMI 30• MRI of the brain shows 2 small lacunar infarcts—age unknown• US of the carotids is WNL• ECG is WNL• CIMT is WNL
Case #166 y/o female with a hx. of a “TIA-like” event 4 years ago with no subsequent symptoms. Hx. of hypertension and hyperlipidemia. BMI 30• MRI of the brain WNL• US of the carotids is WNL• ECG is WNL• CIMT at 90th percentile for age
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
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Lifelong Risk for Rupture of Intracranial AneurysmsTake-HOME MESSAGE•Of 118 people, 34 (29%) had subarachnoid hemorrhage (SAH) during lifelong follow-up after diagnosis of unruptured intracranial aneurysm (UIA). The median age at SAH was 51.3 years. The annual rupture rate per patient was 1.6%. Risk factors for a lifetime SAH included female sex, current smoking, and aneurysm size of ≥7 mm in diameter. Depending on the risk factor burden, the annual rupture rate was from 0% to 6.5%, and the lifetime risk of an aneurysmal SAH varied from 0% to 100%. Of 96 patients with small (<7 mm) UIAs, 24 (25%) had an aneurysmal SAH during the follow-up. Although risk was associated with the risk factor burden, close to 30% of the aneurysms in working-age people ruptured over the course of lifelong follow-up.•The results suggest that maybe risk factor status should drive treatment decisions for individuals with UIAs given that even the small ones in this study ruptured.ABSTRACTBackground and PurposeOur aim was to define for the first time the lifelong natural course of unruptured intracranial aneurysms (UIAs) and identify high-risk and low-risk patients for the rupture.MethodsOne hundred and eighteen patients (61 women) with UIAs were diagnosed between 1956 and 1978 and followed up until death or subarachnoid hemorrhage (SAH). The median age at the diagnosis was 43.5 years (range, 22.6–60.7 years). The median size of the UIA at the diagnosis was 4 mm (range, 2–25 mm). Analyzed risk factors for a rupture included sex, age, cigarette smoking, systolic blood pressure values, diagnosed hypertension, UIA size, and number of UIAs.ResultsThirty four (29%) out of 118 people had SAH during the lifelong follow-up. The median age at SAH was 51.3 years (range, 30.1–71.8 years). The annual rupture rate per patient was 1.6%. Female sex, current smoking, and aneurysm size of ≥7 mm in diameter were risk factors for a lifetime SAH. Depending on the risk factor burden, the lifetime risk of an aneurysmal SAH varied from 0% to 100%, and the annual rupture rate from 0% to 6.5%. Of the 96 patients with small (<7 mm) UIAs, 24 (25%) had an aneurysmal SAH during the follow-up.ConclusionsAlmost 30% of all UIAs in people of working age ruptured during a lifelong follow-up. The risk varied substantially on the basis of risk factor burden. Because even small UIAs ruptured, treatment decisions of UIAs should perhaps be based on the risk factor status.
Stroke; A Journal of Cerebral CirculationLifelong Rupture Risk of Intracranial Aneurysms Depends on Risk Factors: A Prospective Finnish Cohort StudyStroke 2014 May 22;[EPub Ahead of Print], M Korja, H Lehto, S Juvela
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014
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Stroke; A Journal of Cerebral CirculationLong-Term Mortality After First-Ever and Recurrent Stroke in Young AdultsStroke 2014 Jul 24;[EPub Ahead of Print], K Aarnio, Elena Haapaniemi, S Melkas, M Kaste, T Tatlisumak, J PutaalaBackground and PurposeMortality after first-ever stroke, and particularly after recurrent stroke, and predictors of long-term mortality among young and middle-aged stroke patients are not well-known. We assessed 17-year risk of mortality with focus on the effect of recurrence on the risk of death of young and middle-aged patients with stroke.MethodsMortality and recurrent stroke rate of 970 consecutive 30-day survivors of first-ever ischemic stroke aged 15 to 49 years (1994–2007) were studied. Prospective follow-up data came from the Finnish Care Register for Health Care and Statistics Finland. Mean follow-up was 10.2±4.3 years. We compared survival between clinical subgroups and identified factors associated with mortality. Standardized mortality ratio was calculated for demographic and pathogenetic subgroups using mortality data of the general population matched with age, sex, calendar year, and geographical area.ResultsAt the end of follow-up, 152 (15.7%) patients had died (cumulative risk, 23.0%; 95% confidence interval, 19.1%–26.9%) and 132 (13.6%) had experienced a recurrent stroke. After adjusting for baseline characteristics, recurrent stroke was statistically the most important risk factor for mortality after first-ever ischemic stroke (hazard ratio, 16.68; 95% confidence interval, 2.33–119.56; P=0.005). Observed mortality was 7-fold higher than the expected mortality (standardized mortality ratio, 6.94; 95% confidence interval, 5.84–8.04) and particularly high among patients who experienced a recurrent stroke (standardized mortality ratio, 14.43; 95% confidence interval, 10.11–18.74).ConclusionsThe high mortality rates and the striking impact of recurrent stroke on the risk of death should lead to development of more robust primary and secondary prevention strategies for young patients with stroke.
Nebraska Home Office Life Underwriters Meeting Presentation 9/2014