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48
CHAPTER 3 Valvular Heart Disease
43. Roudaut R, Lafitte S, Roudaut MF, et al. Fibrinolysis of mechanical pros-
thetic valve thrombosis: a single-center study of 127 cases. J Am Coll Cardiol
2003; 41 (4): 653–658 .
44. Leon MB. Transcatheter aortic valve replacement: a breakthrough medical ther-
apy! The 20-year odyssey, and now, a 10-year anniversary. Arch Cardiovasc Dis
2012; 105 (3): 129–131 .
45. Holmes DR, Jr., Mack MJ, Kaul S, et al. 2012 ACCF/AATS/SCAI/STS expert
consensus document on transcatheter aortic valve replacement: developed
in collaboration with the American Heart Association, American Society
of Echocardiography, European Association for Cardio-Thoracic Surgery,
Heart Failure Society of America, Mended Hearts, Society of Cardiovascular
Anesthesiologists, Society of Cardiovascular Computed Tomography, and
Society for Cardiovascular Magnetic Resonance. Catheter Cardiovasc Interv
2012; 79 (7): 1023–1082 .
46. Thomas M, Schymik G, Walther T, et al. One-year outcomes of cohort 1 in the
Edwards SAPIEN Aortic Bioprosthesis European Outcome (SOURCE) regis-
try: the European registry of transcatheter aortic valve implantation using the
Edwards SAPIEN valve. Circulation 2011; 124 (4): 425–433 .
47. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation
for aortic stenosis in patients who cannot undergo surgery. N Engl J Med
2010; 363 (17): 1597–1607 .
48. Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve
replacement in high-risk patients. N Engl J Med 2011; 364 (23): 2187–2198 .
49. Leon MB, Piazza N, Nikolsky E, et al. Standardized endpoint definitions
for Transcatheter Aortic Valve Implantation clinical trials: a consensus
report from the Valve Academic Research Consortium. J Am Coll Cardiol
2011; 57 (3): 253–269 .
50. http://www.fda.gov/downloads/AdvisoryCommittees/Committees-
MeetingMaterials/MedicalDevices/MedicalDevicesAdvisoryCommittee/
CirculatorySystemDevicesPanel/UCM269472.pdf. (Transcript for the July 20,
2011 Circulatory System Devices Panel meeting).
51. Moat NE, Ludman P, de Belder MA, et al. Long-term outcomes after transcathe-
ter aortic valve implantation in high-risk patients with severe aortic stenosis: the
U.K. TAVI (United Kingdom Transcatheter Aortic Valve Implantation) Registry.
J Am Coll Cardiol 2011; 58 (20): 2130–2138 .
52. Kahlert P, Knipp SC, Schlamann M, et al. Silent and apparent cerebral ischemia
after percutaneous transfemoral aortic valve implantation: a diffusion-weighted
magnetic resonance imaging study. Circulation 2010; 121 (7): 870–878 .
53. Cerillo AG, Murzi M, Glauber M, Berti S. Quality control and the learning curve
of transcatheter aortic valve implantation. JACC Cardiovasc Interv 2012; 5 (4): 456 ;
author reply 456–457.
54. Tommaso CL, Bolman RM, 3rd, Feldman T, et al. Multisociety (AATS, ACCF,
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ments for transcatheter valve repair and replacement, part 1: transcatheter aor-
tic valve replacement. J Am Coll Cardiol 2012; 59 (22): 2028–2042 .
55. Naber CK, Ghanem A, Abizaid AA, et al. First-in-man use of a novel embolic
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56. Tuzcu EM, Kapadia SR, Svensson LG. Valve in valve: another milestone for tran-
scatheter valve therapy. Circulation 2012; 126 (19):2280–2282.
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4949
Chapter 4
Cerebrovascular Disease:
Ischemic Syndromes Due
to Atherothrombosis
Mark J. Alberts
Overview of stroke types, epidemiology,
and risk factors
Stroke is a common and serious disease. On a global basis, stroke is the second
leading cause of death (fourth in the United States).
1,2
It is estimated that each
year between 6 and 7 million people die due to stroke, and more than one third
were disabled for 1 year or longer.
3
Since in some cases stroke may be chal-
lenging to diagnose without specialty medical care and brain imaging, the above
numbers may be gross underestimates of the annual deaths due to stroke. In
many cases these strokes could have been prevented.
We generally divide stroke syndromes and mechanisms into ischemic and
hemorrhagic events, and in this chapter we will focus on the ischemic types of
stroke. In most cases an ischemic stroke is due to atherothrombotic disease in
a cerebral blood vessel (cervical or intracranial), although in some cases it can
be due to disease in another organ system (i.e., a cardioembolic process such as
atrial fi brillation, a hypercoagulable blood process).
It is clear that different ethnic and racial groups have different patterns of
stroke and cerebrovascular disease. For example, Asian populations and African
Americans have relatively higher rates of cerebral hemorrhages compared to
non-Asian groups. Also, African Americans and Asians tend to have lower rates
of extracranial atherothrombotic disease and higher rates of intracranial disease
compared to Caucasians.
4
These differences can be only partially explained by
standard risk factor profi les, and suggest that other factors (environmental,
genetic) may be playing a role.
Prior studies have defi ned several risk factors for stroke and cerebrovascular
disease that generally mirror the risk factors for cardiovascular disease, with
some adjustments and differences. Age is the most powerful nonmodifi able risk
factor for stroke, and hypertension is the most signifi cant treatable risk factor.
Lipid disorders play a less prominent role for stroke than for cardiovascular
disease, but diabetes and obesity are signifi cant risk factors for stroke. Other
well-recognized risk factors for ischemic stroke include atrial fi brillation (and
other forms of heart disease), smoking, elevated homocysteine levels, lack of
exercise, sleep apnea, genetics, and drug/alcohol abuse.
5,6
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50
CHAPTER 4 Cerebrovascular Disease
The large INTERSTROKE study enrolled 3,000 stroke patients (78 percent
ischemic) from 22 countries. They found that 88 percent of the population
attributable risk for stroke could be explained by 10 risk factors (Table 4.1).
7
A study of over 40,000 patients with fi rst-time ischemic stroke reported gender
differences for risk factors, with men having more diabetes, cardiac disease,
alcohol consumption, and peripheral arterial disease, and women having higher
rates of hypertension and obesity.
8
An elevated homocysteine level is also a risk
factor for ischemic s troke.
9
The risk factor profi le appeared to infl uence the
type of stroke seen in different groups. For example, the Atherosclerosis Risk
in Community study (ARIC), which included more than 14,400 patients, found
that small vessel lacunar strokes were more common in blacks (mostly African
Americans) compared to Caucasians. Diabetes and smoking were associated
with a higher risk of lacunar events, while other risk factors were associated
with non-lacunar stroke.
4
In the United States, African Americans are at increased risk of having a
stroke and of dying due to stroke.
5,10
About half of this disparity can be explained
by typical stroke risk factors and socioeconomic status.
11
Perhaps genetic fac-
tors along with as-yet-unidentifi ed novel medical risk factors and environmen-
tal factors explain some of the remaining disparity. A study of over 22,400 men
and women in the United Kingdom reported that social class was a signifi cant
stroke risk factor, with higher risks being seen in lower social classes.
12
This
increase persisted after adjustments for traditional stroke risk factors. Recent
studies have also suggested that stress may be a risk factor for stroke.
7
A very powerful and prevalent risk factor for ischemic stroke is the pres-
ence of symptomatic atherothrombotic disease in one or more vascular beds.
Data from the REACH registry showed that individuals with prior ischemic
events (strokes, cardiac events, or symptomatic arterial vascular disease) have
a three- to four-fold increased risk of a subsequent vascular event compared to
asymptomatic individuals.
13
This increased risk became apparent soon after the
initial event and persisted for at least 4 years. Patients with a recent transient
ischemic attack (TIA) have a 10 percent risk at 3 months of having a stroke,
Table 4.1 Risk Factors of Stroke
Risk Factor Odds Ratio PAR
Hypertension 2.64 34.6
Current smoking 2.09 18.9
Waist–hip ratio 1.65 26.5
Diet 1.35 18.8
Physical activity 0.69 28.5
Diabetes mellitus 1.36` 5.0
Alcohol intake 1.51 3.8
Stress 1.30 4.6
Depression 1.35 5.2
Cardiac disease 2.38 6.7
Apolipoprotein B/A1 1.89 24.9
Data derived from reference 7. PAR, population attributable risk.
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CHAPTER 4 Cerebrovascular Disease
and a 21 percent risk of having a stroke, recurrent TIA, cardiac event, death, or
hospital admission.
14
These data highlight the importance of primary prevention
as well as the need for highly effi cacious secondary prevention therapies.
A topic of much discussion and research over the past decade has been
genetic factors causing or contributing to stroke. There are rare instances of
specifi c mutations causing high stroke risk and unusual stroke syndromes (i.e.,
CADASIL and related disorders, MELAS). There are also rare mutations that
cause malignant and hard-to-treat stroke risk factors (i.e., extreme hyperten-
sion, familial dyslipidemias). However, these purely genetic etiologies are rela-
tively rare and account for only a small minority of strokes and stroke risk.
Much of the genetic or familial risk of stroke (and heart disease) may be due to
the familial aggregation of standard cardiovascular disease risk factors.
15
Genome-wide searches for a so-called “stroke gene” have yielded mixed
results, with a few genotypes or markers having modest statistical signifi cance,
which is often not confi rmed when attempts are made to validate them in
other populations.
16
The DECODE group from Iceland has reported some
markers that correlated with non-cardioembolic strokes, and other markers
related to atrial fi brillation.
17,18
These await confi rmation in other more diverse
datasets. Overall it appears unlikely there is a magical “stroke gene” lurking in
the genome. Whether dozens of single nucleotide polymorphisms combined
will contribute to a stroke phenotype remains unclear but is an area under
active study.
Geographic factors may be important for stroke risk. Throughout the world
there are well-defi ned areas where the risks of cardiovascular events and
stroke are increased in comparison to other areas. One of the oldest and best
studied is the Stroke Belt, which encompasses the southeastern region of the
United States. This area has, on average, a 25 percent increase in the incidence
and mortality of stroke compared to other regions of the United States.
19,20
Part
of the increased risk in the Stroke Belt is explained by traditional risk factors,
but about 30 percent cannot be explained.
21
Eastern Europe is another area
with higher rates of cardiovascular disease, including stroke. These geographic
areas might provide important insights into new stroke risk factors as well as be
a focus for stroke prevention strategies and programs.
Traditional stroke risk factors tend to lose their infl uence over time, as was
shown in a Swedish study of over 7,400 patients who were followed for several
decades. Over time, only two risk factors, hypertension and diabetes, main-
tained their risk association into old age, whereas other traditional risk factors
tended to lose their infl uence over several years.
22
Of course, since age is the
most powerful nonmodifi able risk factor for strokes, the attenuation of other
risk factors with age is of little comfort.
Extracranial cerebrovascular disease
Extracranial cerebrovascular disease is very common, whether it be symptom-
atic or asymptomatic. Increased thickness of the carotid intima–media layer
is strongly associated with cardiovascular disease risk factors and is a com-
mon precursor to carotid atherosclerotic disease as well as a risk factor for
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52
CHAPTER 4 Cerebrovascular Disease
coronary artery disease.
23
Population-based studies of asymptomatic individuals
have found some degree of carotid plaque formation in 60 to 87 percent of
adults with low or intermediate Framingham scores in the more-than-18-years
to less-than-90-years age group.
24
The presence of carotid plaques is not always
associated with the risk factors described above.
There are a number of locations in the extracranial vasculature where athero-
sclerotic and atherothrombotic lesions commonly occur and may cause a TIA or
ischemic stroke. The most common is at the bifurcation of the common carotid
artery (CCA) in the neck into the internal carotid artery (ICA) and the external
carotid artery (ECA). The distal portion of the CCA and the proximal 1 to 2 cm
of the ICA are common locations for atherosclerotic plaques and atherothrom-
botic lesions.
25
Other common locations include the aortic arch in the upper
thorax and the proximal vertebral arteries as they arise from the aorta, although
atherosclerotic lesions can occur anywhere in the extracranial vasculature.
Plaque formation and composition is a complex and gradual process.
Advances in imaging techniques have permitted serial analysis of plaque com-
position and progression. There is a classifi cation system for human carotid
lesions based on gross pathological changes and in vivo magnetic resonance
imaging (Table 4.2). This system classifi es plaques based on size, morphology,
and composition. A type VI plaque is defi ned as having complex morphology
with surface defects, hemorrhage, and/or thrombus formation. Overall, increas-
ing plaque size and the degree of stenosis correlate with the risk of ipsilateral
ischemic events.
26
A recent study using computed tomography (CT) angiography reported
that in 193 carotid arteries studied over 5 years, plaque volume increased in
69 percent of cases but also decreased in 31 percent.
27
Another study used
magnetic resonance imaging (MRI) plaque classifi cation of 78 patients with 156
carotid arteries. About half of these patients had one or more TIAs or ischemic
strokes. They found that type VI plaque morphology at the carotid bifurcation
was highly correlated with symptomatic status, even after controlling for typical
Framingham vascular risk factors.
25
Clinical manifestations of disease in the above arteries can range from no symp-
toms to minor TIAs lasting a matter of seconds or minutes, to catastrophic strokes
Table 4.2 Classifi cation of Atherosclerotic and Atherothrombotic
Plaques
Type Grade Characteristics*
I–II Minor fatty streak, near-normal wall thickness; no calcifi cation
III Preatheroma with extracellular lipids; diffuse intima thickening,
small plaques; no calcifi cation
IV–V Atheroma with confl uent lipid core; plaque with lipid or necrotic
core; calcifi cation possible
VI Complex plaque with surface defect, hemorrhage, or thrombus
VII Calcifi ed plaque
VIII Fibrotic plaque; no lipid core
*These characteristics include morphologic and MRI fi ndings.
Data derived from reference 25.
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CHAPTER 4 Cerebrovascular Disease
involving large regions of a cerebral hemisphere.
26
One of the classic presentations
of atherothrombotic disease in the ICA is amaurosis fugax (transient blindness in
one eye). This is almost always painless and presents with a shade coming down
over one eye or a “graying out” of vision in one eye.
28
The symptoms typically last
only 1 to 10 minutes, and they resolve over 5 to 10 minutes. The usual mechanism
is the embolization of a platelet-rich thrombus to the ophthalmic artery or retinal
artery, although in many cases no proximate cause can be found.
29
If a monocular
scotoma occurs, then the presumed mechanism is embolization to a branch of the
retinal artery. If the embolism is persistent or permanent, the patient may have a
retinal infarction with partial or total monocular vision loss that does not resolve.
If an embolism from a plaque in the proximal ICA travels to the intracranial
vasculature (other than the eye), a hemispheric TIA or stroke will occur. The
symptomatology can range from transient numbness or weakness of an arm,
hand, or leg to permanent hemiparesis or hemiplegia, speech disturbance (dys-
arthria or aphasia), visual fi eld defi cits, and a neglect syndrome. Due to the rela-
tively small size of most cerebral vessels, an embolism only 2 to 3 mm in size can
completely occlude the middle cerebral artery (MCA) and/or its branches and
produce a large stroke with life-threatening and life-changing consequences.
30
A high-grade stenosis or occlusion of the CCA or ICA can also produce a TIA
or stroke. In this case the mechanism is hypoperfusion of the eye or all or part of
a cerebral hemisphere. Symptoms may be precipitated by a drop in the systemic
blood pressure, although this is not always present. Based on the intracranial
cerebral circulation, there are watershed zones between the circulations of the
MCA and anterior cerebral artery (ACA), and another one between the MCA
and posterior cerebral artery (PCA).
31
In the setting of high-grade ICA stenosis,
ischemia in the MCA/ACA watershed could produce weakness and numbness
of the distal arm and hand. Ischemia in the MCA/PCA watershed could produce
speech changes, sensory changes, agnosia, and vision changes.
Emboli from an aortic arch plaque could travel to the CCA, ECA, or ICA, as
well as the vertebral arteries (left more likely than right) and basilar artery.
32
If the
embolism goes to the anterior circulation (i.e., CCA, ICA, ECA), then symptoms
as described above can occur. If it goes to the vertebral arteries and/or basilar
artery, then symptoms related to the posterior fossa could occur. These include
cerebellar abnormalities, dizziness/vertigo, diplopia, bilateral motor fi ndings,
severe dysarthria, and even altered levels of consciousness. In situ atherothrom-
botic lesions in the vertebral arteries can produce similar clinical fi ndings.
Rupture of an atherosclerotic plaque with formation of a thrombus on the
plaque surface has been described as a common mechanism that is responsible
for the transition of an asymptomatic lesion into one that can produce clini-
cal symptoms such as a TIA or ischemic stroke.
33
Thinning and rupture of the
fi brous cap on the surface of a plaque leads to exposure of the thrombogenic
plaque core, thereby precipitating platelet aggregation and thrombus forma-
tion. A number of clinical factors and laboratory fi ndings have been correlated
with plaque rupture, including infl ammation, recent infections and various infec-
tious agents, recent surgery, dental disease, high levels of C-reactive protein,
and high PLA2 levels, to name but a few.
34
Dissections of the extracranial vasculature occur when there is a separation
or ripping between one or more layers (intima, media, adventitia) of the vessel
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54
CHAPTER 4 Cerebrovascular Disease
wall. Such dissections can produce local clots that embolize distally or can
cause occlusion of the vessel, with clinical consequences as noted above. About
50 percent of dissections occur without any obvious or signifi cant trauma to
the head or neck. Almost all cases of dissection are accompanied by moderate
to severe head and/or neck pain.
35
Intracranial cerebrovascular disease
Atherothrombotic disease can affect any of the intracranial vessels, but some areas
appear to be more commonly affected than others. These include the proximal
MCA, midportions of the ACA, proximal PCA, and midbasilar artery. It is hypothe-
sized that turbulent fl ow and pressure gradients may be causative factors that pro-
mote the development of atherosclerotic lesions in these particular areas. These
lesions begin as atherosclerotic plaques, which may enlarge and rupture over time.
Rupture of the atherosclerotic plaque can lead to thrombus formation with vessel
occlusion or artery-to-artery embolization of material to a distal vessel.
The symptoms produced by lesions in the intracranial vessels noted above
are similar to those due to extracranial atherothrombotic disease and embolic
events. The one exception is disease in the basilar artery, which can produce a
brainstem syndrome with altered mentation, abnormal eye movements, weak-
ness of all four extremities, severe dysarthria, dysphagia, and ataxia.
In addition to these large vessels, the small intracranial arteries (100 to 300
microns in diameter) are also commonly involved. Typically the involved vessels
arise at a 90-degree angle from a larger vessel (i.e., MCA, basilar artery), and the
abrupt change in vessel diameter may allow a high blood pressure to be trans-
mitted into the smaller artery, with resulting damage to the vessel wall. Over
time microatheromas may form in these vessels, with subsequent vessel occlu-
sion.
36
The clinical manifestations of small vessel disease are described below.
Besides atherothrombosis, another process termed lipohyalinosis also com-
monly affects these small intracranial vessels. Lipohyalinosis is a form of fi brinoid
damage to the vessels than can lead to vessel occlusion or weakness in the vessel
wall with the formation of small outpouchings (Charcot-Bouchard aneurysms).
36
Occlusion of these small vessels will cause a lacunar stroke, of which there are fi ve
classic syndromes (Table 4.3).
37
These lacunar strokes typically occur in specifi c
Table 4.3 Classic Lacunar Stroke Syndromes and Anatomic
Location of Stroke
Clinical Syndrome Common Location(s)
Pure motor hemiparesis Internal capsure, basis pontis
Mixed motor–sensory Internal capsule, corona radiata
Pure hemisensory loss Thalamus
Ataxic–hemiparesis Basis pontis, internal capsule
Dysarthria–clumsy hand Internal capsule, basis pontis
These represent only the most common syndromes and locations; this information is not meant to
be all inclusive.
Data derived in part from reference 37.
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CHAPTER 4 Cerebrovascular Disease
brain areas (basal ganglia, pons) that get their blood supply primarily from small
blood vessels. Rupture of these small vessels will lead to a deep intracerebral hem-
orrhage. This typically occurs in the setting of longstanding hypertension as well as
other risk factors, such as diabetes, and smoking.
Diagnosis and screening for cerebrovascular disease
Medical science has provided us with excellent tools for diagnosing extracranial
and intracranial disease due to atherosclerotic lesions and related processes.
As noted above, most patients who present for medical care in this realm
have had some symptom or event related to cerebrovascular disease (i.e., TIA,
stroke). Auscultation of the neck for a cervical bruit may indicate the presence
of extracranial internal carotid disease, although the specifi city and sensitivity
of this exam is limited.
38,39
Cervical bruits can be transmitted from other vessels
(i.e., external carotid artery, subclavian artery) as well as from cardiac valvular
disease (particularly aortic stenosis). Current guidelines recommend a number
of diagnostic tests that can be performed with high sensitivity and specifi city for
the detection of such lesions; these include carotid artery Doppler ultrasound,
magnetic resonance angiography (MRA), computed tomographic angiography
(CTA), and transcranial Doppler (TCD). The advantages and limitations of each
are detailed in Table 4.4 and the references.
40,41
In general, some clinicians prefer to use MRA of the extracranial and intrac-
ranial vessels as an initial approach, since it can be done at the time of a brain
MRI, it is noninvasive, has no radiation, and it provides fairly complete imaging
of the entire cerebral vasculature. CTA provides somewhat greater anatomical
detail and more precise information about the degree of stenosis, but it does
expose the patient to some radiation. Carotid Doppler ultrasound is clearly
safe and noninvasive, but it images only a relatively small amount of the cerebral
vasculature in the cervical region.
The issue of screening asymptomatic individuals for the presence of cervical
carotid artery disease has been the topic of much debate among clinicians. The
overall concept is to identify patients with carotid disease before it becomes
symptomatic and to intervene with medical therapy as well as either surgery
(carotid endarterectomy) or carotid artery stenting in an attempt to prevent
a devastating stroke. However, data from various studies as well as published
guidelines do not support this approach in the general population due to the
low prevalence of signifi cant carotid disease and the risk of complications for
surgical and endovascular interventions.
42
The benefi ts from screening may be
greater if a high-risk patient population is the focus of such efforts.
43,44
Prevention and treatment of
atherothrombotic cerebrovascular disease
This section will discuss primary and secondary prevention of atherothrombotic
disease and ischemic strokes/TIAs and will briefl y touch on acute therapies. The
concept of primary prevention for ischemic stroke is of vital importance, since
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CHAPTER 4 Cerebrovascular Disease
Table 4.4 Characteristics of Vascular Testing Techniques for Cerebrovascular Disease
Test Carotid Doppler MRA (head and neck) CTA (head and neck) TCD Digital Angiogram
Vessels imaged Carotid and
vertebral neck
vessels
Large and medium-sized
extra- and intracranial
Large, medium, and small
extra- and intracranial
Large intracranial All types in all locations
Advantages Safe, noninvasive,
low cost
Safe, noninvasive; can
be done at time of brain
MRI; can be done without
contrast using time-of-fl ight
techniques
Safe, noninvasive, rapid;
high accuracy for degree
of stenosis and structural
lesions; can be done at
time of head CT
Safe, noninvasive;
accurate measures
of cerebral fl ow
velocities
Considered “gold standard”
for vascular imaging; high
sensitivity and anatomical
detail
Disadvantages Only images
extracranial vessels
in neck region;
variable accuracy for
degree of stenosis
Not used in patients
with pacemakers, severe
claustrophobia; cannot use
contrast in renal failure
Use of contrast limited in
renal failure
Poor anatomical
detail; cannot image
most structural
lesions
Invasive, 1% risk of serious
complications; limited in
renal failure; may require
anesthesia
Typical use Good for patient
screening
Evaluation of strokes, TIAs Evaluation of strokes, TIAs,
aneurysms, arteriovenous
malformations
Vasospasm and vaso-
occlusive disease
Confi rmation of degree of
stenosis; assess collateral
fl ow and structural lesions
Data derived in part from reference 40.
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CHAPTER 4 Cerebrovascular Disease
more than 600,000 of the almost 800,000 strokes each year in the United States
are fi rst-time (not recurrent) strokes.
5
While this implies that primary prevention
is the optimal approach, this has proven problematic. It requires treating large
numbers of patients for many years to prevent a relatively small number of events.
This exposes many patients to the costs and side effects of one or more therapies.
Perhaps a better approach is to identify and aggressively target high-risk asymp-
tomatic individuals for comprehensive risk factor control and other interventions.
Preventing the formation of atherosclerotic plaques can be accomplished
(in some cases) by aggressive identifi cation and treatment of risk factors such
as hypertension, diabetes, hyperlipidemia, and smoking. Studies have estimated
that proper control of these risk factors could reduce the occurrence of isch-
emic stroke by approximately 80 percent.
45
This is assuming a high level of
compliance with medication and lifestyle changes, which is a challenge even in
populations with easy access to affordable medications and health care.
However, even high levels of adherence to medical regimens may not have
the desired effects. Recent studies have shown that aggressive treatment of
diabetes did not result in a signifi cant reduction in major vascular events.
46,47
The REACH registry found that in some populations with relatively high rates
of medication use and low smoking rates, the risk of recurrent cardiovascu-
lar events remained quite high.
13
On the other hand, studies of high-dose sta-
tin therapy in asymptomatic populations found a reduction in carotid disease
progression along with a 50 percent reduction in the occurrence of stroke
(although the actual number of events was quite low).
34,48
The use of antiplatelet therapy for primary prevention of stroke has pro-
duced mixed results due to the increase in serious bleeding largely outweighing
a reduction in ischemic events. Meta-analyses have suggested that aspirin (81 to
100 mg qod) may be benefi cial for the primary prevention of ischemic strokes
in women and myocardial infarction in men in the 40-to-60-year age range.
49
The overall benefi t was modest, with three cardiovascular events prevented
per 1,000 women treated for 6.4 years, and four events for men treated for the
same time.
50
A recent guideline did recommend such therapy in populations at
high risk for stroke or where the benefi ts outweigh the risk.
6
The same is true for surgical and endovascular approaches. For example,
carotid endarterectomy can reduce strokes in patients with 60 to 99 percent
asymptomatic carotid stenosis, with a 6 percent absolute risk reduction over
5 years for ipsilateral strokes and periprocedure stroke and death.
51
This
amounts to slightly more than a 1 percent absolute risk reduction per year,
assuming a perioperative risk of stroke or death of 3 percent or less. Carotid
stenting for asymptomatic carotid lesions may have a similar profi le and benefi t,
but data from well-controlled trials comparing stenting to medical therapy in
patients with asymptomatic lesions are lacking.
The data on secondary prevention are more robust, with many large studies
proving the effi cacy and safety of a variety of medical, surgical, and endovascular
therapies. Aggressive treatment of important risk factors such as hypertension
and hyperlipidemia is benefi cial, with relative risk reductions in the 10 to 20 per-
cent range for each intervention (Table 4.5).
52
Some of the benefi ts of statin
therapy appear to be independent of their ability to reduce LDL cholesterol
and raise HDL levels. The SPARCL study of high-dose atorvastatin showed
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