Guidelines for the Primary Prevention of Stroke
A Guideline for Healthcare Professionals From the American Heart
Association/American Stroke Association
The American Academy of Neurology affirms the value of this guideline as an educational
tool for neurologists.
Larry B. Goldstein, MD, FAHA, Chair; Cheryl D. Bushnell, MD, MHS, FAHA, Co-Chair;
Robert J. Adams, MS, MD, FAHA; Lawrence J. Appel, MD, MPH, FAHA;
Lynne T. Braun, PhD, CNP, FAHA; Seemant Chaturvedi, MD, FAHA; Mark A. Creager, MD, FAHA;
Antonio Culebras, MD, FAHA; Robert H. Eckel, MD, FAHA; Robert G. Hart, MD, FAHA;
Judith A. Hinchey, MD, MS, FAHA; Virginia J. Howard, PhD, FAHA;
Edward C. Jauch, MD, MS, FAHA; Steven R. Levine, MD, FAHA; James F. Meschia, MD, FAHA;
Wesley S. Moore, MD, FAHA; J.V. (Ian) Nixon, MD, FAHA; Thomas A. Pearson, MD, FAHA; on
behalf of the American Heart Association Stroke Council, Council on Cardiovascular Nursing, Council
on Epidemiology and Prevention, Council for High Blood Pressure Research, Council on Peripheral
Vascular Disease, and Interdisciplinary Council on Quality of Care and Outcomes Research
Background and Purpose—This guideline provides an overview of the evidence on established and emerging risk factors
for stroke to provide evidence-based recommendations for the reduction of risk of a first stroke.
Methods—Writing group members were nominated by the committee chair on the basis of their previous work in relevant
topic areas and were approved by the American Heart Association (AHA) Stroke Council Scientific Statement Oversight
Committee and the AHA Manuscript Oversight Committee. The writing group used systematic literature reviews
(covering the time since the last review was published in 2006 up to April 2009), reference to previously published
guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and
when appropriate, formulate recommendations using standard AHA criteria (Tables 1 and 2). All members of the writing
group had the opportunity to comment on the recommendations and approved the final version of this document. The
guideline underwent extensive peer review by the Stroke Council leadership and the AHA scientific statements
oversight committees before consideration and approval by the AHA Science Advisory and Coordinating Committee.
Results—Schemes for assessing a person’s risk of a first stroke were evaluated. Risk factors or risk markers for a first
stroke were classified according to potential for modification (nonmodifiable, modifiable, or potentially modifiable) and
strength of evidence (well documented or less well documented). Nonmodifiable risk factors include age, sex, low birth
weight, race/ethnicity, and genetic predisposition. Well-documented and modifiable risk factors include hypertension,
exposure to cigarette smoke, diabetes, atrial fibrillation and certain other cardiac conditions, dyslipidemia, carotid artery
stenosis, sickle cell disease, postmenopausal hormone therapy, poor diet, physical inactivity, and obesity and body fat
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside
relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required
to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on August 18, 2010. A copy of the
statement is available at http://www.americanheart.org/presenter.jhtml?identifier?3003999 by selecting either the “topic list” link or the “chronological
list” link (No. KB-0080). To purchase additional reprints, call 843-216-2533 or e-mail firstname.lastname@example.org.
The online-only Data Supplement is available at http://stroke.ahajournals.org/cgi/content/full/STR.0b013e3181fcb238/DC1.
The American Heart Association requests that this document be cited as follows: Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT,
Chaturvedi S, Creager MA, Culebras A, Eckel RH, Hart RG, Hinchey JA, Howard VJ, Jauch EC, Levine SR, Meschia JF, Moore WS, Nixon JV, Pearson
TA; on behalf of the American Heart Association Stroke Council, Council on Cardiovascular Nursing, Council on Epidemiology and Prevention, Council
for High Blood Pressure Research, Council on Peripheral Vascular Disease, and Interdisciplinary Council on Quality of Care and Outcomes Research.
Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2011;42:517–584.
Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development,
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
permission of the American Heart Association. Instructions for obtaining permission are located at http://www.americanheart.org/presenter.jhtml?
identifier?4431. A link to the “Permission Request Form” appears on the right side of the page.
© 2011 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.orgDOI: 10.1161/STR.0b013e3181fcb238
distribution. Less well-documented or potentially modifiable risk factors include the metabolic syndrome, excessive
alcohol consumption, drug abuse, use of oral contraceptives, sleep-disordered breathing, migraine, hyperhomocysteine-
mia, elevated lipoprotein(a), hypercoagulability, inflammation, and infection. Data on the use of aspirin for primary
stroke prevention are reviewed.
Conclusion—Extensive evidence identifies a variety of specific factors that increase the risk of a first stroke and that
provide strategies for reducing that risk. (Stroke. 2011;42:517-584.)
Key Words: AHA Scientific Statements ? stroke ? risk factors ? primary prevention
ple in the United States have a stroke each year, of which
about 610 000 are a first attack; and 6.4 million Americans
are stroke survivors.1Stroke is also estimated to result in
134 000 deaths annually and is the third leading cause of
death in the nation behind heart disease and cancer.1Progress
has been made in reducing deaths from stroke. Along with
other healthcare organizations, the American Heart Associa-
tion (AHA) set the goal of decreasing cardiovascular and
stroke mortality by 25% over 10 years.1Between 1996 and
2006 the death rate for stroke fell by 33.5%, with the total
number of stroke deaths declining by 18.4%.1The goal of a
25% reduction was exceeded in 2008. The declines in stroke
death rates, however, were greater in men than in women
(age-adjusted male-to-female ratio decreasing from 1.11 to
may be increasing.2From 1988 to 1997 the age-adjusted stroke
hospitalization rate grew 18.6% (from 560 to 664 per 10 000),
while the total number of stroke hospitalizations increased
38.6% (from 592 811 to 821 760 annually).3In 2010, the cost of
stroke is estimated at $73.7 billion (direct and indirect costs),1
with a mean lifetime cost estimated at $140 048.1
Stroke is also a leading cause of functional impairments,
with 20% of survivors requiring institutional care after 3
months and 15% to 30% being permanently disabled.1
Stroke is a life-changing event that affects not only stroke
patients themselves but their family members and caregiv-
ers as well. Utility analyses show that a major stroke is
viewed by more than half of those at risk as being worse
than death.4Despite the advent of treatment of selected
patients with acute ischemic stroke with intravenous
tissue-type plasminogen activator and the promise of other
acute therapies, effective prevention remains the best
approach for reducing the burden of stroke.5–7Primary
prevention is particularly important because ?77% of
strokes are first events.1The age-specific incidence of
major stroke in Oxfordshire, United Kingdom, fell by 40%
over a 20-year period with increased use of preventive
treatments and general reductions in risk factors.9Those
who practice a healthy lifestyle have an 80% lower risk of
a first stroke compared with those who do not.8As
discussed in detail in the sections that follow, persons at
high risk for or prone to stroke can now be identified and
targeted for specific interventions.
This guideline provides an overview of the evidence on
various established and emerging stroke risk factors and repre-
sents a complete revision of the 2006 statement on this topic.9
troke remains a major healthcare problem. Its human and
economic toll is staggering. Approximately 795 000 peo-
Whereas the 2006 statement focused on ischemic stroke, be-
cause of the overlap of risk factors and prevention strategies, this
guideline also addresses hemorrhagic stroke, primarily focusing
on an individual patient–oriented approach to stroke prevention.
entire distribution of risk factors in the population is shifted to
lower levels through population-wide interventions” and is
reflected in the AHA statement on improving cardiovascular
health at the community level.10
Writing group members were nominated by the commit-
tee chair on the basis of their previous work in relevant
topic areas and were approved by the AHA Stroke Council
Scientific Statement Oversight Committee and the AHA
Manuscript Oversight Committee. The writing group used
systematic literature reviews covering the time since the
last statement was published in 2006 up to April 2009,
reference to previously published guidelines, personal
files, and expert opinion to summarize existing evidence,
indicate gaps in current knowledge, and when appropriate,
formulate recommendations using standard AHA criteria.
All members of the writing group had the opportunity to
comment on the recommendations and approved the final
version of the document. The guideline underwent exten-
sive peer review by the AHA Stroke Council leadership
and the AHA Manuscript Oversight Committee before
consideration and approval by the AHA Science Advisory
and Coordinating Committee (Tables 1 and 2). Because of
the diverse nature of the topics, it was not possible to
provide a systematic, uniform summary of the magnitude
of the effect associated with each recommendation. As
with all therapeutic recommendations, patient preferences
must be considered. As seen in Tables 3 through 5, risk
factors (directly increase disease probability or, if absent
or removed, reduce disease probability) or risk markers
(attribute or exposure associated with increased probability
of disease, but relationship is not necessarily causal)11of a
first stroke were classified according to their potential for
modification (nonmodifiable, modifiable, or potentially
modifiable) and strength of evidence (well documented,
less well documented).7Although this classification sys-
tem is somewhat subjective, for well-documented and
modifiable risk factors (Table 4) there was clear, support-
ive epidemiological evidence in addition to evidence of
risk reduction with modification as documented by ran-
domized trials. For less well-documented or potentially
modifiable risk factors (Table 5), the epidemiological
evidence was less clear or evidence was lacking from
randomized trials that demonstrated reduction of stroke
risk with modification. The tables give the estimated
prevalence, population-attributable risk (ie, the proportion
of ischemic stroke in the population that can be attributed
toa particular riskfactor,
Risk?1)?1]),12relative risk, and risk reduction with treatment
for each factor when known. Gaps in current knowledge are
indicated by question marks. When referring to these data, it
should be noted that comparisons of relative risks and
population-attributable risks between different studies should be
made with caution because of differences in study designs and
patient populations. Precise estimates of attributable risk for
factors such as hormone replacement therapy are not available
because of variations in estimates of risk and changes in
Other tables summarize endorsed guideline or consensus
statements on management recommendations as available.
Recommendations are indicated in the text and tables.
Generally Nonmodifiable Risk Factors
These factors are generally not modifiable but identify
persons who are at increased risk of stroke and who may
benefit from rigorous prevention or treatment of other mod-
ifiable risk factors (Table 3). In addition, although genetic
predisposition itself is not modifiable, treatments for specific
genetic conditions are available.
Stroke is thought of as a disease of the elderly, but incidence
rates for pediatric strokes have increased in recent years.13,14
Although younger age groups (25 to 44 years) are at lower
stroke risk,15the public health burden is high in these
populations because of a relatively greater loss of prod-
uctivity and wage-earning years. The cumulative effects of
aging on the cardiovascular system and the progressive nature
of stroke risk factors over a prolonged period substantially
Table 1.Applying Classification of Recommendations and Level of Evidence
*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior
myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak.
Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may
be a very clear clinical consensus that a particular test or therapy is useful or effective.
†For recommendations (Class I and IIa; Level of Evidence A and B only) regarding the comparative effectiveness of one treatment with respect to another, these
words or phrases may be accompanied by the additional terms “in preference to” or “to choose” to indicate the favored intervention. For example, “Treatment A is
recommended in preference to Treatment B for. . . ” or “It is reasonable to choose Treatment A over Treatment B for. . . . ” Studies that support the use of comparator
verbs should involve direct comparisons of the treatments or strategies being evaluated.
Goldstein et al Guidelines for the Primary Prevention of Stroke
increase the risks of both ischemic stroke and intracerebral
hemorrhage (ICH). The risk of ischemic stroke and ICH
doubles for each successive decade after age 55.2,16–20
Stroke is more prevalent in men than in women.2,21Men
also generally have higher age-specific stroke incidence
rates than women have (based on age-specific rates calcu-
lated from strata defined by race/ethnicity), and this is true
for ischemic as well as hemorrhagic stroke.2,16–20,22,23The
exceptions are those 35 to 44 years of age and those ?85
years of age.23,24
Factors such as use of oral contraceptives (OCs) and preg-
nancy contribute to the increased risk of stroke in young
women.25–27The earlier cardiac-related deaths (ie, competing
causes of death) of men with cardiovascular disease (CVD) may
contribute to the relatively greater risk of stroke in older women.
Women accounted for 60.6% of US stroke deaths in 2005.28
Overall, 1 in 6 women die of stroke, compared with 1 in 25 who
were 44.0 per 100 000 among white women and 60.7 per
100 000 among black women, versus rates of 44.7 and 70.5 per
100 000 among white and black men, respectively.28
Low Birth Weight
Stroke mortality rates among adults in England and Wales are
higher among people with lower birth weights.30The mothers
of these low-birth-weight babies were typically poor, were
malnourished, had poor overall health, and were generally
socially disadvantaged.30A similar study compared a group
of South Carolina Medicaid beneficiaries ?50 years of age
who had stroke with population controls.31The odds of stroke
were more than double for those with birth weights of ?2500 g
compared with those weighing 4000 g (with a significant
linear trend for intermediate birth weights). Regional differ-
ences in birth weight may partially underlie geographic
differences in stroke-related mortality, which is also associ-
ated with birthplace.32The potential reasons for these rela-
tionships remain uncertain, and statistical association alone
does not prove causality.
Race/ethnic effects on disease risk can be difficult to consider
separately. Blacks23,24,33and some Hispanic/Latino Ameri-
cans23,34–36have a higher incidence of all stroke types and
higher mortality rates compared with whites. This is partic-
ularly true for young and middle-aged blacks, who have a
substantially higher risk of subarachnoid hemorrhage (SAH)
and ICH than whites of the same age.24,33In the Atheroscle-
rosis Risk In Communities (ARIC) Study, blacks had an
incidence of all stroke types that was 38% higher [95%
confidence interval (CI), 1.01 to 1.89] than that of whites.22
Possible reasons for the higher incidence and mortality rate of
stroke in blacks are a higher prevalence of hypertension,
obesity, and diabetes.37–40Higher prevalence of these risk
factors, however, does not explain all of the excess risk.37
Data from the Strong Heart Study (SHS) show that American
Indians had a higher incidence of stroke compared with
African-American and white cohorts.41
A meta-analysis of cohort studies showed that a positive
family history of stroke increases risk of stroke by approxi-
mately 30% [odds ratio (OR), 1.3; 95% CI, 1.2 to 1.5,
P?0.00001].42The odds of both monozygotic twins having
strokes are 1.65-fold higher than those for dizygotic twins.42
Cardioembolic stroke appears to be the least heritable type of
stroke compared with other ischemic stroke subtypes.43
Women with stroke are more likely than men to have a
parental history of stroke.44The increased risk of stroke
imparted by a positive family history could be mediated
through a variety of mechanisms, including (1) genetic
heritability of stroke risk factors, (2) inheritance of suscepti-
bility to the effects of such risk factors, (3) familial sharing of
cultural/environmental and lifestyle factors, and (4) interac-
tion between genetic and environmental factors.
Genetic influences on stroke risk can be considered on the
basis of individual risk factors, genetics of common stroke
types, and uncommon or rare familial stroke types. Many of
the established and emerging risk factors described in the
sections that follow, such as hypertension, diabetes, and hyper-
ponents.45–47Elevations of blood homocysteine occur with 1
AHA Stroke Council Recommendations
Definition of Classes and Levels of Evidence Used in
Class IConditions for which there is evidence for
and/or general agreement that the
procedure or treatment is useful and
Conditions for which there is conflicting
evidence and/or a divergence of opinion
about the usefulness/efficacy of a
procedure or treatment.
The weight of evidence or opinion is in
favor of the procedure or treatment.
Usefulness/efficacy is less well established
by evidence or opinion.
Conditions for which there is evidence
and/or general agreement that the
procedure or treatment is not
useful/effective and in some cases may be
Level of Evidence AData derived from multiple randomized
clinical trials or meta-analyses
Data derived from a single randomized
trial or nonrandomized studies
Consensus opinion of experts, case
studies, or standard of care
Level of Evidence B
Level of Evidence C
Level of Evidence A Data derived from multiple prospective
cohort studies using a reference standard
applied by a masked evaluator
Data derived from a single grade A study,
or ?1 case-control studies, or studies
using a reference standard applied by an
Consensus opinion of experts
Level of Evidence B
Level of Evidence C
or more copies of the C677T allele of the methylenetetrahydro-
folate reductase gene.48Many coagulopathies are inherited as
autosomal dominant traits.49These disorders, including protein
C and S deficiencies, factor V Leiden mutations, and various
other factor deficiencies, can lead to an increased risk of venous
thrombosis.50–53As discussed below, there has not been a strong
association between several of these disorders and arterial
events, such as myocardial infarction (MI) and stroke.54,55Some
apparently acquired coagulopathies, such as the presence of a
lupus anticoagulant or anticardiolipin antibody, can be familial
in approximately 10% of cases.56,57Inherited disorders of vari-
ous clotting factors (ie, factors V, VII, X, XI, and XIII) are
childhood or the neonatal period.50Arterial dissections, moya-
moya disease, and fibromuscular dysplasia have a familial
component in 10% to 20% of cases.58,59
Common variants on chromosome 9p21 adjacent to the
tumor suppressor genes CDKN2A and CDKN2B, which
were initially found to be associated with MI,60–62have
been found to be associated with ischemic stroke as well.63
Common variants on 4q25 adjacent to the PITX2 gene
involved in cardiac development were first shown to be
associated with atrial fibrillation.64This locus was subse-
quently associated with ischemic stroke, particularly car-
dioembolic stroke.65Although commercially available
tests exist for the 9p21 and 4q25 risk loci, studies have yet
to show that knowledge of genotypes at these loci leads to
an improvement in risk prediction or measurable and
cost-effective improvements in patient care.
Several rare genetic disorders have been associated with
stroke. Cerebral autosomal dominant arteriopathy with sub-
cortical infarcts and leukoencephalopathy (CADASIL) is
characterized by subcortical infarcts, dementia, and migraine
headaches.66CADASIL can be caused by any of a series of
mutations in the Notch3 gene.66,67Marfan syndrome (caused
by mutations in the fibrillin gene) and neurofibromatosis
types I and II are associated with an increased risk of
ischemic stroke. Gene transfer therapy has been attempted to
correct the genetic defect in Marfan syndrome.68
Fabry disease is a rare inherited disorder that can also lead
to ischemic stroke. It is caused by lysosomal ?-galactosidase
A deficiency, which causes a progressive accumulation of
globotriaosylceramide and related glycosphingolipids.69De-
position affects mostly small vessels in the brain and other
Table 3. Generally Nonmodifiable Risk Factors and Risk Assessment
Factor Incidence/PrevalenceRelative Risk
Prevalence of first stroke
(percent per 100 000)
Incidence of first stroke (per 1000)1†
Prevalence (percent per 100 000)
. . .
Sex (age adjusted)21
. . .
Low birth weight30,31
Race/ethnicity (age adjusted)21
. . .
?2 for birth weight ?2500 g vs ?4000 g
. . . Prevalence (percent per 100 000)
. . . Family history of stroke/TIA725
RR, paternal history: 2.4 (95% CI, 0.96–6.03)
RR, maternal history
1.4 (95% CI, 0.60–3.25)
CI indicates confidence interval; RR, relative risk; and TIA, transient ischemic attack.
*Incidence rates for black men and women 45 to 54 y of age and black men ?75 y of age are considered unreliable.
†Unpublished data from the Greater Cincinnati/Northern Kentucky Stroke Study.
Goldstein et al Guidelines for the Primary Prevention of Stroke
Table 4. Well-Documented and Modifiable Risk Factors
Risk, %¶Relative RiskRisk Reduction With Treatment
50% within 1 y; baseline after 5 y
Men WomenMen Women†
Diabetes7.3 5–27 1.8–6.0 Reduction of stroke risk in hypertensive
diabetics with BP control. No
demonstrated benefit in stroke
reduction with tight glycemic control;
however, reduction in other
complications (see text).
Reduction of stroke with statins
0.81 (95% CI, 0.75–0.87) High total cholesterolData calculated for
highest quintile (20%)
vs lowest quintile
Continuous risk for
9.1 (5.7–13.8)1.5 (95% CI
. . . 1.25/1 mmol/L
Low HDL cholesterol:
Data calculated for
highest quintile (20%)
vs lowest quintile
?35 mg/dL20.6 (10.1–30.7)2.00 (95% CI,
each 1 mmol/L
Continuous risk for
Atrial fibrillation (nonvalvular)235,236,252
Adjusted-dose warfarin vs control:
64% (CI, 49%–74%); 6 trials, 2900
Aspirin vs placebo: 19% (CI, ?1% to
35%); 7 trials, 3990 patients
Adjusted-dose warfarin vs aspirin: 39%
(CI, 19% to 53%): 9 trials, 4620 patients
Overall age, y
organs, although involvement of the larger vessels has been
reported. Two prospective randomized studies using human
recombinant lysosomal ?-galactosidase A found a reduction in
microvascular deposits as well as reduced plasma levels of
globotriaosylceramide.70–72These studies had short follow-up
periods, and no effects on stroke incidence were found. Enzyme
replacement therapy also appears to improve cerebral vessel
function.73Agalsidase alpha and agalsidase beta given at the
same dose of 0.2 mg/kg have similar short-term effects in
disease (discussed later), no treatment based specifically on
genetic factors has yet been shown to reduce incident stroke.
Intracranial aneurysms tend to be more common within
families.75–78One study using historical controls found that
persons with a familial history of unruptured intracranial
aneurysms had a 17-fold higher risk of rupture than persons
with sporadic aneurysms of comparable size and location.79
One study calls into question anticipation.80
Intracranial aneurysms are a feature of certain Mendelian
disorders, including autosomal dominant polycystic kidney
Table 4. Continued
%¶Relative Risk Risk Reduction With Treatment
Asymptomatic carotid stenosis2–8 2–7‡ 2.0
?50% reduction with endarterectomy
(see text). Aggressive management of
other identifiable vascular risk factors
91%|| with transfusion therapy
Treatment increases risk.
SCD0.25 (of blacks) . . .200–400§
Postmenopausal hormone therapy 25 (women 50–74 y)372,729,730
OC use13 (women 25–44 y)731
None; may increase risk.
Dietary-nutritionObservational studies show 8%
reduction in stroke mortality from a
3 mm Hg reduction in SBP. Extent of
SBP reduction from reduced Na and
increased K can exceed 3 mm Hg
depending on baseline intake levels
and other factors.
Na intake ?2300 mg
K intake ?4700 mg
Obesity1.39 stroke death
per increase of 5
Other CVD, CHD#Overlap with risk factors for first
stroke; see text.
Other CVD, heart failure
Other CVD, PAD
CHD indicates coronary heart disease; N/A, not applicable; NOMASS, Northern Manhattan Stroke Study; PAD, peripheral artery disease; and PAR,
*PAR is for stroke deaths, not ischemic stroke incidence.120,124,125
†PAR?100727((prevalence (RR-1)) /(prevalence (RR-1) ?1).
‡Calculated based on referenced data provided in table or text.
§Relative to stroke risk in children without SCD.
?For high-risk patients treated with transfusion.
#CVD includes CHD, cardiac failure, and PAD. PFO is discussed in text.
¶PAR is proportion of ischemic stroke in population that can be attributed to a particular risk factor (see text for formula).
¶¶Calculated based on point estimates of referenced data provided in table; PAD calculation based on average relative risk for men and women.
Goldstein et alGuidelines for the Primary Prevention of Stroke
Table 5. Less Well-Documented or Potentially Modifiable Risk Factors
FactorPrevalence, % Population-Attributable Risk, %Relative Risk or Odds RatiosRisk Reduction With Treatment
Migraine with aura
?5 drinks per day
. . .
. . .
. . .
HR, 1.97; 95% CI, 1.12–3.48; P?0.01
(adjusted for age, sex, race, smoking
status, alcohol consumption status,
BMI, and presence or absence of
diabetes mellitus, hyperlipidemia,
atrial fibrillation, and hypertension)541
HR in the elderly, 2.52 (95% CI,
3.08; 95% CI, 0.74–12.81; P?0.12543
Hyperhomocysteinemia Data calculated for
?mol/L) vs lowest
Continuous risk for
Data calculated for
highest (33%) vs
17.0 (3.4–32.3)1.82 (1.14–2.91) Not established with B-vitamin
1.59 (95% CI, 1.29–1.96) per
5 ?mol/L increase
1.22 (95% CI, 1.04–1.43)High Lp(a) 6.8 (95% CI, 1.3–12.4)Unknown
Women 15–44 y
Women 15–44 y
6 1.3 (0.7–2.3)*
0.99 (0.69–1.41)† Warfarin
2.89 1.80 (1.06–3.06)0.78 (0.50–1.21)†
1.47 (0.91–2.36)† (aCL/LA)
HR, 1.04 (0.69–1.56) for aspirin
(81 mg/d) vs placebo in
. . . . . .
Factor V Leiden
Protein C deficiency
Protein S deficiency
162.11 (1.30–3.42) Effects of medical therapy on
periodontal disease remain to
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