Women and Coronary Artery Diseases

Women and Coronary
Artery Diseases
Rashed J. Al-Hamdan MD. FRCP(C)
General Considerations
• There are 2 important challenges for
physicians specializing in cardiology
and women’s health:
(1) To educate women on the risk of
CVD, and
(2) To update the medical community
on the true impact of CVD.
• CVD is gaining recognition as a
disease that does not
discriminate based on sex.
• By age 65, the number of deaths from
CVD in women surpasses deaths in
men by 11%.
• Results of a recent AHA survey reveal that
many women do not know their risk of
CVD.
• Among women surveyed, 61% in all
age groups and 72% of those
between the ages of 25 and 34 years
responded that cancer was their
primary health concern.
• Although the women surveyed
considered themselves to be well
informed about heart disease, ≤10%
considered CVD to be the greatest
risk to their well-being.
• Many people are familiar with the
quoted “1-in-9” statistic for breast
cancer.
• This is misleading. It refers to the
cumulative lifetime risk of developing
breast cancer in a woman living past
the age of 85.
• In 50% of cases, the 1 woman in 9 who
will be diagnosed with breast cancer
will not develop the disease until 65
years of age.
“Breast Cancer is the REAL issue!”
• What about the so called greatest fear for
women, the women’s KILLER:
BREAST CANCER and lung cancer
• In a recent survey, 75% of women
identified cancer as their leading cause of
death…
Statistics
• Heart Disease and Stroke
– First and third leading causes of death in US
– More women die every year from CVD than
from any other cause
– Accounts for more than 40% of all deaths
• About 95,000 Americans die of heart
disease or stroke each year
– Amounts to one death every 33 seconds
• Heart Disease is the leading cause of
disability among working adults
Statistics
A Total CVD D Chronic Lower Respiratory

B Cancer Diseases E
C Accidents Diabetes Mellitus F
Influenza and Pneumonia
Statistics
• Leading Causes of Death for - White Males and Females
US: 2000
A Total CVD D Accidents

B Cancer E Diabetes Mellitus
C Chronic Lower F Alzheimer’s Disease
Respiratory Diseases G Influenza and Pneumonia
Statistics
• Prevalence of Cardiovascular Diseases in Americans
Age 20 and Older by Age and Sex US: 1988-94
Leading causes of Death - USA 2000
• Heart disease is far more age
dependent in women than in men
• Women with CVD are older and have
more comorbidities.
• Many effective pharmacological and
non- pharmacological strategies are
underutilized.
• There is a lack of gender-specific data
on numerous therapies.
• Heart disease is on the decline in men but
not women highlighting our failure.
Heart Disease is the #1 Killer of Women
• Coronary heart disease is the single

leading cause of death and a
significant cause of morbidity among
American women.
• In 1997 CHD claimed the lives of
502,938 women (men had less
deaths)
• Since 1984, CVD has killed more
American women than men each
year.
In perspective:
• 1 in 25 women will die of breast
cancer.
• 1 in 2 women will die of heart
disease.
Economics
• In 2001 the US Nationwide cost for all
CVD was $300 billion
• For heart disease, the cost was $105
billion and for stroke, $28 billion.
• Lost productivity due to stroke and
heart disease cost more than $129
billion
Are Women Different?
• Differences between men and women
in the circulatory system have been
noted for a long time. These
differences were attributed mostly to
gonadal hormones.
• Gonadal hormones alter many
pathophysiological processes thought
to be fundamental to the development
of atherosclerosis, including
thrombosis and inflammation
• Estrogen receptors are present in
cardiac myocytes of both males and
females, a potential explanation for
gender differences in gene regulation.
• The differences between men and
women in atherosclerosis are not limited
to gonadal hormones.
• Research has shown some major
variation in the underlying mechanisms
of disease.
• In a study, a large population of MI
survivors were examined for the
presence of 71 single-nucleotide
polymorphisms in candidate genes
known to be relevant to the
pathophysiology of atherosclerosis.
• Two genes were found to be
significantly more prevalent in men—
connexin37 and p22phox.
• Two different genes were relevant in
women—plasminogen activator
inhibitor 1 (PAI-1) and stromelysin-1
• The findings suggested that the
genetic basis underlying coronary
heart disease (CHD) varies by
gender.
• Such genetic differences are manifest
in the physiology of atherosclerosis,
including:
♦ Plaque components (more cellular and
fibrous tissue in women),
♦ Endothelial function (estrogen-induced
coronary vasodilation),
♦ Hemostasis (higher fibrinogen and factor
VII levels in women).
• Coronary thrombosis is the most likely
cause of MI in both genders (only
rarely are infarctions due to spasm or
syndrome X).
• However, women are twice as likely to
have plaque erosion (37% in women
vs. 18% in men), whereas men have
plaque rupture as the underlying
cause of the infarction (82% in men
vs. 63% in women).
• Once the cardiovascular disease is
established, the two genders show 2
different compensatory mechanisms.
• In increased afterload conditions,
women tend to have more vigorous
hypertrophy, with greater LV mass,
and better preserved systolic function
and contractile reserve than men.
• In ischemic syndromes, animal
studies suggest that females show
less hypertrophy but also less
pathological remodeling and dilation.
• Apoptosis and myocyte necrosis in
response to aging, injury, or stress
are more pronounced in males than in
females.
• Because women are older and have a
greater burden of risk factors and
concomitant disease, they are more
frail and less likely to recover fully
from cardiovascular events.
• Women, may underestimate the
importance of atherosclerotic disease
and fail to implement preventive
strategies fully or even recognize and
act on symptoms appropriately.
CAD in Women
Risk Factors
• DM
• Hypertension
• Dyslipidemias
• Smoking
• Menopause
• Obesity
• Psychosocial Factors
Risk Factors - DM
• Diabetes is associated with a greater
risk in women, completely eliminating
the female gender advantage and
increasing their risk by 5 to 7 folds.
• The AHA awards double weight to
DM in women when calculating CHD
risk, similar to the weight given a
systolic BP of ≥173 mm Hg, or a
cholesterol level of ≥ 8.4 mmol/l or
above.
Risk Factors - DM
• More than in men, DM increases the
mortality of MI in women.
Risk Factors - DM
• Type 2 DM is associated with obesity,
abdominal body fat distribution,
hypertension, dyslipidemia, and
insulin resistance, all of which have
been associated with higher CHD
risk.
• This complex of abnormalities, termed
"metabolic syndrome”.
• It alters hepatic metabolism,
lipoprotein levels, and circulating
insulin levels
Risk Factors - DM
• Obesity and body fat distribution appear
to be independent CAD risk factors in
women more than in men.
• DM is also linked with endothelial
dysfunction and platelet abnormalities.
• Data from the Diabetes Control and
Complications Trial suggest that
intensive DM therapy reduces CVD
complications in men and women
younger than 40 years.
Risk Factors - Hypertension
• More than 25 million American women
have high BP.
• Cardiovascular risk related to hypertension
rises steeply with age in females.
• Although women have fewer cardiovascular
events, the population risk attributable to
hypertension is higher for women than men
because of the increased incidence with
age and the longevity of women.
• Most trials have shown equal efficacy
of blood BP lowering to prevent CVD
events in men and women.
• The JNC-VII includes a single set of
guidelines for both men and women.
• Although it is clear that hypertension
in women should be treated as
aggressively as in men, it is possible
that the optimal choice of
antihypertensive agent may differ.
• In the ALLHAT the superiority of diuretic
therapy in the prespecified female
cohort, as in the trial as a whole was
evident.
• The Second Australian National Blood
Pressure Study Group found that ACE-I
therapy decreased cardiovascular
endpoints relative to HCTZ in men but
not in women.
• However, the numbers of women
included in trials are often too small to
draw conclusions.
Risk Factors - Lipids
• The average lipid profile in women is
affected by hormonal status and
changes throughout life.
• Young women have lower LDL levels
and higher HDL levels than men of
the same age.
• As women age, HDL decreases, LDL
increases, along with the risk of CHD.
• However, elevated total cholesterol
and LDL levels are only weakly
associated with CHD in women and
only in women ≤ 65 years old.
• Instead, HDL is closely and inversely
associated with CHD risk.
• TGs are an independent predictor of
CHD, particularly in older women.
• Lipoprotein(a), a composite of LDL,
apolipoprotein B-100, and
apolipoprotein(a), is also associated
with higher cardiac risk in women.
• Initial modification of a high-risk
lipoprotein profile is generally
accomplished by the same life-style
changes and medications in men and
women, although dietary interventions
may be less effective in women.
• Multiple trials have demonstrated
efficacy of statins, in both primary and
secondary prevention of coronary
events and death in women with both
elevated and normal cholesterol,
supporting the theory about the
benefits of these agents independent
of LDL-lowering effects.
• However, women have generally
not been included in trials of other
classes of lipid-lowering agents.
• Also, there are no data from large
trials on the efficacy of lipid-lowering
agents targeted more specifically at
altering the HDL and TGs which
appear more important in women.
Risk Factors - Smoking
• Tobacco contributes to 17% of all female
deaths in the US and results in more
deaths from CHD and stroke than any
other cause.
• This results from a combination of
accelerated atherosclerosis and
propensity to thrombosis induced by
smoking.
• Cigarettes have an antiestrogenic effect
and induce an unfavorable lipid profile,
leading women to lose their "natural"
protection.
• As a result, there is a six- to nine-fold
increased risk of MI among female
smokers compared with nonsmokers.
• Smoking yields a similar increase in
stroke risk.
• The combination of smoking and oral
contraceptives appears to be
particularly potent at increasing the
risk of arterial thrombosis.
• Currently available methods to assist
with quitting may be less effective in
women, perhaps because of a greater
behavioral component and less
nicotine addiction in women.
• Environmental exposure to tobacco
smoke increases the risk of CVD in
women, and assessment of
environmental exposure is an
important part of risk assessment.
Risk Factors – Menopause
• The presence of estrogen in the
premenopausal female population is the
presumed cause of the obvious
protection this group enjoys against
cardiovascular events.
• The documentation of estrogen
receptors in cardiomyocytes and
vascular tissues in both men and women
led to tremendous enthusiasm for use of
postmenopausal hormone replacement
therapy ( HRT )as a preventive measure.
• The enthusiasm for HRT was further
consolidated by multiple observational
studies suggesting improved longevity
and decreased CVD events in
postmenopausals receiving HRT.
• However, Multiple randomized controlled
trials in the past few years have refuted
this hypothesis and provided strong
evidence of an increase in
cardiovascular risk particularly in the first
year after beginning HRT.
• That increase in CVD risk was accompanied with
increased risk of breast cancer, thromboembolic
disease, and stroke, resulting in a withdrawal of
prior recommendations.
• The results of 2 large trials have left us
with few answers and many more
questions:
♦ Would alternative formulations of either
estrogen or progesterone be of benefit?
♦ Does starting therapy immediately at
menopause eliminate risk?
♦ Can genotype predict the risk-benefit profile
of estrogen therapy?
♦ If the estrogen hypothesis is a fallacy, what is
the underlying cause of the protection in the
premenopausal female population?
Risk Factors – Obesity
• Excess caloric intake and obesity are
a growing epidemic worldwide, and
more than 33% of American women
are classified as obese.
• The Nurses' Health Study revealed a
sevenfold higher CVD mortality in the
heaviest women.
• The Framingham Offspring study
demonstrated a dramatic rise in risk
factors for cardiovascular disease at
body mass indices above 20.
The Nurses' Health Study
6
Rel- 5
ative
Risk of 4
CHD
Morta- 3
lity
2
0
<19 19.0- 22.0- 25.0- 27.0- 29.0- >32.0
21.9 24.9 26.9 28.9 31.9
Body Mass Index (kg/m2)

• The combination of obesity and DM
appears particularly deadly in women, as
does the pattern of fat distribution.
• Abdominal fat accumulation is an
important predictor of type 2 DM,
hypertriglyceridemia, high BP, and CHD.
• Among women, a waist-to-hip ratio
greater than 0.88 is predictive of a
substantially increased risk of
cardiovascular events, as is a waist
circumference of more than 38 inches
( 97 cm ).
• There is also some evidence linking
obesity to myocardial structural and
functional alterations related to insulin
resistance and to LV volume overload.
• These findings could be considered the
very early stage of incipient obesity
cardiomyopathy.
( Data pertaining to pts with extreme obesity, i.e. BMI of ≥ 40 ).
• Physical inactivity is more prevalent among
women than men. There is a strong inverse
association between physical activity and
coronary events in women.
• Physical activity also has a strong effect on
other cardiovascular risk factors, including
hypertension, obesity, and DM.
• The effect of regular exercise to increase
HDL cholesterol and induce weight loss
may be less in women than in men.
Risk Factors- Metabolic Syndrome
RISK FACTOR DEFINING LEVEL
Abdominal Obesity Waist Circumference
Men >40 inches
Women >35 inches
TG’s >1.7 mmol/L
HDL
Men <1.03 mmol/L
Women <1.3 mmol/L
BP >130/85
Fasting Glucose >5.55 mmol/L
Risks – Psychosocial Factors.
• The interaction of psychosocial and
behavioral factors and heart disease
is complex and has not been
rigorously studied.
• Several CVD risk factors are related
to behavior (obesity, smoking,
exercise), yet modification may be
more difficult for women than for men.
• Perceived stress and lack of
situational control have been found to
increase CHD risk in both genders.
Summary of Risk Factors
• DM
• Hypertension
• Dyslipidemias
• Smoking
• Menopause
• Obesity
• Psychosocial Factors
CHD Mortality in Younger Women
Women under 65 suffer the highest relative sexspecific CHD mortality
30
25.3
25 24.2
Men 21.8 21.5
20 19.1
Women 18.4
Death during Hospitalization (%)
16.6
14.4
15 13.4
11.1 10.7
9.5
10
8.2
7.4
6.1 5.7
5 4.1
2.9
0
< 50 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85-89
Figure 1. Rates of death during hospitalization for Myocardial Infarction among w omen and men, according to age. The interaction betw een sex
and age w as significant (P<0.001).
Evaluation of Females
with Suspected CAD
Evaluation of CAD in General
• One has to standardize the approach
to patients with suspected CAD.
• A good understanding of the
pathogenesis of CAD is mandatory for
any physician who encounters the
condition in order to address the
underlying problem.
• The progression of atherosclerosis is
accelerated by three processes:
♦ Endothelial dysfunction,
♦ Inflammation, and
♦ Thrombosis.
• The advanced atherosclerotic lesion has
a core of lipid and necrotic tissue
surrounded by a fibrous cap.
• This cap contains collagen, and its
characteristics are related to the risk of
plaque rupture, the most common cause
of acute coronary syndromes.
• Specifically, the thinner the cap, the
more likely it is to rupture.
• Shear stress at the edge or ‘‘shoulder’’
region of a plaque, inflammation at the
endothelial surface of the cap, or
internal degradation of the cap by
enzymes known as metalloproteinases
are other major determinants of the
likelihood of plaque rupture.
• A ruptured plaque leads very quickly to
thrombus formation.
• The complete occlusion of a coronary
vessel by ruptured plaque manifests as
an acute transmural or ST elevation
myocardial infarction (ie, STEMI).
• Non-occlusive thrombus can cause
unstable angina or non–ST elevation
MI (ie, NSTEMI). Non-occlusive
thrombus may not cause symptoms
but, instead, may change plaque
geometry, leading to rapid plaque
growth.
• Typical or classic angina (defined as
exertional substernal discomfort relieved
rapidly by rest or NTG) is commonly
due to atherosclerosis in women,
particularly older women.
• Atypical C/P (exertional substernal
discomfort with atypical radiation or not
relieved rapidly by rest or NTG) is less
likely to be associated with angio-
graphic CAD in women, particularly
younger women, than in men.
• Although equally likely to have effort
angina, women with CHD are more
likely than men to experience atypical
symptoms, e.g. pain at rest, during
sleep, or with mental stress.
• Also, noncoronary chest pain
syndromes are more common in
women, further complicating clinical
assessment of chest pain in females.
Evaluation of CAD in Women
• Chest discomfort, although present in
the majority of women when
experiencing an MI, is not as
predictive in less acute settings.
• Noncardiac reasons for chest
discomfort should be evaluated only
after coronary disease has been ruled
out.
• Abnormalities in the coronary
circulation caused by microvascular
disease, endothelial dysfunction, or
abnormalities in coronary flow reserve
are being identified as potential
causes for symptoms in women but
should not to be considered the
primary initial focus of a disease
evaluation strategy.
• Although most women have typical
angiographic findings of
atherosclerosis, women have higher
prevalences of vasospastic angina,
microvascular angina, and abnormal
coronary vasodilator reserve.
• These syndromes are associated with
atypical chest pain, have distinct
treatments, and have a more
favorable prognosis than epicardial
CAD.
• These differences make a gender-
based approach essential in the
recognition and assessment of acute
and chronic ischemic syndromes.
• Canto et al in JAMA in 2000 showed
that up to 33% of pts with MI had no
chest pain. These patients were more
likely to be older, or females or
diabetics.
• Women with undiagnosed chest pain
have a better prognosis than men
with chest pain because of a lower
prevalence of atherosclerosis in
women with chest pain.
• However, when a diagnosis of
atherosclerotic disease is made
conclusively (e.g., by a history of MI),
women are at equal and perhaps
greater risk for adverse outcomes.
• In subjects older than 65 with exertional
chest pain, women and men have the
same relative risks of CHD death (2.7
versus 2.4).
• Mortality after myocardial infarction is
worse in women younger than 60 than
that in men, indicating that once an
atherosclerotic etiology for the C/P
syndrome is identified, the prognosis is
no different between the genders.
• The presence of elevated troponin in
a woman with unstable angina
predicts a worse outcome.
• The positive serum troponin
predicting a greater increase in risk of
death or MI in women than in men.
• Women should be assessed for their
overall level of risk for CAD and the
severity and nature of symptoms.
• Noninvasive testing is best applied to
women at intermediate risk.
• There are strengths and weaknesses for
each of the available imaging modalities,
but both nuclear scans and
echocardiography have reasonable
accuracy and reliability for detecting
serious CAD in women.
Milner Am J Cardiol 1999;84:396 Women have More atypical Symptoms of MI

• Low risk is considered <10% and
High risk is considered >80%.
• Anything in between is intermediate
risk.
• It is useless to apply a test to a
subject with a pre-test probability of
higher than 80% or lower than 10%.
• Instead, tests should be for the
intermediate risk group.
• One has to choose the best test modality that
achieves the best diagnostic results at the lowest
cost.
• When it comes to women, tests which include a
visualization modality like stress nuclear or stress
echo are superior to regular stress ECG.
• Stress ECG has a high negative predictive value.
• EST is associated with a higher false-
positive rate and a lower false-negative
rate than in men (12% vs 40%),
suggesting that routine testing reliably
excludes the presence of CHD in women
with negative tests.
• Variables that may alter test accuracy
are resting ST-T wave abnormalities,
peak exercise HR, number of diseased
vessels, age, drug use (digitalis,
diazepam), hyperventilation, conduction
abnormalities, LVH, MVP, vasospasm,
and hormons.
• The addition of imaging to
electrocardiographic stress testing
markedly improves its accuracy in
women, as noted by meta-analyses.
• SPECT may not improve accuracy in
women as much as it does in men.
• Exercise echo improves diagnostic
accuracy in women, even more so
than in men.
Type of Sensitivity Specificity Likelihood Likelihood
Ratio for Ratio for
Study Positive Negative
Test
Test
Stress 0.77 (0.69– 0.71 (0.69– 2.54 (1.95– 0.36 (0.28–
Nuclear 0.81) 0.78) 3.32) 0.46)
Stress 0.82 (0.73– 0.60 (0.48– 2.06 (1.53– 0.29 (0.18–

Echo 0.89) 0.71) 2.77) 0.47)
• Women are more likely than men to
experience vascular and renal
complications from diagnostic
angiography, possibly because of
more advanced age, higher
prevalence of diabetes, and smaller
body size.
• The incidences of myocardial
infarction, stroke, and death
complicating coronary angiography
are similar in men and women.
• Because of atypical symptoms,
women seek medical care later than
men and are more likely to be
misdiagnosed.
• Women presenting with MI and CAD
are more likely to be older, have a
history of DM, HTN, Hyperlipids, CHF,
and U/A than male counterparts. (JACC)
• Because of comorbid conditions,
there tends to be diagnostic
confusion.
• Women were less likely to have an
ECG or be admitted to the telemetry
floors.
• Women are under-diagnosed and can
therefore get a false sense of
security.
• Less ASA, β-B, statins, cath, PTCA
Antiarrhythmic Rx, CABG.
• Women were less likely to enroll in
cardiac rehabilitation after an MI or
bypass surgery.
Prevalence of angiographically significant CAD (70% or more luminal

narrowing of one or more major epicardial arteries) CASS trial
Management of CAD
in Women
Management of CAD in Women
• Women have a different clinical

presentation and hospital course
following acute coronary syndromes
and acute myocardial infarction and
respond differently to medical and
procedural therapies.
• Women suffering from an ACS or MI are
likely to be older; are more likely to have
a history of hypertension, DM, unstable
angina, hyperlipidemia, and congestive
heart failure; and are less likely to be
smokers than men.
• They are also more likely to experience
jaw, neck, and shoulder pain; abdominal
pain; nausea; vomiting; palpitations;
fatigue; and dyspnea in addition to chest
pain and are less likely to report
diaphoresis than men.
• Although chest pain is the single most
common presenting symptom of MI in
women, women seem more
susceptible to "silent" MI, particularly
elderly women.
• At least in part due to these atypical
symptoms, women seek medical
attention more slowly and even after
hospital arrival may experience
greater delays in receiving care.
• Women with MI have higher risk initial

presentations, with greater
prevalences of tachycardia, rales,
heart block, and a higher Killip class.
• They are less likely to be admitted to
a CCU or to be hospitalized in an
institution in which catheterization is
available.
• Most studies, but not all, find that

women with acute MI are less likely to
undergo diagnostic catheterization
during their hospital stay, even after
controlling for age and a variety of
clinical characteristics.
• Women have higher rates of in-

hospital complications from infarction,
including bleeding, stroke, shock,
myocardial rupture, and recurrent
chest pain, than do men, although
most of these differences appear
attributable to age and comorbidities.
• Mortality in NSTEMI appears to be
similar to that in men.
• Women with unstable angina are less
likely to have angiographic CHD, re-
infarction, or death.
• In STEMI, early or in-hospital
mortality in women is greater than in
men, and adjustment for age or
clinical characteristics, or both,
reduces but does not eliminate this
difference.
• This gap may be due to a higher rate
of prehospital sudden death in men,
but this cannot explain the twofold
greater mortality in women younger
than 50 years compared with similarly
aged men.
• Mortality 1 to 3 years after hospital
discharge is also increased in
younger women, although it is similar
in postmenopausal women and men
• Men and women show similar rates of

coronary thrombosis on pretreatment
angiography.
• The efficacy of lysis is equivalent with
similar infarct-related artery patency and
preservation of LVEF.
• Although mortality is similar,
complication rates, particularly
hemorrhagic stroke and recurrent
myocardial infarction, appear to be
higher in women.
• Primary angioplasty is equally, if not

more, effective in women, in part
because of the greater reduction in
hemorrhagic stroke.
• Despite a greater risk profile in
women, PCI is as safe and effective
in women as it is in men.
• There are physiological reasons to
suspect that women may benefit from
use of LMWH and clopidogrel, adequate
trial data assessing efficacy in women
are unavailable.
• Use of GP IIb/IIIa inhibitors confers
benefit in addition to that of aspirin in
unstable coronary syndromes in women
but not in men, provided there is
evidence of injury. Women do not
appear to benefit in the absence of
positive biomarkers.
• Data show the efficacy of stenting to be
similar in men and women in both the
short and long term.
• The likelihood of angiographic success
is similar in men and women in newer
series, with lower success rates in
women reported in older studies.
However, the proportional risk of death
from procedural complications remains
greater in women.
• The difference in outcome has been

variously attributed to women's older
age, smaller body size, greater
severity of angina, more fragile
vessels, and greater burden of
comorbidity.
• Gender differences in outcome

following CABG are well established
and, although decreasing, are
persistant.
• In-hospital mortality is 1.4 to 4.4 times
higher, particularly for younger
women (<60 years) and low- and
medium-risk patients, with no
difference in highest risk patients.
• Women are less likely to receive IMA
grafts or undergo complete
revascularization and are more likely to
experience the complications of heart
failure, periop. MI, and hemorrhage.
• Neurological complications of CABG,
including stroke, TIA, and coma, are
more frequent in women.
• Rehospitalization rates for women are
two times those for men in the first 2
months after CABG.
• The causes of higher operative mortality
and morbidity appear to be multiple,
including technical factors such as
smaller body size and coronary
diameter, age, comorbidities such as
diabetes and hypertension, and clinical
factors such as the urgency of the
procedure.
• Controlling for these factors eliminates
only a small portion of the excess risk,
with about 70 percent of the risk
unaccounted for.
• Women with MI are more likely than

men to be treated with nitrates,
digoxin, and diuretics and less likely
to receive thrombolytics,
antiarrhythmics, antiplatelet agents,
ACE-I, and BB’s despite evidence for
similar benefit in women.
• Although in the CASS, women treated

medically had better 12-year survival
with angiographically documented
zero-, 1-, or 2-vessel disease than
men with similar anatomy, other
studies suggest that under treatment
of women is related to a worse
outcome.
• Data from the Heart and

Estrogen/progestin Replacement
Study (HERS) are the most extensive
and distressing.
• At the start of the study, only 33% of
patients were receiving beta blockers,
53% were receiving lipid-lowering
drugs, and 83% were receiving ASA
or other antiplatelet agents.
• Women at greatest risk were less

likely to be taking aspirin (p < 0.001)
or lipid-lowering drugs (p = 0.006).
• During the study period, the rate of
ASA use by participants actually fell.
• Lipid lowering is efficacious in women
with atherosclerotic disease, with
several statin trials showing
reductions in cardiac events and
death.
• Diabetic, elderly, and symptomatic

women appeared to benefit most, as
did women with prior MI.
• ASA and other antiplatelet agents
also reduced vascular events in
women.
• Administration of a BB agent clearly
provides substantial improvement in
post MI survival in women equal to, if
not greater than, that in men.
• After hospital discharge, women are

less likely to be scheduled for
exercise tests or referred for cardiac
rehabilitation, and recovery from
infarction appears delayed with
slower return to work and full
resumption of all activities and more
sleep disturbance and psychiatric and
psychosomatic complaints.
• Now we know that although women

present somewhat differently from
men who have CAD, they tend to
benefit from the same lines of
management.
• We also know that women as a
group, are underserved in the health
care systems of almost all developed
nations.
• The question is whether there is a

modality by which CAD could be
prevented in women.
• Physiologically, the best and clearest
answer was HORMONES.
• As it was seen in numerous
observational studies, pre-
menopausal women have less CAD.
Women and CAD - HRT
• It is important to note that there is a
substantial time lapse between study
initiation and completion in observational
studies, and then again before the data are
fully analyzed and presented. A given
study, therefore, usually reflects clinical
practice of some 5 to 15 years before the
date of publication.
• It is impossible to eliminate all biases from
observational studies. The results,
therefore, should be interpreted cautiously.
Women and CAD - HRT
• The use of hormonal replacement
therapy (HRT) gained scientific
approval as a result of multiple
observational studies.
• In all studies except one, HRT was
found to be cardioprotective.
• In several studies, the risk was
significantly reduced.
Management of CAD - HRT
• The general trend indicates more protection in
the early studies and less in later trials.
• The later studies included more exposure to
combined HRT.
Women and CAD - HRT
• In the later trials, the estrogen component
of HRT was mostly 0.625 mg of conjugated
estrogens or equivalent. In contrast, earlier
studies reflected the use of higher doses of
unopposed estrogen.
• A meta-analysis of studies conducted from
1976-1996 showed that postmenopausal
treatment with estrogen plus progestin was
associated with a similar reduction in CVD
risk (RR, 0.66; 95%; CI 0.53 to 0.84) as
with ERT alone (RR, 0.70; 95% CI, 0.65 to
0.75).
Women and CAD - HRT
• Some observational studies have
been conducted in specific high risk
patient subpopulations.
• Sullivan et al. determined the risk of
CVD events with ERT use in women
with established CAD. Women who
had undergone coronary angiograms
were observed for 10 years for
estrogen use and survival outcome.
Women and CAD - HRT
• After 10 years, survival rates were >96% in
women who had received ERT at some
time during the 10-year period, regardless
of the degree of CAD.
• In contrast, in women who had never used
ERT, survival rates decreased to around
90% in those with normal coronary arteries,
and to 85% and 60% in those with
moderate or severe CAD.
• These results suggested that estrogen use
provided benefit for survival in women with
CAD, especially in women with more
advanced disease.
Women and CAD - HRT
• A drawback to this study was that,
although the population initially
enrolled was large (2,268 women),
only 160 patients remained at the end
of the follow-up period.
• Non-HRT users were more likely to
have CVD risk factors, such as DM,
advanced age, and poorer health in
general.
Women and CAD - HRT
• Newton et al. conducted a retrospective
analysis of 726 women (mean age, 66
years) who had survived a first MI,
examining the risks of reinfarction and
death in relation to ERT use.
• The relative risk for both outcomes was
lower in current ERT users versus past
users, and in both groups versus women
who had never used ERT.
Women and CAD - HRT
• Adjustment such for factors as DM
and CHF did not have a substantial
effect on the results.
• These findings were not significant,
however: For current-user versus
never-user subjects, the odds ratios
were 0.64 (95% CI, 0.32 to 1.30) for
reinfarction and 0.50 (95% confidence
interval, 0.25 to 1.00) for death.
Women and CAD - HRT
• 3 major prospective trial have
examined the effects of HRT on CAD.
• These are the:
HERS (Heart and Estrogen/progestin
Replacement Study),
ERA ( Estrogen Replacement and
Atherosclerosis) trial, and
WHI (Women’s Health Initiative).
Women and CAD - HRT
• The HERS trial tested only the effects
of conjugated equine estrogen (CEE)
plus medroxyprogesterone acetate
(MPA) combination for the secondary
prevention of heart diseases in older
women.
• The ERA trial investigated the effects
of CEE or CEE plus MPA on the
progression of atherosclerosis.
Women and CAD - HRT
• The Women’s Health Initiative (WHI)
is a primary prevention trial that is
investigating the effects of CEE or
CEE plus MPA on the incidence of
coronary events.
Women and CAD - HERS
• HERS was the first controlled trial to
investigate the effect of HRT on the
risk for subsequent cardiovascular
events in postmenopausal women
with established coronary disease.
• The mean age of the 2,763 women
enrolled was 66.7 years, with an
average time since menopause of 18
years. This population was not
representative of the typical woman
considered for HRT.
• Subjects were randomized to receive
placebo or CEE 0.625 mg/day plus
MPA 2.5 mg/day.
• A wide range of cardiovascular
outcomes were assessed in HERS,
including fatal and nonfatal MI,
CABG, angioplasty, CHF, angina,
stroke, and peripheral arterial
disease.
• There were no significant differences between
groups in any of the CVD outcomes. The data
showed a null effect of HRT on overall CVD
events.
• Treatment arm was associated with significant
effects on the lipid profile, including lower LDL
cholesterol and higher HDL cholesterol levels.
It was also associated with significantly higher
TGs levels (p < 0.001 vs placebo in all 3).
• A post-hoc analysis of the time trend of relative
risks for second coronary events indicated that the
risk was greater in the HRT group than in the
placebo group in the first year of the trial, similar to
placebo in the second year, and then lower than in
the placebo group thereafter. This trend was
significant (p <0.009).
Women and CAD - ERA
• The ERA trial, was a randomized,
controlled trial to test the effects of HRT on
the progression of CAD.
• The primary endpoint of the ERA trial was
angiographic change rather than coronary
events, to assess the effects of therapy on
the underlying progression of
atherosclerosis.
• This trial was also designed to address the
effect of unopposed estrogen.
• In addition to the CEE/MPA and placebo
groups, a third arm was included to
examine the effect of unopposed CEE.
Women and CAD - ERA
• The study population in the ERA trial
(N 309) was similar to that in HERS:
Women older than those typically
considered for initiation of ERT/HRT
today (average age, 65.8 years) and
2 decades after menopause (average
time, 22 to 24 years after
menopause), with established CVD.
Women and CAD - ERA
• Levels of LDL cholesterol decreased
and levels of HDL cholesterol and
TGs increased with therapy.
• However, at the average follow-up
time of 3.2 ± 0.6 years, there was no
effect on vessel diameter, or on the
secondary outcomes of the
percentage of women who developed
new lesions or the incidence of
cardiovascular events.
Women and CAD - ERA
• These results demonstrate an
agreement between angiographic
markers in the ERA study and clinical
outcome in the HERS trial.
• Neither CEE 0.625 mg/day alone nor
CEE 0.625 mg/day plus MPA 2.5
mg/day offered cardioprotection in
this study of secondary prevention.
Women and CAD - ERA
• Possible explanations for the lack of a
cardioprotective effect are:
(1) the older age of the study
population,
(2) the particular hormone combination
that was used, or
(3) simply that there was no benefit in
terms of secondary prevention for
HRT.
Women and CAD - ERA
• As in HERS, the ERA trial results
emphasize that dyslipidemia and the
progression of atherosclerosis are not
the only cardiovascular concerns.
• Vasospasm, thrombosis,
inflammation, and ulcerative effects
on current lesions should also be
taken into consideration.
Women and CAD - WHI
• WHI is a large, complex study designed to
examine the primary prevention of CAD
breast cancer, fractures from osteoporosis,
and bowel cancer among other common
causes of mortality and morbidity in
women.
• There are 2 distinct populations in this
study: (1) the observational cohort, which
includes approximately 94,000 women, and
(2) the clinical trial, which includes
approximately 68,000 women enrolled in 3
overlapping components (low-fat diet, HRT,
and calcium/vitamin D supplementation).
Women and CAD - WHI
• The main aim of the observational study is
to gather longitudinan infor-mation from a
large cohort of women whose health habits
and disease outcomes may reflect long-
term trends in US women of similar age.
• The observational study will: (1) serve as
an external control for the clinical trial, (2)
allow exploration of rare diseases, and (3)
provide opportunities to examine novel and
emerging risk factors for common diseases.
Women and CAD - WHI
• The WHI was designed in 1991-1992
using cumulate data and knowledge
up till then.
• The WHI study enrolled 161,809
postmenopausal women who were 50
to 79 years of age at study entry. Only
a small number of women in any WHI
component had evidence of CVD
when they entered the study.
Women and CAD - WHI
• The WHI study includes
postmenopausal women who were 50
to 79 years of age at study entry. Only
a small number of women in any WHI
component had evidence of CVD
when they entered the study.
Women and CAD - WHI
• Women were divided into those who
had and those who had not have
hysterectomy.
• Women with hysterectomy were
eligible for the unopposed estrogen
arm, while those with intact uterus
were randomized only in the
combined estrogen/progesterone
arm.
Women and CAD - WHI
• The women were enrolled in a set of
trials including:
2. Dietary habits,
3. Vitamin D Supplementation,
4. 2 sets of HRT, and
5. An observational study in 40
centers in the US.
Women and CAD - WHI
16606 Randomized
18845 Provided
consent & had no
hysterectomy
373092 Women
screened
initially
8506 Received 8102 Received

CEE + MPA Placebo
7968 Alive 7608 Alive

307 Unknown 276 Unknown
231 Dead 218 Dead
Women and CAD - WHI
• The trial was stopped early at year
5.2 due to an excess rate of invasive
breast cancer in the treatment arm
group more than placebo with
statistics of risk exceeding benefits.
Women and CAD - WHI
Women and CAD - WHI
Women and CAD - WHI
• Blood levels of LDL, HDL and TGs
changed in a similar manner as with
the HERS.
• Systolic blood pressure was 1mmHg
higher in the treatment arm at year 1
increasing to 1.5mmHg in year 2. But,
the diastolic blood pressure did not
change.
Women and CAD - WHI
• The overall rate of CVD was low.
• The rate of CVD events was 29%
higher in the HRT arm and this JUST
reached statistical significance.
• Most of the change was in the rate of
nonfatal MI with n difference in the
fatal ones nor in the revascularization
rates.
• Stroke rates and VTEs were also
higher in the HRT arm.
Women and CAD - WHI
• For every 10,000 women taking HRT
for a year there will be:
7 more CHD events,
8 more invasive breast cancer cases,
8 more strokes, and
8 more pulmonary emboli
6 fewer colorectal cancers, and
5 fewer hip fractures
Women and CAD - WHI
• Although the absolute risks for
women’s health are small, the reality
is that more women taking HRT will
do more harm than good to their
health.
• Based on these results and untill
further issues are addressed, we
should refrain from prescribing HRT
for long term use.
Women and CAD - WHI
• Primum non nocere.
• What about short term use?
• The results suggest an increases
absolute risks of CVD and VTE
events with short term use ( ≤1 year ).
• The possibilities of these short term
results must be weighed against the
benefits of alleviating menopausal or
osteoperotic symptoms.
Women and CAD – Now What?
• Women have their unique physio-

pathology when it comes to CAD.
• They present differently, at different
means of age than men and tend to
be more vague in terms of their
symptoms.
• They usually require a different lines
of diagnostic work-up.
• Women also respond generally to the

same treatment modalities like men
with few exceptions.
• The problem with women is us
physicians.
• As a group, they are under-
represented in clinical trials, under-
diagnosed in the ERs, and under-
treated in CCUs.
• Prevention, prevention, prevention.
• CAD is the No. 1 women killer despite
them thinking otherwise.
• Womn do much worse than men
when they have the disease, it is thus
more prudent to prevent them from
getting it in the first place.
• Prevention is the key.
• HRT is a no no, until further notice.
• Exercise for 30-45 mins of walking

5x’s/week reduces risk of MI in
women by 50%.
• It helps control BP, increases HDL,
decreases body fat, DM risk, possibly
prostate, breast and uterine cancers.
• Life style modifications include
smoking cessation, weight reduction,
reduction of alcohol intake.
• When you get a woman with a high

risk score of CAD, be aggressive in
the diagnosis as well as in the
treatment.
• Spend enough time with the patient.
Your patient can help you a lot in
taking care of his or her health if
he/she knew what to do and what not
to do.
• An individualized approach based on
cardiovascular risk-
• First-Assess and stratify women into
high, intermediate, lower/optimal risk
categories.
• The aggressiveness of treatment
should be linked with your risk of
having a heart attack or event in the
next 10 years- based on the
Framingham Heart Study.
Framingham Risk Score
• You get points for:
• Age
• Total Cholesterol
• HDL Cholesterol
• Smoking
• Systolic Blood Pressure
• Add these numbers --you get a 10 yr
CHD risk % (category):
Low Risk
• A. Low Risk : 10% or less risk of
having a heart attack or dying of heart
disease in the next 10 years.
• May include women with multiple risk
factors, Metabolic Syndrome, or 1 or
no risk factors.
Low Risk
• Low Risk Women <10%:
• Class I recommendations:
Intervention is useful and effective:
• Lifestyle Interventions”
Smoking Cessation
Physical Activity
Heart Healthy Diet- DASH Diet
Weight Reduction
Treat Individual CVD risk factors
Intermediate Risk
• Those with a 10-20% chance of a
heart attack in the next 10 yrs.
• Pts with the obesity, multiple risk
factors, marked elevations of a single
risk factor, first degree relative with
CHD (male<55, female<65)
Intermediate Risk
• Intermediate Risk Women (10-20%):
Smoking Cessation
Physical Activity Heart
Healthy Diet- DASH Diet Weight
Reduction Control
BP and Lipids
• Class Ila- most scientific evidence
favors this type of therapy:
ASA Rx-as long as BP is controlled
(hemorrhagic stroke) and minimal risk of GI bleed
High Risk
• You are automatically considered
high risk if you have:
2. PAD
3. CRF
4. AAA
5. DM
6. History of stroke
High Risk
• High Risk Women (>20%): Class I
Smoking Cessation
Physical Activity/cardiac rehab
Heart Healthy Diet- DASH
Diet Weight Reduction
Control BP and Lipids- statin
ASA therapy
β blocker therapy-esp in all s/p
MI ACE-I or ARBS
Glycemic control in DM
Women with
Diastolic Heart
Failure
Women and DHF
• Most men with CAD have depressed
heart function while most women
have PRESERVED heart function.
• In the Cardiovascular Health Study
(CHS), a populationbased
observational study of CVD risk in the
elderly, CHF prevalence increased in
women from 4.1% at age 70 years to
14.3% at age 85 years.
Women and DHF
• During 6 years of follow-up, the
incidence of CHF in CHS was
10.6/1000 personyears at age 65 and
was 42.5/1000 person-years at age
≥80 years.
• Women who develop HF,particularly
those in the older age range,
frequently have preserved LVEF, a
syndrome commonly termed diastolic
heart failure.
Women and DHF
• Prevalence of CHF vs. age in elderly men (dark bars) and women
(light bars) in the Cardiovascular Health Study.
Women and DHF
• Numbers of patients in Olmsted County Minnesota

hospitalized with CHF in 1991 vs. age with normal (dark bars)
and reduced (light bars) LVEF.
Women and DHF
• There is a remarkable sex-related
difference in DHF.
• In the cross-sectional analysis of
CHS, 67% of elderly women with
prevalent CHF had a normal EF,
whereas this finding was present in
only 42% of men.
Women and DHF
• During the longitudinal analysis of 6-
year follow-up in CHS, over 90% of
women who developed heart failure
had normal systolic function.
• Since women significantly outnumber
men in the older population, the
population-attributable risk of reduced
systolic function was relatively small
compared with those with normal
systolic function.
Women and DHF
• Other large population-based reports,
including the Framingham Heart
Study, the Strong Heart Study of
American Indians, the Helsinki Ageing
Study, and large Medicare studies,
have found a similarly profound sex
differential in this disorder.
Women and DHF
• Thus, the typical person with heart
failure living in the community is an
older woman with normal LVEF and
systolic hypertension.
• This contrasts significantly with the
typical patient seen in referral heart
failure clinics, who is a middle-aged
man with severely reduced LVEF and
CAD.
Women and DHF
• Relatively few data are available regarding
the pathophysiology of DHF, and even
fewer regarding women specifically.
• Three large populationbased studies –
Framingham, CHS, and HyperGEN
(Hypertension Genetic Epidemiology
Network) – have reported that Doppler LV
diastolic filling velocities are significantly
different in women compared with men,
with increased early and atrial filling
velocities in women.
Women and DHF
• Women, particularly older women,
tend to have higher LVEFs, indepen-
dent of their smaller chamber size.
• The female LV in mammals has a
distinctly different response to
pressure load, such as is typical of
hypertension, compared with males.
Women and DHF
• Evaluation of new-onset heart failure
in an elderly patient should include an
imaging test, usually an echo.
• This will not only assess systolic
function, but will also exclude
unexpected but important diagnoses,
such as AS, severe regurgitant
lesions, HCM, …,etc.
• However, a definitive noninvasive
measure is not available for diastolic
dysfunction.
Women and DHF
Diastolic indexes included: 1--transmitral early (E) and late (A) velocities and early
deceleration time (DT); 2--pulmonary vein systolic (S), diastolic (D), and atrial
reversal (AR) velocities; 3--systolic (Sa) and early (Ea) and late (Aa) diastolic
mitral annular velocities measured from TDI of the septal annulus; 4--the velocity
of propagation (Vp) of early filling (from mitral annulus to left ventricular apex)
measured from the slope of the first aliasing velocity.
Women and DHF
• The severity of exercise intolerance
and the frequency of hospitalization
appear to be similar in patients with
SHF versus DHF.
• This high rate of hospitalization is
associated with poor quality of life and
high health-care costs.
Women and DHF
• The annual mortality rate for diastolic
heart failure in the Framingham Study
was 8.9% per year, a rate about half
that reported for systolic heart failure
(19.6%). Similar results were found in
CHS.
• However, in hospitalized patients,
mortality is similar with DHF and SHF.
Women and DHF
• The approach to the patient with heart
failure and a normal EF should begin
with a search for a primary etiology.
• Most such patients will be found to
have hypertension as their main
underlying condition.
• Of course, if one found an underlying
cause like CAD or HCM, adequate
control of this factor is of paramount
importance.
Women and DHF
• Control of hypertension may be the
single most important treatment
strategy for DHF.
• Meta-analyses indicate that therapy of
chronic, mild systolic hypertension in
the elderly is a potent means of
preventing the development of heart
failure, and it is likely that a major
proportion of cases prevented are due
to DHF
Women and DHF
• Management goals in women with
DHF include relief of symptoms,
improvement in functional capacity
and quality of life, prevention of acute
exacerbations and related hospital
admissions, and prolongation of
survival.
Women and DHF
• Drug used are diuretics, digoxin,
ACE-I, ARB, CCB.
• Although BB are used in the
treatment of hypertension, their role in
DHF is still awaiting delineation
because they impair early myocardial
relaxation.
• The use of aldosterone antagonists,
although important in SHF, it is till not
well established in DHF.
Women with Systolic
Heart Failure and
PPCMP
Women and SHF-PPCMP
• More than half of all patients in the
US with heart failure are women.
• Among persons older than 70 years,
the incidence of CHF in women is
higher than in men, with the largest
increase in prevalence occurring in
the 65–74-yearold age group.
Women and SHF-PPCMP
• The incidence of heart failure in
women, however, has declined in the
past 40 years, perhaps due to better
BP control or perhaps due to a
reduction in rheumatic heart disease.
• The incidence in men during the
same period has remained
unchanged.
Women and SHF-PPCMP
Prevalence of congestive heart failure by sex and age according to

National Health and Nutrition Examination Survey, 1999–2002.
Women and SHF-PPCMP
• Hypertension is a stronger risk factor for
the development of HF in women than in
men.
• Although the incidence of MI is lower in
women, women who sustain an MI are
more likely to develop CHF, (46%)
compared with men (22%).
• In addition, DM is a more potent risk factor
in women than in men for the development
of CHD, and diabetes increases the risk of
death following an acute MI.
Women and SHF-PPCMP
Differences in characteristics between women and men in several heart
failure trials and in a specialty CHF clinic.
Women and SHF-PPCMP
• In the early literature, there were
conflicting data regarding the survival
of women with CHF.
• More recent data suggest that
mortality has been is lower for women
with heart failure in several large
clinical trials following adjustment for
differences in baseline variables.
Women and SHF-PPCMP
• Treatment of CHF in women is the
same as in men with some cautions.
• Women tend to get more side effects
out of the ACE-I and ARB is good for
them.
• Digoxin is good to reduce admissions
and not to improve mortality. Serum
levels should be kept below 1.0 ng/ml.
Women and SHF-PPCMP
• PPCMP can be defined as an
unexplained LV systolic dysfunction
confirmed by echo and developing in
the last month of pregnancy or within
5 months of delivery.
• It requires that there be no other
identifiable cause for the HF and that
the LV systolic dysfunction be
demonstrated echocardiographically.
Women and SHF-PPCMP
• A consensus opinion was of an
incidence of between 1 in 3000 and 1
in 4000, which gives an estimated
250–300 cases each year in the UK.
• This would make it far more common
than is generally realized.
• The apparent rarity of PPCM in the
developed world and the near
certainty of serious under-reporting of
it have made it difficult to study.
Women and SHF-PPCMP
• Diagnostic Criteria:
• Development of cardiac failure in the last
month of pregnancy or within 5 months of
delivery
• Absence of another identifiable cause
• Absence of identifiable heart disease
before the last month of pregnancy
• LV systolic dysfunction demonstrated by
echocardiography
• • EF less than 45% or
• • M-mode FS less than 30% or both and
• • EDD more than 2.7 cm/m2
Women and SHF-PPCMP
• Etiology:
Myocarditis?
Autoimmunity?
Infection?
Women and SHF-PPCMP
• Diagnosis:
• CHF
• Embolism
• Arrhythmias
• Chest pain
Women and SHF-PPCMP
• Diagnosis
Same as CHF
Women and SHF-PPCMP
• Treatment:
Same
Anticoagulation!!
Recurrence in future pregnancies ( as
high as 21% ). Mortality is higher
when LVEF is not fully recovered.
Continue meds for 1 year after
recovery! Future pregnancies and
contraception.
Women and SHF-PPCMP
Women and SHF-PPCMP
Women and SHF-PPCMP
Women and SHF-PPCMP
Women and SHF-PPCMP
Women and SHF-PPCMP

Women and Coronary Artery Diseases

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Women and Coronary

A Total CVD D Chronic Lower Respiratory

A Total CVD D Accidents

• Coronary heart disease is the single

Body Mass Index (kg/m2)

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Milner Am J Cardiol 1999;84:396 Women have More atypical Symptoms of MI

Stress 0.82 (0.73– 0.60 (0.48– 2.06 (1.53– 0.29 (0.18–

Prevalence of angiographically significant CAD (70% or more luminal

• Women have a different clinical

• Women with MI have higher risk initial

• Most studies, but not all, find that

• Women have higher rates of in-

• Men and women show similar rates of

• Primary angioplasty is equally, if not

• The difference in outcome has been

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• Women with MI are more likely than

• Although in the CASS, women treated

• Data from the Heart and

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• Diabetic, elderly, and symptomatic

• After hospital discharge, women are

• Now we know that although women

• The question is whether there is a

8506 Received 8102 Received

7968 Alive 7608 Alive

• Women have their unique physio-

• Women also respond generally to the

• Exercise for 30-45 mins of walking

• When you get a woman with a high

• Numbers of patients in Olmsted County Minnesota

Prevalence of congestive heart failure by sex and age according to

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