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Overview of the management

of stable angina pectoris
Authors
Joseph P Kannam, MD
Julian M Aroesty, MD
Bernard J Gersh, MB,
ChB, DPhil, FRCP

Section Editor
Christopher P Cannon,
MD

Deputy Editor
Gordon M Saperia,
MD, FACC

Last literature review version 17.3: September 2009 | This topic last
updated: August 12, 2009 (More)
INTRODUCTION Angina pectoris occurs whenever myocardial oxygen
demand exceeds oxygen supply; the clinical manifestation is chest discomfort
caused by transient myocardial ischemia. A clinical diagnosis of angina has a
90 percent predictive accuracy for the presence of coronary heart disease
(CHD). The management of stable angina involves pharmacologic intervention
to prevent or minimize ischemia, reduction of risk factors for CHD and
revascularization in some patients.
Our recommendations for the management of stable angina are generally in
accord with those made in the 2002 American College of Cardiology/American
Heart Association (ACC/AHA) guidelines for the management of patients with
chronic stable angina and the limited revisions in the 2007 ACC/AHA chronic
angina focused update [ 1,2] .
The initial diagnosis of angina, patients with angina that is refractory to
conventional therapeutic approaches, and unstable angina are discussed
separately. ( See "Diagnostic approach to chest pain in adults" and see "New
therapies for angina pectoris" and see "Overview of the management of
unstable angina and acute non-ST elevation myocardial infarction" ).
DEFINITIONS There are two types of angina:
Stable angina, which refers to chest discomfort that occurs predictably
and reproducibly at a certain level of exertion and is relieved with rest
or nitroglycerin .
Unstable angina, which is an acute coronary syndrome that
encompasses a variety of clinical conditions including the new onset of

chest pain, rest angina, an accelerating pattern of previously stable

angina, post-myocardial infarction (MI) angina, and angina after a
revascularization procedure. ( See "Classification of unstable angina and
non-ST elevation myocardial infarction" ).
GENERAL PRINCIPLES The treatment of angina is aimed at decreasing
oxygen demand and/or increasing oxygen supply [ 3] . (See "Pathophysiology
and clinical presentation of ischemic chest pain" ).
Myocardial oxygen demand varies with:
Heart rate
Systolic blood pressure (afterload)
Contractility
Left ventricular (LV) wall stress, which is proportional to LV end-diastolic
volume (preload) and myocardial mass
Myocardial oxygen supply is dependent upon:
Coronary blood flow
Perfusion pressure
Both of these are limited in patients with critical ( 70 percent) coronary artery
stenoses or prominent coronary vasoconstriction [ 3] . The subendocardium,
which is most vulnerable to ischemia, receives most of its blood supply during
diastole [ 4] ; conditions that decrease the duration of diastole, such as
tachycardia, enhance the potential for subendocardium ischemia.
In addition to severe obstructive lesions that cause stable angina, there are
also nonobstructive (ie, non-flow-limiting) may remain silent, progress slowly
to obstructive symptomatic lesions, or rupture, causing an acute coronary
syndrome that may be manifested as unstable angina, an acute MI, or
ischemic sudden death [ 3] . (See "The role of plaque rupture in acute coronary
syndromes" ).
Goals of therapy The goals of the therapy of stable angina include:
Relief of symptoms
Prevention or slowing of disease progression
Prevention of future cardiac events, such as MI, unstable angina, or the
need for revascularization
Improvement in survival
These goals can be achieved with a variety of modalities including medical
therapy, nonpharmacologic and lifestyle measures, percutaneous coronary
intervention (PCI), and surgical revascularization with a coronary artery
bypass graft (CABG).

RECOMMENDATIONS FOR ANTIANGINAL THERAPY There are currently

three major classes of antiischemic drugs used in the medical management of
angina pectoris: nitrates (short and long acting), beta blockers, and calcium
channel blockers [ 1] . Most commonly, a combination of these agents is used
for management.
Nitrates For patients with stable angina, the various nitrate preparations
are useful both to treat acute episodes and to prevent new episodes and
improve exercise capacity ( show table 1 ).
Nitrates , usually in the form of a sublingual preparation, are a first-line
therapy for the treatment of acute anginal symptoms. While they act as
venodilators, coronary vasodilators, and modest arteriolar dilators [ 5,6] , the
primary antiischemic effect of nitrates is to decrease myocardial oxygen
demand by producing systemic vasodilation more than coronary vasodilation.
In patients with exertional stable angina, chronic nitrate therapy, with oral or
dermal preparations, improves exercise tolerance, time to onset of angina,
and ST-segment depression during exercise testing. In combination with beta
blockers or calcium channel blockers, nitrates produce greater antianginal and
antiischemic effects.
There are various preparations of nitrates available; there is no difference in
efficacy among these preparations.
The use of the various preparations as well as their side effects, including
nitrate tolerance, is discussed elsewhere. ( See "Nitrates in the management
of stable angina pectoris" ).
Beta blockers Beta blockers relieve anginal symptoms by competitively
inhibiting sympathetic stimulation of the heart, reducing both heart rate and
contractility. Since beta blockers reduce the heart rate-blood pressure product
during exercise, the onset of angina or the ischemic threshold during exercise
is delayed or avoided. All types of beta blockers appear to be equally effective
in exertional angina.
Choice of agents In patients with chronic stable angina, important
considerations in the choice of which beta blocker to use are ancillary
properties, such as side effects, dosing interval, and cost. In general
propranolol is less expensive than other beta blockers.
Lower doses of the cardioselective beta blockers (such as
atenolol and
metoprolol ) have the advantage of blocking beta-1-receptor mediated
stimulation of the heart with lesser inhibition of the peripheral vasodilation
and bronchodilation induced by the beta-2 receptors. As a result, a long acting
cardioselective agent (atenolol or metoprolol) is preferred for the treatment of
stable angina. There are no major advantages of a nonselective agent, other
than the low cost of propranolol , and there are potential disadvantages in

patients with certain underlying diseases such as obstructive lung disease,

asthma, peripheral vascular disease, diabetes, and depression.
The starting dose of atenolol is 25 mg once daily which can be increased as
tolerated to a maximum of 200 mg once a day (assuming renal function is
relatively normal) until the resting heart rate is 50 to 60 beats/min and does
not exceed 100 beats/min with ordinary activity.
The starting dose of metoprolol is 25 mg BID, which can be increased to 200
mg BID as tolerated. An extended release form of metoprolol, given once per
day, can substituted once an effective dose has been established.
Beta blockers are generally well tolerated and extremely effective in reducing
anginal episodes and improving exercise tolerance. In addition, beta blockers
are the only antianginal drugs proven to prevent reinfarction and to improve
survival in patients who have sustained an MI [ 7] . (See "Beta blockers in the
management of stable angina pectoris" and see "Beta blockers in the
management of acute coronary syndrome" ).
In comparison to these benefits, beta blockers do not appear to improve
survival or reduce the incidence of MI in patients with chronic stable angina
who have never had an MI, as in trials on mild hypertension. As a result, the
primary therapeutic goal with beta blockers in such patients is to reduce the
frequency and severity of angina and to improve exercise capacity without
significant side effects. ( See "Choice of therapy in essential hypertension:
Clinical trials" , section on Beta blockers as initial therapy?).
We agree with the 2007 ACC/AHA chronic angina focused update, which
recommends beta blockers in all patients with stable angina who have had an
ACS or who have left ventricular dysfunction, unless contraindicated [ 2] .
Achieving adequate beta blockade The efficacy of beta blockers in
relieving angina is dose-dependent. Thus, it is important to be certain that
adequate beta blockade has been attained. Reasonable goals when titrating
the dose include:
Resting heart rate between 50 and 60 beats/min. The target heart rate
for some patients with more severe angina can be <50 beats/min, as
long as the bradycardia is asymptomatic and heart block does not
develop.
Patients with resting bradycardia prior to therapy can be treated with a
calcium channel blocker (such as diltiazem or nifedipine ), nitrates , or a drug
with intrinsic sympathomimetic activity if a beta blocker is necessary. Similar
considerations apply to patients with atrioventricular conduction delay.
Blunting of peak heart rate and blood pressure during exercise, which
can be measured by the patient or during exercise testing, if performed.

Reduction in the frequency and severity of angina and in the use of

sublingual nitroglycerin .
Side effects The most frequent side effects associated with beta
blockers include: bradycardia, conduction disturbances, bronchoconstriction,
worsening of symptoms of peripheral vascular disease, fatigue, central
nervous system side effects, and impotence. As a result, beta blockers should
be used with caution in patients with obstructive airways disease or
peripheral vascular disease and, initially at very low doses in patients with
heart failure. ( See "Major side effects of beta blockers" and see "Use of beta
blockers in heart failure due to systolic dysfunction" ).
Beta blockers should not be used in patients with vasospastic or variant
(Prinzmetal) angina. In such patients, they are ineffective and may increase
the tendency to induce coronary vasospasm from unopposed alpha-receptor
activity. (See "Variant angina" ).
Calcium channel blockers Calcium channel blockers prevent calcium entry
into vascular smooth muscle cells and myocytes, which leads to coronary and
peripheral vasodilatation, decreased atrioventricular (AV) conduction, and
reduced contractility [ 8] . In patients with angina, these effects result in
decreased coronary vascular resistance and increased coronary blood flow.
Calcium blockers also decrease myocardial oxygen demand by reducing
systemic vascular resistance and arterial pressure and a negative inotropic
effect.
Choice of agent The degree to which these changes occur varies with
the type of calcium channel blocker given.
Verapamil is a negative inotrope that also slows sinus rate and
decreases AV conduction (negative chronotrope). It is a much less
potent vasodilator than the dihydropyridines.
The dihydropyridines (eg, nifedipine , nicardipine , felodipine , amlodipine )
have a greater selectivity for vascular smooth muscle than for the
myocardium. They are potent vasodilators with less effect on
contractility and AV conduction.
Diltiazem is a modest negative inotropic and chronotropic agent and
vasodilator and has intermediate effects between the dihydropyridines
and verapamil.
If a calcium channel blocker is used, long-acting diltiazem or verapamil or a
second generation dihydropyridine ( amlodipine or felodipine ) should be
selected. Short-acting dihydropyridines, especially nifedipine , should be
avoided unless used in conjunction with a beta blocker in the management of

CHD because of evidence of an increase in mortality after an MI and an

increase in acute MI in hypertensive patients. ( See "Major side effects and
safety of calcium channel blockers" ).
When to use All of the calcium channel blockers reduce anginal
symptoms and increase exercise tolerance and exercise time before the onset
of angina or ischemia, especially when used in conjunction with other
antianginal agents. ( See "Calcium channel blockers in the management of
stable angina pectoris" ).
They should be used in combination with beta blockers when initial
treatment with beta blockers is not successful.
They may be a substitute for a beta blocker when beta blockers are
contraindicated or cause side effects.
Calcium channel blockers (eg, diltiazem at a dose of 240 to 360 mg per
day) are effective in patients with vasospastic or variant (Prinzmetal)
angina; they are the preferred agents in this setting. ( See "Variant
angina" ).
Side effects Potential side effects include symptomatic bradycardia,
heart block, worsening heart failure, constipation, flushing, headache,
dizziness, and pedal edema. ( See "Major side effects and safety of calcium
channel blockers" ).
Relative effectiveness of medical therapies Beta blockers and calcium
channel blockers generally have equal efficacy in the management of stable
angina [ 1,9] . A meta-analysis was performed of 90 randomized or crossover
studies comparing at least two of the classes of beta blockers, calcium
channel blockers, and long-acting nitrates for efficacy and tolerability in the
treatment of patients with stable angina [ 9] . The following observations were
noted:
There were no observed differences in outcome (eg, cardiac death and
MI) between beta blockers and calcium channel blockers. Too few
patients received long-acting nitrates for efficacy analysis of these
drugs against either of the other classes.
For the variables where differences existed between beta blockers and
calcium blockers (eg, episodes of angina per week and side effects), the
major effect was observed with beta blockers compared to
nifedipine .
As an example, there were 0.31 fewer episodes of angina per week
with beta blockers than with calcium channel blockers as a group and
0.63 fewer episodes per week than with nifedipine. However, as noted
above, nifedipine is typically avoided now in the treatment of patients
with CHD. Short-acting calcium channel blockers were also associated

with a 0.44 increase in weekly angina episodes compared to beta

blockers, while long-acting calcium channel blockers decreased angina
frequency by 0.08 episodes per week.
Beta blockers were discontinued because of adverse reaction less often than
calcium channel blockers (odds ratio 0.72). Again, this difference was most
striking with nifedipine .
Despite the differences in angina frequency, there were no differences
in nitroglycerin use or exercise time between beta blockers and calcium
channel blockers.
Angina that persists with monotherapy Addition of a second drug is
indicated if angina persists with monotherapy. If, for example, the patient is
already taking a beta blocker, a long-acting calcium channel blocker,
particularly if the patient is also hypertensive, or a long-acting nitrate can be
started. The efficacy of combination therapy was illustrated in a study that
randomly assigned 397 patients to four weeks of monotherapy with
felodipine
or metoprolol or a combination of felodipine and metoprolol [ 10] . Combination
therapy was more effective for increasing exercise duration and better
tolerated than monotherapy.
Although a third class of antianginal drug can be added in patients who have
limiting angina on two agents, many physicians would consider coronary
angiography in such patients and revascularization if indicated.
ACE inhibitors Angiotensin converting enzyme (ACE) inhibitors are not
considered a usual treatment for angina pectoris. There are conflicting data
regarding a possible benefit in reducing exercise-induced ischemia. A small
randomized trial noted an improvement in time to 0.1 mV ST depression on
treadmill testing with an ACE inhibitor [ 11] . In contrast, ACE inhibitors had no
effect on the development of myocardial ischemia in the QUASAR trial [ 12] .
It has also been suggested that ACE inhibitors have a specific benefit in
patients at high risk for cardiovascular disease [ 13] . However, as described in
detail elsewhere, the available evidence suggests that the attained blood
pressure not the drug used is of primary importance in such patients. ( See
"Choice of antihypertensive drug and blood pressure goal in patients at
increased risk for a cardiovascular event" ).
The 2007 ACC/AHA chronic angina focused update makes the following
recommendations regarding the use of angiotensin inhibitors in patients with
stable angina unless contraindicated [ 2] :
ACE inhibitors are recommended for patients with myocardial infarction,
left ventricular ejection fraction (LVEF) less than 40 percent,
hypertension, diabetes, or chronic kidney disease

ACE inhibitors are recommended for patients with stable angina who
are not lower risk as defined as those with normal LVEF in whom
cardiovascular risk factors are well controlled and revascularization has
been performed
ACE inhibitors may be considered for lower risk patients with mildly
reduced or normal LVEF in whom risk factors are well controlled and
revascularization has been performed
Angiotensin receptor blockers (ARBs) are recommended for patients
who have hypertension, have indications for but are intolerant of ACE
inhibitors, have heart failure, or have had and MI with LVEF 40 percent
ARBs may be considered in combination with ACE inhibitors for heart
failure due to left ventricular systolic dysfunction
Aldosterone antagonists ( spironolactone or eplerenone ) are
recommend for post MI patients without significant renal dysfunction or
hyperkalemia who are already receiving therapeutic doses of an ACE
inhibitor and a beta blocker, have an LVEF 40 percent and have either
diabetes or heart failure (strong recommendation)
New therapies A number of new medical and invasive therapies have been
evaluated for use in patients with stable angina. Only
ranolazine , a fatty acid
oxidation inhibitor, has been approved for clinical use and its role is evolving
[14] . The absence of a proarrhythmic effect of ranolazine in the MERLIN-TIMI
36 trial has mitigated concerns of possible QT interval prolongation. We
believe ranolazine can be used as an option for angina patients who have
failed all other antianginal therapies. ( See "Clinical features and treatment of
ventricular arrhythmias during acute myocardial infarction" , section on
Ranolazine).
Other potential therapies include ivabradine and fasudil, and mechanical
therapies such as enhanced external balloon counterpulsation, spinal cord
stimulation, and transmyocardial laser revascularization. These approaches
are discussed separately. ( See "New therapies for angina pectoris" ).
Exacerbating factors Treatment of any underlying medical conditions that
might aggravate myocardial ischemia, such as hypertension, fever,
tachyarrhythmias (eg, atrial fibrillation), thyrotoxicosis, anemia or
polycythemia, hypoxemia, or valvular heart disease should be undertaken.
Asymptomatic low grade arrhythmias are not treated routinely, but may
require therapy under circumstances, such as left ventricular dysfunction.
There should also be modification of activities that exacerbate angina, such as
exercise in cold weather or after a meal.
Summary Since beta blockers and calcium channel blockers appear to be of

equivalent efficacy, the choice of one or another as initial therapy is usually

based upon other factors, such as associated medical conditions (
show table
2). As examples, beta blockers should, in the absence of a contraindication, be
given to virtually all patients who have had a prior MI or who have stable
heart failure on an ACE inhibitor. ( See "Beta blockers in the management of
acute coronary syndrome" and see "Use of beta blockers in heart failure due
to systolic dysfunction" ).
Combination therapy using beta blockers and calcium blockers, with or without
long acting nitrates , is often beneficial in patients who are not controlled with
monotherapy.
OTHER INTERVENTIONS The optimal management of stable angina
requires more than antianginal medical therapy. Reducing myocardial oxygen
demand and preventing both the development of symptomatic lesions and
cardiovascular events are also central to long term care. Most
nonpharmacologic measures relieve angina primarily by reducing myocardial
oxygen demand; other measures are of importance for the treatment of risk
factors associated with the development and progression of coronary artery
disease and its sequelae [ 1,3] . (See "Secondary prevention of cardiovascular
disease: Risk factor reduction" ).
Antiplatelet therapy In the absence of a contraindication, all patients
should be treated with aspirin (81 to 325 mg/day). Patients who have a
gastrointestinal bleed on low dose aspirin should, after the episode is
controlled, be treated with aspirin (81 mg/day) plus a proton pump inhibitor.
Clopidogrel is an alternative in patients who are allergic to aspirin. There is no
role for dipyridamole . (See "Benefits and risks of aspirin in secondary and
primary prevention of cardiovascular disease" ).
Risk factor reduction Risk factor reduction should be a central component
of the management of patients with stable angina. This includes treatment of
hypertension, cessation of smoking, lipid lowering with a regimen that
includes statin therapy, weight reduction, and glycemic control in diabetics. In
addition to contributing to chronic progression of atherosclerosis, smoking and
hypertension can precipitate acute coronary ischemia by increasing
oxygen
demands and reducing oxygen supply [ 15,16] . The specific goals are
described elsewhere. ( See "Secondary prevention of cardiovascular disease:
Risk factor reduction" and see "Choice of antihypertensive drug and blood
pressure goal in patients at increased risk for a cardiovascular event"
, section
on Goal blood pressure, and see "Cardiovascular risk of smoking and benefits
of smoking cessation" and see "Intensity of lipid lowering therapy in
secondary prevention of coronary heart disease" ).
Stress reduction should also be encouraged and treatment of underlying
depression and anxiety should be considered, if appropriate. The impact of

these interventions in patients with chronic CHD and stable angina is

unknown, although their role in patients with a prior MI is better established.
(See "Psychosocial factors in coronary and cerebral vascular disease"
and see
"Psychosocial and other social factors in acute myocardial infarction" ).
Exercise program Gradual institution of a regular aerobic exercise program
should be encouraged. Exercise can result in a lower
oxygen requirement for
a given workload, thereby improving exercise tolerance and a sense of
well-being, and reducing symptoms [ 17-19] . An exercise program is also
beneficial in the management of risk factors for CHD such as lipids, blood
pressure, obesity, and diabetes mellitus.
The potential efficacy of exercise training was illustrated in a trial of 101 men
age 70 with class I to III angina ( show table 3 ) and angiographic evidence
of coronary disease; higher risk patients were excluded [ 20] . The patients
were randomly assigned to PCI with stenting or an exercise training program.
At 12 months, survival free of cardiac events (cardiac death, cardiac arrest, MI,
stroke, revascularization, or hospitalization for worsening angina) was
significantly higher with exercise training than with PCI (88 versus 70 percent).
Recommendations for referral to cardiac rehabilitation programs and routine
physical activity for patients with stable angina pectoris are discussed
separately. ( See "Components of cardiac rehabilitation and exercise
prescription" and see "Exercise and fitness in the prevention of cardiovascular
disease" ).
Optimal medical care The potential benefit of utilizing all of the
interventions discussed above was evaluated in the COURAGE trial, which is
discussed separately. ( See "Medical versus interventional therapy in the
management of stable angina pectoris" , section on PCI versus medical
therapy).
Influenza vaccination The 2007 ACC/AHA chronic angina focused update
and the 2007 Advisory Committee on Immunization Practices report
recommend annual influenza vaccination for all patients with cardiovascular
disease, excluding hypertension [ 2,21] . (See "Seasonal influenza vaccination
in adults" , section on Target groups for immunization).
MEASUREMENT OF LV SYSTOLIC FUNCTION Most patients with chronic
stable angina do not need measurement of LV systolic function. However, it
may be useful in selected patients to determine optimal medical, the role of
interventional or surgical therapy, or in making recommendations about
activity level, rehabilitation, and work status. This assessment may be
appropriate at the time of diagnosis, later in the patient's course, or both.
The 2002 ACC/AHA guidelines on the management of patients with chronic
stable angina strongly recommends measurement of LV systolic function in

patients with the following [ 1] :

A history of prior MI, pathologic Q waves, or symptoms or signs of heart
failure.
A systolic murmur suggesting mitral regurgitation.
Complex ventricular arrhythmias.
The methodology for the measurement of LV systolic function is discussed
separately. ( See "Noninvasive methods for measurement of left ventricular
systolic function" ).
STRESS TESTING We agree with the 2005 ACC/AHA/SCAI guideline update
for PCI which recommends that most patients with stable angina undergo
stress testing to evaluate the efficacy of the antiischemic program, for
prognostic information and perhaps as a prelude to PCI [ 22] . (See "Stress
testing to determine prognosis and management of patients with known or
suspected coronary heart disease" ).
The choice of initial stress test, eg, exercise ECG, exercise with perfusion
imaging, pharmacologic stress testing with imaging (echocardiography or
myocardial perfusion scan), may be influenced the patient's resting ECG,
physical ability to perform exercise, local expertise, and available technologies.
A standard exercise ECG is preferred as the initial test in patients with a
normal resting ECG who are able to exercise and are not taking
digoxin . (See
"Advantages and limitations of different stress testing modalities"
).
Exercise testing can identify a subset of high-risk patients who have an
annual mortality of more than 3 per cent ( show table 4 ) [23,24] . In
comparison, low-risk patients, with an annual mortality below one per cent,
are able to exercise into stage 3 of a Bruce protocol with a normal ECG. ( See
"Exercise ECG testing to determine prognosis of coronary heart disease"
,
section on Treadmill scores).
Once this information has been obtained, the therapeutic approach is
determined by the individual patient characteristics. Low- and
intermediate-risk patients are generally treated medically, while high-risk
patients or those with angina refractory to medical therapy undergo coronary
angiography and revascularization with either PCI or CABG.
CORONARY ANGIOGRAPHY AND REVASCULARIZATION The 2002
ACC/AHA guidelines on the management of chronic stable angina
recommended coronary angiography in selected patients ( show table 5 ) [1] .
There are two primary indications for coronary angiography followed by
revascularization of appropriate lesions:
Angina that significantly interferes with a patient's lifestyle despite

maximal tolerable medical therapy. This includes active patients who

desired improved quality of life compared to medical therapy.
Patients with high-risk criteria and selected patients with
intermediate-risk criteria on noninvasive testing, regardless of anginal
severity. (See "Stress testing to determine prognosis and management
of patients with known or suspected coronary heart disease"
, section
on Choice of therapy).
Although coronary angiography is the traditional gold standard for the
diagnosis of coronary atherosclerosis, it is not a reliable indicator of the
functional significance of a coronary stenosis [ 25] . However, the extent and
severity of CHD and LV dysfunction identified on coronary angiography are
powerful clinical predictors of prognosis and the findings are often used to
guide further therapy in patients with angina pectoris [ 26,27] .
Revascularization is performed in appropriate patients in whom angiography
reveals anatomy for which revascularization has a proven benefit or in whom
medical therapy has failed. ( See "Medical versus interventional therapy in the
management of stable angina pectoris" , section on Factors that favor an
interventional approach).
Since the rates of MI and overall survival are generally similar, the choice
between PCI and CABG is based upon anatomy and other factors such as left
ventricular function and the presence or absence of diabetes. With the
availability of drug-eluting stents, PCI is increasingly performed for most
lesions. These issues are discussed in detail separately. ( See "Bypass surgery
versus percutaneous intervention in the management of stable angina
pectoris: Recommendations" and see "Bypass surgery versus percutaneous
intervention in the management of stable angina pectoris: Clinical trials" ).
CONSIDERATIONS IN OLDER ADULTS Individuals over the age of 65
years represent a growing proportion of the population in developed
countries; as the population ages, the frequency of both coronary heart
disease (CHD) and myocardial infarction (MI) increases [ 28,29] . The
Cardiovascular Health Study reported that the incidence of CHD in older adults
was 16.3 and 5.8 per 1000 person-years in men and women, respectively
between the ages of 65 and 74; the respective values between the ages of
75 and 84 were 28.7 and 12.9 [ 28] . In addition, elderly patients who have
CHD have more severe disease than younger subjects.
The approach to the management of angina in older adults should not differ
substantially from that advocated for younger patients. However, both
medical and especially interventional therapy have been underutilized in this
population [ 30] . This occurs for several reasons:
Elderly patients with CHD often present with atypical symptoms,

including exertional dyspnea. Silent myocardial ischemia is also common.

The efficacy of therapies for CHD in older adults is often unrecognized or
underestimated, in part because older adults are usually
underrepresented in randomized controlled studies [ 31] .
The presence of comorbid conditions and difficulties managing
medications in older adults also complicate care.
In addition to medical and revascularization therapies, stress testing has
been underutilized in older patients. This point was illustrated in a
retrospective study of nearly 24,000 Medicare (United States) beneficiaries
aged 65 or older of whom only 44.5 percent underwent stress testing within
the 90 days prior to PCI [ 32] . Factors associated with a decreased likelihood
of testing were age greater than age 85 years, female sex, a history of heart
failure, and prior cardiac catheterization.
In addition, physician characteristics predicting a lower likelihood of stress
testing were older physician age and the volume of PCI performed. Marked
regional variability in the utilization of stress testing was also noted. These
findings suggests that many decisions regarding stress testing prior to PCI
are not based upon guidelines and demographic factors, but are related to
other factors.
As mentioned above, most patients with stable angina, including older
individuals, should undergo stress testing. ( See "Stress testing" above ).
Medical treatment of angina The cornerstones of medical management of
chronic angina in patients of any age are aspirin (81 to 325 mg/day) and beta
blockers [ 1] . Both are underutilized in older adults, particularly as secondary
prevention in those who have had a recent MI [ 33,34] . (See "Benefits and
risks of aspirin in secondary and primary prevention of cardiovascular
disease" ).
All of the drugs used in younger patients for the control of anginal symptoms
are appropriate for older adults. However, older adults may experience more
side effects, particularly hypotension from nitrates and calcium channel
blockers and central nervous system effects from beta blockers. Elderly
patients may need to be started on lower doses initially and should be
monitored carefully for side effects.
Revascularization Percutaneous coronary intervention (PCI) or coronary
artery bypass grafting (CABG) can be used to treat stable angina in older
adults, but are typically performed less often, in part due to concerns about
age specific risk [ 35] . However, decision making should make an attempt at
weighing risk with potential advantages as is done in younger patients.
Elderly patients undergoing a PCI are at an increased risk for a complication

compared to younger patients [ 36-40] . The magnitude of this effect was

illustrated in a report that compared 7472 octogenarians (mean age 83) and
102,236 younger patients (mean age 62) undergoing an intervention
between 1994 and 1997 [ 39] . The octogenarians had an increased risk of
death (3.8 versus 1 percent), ST elevation infarction (1.9 versus 1.3 percent),
renal failure (3.2 versus 1 percent), and vascular complications (6.7 versus 3.3
percent).
The long-term outcome after PCI is also less favorable in elderly patients, with
a higher incidence of death from all causes, cardiac death, and angina
compared to younger patients [ 36-38] . The increase in adverse outcomes
with PTCA alone is most prominent in patients with incomplete
revascularization [ 36,37] .
The risk of bleeding requiring transfusion is higher in elderly patients
undergoing PCI, whether or not they receive a glycoprotein (GP) IIb/IIIa
inhibitor. This issue was examined in a series of 1392 patients 80 years of
age undergoing PCI (more than two-thirds with stenting) at a single
institution [ 41] . There were no intracranial hemorrhages. The incidence of
bleeding requiring transfusion was 8.6 percent without a GP IIb/IIIa inhibitor
versus 9.8 percent with such therapy ( eptifibatide in 73 percent). Transfusion
rates were much lower in randomized trials of younger patients such as
EPISTENT (2.2 percent without versus 2.8 percent with abciximab) or ESPRIT
(1 percent with or without eptifibatide).
CABG is usually well tolerated in older adults, including those over 80 years of
age [ 42-45] . However, Medicare data comparing 24,461 CABG patients 80
years of age to those 65 to 70 years of age undergoing CABG found that the
older patients had a longer hospital stay (14.3 versus 10.4 days) and higher
mortality rates in-hospital (11.5 versus 4.4 percent), at one year (19.3 versus
7.9 percent), and at three years (28.8 versus 13.1 percent) [ 46] . As in
younger subjects, the outcome of CABG is improved with the use of an arterial
compared to a saphenous vein graft [ 47,48] .
Despite the initial increase in surgical risk, elderly subjects, including
octogenarians, who undergo CABG have a long-term survival rate similar to
that of an age-matched control population [ 46,49] and an improvement in
quality of life similar to that in younger patients [ 45,50] . (See "Long-term
outcome after coronary artery bypass graft surgery" ).
Coronary artery reoperation Elderly patients are increasingly being
considered for CABG reoperation, but the outcome from a second CABG is
usually not as good as with the first surgery. The short- and long-term
outcome of elderly patients undergoing a second CABG was examined in a
review of 739 patients 70 years of age (mean age 74 ) [ 51] . In-hospital
mortality was 7.6 percent. Perioperative factors associated with an increased

risk included emergency surgery, left main disease, and left ventricular
dysfunction.
Actuarial survival at 5 and 10 years was 75 and 49 percent, respectively, and
cardiac-event free survival was 60 and 27 percent, respectively. Mortality was
associated with comorbidities such as diabetes mellitus, left ventricular
dysfunction, peripheral vascular disease, and postoperative stroke.
Summary While older adults have been underrepresented in clinical trials,
there are sufficient data that medical and revascularization therapies are
effective in older adults. The decision whether to continue with optimal
medical therapy or perform revascularization requires the elderly patient's
understanding of the strengths and weaknesses of each approach and a
respect by the health care delivery team of that patient's subsequent
preferences.
FOLLOW-UP Patients with chronic stable angina that is effectively
managed require follow-up on a regular basis, eg, every four to six months
during the first year, and every 4 to 12 months thereafter [ 1] . At each visit, a
detailed history should be obtained and physical examination performed. In
particular, it is important to establish:
A change in physical activity
Any change in the frequency, severity, or pattern of angina
Tolerance of and compliance with the medical program
Modification of risk factors
The development of new or worsened comorbid illnesses
Routine laboratory examination includes glucose, lipid profile, and hematocrit.
An assessment of electrolytes and renal and thyroid function is guided by
symptoms or history. An ECG should be obtained if medications are altered or
if the history or physical examination have changed.
The ACC/AHA Task Force has published recommendations for noninvasive
testing and angiography during follow-up [ 1] . These studies are primarily
indicated when there is a change in clinical status, such as a change in anginal
frequency, severity, or pattern; a new MI; new or worsening heart failure; or
the appearance of a new murmur suggesting significant valvular disease.
Use of UpToDate is subject to the Subscription and License Agreement .
REFERENCES
1. Gibbons, RJ, Abrams, J, Chatterjee, K, et al. ACC/AHA 2002 guideline
update for the management of patients with chronic stable angina.

2.

3.
4.

5.

6.
7.

8.
9.

10.

11.

12.

13.

Available at: www.acc.org/qualityandscience/clinical/statements.htm

(accessed August 24, 2006).
Fraker, TD Jr, Fihn, SD, Gibbons, RJ, et al. 2007 chronic angina focused
update of the ACC/AHA 2002 guidelines for the management of patients
with chronic stable angina: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines
Writing Group to develop the focused update of the 2002 guidelines for
the management of patients with chronic stable angina. J Am Coll
Cardiol 2007; 50:2264.
Abrams, J, Thadani, U. Therapy of stable angina pectoris: the
uncomplicated patient. Circulation 2005; 112:e255.
Lewis, FB, Coffman, JD, Gregg, DE. Effect of heart rate and intracoronary
isoproterenol, levarterenol, and epinephrine on coronary flow and
resistance. Circ Res 1961; 9:89.
Kaski, JC, Plaza, LR, Meran, DO, et al. Improved coronary supply:
Prevailing mechanism of action of nitrates in chronic stable angina. Am
Heart J 1985; 110:238.
Parker, JO. Nitrates and angina pectoris. Am J Cardiol 1993; 72:3C.
Teo, KK, Yusuf, S, Furberg, CD. Effects of prophylactic antiarrhythmic
drug therapy in acute myocardial infarction: An overview of results from
randomized controlled trials. JAMA 1993; 270:1589.
Braunwald, E. Mechanism of action of calcium-channel-blocking agents.
N Engl J Med 1982; 307:1618.
Heidenreich, PA, McDonald, KM, Hastie, T, et al. Meta-analysis of trials
comparing -blockers, calcium antagonists, and nitrates for stable
angina. JAMA 1999; 281:1927.
Emanuelsson, H, Egstrup, K, Nikus, K, et al, for the TRAFFIC Study
Group. Antianginal efficacy of the combination of felodipine-metoprolol
10/100 mg compared with each drug alone in patients with stable
effort-induced angina pectoris: A multicenter parallel group study. Am
Heart J 1999; 137:854.
van den Heuvel AF, Dunselman, PH, Kingma, T, et al. Reduction of
exercise-induced myocardial ischemia during add-on treatment with the
angiotensin-converting enzyme inhibitor enalapril in patients with
normal left ventricular function and optimal beta blockade. J Am Coll
Cardiol 2001; 37:470.
Pepine, CJ, Rouleau, JL, Annis, K, et al. Effects of angiotensin-converting
enzyme inhibition on transient ischemia: the Quinapril Anti-Ischemia and
Symptoms of Angina Reduction (QUASAR) trial. J Am Coll Cardiol 2003;
42:2049.
Yusuf, S, Sleight, P, Pogue, J, et al. Effects of an
angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular

14.

15.

16.

17.
18.

19.
20.

21.

22.

23.

24.

25.

events in high-risk patients. The Heart Outcomes Prevention Evaluation

Study Investigators. N Engl J Med 2000; 342:145.
Chaitman, BR. Ranolazine for the treatment of chronic angina and
potential use in other cardiovascular conditions. Circulation 2006;
113:2462.
Winniford, MD, Jansen, DE, Reynolds, GA, et al. Cigarette
smoking-induced coronary vasoconstriction in atherosclerotic coronary
artery disease and prevention by calcium antagonists and nitroglycerin.
Am J Cardiol 1987; 59:203.
Winniford, MD, Wheelan, KR, Kremers, MS, et al. Smoking-induced
coronary vasoconstriction in patients with atherosclerotic coronary
artery disease: Evidence for adrenergically mediated alterations in
coronary artery tone. Circulation 1986; 73:662.
Thompson, PD. Exercise prescription and proscription for patients with
coronary artery disease. Circulation 2005; 112:2354.
Dressendorfer, RH, Smith, JL, Amsterdam, EA, Mason, DT. Reduction of
submaximal exercise myocardial oxygen demand post-walk training
program in coronary patients due to improved physical work efficiency.
Am Heart J 1982; 103:358.
Barnard, RJ, MacAlphin, R, Kattus, AA, Buckber, GD. Effect of training on
myocardial oxygen supply/demand balance. Circulation 1977; 56:289.
Hambrecht, R, Walther, C, Mobius-Winkler, S, et al. Percutaneous
coronary angioplasty compared with exercise training in patients with
stable coronary artery disease: a randomized trial. Circulation 2004;
109:1371.
Fiore, AE, Shay, DK, Broder, K, et al. Prevention and control of influenza.
Recommendations of the Advisory Committee on Immunization Practices
(ACIP), 2009. MMWR Recomm Rep 2009; 58:1.
Smith, SC, Feldman, TE, Hirshfeld, JW et al. ACC/AHA/SCAI 2005
guideline update for percutaneous coronary intervention: a report of
the ACC/AHA task force on practice guidelines (ACC/AHA/SCAI writing
committee to update the 2001 guidelines for percutaneous coronary
intervention). American College of Cardiology Web Site. Available at:
www.acc.org/qualityandscience/clinical/statements.htm (accessed May
9, 2007).
Weiner, DA, Ryan, TJ, McCabe, CH, et al. Prognostic importance of a
clinical profile and exercise test in medically treated patients with
coronary artery disease. J Am Coll Cardiol 1984; 3:772.
Mark, DB, Hlatky, MA, Harrell, FE Jr, et al. Exercise treadmill score for
predicting prognosis in coronary artery disease. Ann Intern Med 1987;
106:793.
White, CW, Wright, CB, Doty, DB, et al. Does visual interpretation of the

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

coronary arteriogram predict the physiologic importance of a coronary

stenosis? N Engl J Med 1984; 310:819.
Ringqvist, I, Fisher, LD, Mock, M, Davis, KB. Prognostic value of
angiographic indices of coronary artery disease from the Coronary
Artery Surgery Study (CASS). J Clin Invest 1983; 71:1854.
Emond, M, Mock, MB, Davis, KB, et al. Long-term survival of medically
treated patients in the Coronary Artery Surgery Study (CASS) Registry.
Circulation 1994; 90:2645.
Psaty, BM, Furberg, CD, Kuller, LH, et al. Traditional risk factors and
subclinical disease measures as predictors of first myocardial infarction
in older adults. Arch Intern Med 1999; 159:1339.
Goldberg, RJ, McCormick, D, Gurwitz, JH, et al. Age-related trends in
short- and long-term survival after acute myocardial infarction: A
20-year population-based perspective (1975-1995). Am J Cardiol 1998;
82:1311.
Williams, MA, Fleg, JL, Ades, PA, et al. Secondary prevention of coronary
heart disease in the elderly (with emphasis on patients 75 years of
age): an American Heart Association scientific statement from the
Council on Clinical Cardiology Subcommittee on Exercise, Cardiac
Rehabilitation, and Prevention. Circulation 2002; 105:1735.
Lee, PY, Alexander, KP, Hammill, BG, et al. Representation of elderly
persons and women in published randomized trials of acute coronary
syndromes. JAMA 2001; 286:708.
Lin, GA, Dudley, RA, Lucas, FL, et al. Frequency of stress testing to
document ischemia prior to elective percutaneous coronary intervention.
JAMA 2008; 300:1765.
Krumholz, H, Radford, MJ, Ellerback, EF, et al. Aspirin for secondary
prevention after acute myocardial infarction in the elderly: prescribed
use and outcomes. Ann Intern Med 1996; 124:292.
Soumerai, SB, McLauglin, TJ, Spiegleman, D, et al. Adverse outcomes of
underuse of beta-blockers in elderly survivors of acute myocardial
infarction. JAMA 1997; 277:115.
Bearden, D, Allman, R, McDonald, R, et al. Age, race, and gender
variation in the utilization of coronary artery bypass surgery and
angioplasty in SHEP. SHEP Cooperative Research Group. Systolic
Hypertension in the Elderly Program. J Am Geriatr Soc 1994; 42:1143.
ten Berg, JM, Voors, AA, Suttorp, MJ, et al. Long-term results after
successful percutaneous coronary angioplasty in patients over 75 years
of age. Am J Cardiol 1996; 77:690.
Tan, KH, Sulke, N, Taub, N, et al. Percutaneous transluminal coronary
angioplasty in patients 70 years old or older: 12 years' experience. Br
Heart J 1995; 74:310.

38. Thompson, RC, Holmes, DR, Gersh, BJ, et al. Predicting early and
intermediate-term outcome of coronary angioplasty in the elderly.
Circulation 1993; 88:1579.
39. Batchelor, WB, Anstrom, KJ, Muhlbaier, LH, et al. Contemporary outcome
trends in the elderly undergoing percutaneous coronary interventions:
results in 7,472 octogenarians. National Cardiovascular Network
Collaboration. J Am Coll Cardiol 2000; 36:723.
40. Thompson, RC, Holmes, DR, Grill, DE, et al. Changing outcome of
angioplasty in the elderly. J Am Coll Cardiol 1996; 27:8.
41. Sadeghi, HM, Grines, CL, Chandra, HR, et al. Percutaneous coronary
interventions in octogenarians. glycoprotein IIb/IIIa receptor inhibitors'
safety profile. J Am Coll Cardiol 2003; 42:428.
42. Williams, DB, Carrillo, RG, Traad, EA, et al. Determinants of operative
mortality in octogenarians undergoing coronary bypass. Ann Thorac
Surg 1995; 60:1038.
43. Kolh, P, Kerzmann, A, Lahaye, L, et al. Cardiac surgery in octogenarians.
Peri-operative outcome and long-term results. Eur Heart J 2001;
22:1235.
44. Rosengart, TK, Finnin, EB, Kim, DY, et al. Open heart surgery in the
elderly: results from a consecutive series of 100 patients aged 85 years
or older. Am J Med 2002; 112:143.
45. Conaway, DG, House, J, Bandt, K, et al. The elderly: health status
benefits and recovery of function one year after coronary artery bypass
surgery. J Am Coll Cardiol 2003; 42:1421.
46. Peterson, ED, Cowper, PA, Jollis, JG, et al. Outcomes of coronary artery
bypass graft surgery in 24,461 patients aged 80 years or older.
Circulation 1995; 92:II85.
47. He, GW, Achuff, TE, Ryan, WH, et al. Determinants of operative mortality
in elderly patients undergoing coronary artery bypass grafting.
Emphasis on the influence of internal mammary artery grafting on
mortality and morbidity. J Thorac Cardiovasc Surg 1994; 108:73.
48. Galbut, DL, Traad, EA, Dorman, MJ, et al. Coronary bypass grafting in
the elderly> Single versus bilateral internal mammary artery grafts. J
Thorac Cardiovasc Surg 1993; 106:128.
49. Canver, CC, Nichols, RD, Cooler, SD, et al. Influence of increasing age on
long-term survival after coronary artery bypass grafting. Ann Thorac
Surg 1996; 62:1123.
50. Heijmeriks, JA, Pourrier,S, Dassen, P, et al. Comparison of quality of life
after coronary and/or valvular cardiac surgery in patients 75 years of
age with younger patients. Am J Cardiol 1999; 83:1129.
51. Yamamuro, M, Lytle, BW, Sapp, SK, et al. Risk factors and outcomes
after coronary reoperation in 739 elderly patients. Ann Thorac Surg

2000; 69:464.

GRAPHICS

Common nitrate preparations used in the treatment of stable

angina

Preparation

Onset
of
Route of
action,
administration minutes

Duration
of action

Dose

Sublingual
tablet

2-5

15-30 min

0.15-0.9
mg

Sublingual spray

2-5

15-30 min

0.4 mg

Up to 7
hours

2
percent,
15x15
cm (7.5
to 40
mg)

Ointment

2-5

Nitroglycerin
Transdermal

30

8-14 hours

0.2-0.8
mg/hour
q 12
hours

Oral sustained
release

30

4-8 hours

2.5-13
mg

Intravenous

2-5

During
infusion
tolerance
in 7-8 hrs

5-200
g/min

Sublingual

2-5

Up to 60
min

2.5-15
mg

30

Up to 8
hours

5-80 mg
BID or
TID

Oral

Isosorbide
dinitrate

Spray

2-5

2-3 min

1.25
mg/day

Chewable

2-5

2-2.5 hours

5 mg

30

Up to 8
hours

40 mg
OD or
BID

2-5

During
infusion
tolerance
in 7-8 hrs

1.25-5
mg/hour

Oral slow release

Intravenous

Isosorbide
mononitrate,
extended
release
Isosorbide
mononitrate,
extended
release
Pentaerythroid
tetranitrate

Eyrthritol
tetranitrate

Oral

Oral

Sublingual

30

30-60

2-5

12-24
hours

20-40
mg BID
60-240
mg/day

12 hours

30-120
mg once
daily

Not known

10 mg
as
needed

Sublingual

2-5

Not known

5-10 mg
as
needed

Oral

30

Not known

10-30
mg TID

ACC/AHA/ACP guidelines: recommended drug therapy

(calcium antagonist vs. beta-blocker) in patients with angina
and associated conditions

Condition

Recommended
treatment (and
alternative)

Avoid

Medical conditions
Systemic hypertension

Beta-blockers (calcium
antagonists)

Migraine or vascular
headaches

Beta-blockers
(verapamil or diltiazem)

Asthma or chronic
obstructive pulmonary
disease with
bronchospasm

Verapamil or diltiazem

Hyperthyroidism

Beta-blockers

Raynaud's syndrome

Long-acting
slow-release calcium
antagonists

Insulin-dependent
diabetes mellitus

Beta-blockers
(particularly if prior
myocardial infarction) or
long-acting
slow-release calcium
antagonists

Non-insulin-dependent
diabetes mellitus

Beta blockers or
long-acting
slow-release calcium
antagonists

Depression

Long-acting
slow-release calcium
antagonists

Mild peripheral vascular

disease

Beta-blockers or calcium
antagonists

Beta-blockers

Beta-blockers

Beta-blockers

Severe peripheral
vascular disease with
rest ischemia

Calcium antagonists

Beta-blockers

Cardiac arrhythmias and conduction abnormalities

Sinus bradycardia

Long-acting
slow-release calcium
antagonist that do not
decrease heart rate

Sinus tachycardia (not

due to heart failure)

Beta-blockers

Supraventricular
tachycardia

Verapamil, diltiazem, or
beta-blockers

Atrioventricular block

Long-acting
slow-release calcium
antagonists that do not
slow A-V conduction

Rapid atrial fibrillation

(with digitalis)

Verapamil, diltiazem, or
beta-blockers

Ventricular arrhythmias

Beta blockers

Beta-blockers,
diltiazem,
verapamil

Beta-blockers,
diltiazem,
verapamil

Left ventricular dysfunction

Congestive heart failure
Mild (LVEF

40 percent)

Beta-blockers

Moderate to severe (LVEF

Amlodipine or felodipine

Verapamil,

<40 percent)

(nitrates)

diltiazem

Left-sided valvular heart disease

Mild aortic stenosis
Aortic insufficiency

Mitral regurgitation
Mitral stenosis

Beta-blockers
Long-acting slow-release
dihydropyridines
Long-acting slow-release
dihydropyridines
Beta-blockers

Hypertrophic
cardiomyopathy

Beta-blockers,
non-dihydropyridine
calcium antagonist

Nitrates,
dihydropyridine
calcium
antagonists

NOTE: These guidelines were published before the specific survival

benefits of beta blockers were proven in patients with systolic heart
failure. Thus, current practice may differ from these guidelines in this
and other areas. Reproduced with permission from: ACC/AHA/ACP
Guidelines for the Management of Patients with Chronic Stable Angina.
J Am Coll Cardiol 1999; 33:2092. Copyright 1999 American College
of Cardiology.

Comparison of three methods of assessing cardiovascular

disability

Class

New York
Heart
Association
functional
classification

Canadian
Cardiovascular
Society functional
classification

Specific
activity scale

Patients with
cardiac disease
but without
resulting
limitations of
physical activity.
Ordinary physical
activity does not
cause undue
fatigue,
palpitation,
dyspnea, or
anginal pain.

Ordinary physical
activity, such as
walking and climbing
stairs, does not cause
angina. Angina with
strenuous or rapid
prolonged exertion at
work or recreation.

Patients can
perform to
completion any
activity
requiring 7
metabolic
equivalents, eg,
can carry 24 lb
up eight steps;
do outdoor
work (shovel
snow, spade
soil); do
recreational
activities
(skiing,
basketball,
squash,
handball,
jog/walk 5
mph).

II

Patients with
cardiac disease
resulting in slight
limitation of
physical activity.
They are
comfortable at
rest. Ordinary
physical activity
results in fatigue,
palpitation,
dyspnea, or
anginal pain.

Slight limitation of
ordinary activity.
Walking or climbing
stairs rapidly, walking
uphill, walking or stair
climbing after meals, in
cold, in wind, or when
under emotional
stress, or only during
the few hours after
awakening. Walking
more than two blocks
on the level and
climbing more than
one flight of ordinary
stairs at a normal pace
and in normal
conditions.

Patients can
perform to
completion any
activity
requiring
5
metabolic
equivalents, eg,
have sexual
intercourse
without
stopping,
garden, rake,
weed, roller
skate, dance
fox trot, walk at
4 mph on level
ground, but
cannot and do
not perform to
completion
activities
requiring
7
metabolic
equivalents.

III

Patients with
cardiac disease
resulting in
marked limitation
of physical activity.
They are
comfortable at
rest. Less than
ordinary physical
activity causes
fatigue,
palpitation,
dyspnea, or
anginal pain.

IV

Patient with
cardiac disease
resulting in
inability to carry on
any physical
activity without
discomfort.
Symptoms of
cardiac
insufficiency or of
the anginal
syndrome may be
present even at
rest. If any
physical activity is
undertaken,
discomfort is
increased.

Marked limitation of
ordinary physical
activity. Walking one
to two blocks on the
level and climbing
more than one flight in
normal conditions.

Patients can
perform to
completion any
activity
requiring
2
metabolic
equivalents, eg,
shower without
stopping, strip
and make bed,
clean windows,
walk 2.5 mph,
bowl, play golf,
dress without
stopping, but
cannot and do
not perform to
completion any
activities
requiring > 5
metabolic
equivalents.

Inability to carry on
any physical activity
without discomfort anginal syndrome may
be present at rest.

Patients cannot
or do not
perform to
completion
activities
requiring > 2
metabolic
equivalents.
Cannot carry
out activities
listed above
(Specific activity
scale III).

Noninvasive risk stratification in patients with suspected

ischemic chest pain
High risk (greater than 3 percent annual mortality rate)
1. Severe resting left ventricular dysfunction (LVEF <35 percent)
2. High-risk treadmill score (score

-11)

3. Severe exercise left ventricular dysfunction (exercise LVEF <35 percent)

4. Stress-induced large perfusion defect (particularly if anterior)
5. Stress-induced multiple perfusion defects of moderate size
6. Large, fixed perfusion defect with LV dilation or increased lung uptake
(thallium-201)
7. Stress-induced moderate perfusion defect with LV dilation or increased
lung uptake (thallium-201)
8. Echocardiographic wall motion abnormality (involving greater than two
segments) developing at low dose of dobutamine (
10 mg/kg/min) or at
a low heart rate (<120 beats/min)
9. Stress echocardiographic evidence of extensive ischemia

Intermediate risk (1 percent to 3 percent annual mortality

rate)
1. Mild/moderate resting left ventricular dysfunction (LVEF = 35 percent to
49 percent)
2. Intermediate-risk treadmill score (-11 < score <5)
3. Stress-induced moderate perfusion defect without LV dilation OR
increased lung intake (thallium-201)
4. Limited stress echocardiographic ischemia with a wall motion
abnormality only at higher doses of dobutamine involving less than or
equal to two segments

Low risk (less than 1 percent annual mortality rate)

1. Low-risk treadmill score (score

5)

2. Normal or small myocardial perfusion defect at rest or with stress*

3. Normal stress echocardiographic wall motion or no change of limited
resting wall motion abnormalities during stress*

* Although the published data are limited, patients with these findings
will probably not be at low risk in the presence of either a high-risk
treadmill score or severe resting left ventricular dysfunction (LVEF < 35
percent).
Reproduced with permission from: ACC/AHA/ACP Guidelines for the
Management of Patients with Chronic Stable Angina. J Am Coll Cardiol
1999; 33:2092. Copyright 1999 American College of Cardiology.

ACC/AHA guideline summary: Coronary angiography for risk

stratification in patients with chronic stable angina
Class I - There is evidence and/or general agreement that
coronary angiography should be performed to risk stratify
patients with chronic stable angina in the following settings
Disabling anginal symptoms (Canadian Cardiovascular Society [CCS]
classes III and IV) despite medical therapy.
High-risk criteria on noninvasive testing independent of the severity of
angina.
Survivors of sudden cardiac death or serious ventricular arrhythmia.
Symptoms and signs of heart failure.
Clinical features that suggest that the patient has a high likelihood of
severe coronary artery disease.

Class IIa - The evidence or opinion is in favor of

performing coronary angiography to risk stratify patients
with chronic stable angina in the following settings
Left ventricular ejection fraction less than 45 percent, CCS class I or II
angina, and evidence, on noninvasive testing, of ischemia that does not
meet high-risk criteria.
Noninvasive testing does not reveal adequate prognostic information.

Class IIb - The evidence or opinion is less well established

for performing coronary angiography to risk stratify
patients with chronic stable angina in the following settings
Left ventricular ejection fraction greater than 45 percent, CCS class I or
II angina, and evidence, on noninvasive testing, of ischemia that does
not meet high-risk criteria.
CCS class III or IV angina that improves to class I or II with medical
therapy.
CCS class I or II angina but unacceptable side effects to adequate
medical therapy.

Class III - There is evidence and/or general agreement

that coronary angiography should not be performed to risk
stratify patients with chronic stable angina in the following
settings
CCS class I or II angina that responds to medical therapy and, on
noninvasive testing, shows no evidence of ischemia.
Patient preference to avoid revascularization.

Data from Gibbons, RJ, Abrams, J, Chatterjee, K, et al. ACC/AHA 2002

guideline update for the management of patients with chronic stable
angina--summary article: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee on the Management of Patients With Chronic
Stable Angina). Circulation 2003; 107:149.

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