4 Cardiopatia Isquemica Isquemica

9/2/2019 Stable ischemic heart disease: Overview of care - UpToDate
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Stable ischemic heart disease: Overview of care

Authors: Joseph P Kannam, MD, Julian M Aroesty, MD, Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Section Editor: Christopher P Cannon, MD
Deputy Editor: Jane Givens, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2019. | This topic last updated: Jul 05, 2018.
INTRODUCTION
Ischemic heart disease, also referred to as coronary heart disease, is present when a patient has
one or more symptoms, signs, or complications from an inadequate supply of blood to the
myocardium. This is most commonly due to obstruction of the epicardial coronary arteries due to
atherosclerosis. (See "Pathogenesis of atherosclerosis".) Patients are referred to as stable when
symptoms, if present, are manageable with either medical or revascularization therapy.
Angina pectoris, or angina for short, occurs when myocardial oxygen demand exceeds oxygen
supply; the clinical manifestation is often chest discomfort. (See "Angina pectoris: Chest pain
caused by myocardial ischemia".) Stable angina pectoris, or stable angina, refers to chest
discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved
with rest or nitroglycerin. Most patients with ischemic heart disease will experience angina as part
of the clinical manifestations of the disease. (See "Angina pectoris: Chest pain caused by
myocardial ischemia", section on 'History'.)
The care of patients with ischemic heart disease includes ascertainment of the diagnosis and its
severity, control of symptoms, and therapies to improve survival. This topic will provide an
overview of these issues and will direct the reader to more detailed discussions when appropriate.
In particular, this topic will focus on patients with stable ischemic heart disease. The care of
patients with unstable ischemic heart disease is discussed elsewhere. (See "Overview of the
acute management of non-ST elevation acute coronary syndromes" and "Acute coronary
syndrome: Terminology and classification" and "Overview of the non-acute management of
unstable angina and non-ST elevation myocardial infarction" and "Risk stratification after non-ST
elevation acute coronary syndrome" and "Evaluation of patients with chest pain at low or
intermediate risk for acute coronary syndrome" and "Initial evaluation and management of
suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency
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department" and "Overview of the acute management of ST-elevation myocardial infarction" and
"Overview of the non-acute management of ST elevation myocardial infarction".)
CLINICAL MANIFESTATIONS
Stable angina pectoris, or stable angina, refers to chest discomfort that occurs predictably and
reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. Most patients
with ischemic heart disease will experience angina as part of the clinical manifestations of the
disease. The clinical manifestations of angina pectoris are discussed in detail elsewhere. (See
"Angina pectoris: Chest pain caused by myocardial ischemia", section on 'Clinical features'.)
DIAGNOSIS
Many patients can be given the diagnosis of stable ischemic heart disease (SIHD) based on a
classic history of angina pectoris in the presence of one or more risk factors for atherosclerotic
cardiovascular disease. When first evaluated for possible SIHD patients should receive a thorough
physical examination in addition to a complete history. (See "Overview of established risk factors
for cardiovascular disease" and "Angina pectoris: Chest pain caused by myocardial ischemia",
section on 'History'.)
An electrocardiogram should be performed in all patients. However, most patients will require
diagnostic testing either to secure the diagnosis or to evaluate the extent of disease.
Stress testing — We agree with the 2012 American College of Cardiology Foundation/American
Heart Association/American College of Physicians/American Association for Thoracic
Surgery/Preventive Cardiovascular Nurses Association/Society for Cardiovascular Angiography
and Interventions/Society of Thoracic Surgeons guideline for the diagnosis and management of
patients with SIHD, which recommends that most patients with suspected SIHD undergo stress
testing to secure the diagnosis and to gain prognostic information [1-3]. (See "Stress testing to
determine prognosis of coronary heart disease", section on 'Exercise ECG'.)
The choice of initial stress test, such as with exercise electrocardiogram (ECG), exercise with
imaging, or pharmacologic stress testing with imaging, may be influenced the patient's resting
ECG, physical ability to perform exercise, local expertise, and available technologies. (See
"Selecting the optimal cardiac stress test" and "Stress testing for the diagnosis of obstructive
coronary heart disease".)
Once this information has been obtained, the therapeutic approach is determined by the results of
the test(s) and individual patient characteristics. Low- and intermediate-risk patients whose
symptoms are controlled on medical therapy can be managed without intervention while high-risk
patients or those with angina refractory to medical therapy undergo coronary angiography and
revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypass
graft surgery (CABG).
Coronary angiography and revascularization — In patients with SIHD, 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.
● Patients with high-risk criteria and selected patients with intermediate-risk criteria on
noninvasive testing, regardless of anginal severity.
We also believe coronary angiography is reasonable in patients with atypical symptoms

and equivocal findings on stress testing in whom a diagnosis needs to be established.
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 any single coronary
stenosis [4]. However, the extent and severity of coronary heart disease 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 [5,6].
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 "Stable
ischemic heart disease: Indications for revascularization", section on 'Patients without clear
indications'.)
We agree with the following strong recommendations to perform coronary angiography made in
the 2012 American College of Cardiology Foundation/American Heart Association/American
College of Physicians/American Association for Thoracic Surgery/Preventive Cardiovascular
Nurses Association/Society for Cardiovascular Angiography and Interventions/Society of Thoracic
Surgeons guideline for the diagnosis and management of patients with SIHD [1,2]:
● As an initial test in patients who have survived sudden cardiac arrest or potentially life-
threatening ventricular arrhythmia or in those who develop symptoms and signs of heart
failure.
● When a patient’s clinical characteristics and the results of noninvasive testing indicate a high
likelihood of severe ischemic heart disease.
We also agree with the following weaker recommendations for coronary angiography in patients
with SIHD and:
● Depressed left ventricular systolic function (ejection fraction <50 percent) and moderate risk
criteria on noninvasive testing with demonstrable ischemia.
● Inconclusive prognostic information after noninvasive testing or in patients for whom

noninvasive testing is contraindicated or inadequate.
● An unsatisfactory quality of life due to angina, a left ventricular ejection fraction >50 percent,
and intermediate risk criteria on noninvasive testing.
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 [7]. With the availability of drug-
eluting stents, PCI is increasingly performed for most lesions. These issues are discussed in detail
separately. (See "Revascularization in patients with stable coronary artery disease: Coronary
artery bypass graft surgery versus percutaneous coronary intervention".)
Measurement of left ventricular systolic function — Most patients with SIHD do not need
measurement of left ventricular systolic function. However, it may be useful in selected patients to
determine optimal medical therapy, the role of interventional or surgical therapy, or in making
recommendations about activity level, rehabilitation, and work status.
We suggest that the following patients with SIHD merit an assessment of left ventricular systolic
function (generally with the use of transthoracic echocardiography):
● Prior myocardial infarction, diagnosed either by history or pathologic Q waves on an

electrocardiogram
● Symptoms or signs of heart failure
● Undiagnosed heart murmur
● Complex ventricular arrhythmias
The methodology for the measurement of left ventricular systolic function is discussed separately.
(See "Tests to evaluate left ventricular systolic function".)
ANTIANGINAL THERAPY
There are three classes of antiischemic drugs commonly used in the management of angina
pectoris: beta blockers, calcium channel blockers, and nitrates [8]. Often, a combination of these
agents is used for control of symptoms.
Beta blockers — We agree with the 2012 American College of Cardiology Foundation/American
Heart Association/American College of Physicians/American Association for Thoracic
patients with stable ischemic heart disease (SIHD), which recommends beta blockers as first line
therapy to reduce anginal episodes and improve exercise tolerance [1,2]. The use of these agents
in patients with SIHD is discussed in detail elsewhere. (See "Beta blockers in the management of
stable ischemic heart disease".)
Beta blockers relieve anginal symptoms by 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.
In addition, beta blockers are the only antianginal drugs proven to prevent reinfarction and to
improve survival in patients who have sustained a myocardial infarction [9]. (See "Acute
myocardial infarction: Role of beta blocker therapy".)
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 "Vasospastic angina".)
Calcium channel blockers — In general, calcium channel blockers are used in combination with
beta blockers when initial treatment with beta blockers is not successful or as a substitute for a
beta blocker when beta blockers are contraindicated or cause side effects. (See "Calcium channel
blockers in the management of stable angina pectoris" and 'Angina that persists with
monotherapy' below.)
Calcium channel blockers improve anginal symptomatology by causing coronary and peripheral
vasodilatation and reducing contractility [10]. The degree to which these changes occur varies with
the type of calcium channel blocker given.
Long-acting diltiazem or verapamil or a second generation dihydropyridine (amlodipine or

felodipine) are preferred. Short-acting dihydropyridines, especially nifedipine, should be avoided
unless used in conjunction with a beta blocker in the management of SIHD because of evidence of
an increase in mortality after a myocardial infarction and an increase in acute myocardial infarction
in hypertensive patients. (See "Major side effects and safety of calcium channel blockers".)
Angina that persists with monotherapy — Although beta blockers and calcium channel
blockers have similar efficacy in the management of stable angina [8,11], we prefer starting with
the former. This is based principally on the observation of survival benefit with beta blockers in
patients with prior myocardial infarction or impaired left ventricular systolic function. Such a benefit
has not been observed with calcium channel blockers.
Addition of a second drug (usually either a calcium channel blocker or a nitrate) is indicated if
angina persists with monotherapy. 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 [12]. 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.
Nitrates — Nitrates, usually in the form of a sublingual preparation, are the first-line therapy for
the treatment of acute anginal symptoms. Patients should be instructed to use them at the onset
of angina. They may also be recommended for the prophylaxis of anginal episodes.
The use of nitrates as well as their side effects, including nitrate tolerance, is discussed elsewhere.
(See "Nitrates in the management of stable angina pectoris".)
Newer therapies — A number of newer medical and invasive therapies have been evaluated for
use in patients with stable angina. Of these, ranolazine, a late sodium channel blocker, is the most
widely used [13]. Ranolazine is used either in combination with a beta blocker or as a substitute in
patients who cannot receive one. (See "New therapies for angina pectoris".)
Non-pharmacologic therapies that may benefit patients with angina refractory to the above
medical therapies include enhanced external counterpulsation, spinal cord stimulation, and
transmyocardial revascularization. These are discussed elsewhere. (See "New therapies for
angina pectoris", section on 'Non-medical therapies'.)
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.
PREVENTIVE THERAPIES
The optimal management of patients with stable angina requires more than antianginal therapy.
Therapies aimed at preventing cardiovascular events are central to long-term care [8,14]. (See
"Overview of the prevention of cardiovascular disease events in those with established disease
(secondary prevention) or at high risk".)
We agree with the 2012 American College of Cardiology Foundation/American Heart

Association/American College of Physicians/American Association for Thoracic
patients with stable ischemic heart disease (SIHD), which recommends that all patients with SIHD
should receive education and counseling about issues such as medication compliance, control of
risk factors, and regular exercise [1,2].
Antiplatelet therapy — In the absence of a contraindication, all patients should be treated with
aspirin. We believe that doses of aspirin from 75 to 325 mg daily are associated with the best
risk/benefit ratio. Some experts prefer to stay within the 75 to 162 mg per day range.
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. (See "Aspirin for the secondary prevention of
atherosclerotic 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,
initiation of statin therapy, weight reduction, glycemic control in diabetics, and participation in
regular physical activity. 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
"Overview of the prevention of cardiovascular disease events in those with established disease
(secondary prevention) or at high risk" and "Cardiovascular risk of smoking and benefits of
smoking cessation" and "Management of low density lipoprotein cholesterol (LDL-C) in the
secondary prevention of cardiovascular disease" and "Goal blood pressure in adults with
hypertension".)
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
coronary heart disease and stable angina is unknown, although their role in patients with a prior
myocardial infarction is better established. (See "Psychosocial factors in coronary and cerebral
vascular disease" and "Psychosocial factors in acute myocardial infarction".)
Role of exercise — 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]. An exercise
program is also beneficial in the management of risk factors for coronary heart disease such as
lipids, blood pressure, obesity, and diabetes mellitus.
Recommendations for referral to cardiac rehabilitation programs and routine physical activity for
patients with stable angina pectoris are discussed separately. (See "Cardiac rehabilitation
programs" and "Exercise and fitness in the prevention of atherosclerotic cardiovascular disease".)
ACE inhibitors or ARBs — The potential role for Angiotensin converting enzyme (ACE) inhibitors
and angiotensin receptor blockers (ARBs) as preventive therapy in patients with stable ischemic
heart disease or those at high risk is discussed elsewhere. (See "Overview of the prevention of
cardiovascular disease events in those with established disease (secondary prevention) or at high
risk", section on 'ACE inhibitors or ARBs'.)
There are conflicting data regarding whether ACE inhibitors reduce exercise-induced ischemia
[18,19]. We believe the evidence is not convincing and do not recommend ACE inhibitors (or
angiotensin-receptor blockers) to improve angina. (See "Overview of the prevention of
cardiovascular disease events in those with established disease (secondary prevention) or at high
risk", section on 'ACE inhibitors or ARBs'.)
These agents have been shown to be of benefit in subsets of patients with SIHD, such as those
with hypertension, diabetes mellitus, a left ventricular ejection fraction of less than 40 percent, or
chronic kidney disease. Their use in these patients is discussed elsewhere. (See "Use of
angiotensin converting enzyme inhibitors in heart failure with reduced ejection fraction" and
"Treatment of hypertension in patients with diabetes mellitus" and "Angiotensin converting enzyme
inhibitors and receptor blockers in acute myocardial infarction: Clinical trials" and "Angiotensin
converting enzyme inhibitors and receptor blockers in acute myocardial infarction:
Recommendations for use" and "Antihypertensive therapy and progression of nondiabetic chronic
kidney disease in adults" and "Use of angiotensin II receptor blocker in heart failure with reduced
ejection fraction".)
Influenza vaccine — All patients with SIHD should receive an annual influenza vaccine, unless
contraindicated. (See "Overview of the prevention of cardiovascular disease events in those with
established disease (secondary prevention) or at high risk", section on 'Influenza vaccination'.)
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 stable ischemic heart disease (SIHD)
increases [20,21]. In addition, elderly patients who have SIHD 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, diagnostic testing and both medical and interventional
therapy have been underutilized in this population [22-24]. This occurs for several reasons:
● Elderly patients with coronary heart disease often present with atypical symptoms, including
exertional dyspnea. Silent myocardial ischemia is also common.
● The efficacy of therapies for coronary heart disease in older adults is often unrecognized or
underestimated, in part because older adults are usually underrepresented in randomized
controlled studies [23].
● The presence of comorbid conditions and difficulties managing medications in older adults
also complicate care.
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.
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 healthcare
delivery team of that patient's subsequent preferences.
FOLLOW-UP
Patients with chronic stable angina require follow-up on a regular basis. We suggest follow-up
every 6 to 12 months. 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
In addition to laboratory studies such as blood glucose or a lipid profile, an electrocardiogram

should be obtained if medications are altered or if the history or physical examination have
changed.
RECOMMENDATIONS OF OTHERS
Recommendations made in this topic, including those for follow-up, are consistent with those
made in the 2013 European Society of Cardiology guidelines on the management of stable
coronary artery disease [25].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Primary prevention of
coronary heart disease" and "Society guideline links: Secondary prevention of coronary heart
disease" and "Society guideline links: Stable ischemic heart disease".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.”
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Coronary heart disease (The Basics)" and "Patient
education: Cardiac catheterization (The Basics)" and "Patient education: Medicines for angina
(chest pain) (The Basics)" and "Patient education: Stenting for the heart (The Basics)" and
"Patient education: Treatment choices for angina (chest pain) (The Basics)")
SUMMARY
The principal goals in the care of patients with stable ischemic heart disease, also referred to as
coronary heart disease, are to secure the diagnosis, relieve symptoms, and to prevent future
cardiac events such as acute coronary syndromes, revascularization, or death. The following is a
summary of the strategy to achieve these goals:
● Patients in whom the diagnosis of ischemic heart disease is suspected but not previously
secured should undergo a complete history and physical examination and receive a 12 lead
electrocardiogram. Most patients should undergo some form of stress testing to either secure
the diagnosis or evaluate its severity. (See 'Diagnosis' above.)
● Beta blockers are preferred for initial treatment of symptoms. Calcium channel blockers and
nitrates are used routinely to relieve symptoms when initial treatment with beta blockers is not
successful or if beta blockers are contraindicated or cause side effects. Ranolazine has been
used successfully to improve anginal symptoms in patients who have not been successfully
treated with nitrates, beta blockers, or calcium channel blockers. Regular exercise may
reduce anginal symptoms. (See 'Antianginal therapy' above.)
● Therapies known to reduce the incidence of adverse cardiovascular events such as death
and myocardial infarction should be started. These include aspirin, statin, smoking cessation,
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control of blood pressure and excess weight, and optimal management of diabetes. Regular
exercise and stress reduction are also recommended. (See 'Preventive therapies' above.)
● The optimal management of these patients also requires periodic evaluation of the patient's
clinical status, using the history, physical examination, and on occasion the
electrocardiogram. (See 'Follow-up' above.)
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Topic 1483 Version 43.0
Contributor Disclosures
Joseph P Kannam, MD Nothing to disclose Julian M Aroesty, MD Nothing to disclose Bernard J Gersh,
MB, ChB, DPhil, FRCP, MACC Consultant/Advisory Boards: Boston Scientific Corporation [REPRISE study];
Cardiovascular Research Foundation [RELIEVE-HF Trial]; Coretherapix [General consulting]; Duke Clinical
Research Institute [PIONEER HCM]; Duke University [ADAPTABLE study]; Icahn School of Medicine at
Mount Sinai [ENVISAGE-TAVI study]; Janssen Research and Development [GEMINI study]; Janssen
Scientific Affairs [General consulting]; Kowa Research Institute, Inc. [PROMINENT study]; Medtronic
[REVEAL AF study]; Mount Sinai St. Luke's [TWILIGHT study]; Sirtex Medical Limited [General consulting];
Teva Pharmaceutical Industries [Teva Revascor Phase 3 Congestive Heart Failure Stem Cell Study];
Thrombosis Research Institute [GARFIELD study]. Christopher P Cannon, MD Grant/Research/Clinical
Trial Support: Amgen [Lipids (Evolocumab), heart failure (Ivabradine)]; Boehringer-Ingelheim [AF
(Dabigatran), DM (Empaglifozin, Linagliptin)]; Bristol-Myers Squibb [AF (Apixaban)]; Daiichi Sankyo [AF
(Edoxaban)]; Janssen [AF (Rivaroxaban), DM (Canagliflozin)]; Merck [Lipids (Ezetimibe), DM (Ertugliflozin,

Sitaglipitin)]. Consultant/Advisory Boards: Alnylam [Lipids (Inclisiran)]; Amarin [Lipids (Vascepa icosapent
ethyl)]; Amgen [Lipids (Evolocumab), heart failure (Ivabradine)]; BI [AF (Dabigatran), DM (Empaglifozin,
Linagliptin)]; Bristol-Myers Squibb [AF (Apixaban)]; Eisai [Lipids/obesity (Locaserin)]; Janssen [AF
(Rivaroxaban), DM (Canagliflozin)]; Kowa [Lipids (Pitavastatin)]; Lipimedix [Lipids]; Merck [Lipids (Ezetimibe),
DM (Ertugliflozin, Sitaglipitin)]; Pfizer [AF (Apixaban), DM (Ertugliflozin), lipids (Atorvastatin)]; Regeneron
[Lipids (Alirocumab)]; Sanofi [Lipids (Alirocumab), ACS (Clopidogrel)], diabetes (Lixisenatide,
Sotagliflozin). Jane Givens, MD Consultant/Advisory Boards (Partner): CVS Health/CVS Omnicare
[Pharmaceutical management of formulary decision-making].
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
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9/2/2019 Stable ischemic heart disease: Overview of care - UpToDate

Official reprint from UpToDate®

Stable ischemic heart disease: Overview of care

We also believe coronary angiography is reasonable in patients with atypical symptoms

Revascularization is performed in appropriate patients in whom angiography reveals anatomy for

● Inconclusive prognostic information after noninvasive testing or in patients for whom

● Prior myocardial infarction, diagnosed either by history or pathologic Q waves on an

● Symptoms or signs of heart failure

● Undiagnosed heart murmur

● Complex ventricular arrhythmias

Long-acting diltiazem or verapamil or a second generation dihydropyridine (amlodipine or

We agree with the 2012 American College of Cardiology Foundation/American Heart

Role of exercise — Gradual institution of a regular aerobic exercise program should be

CONSIDERATIONS IN OLDER ADULTS

● A change in physical activity

In addition to laboratory studies such as blood glucose or a lipid profile, an electrocardiogram

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1. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS

2. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS

3. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS

10. Braunwald E. Mechanism of action of calcium-channel-blocking agents. N Engl J Med 1982;

12. Emanuelsson H, Egstrup K, Nikus K, et al. Antianginal efficacy of the combination of

Topic 1483 Version 43.0

(Edoxaban)]; Janssen [AF (Rivaroxaban), DM (Canagliflozin)]; Merck [Lipids (Ezetimibe), DM (Ertugliflozin,

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