Initial assessment involves a thorough history, including chest discomfort and related symptoms as well as risk factors, in order to assess the likelihood of coronary artery disease. This is followed by appropriate non-invasive testing guided by the probability of disease.
Management should focus on lifestyle modification, with emphasis on smoking cessation, weight management, physical activity, lipid control, and blood pressure control.
Antiplatelet therapy should be prescribed for all patients and dual antiplatelet therapy may be considered in selected patients.
A stepwise addition of beta-blockers, calcium-channel antagonists, and/or long-acting nitrates should be provided to patients with chronic anginal symptoms.
Patients with persistent angina despite lifestyle modification and guideline-directed medical therapy may warrant revascularisation for reduction of symptoms.
Additionally, patients with high risk of ischaemia may benefit from revascularisation concurrent with initiation of lifestyle modification and medical therapy.
Stable ischaemic heart disease (SIHD) and low-risk unstable angina are most commonly caused by atheromatous plaques in the coronary arteries that obstruct blood flow. Anginal symptoms are a clinical manifestation of ischaemia. Key contributory factors to progression of atheromatous disease include smoking, hypertension, hyperlipidaemia, diabetes, and obesity. In a substantial number of patients, especially women, ischaemia may also be caused by vascular dysfunction of smaller myocardial vessels without significant obstruction of large epicardial vessels. The pathology of this process may differ from that of atheroma formation. Chest discomfort in the setting of exertion or emotional stress is the predominant clinical presentation of chronic stable angina. Atypical presentations, including pain in the epigastrium, jaw, neck, or arms are also common, particularly in women, people with diabetes, and older people. Associated symptoms for typical and atypical angina, or 'ischaemic equivalents', include dyspnoea, nausea, vomiting, perspiration, light-headedness, and fatigue.
The guidelines described here specifically address the clinical syndrome of SIHD, which is defined by the presence of confirmed obstructive coronary artery disease without recent (<1 year) acute coronary syndrome or percutaneous intervention. This clinical syndrome includes patients with stable angina pain syndromes and patients with low-risk unstable angina. Angina is considered unstable if it occurs at rest, is new in onset, and is severe (occurs with walking 1 flight of stairs, or similar low level of exertion), or if it is increasing in severity or frequency requiring markedly less provocation in patients with previous angina. Features of low-risk unstable angina include pain from exertion lasting less than 20 minutes, pain not rapidly increasing, and normal/unchanged ECG. Patients with more severe symptoms consistent with intermediate or high-risk unstable angina or acute coronary syndrome are at increased short-term risk of death or non-fatal myocardial infarction, and should be evaluated urgently.
History and exam
- known medical history of exacerbating factor
- non-anginal chest pain
- epigastric discomfort
- jaw pain
- arm pain
- dyspnoea on exertion
- perspiration (diaphoresis)
- mitral regurgitation murmur
- bibasilar rales
- aortic outflow murmur
- carotid bruit
- diminished peripheral pulses
- signs of abdominal aortic aneurysm
- retinopathy seen on fundoscopic examination
- xanthomas or xanthelasma
- thyroid-stimulating hormone
- stress exercise ECG without imaging
- stress single photon emission computed tomography (SPECT), stress echocardiography, stress cardiac magnetic resonance (CMR), stress positron emission tomography (PET)
- cardiac computed tomographic angiography (CCTA)
- invasive coronary angiography
General Medicine Service
Veterans Affairs (VA) Puget Sound Health Care System
University of Washington
DB declares that he has no competing interests.
Dr Douglas Berger would like to gratefully acknowledge Dr Stephan D. Fihn, Dr Karen E. Segerson, Dr Mark C. Zaros, Dr Joy Bucher, and Dr Steven M. Bradley, previous contributors to this topic. SDF, KES, MCZ, JB, and SMB declare that they have no competing interests.
University of Texas MD Anderson Cancer Center
Department of Cardiology
SWY declares that he has no competing interests.
Associate Professor of Pediatrics
Pediatric Cardiothoracic Intensive Care Unit
University of Michigan Congenital Heart Center
C.S. Mott Children's Hospital
JRC declares that he has no competing interests.
Albert Einstein College of Medicine
Montefiore Medical Center
MAS declares that he has no competing interests.
Associate Professor of Medicine
Division of Cardiology
Johns Hopkins Medical Institutions
KW declares that she has no competing interests.
Professor of Cardiovascular Medicine
Director of Clinical Research
DL declares that he has no competing interests.
Section of Transcatheter Treatment of Congenital Heart Disease in the Adult
Rovigo General Hospital
GR declares that he has no competing interests.
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