Initial assessment of stable ischaemic heart disease 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.
Beta-blockers may improve survival in selected patients. Addition of short- and long-acting nitrates, beta-blockers, and calcium-channel blockers can reduce chronic anginal symptoms.
Patients with persistent angina despite lifestyle modification and guideline-directed medical therapy may warrant percutaneous or surgical revascularisation for reduction of symptoms.
It is possible that for carefully selected patients, revascularisation in addition to lifestyle modification and medical therapy may improve survival.
Ischaemic heart disease, an inability to provide adequate blood supply to the myocardium, is primarily caused by atherosclerosis of the epicardial coronary arteries. For this reason the terms ischaemic heart disease, chronic coronary syndrome, coronary heart disease, and coronary artery disease are often used interchangeably, although the true pathophysiology is more complex.
Complications of ischaemic heart disease include myocardial infarction, ischaemic cardiomyopathy, and sudden cardiac death. Exertional angina is the classic symptom of ischaemic heart disease, but patients may have atypical or no symptoms. Although routine screening is discouraged, testing may reveal ischaemic heart disease in patients without symptoms or complications.
Ischaemic heart disease is said to be stable when symptoms, if any, are manageable and not rapidly progressive; there must also be no recent infarction, procedural intervention, or signs of significant ongoing cardiac necrosis. Stable ischaemic heart disease (SIHD) stands in contrast to acute coronary syndrome (ACS), a term that encompasses unstable angina, ST-elevation myocardial infarction, and non-ST-elevation myocardial infarction. Although ACS is a manifestation of the same general disease process as SIHD, risk stratification, diagnostic testing, and medical and procedural management usually differ significantly between the two conditions. In some circumstances patients with low-risk unstable angina may be managed similarly to patients with SIHD.
History and exam
Key diagnostic factors
- presence of risk factors
- typical angina symptoms
- atypical angina symptoms
- symptoms of low-risk unstable angina
- normal examination
Other diagnostic factors
- 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
- advancing age
- elevated LDL cholesterol
- isolated low HDL cholesterol
- illicit drug use
- male sex
- family history of ischaemic heart disease
- mental stress/depression
- plasma biomarkers
- polluted air
1st investigations to order
- resting ECG
- lipid profile
- fasting blood glucose or HbA1c
Investigations to consider
- exercise ECG (without imaging)
- exercise or pharmacological stress with imaging
- coronary CT angiography (CCTA)
- invasive coronary angiography
- thyroid-stimulating hormone
- rest echocardiography
- CT myocardial perfusion (CTP) and fractional flow reserve CT (FFRCT)
- coronary artery calcium (CAC) scoring
- tests for vasospasm and microcirculatory dysfunction
Douglas Berger, MD, MLitt
General Medicine Service
Veterans Affairs (VA) Puget Sound Health Care System
University of Washington
DB declares that he has no competing interests.
Stephan D. Fihn, MD, MPH
Professor of Medicine and Health Services
University of Washington
SDF declares that he has no competing interests.
Dr Douglas Berger and Dr Stephan D. Fihn would like to gratefully acknowledge Dr Karen E. Segerson, Dr Mark C. Zaros, Dr Joy Bucher, and Dr Steven M. Bradley, previous contributors to this topic.
KES, MCZ, JB, and SMB declare that they have no competing interests.
Syed Wamique Yusuf, MD, MRCPI, FACC
University of Texas MD Anderson Cancer Center
Department of Cardiology
SWY declares that he has no competing interests.
John R. Charpie, MD, PhD
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.
Michael A. Spinelli, MD
Albert Einstein College of Medicine
Montefiore Medical Center
MAS declares that he has no competing interests.
Katherine Wu, MD
Associate Professor of Medicine
Division of Cardiology
Johns Hopkins Medical Institutions
KW declares that she has no competing interests.
Daniel Lenihan, MD
Professor of Cardiovascular Medicine
Director of Clinical Research
DL declares that he has no competing interests.
Gianluca Rigatelli, MD, PhD, FACP, FACC, FESC, FSCAI
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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