Angina: contemporary diagnosis and management

Ford TJ, Berry C. Angina: contemporary diagnosis and management.Heart 2020;106:387-398.

Learning objectives

  • Around one half of angina patients have no obstructive coronary disease; many of these patients have microvascular and/or vasospastic angina.
  • Tests of coronary artery function empower clinicians to make a correct diagnosis (rule-in/rule-out), complementing coronary angiography.
  • Physician and patient education, lifestyle, medications and revascularisation are key aspects of management.


Ischaemic heart disease (IHD) remains the leading global cause of death and lost life years in adults, notably in younger (<55 years) women. Angina pectoris (derived from the Latin verb ‘angere’ to strangle) is chest discomfort of cardiac origin. It is a common clinical manifestation of IHD with an estimated prevalence of 3%–4% in UK adults. There are over 250 000 invasive coronary angiograms performed each year with over 20 000 new cases of angina. The healthcare resource utilisation is appreciable with over 110 000 inpatient episodes each year leading to substantial associated morbidity. In 1809, Allen Burns (Lecturer in Anatomy, University of Glasgow) developed the thesis that myocardial ischaemia (supply:demand mismatch) could explain angina, this being first identified by William Heberden in 1768. Subsequent to Heberden’s report, coronary artery disease (CAD) was implicated in pathology and clinical case studies undertaken by John Hunter, John Fothergill, Edward Jenner and Caleb Hiller Parry. Typically, angina involves a relative deficiency of myocardial oxygen supply (ie, ischaemia) and typically occurs after activity or physiological stress.

Box 1

Definition of angina (NICE guidelines)

Typical angina: (requires all three)
  • Constricting discomfort in the front of the chest or in the neck, shoulders, jaw or arms.
  • Precipitated by physical exertion.
  • Relieved by rest or sublingual glyceryl trinitrate within about 5 min
    • Presence of two of the features is defined as atypical angina.
    • Presence of one or none of the features is defined as non-anginal chest pain.
    • Stable angina may be excluded if pain is non-anginal provided clinical suspicion is not raised based on other aspects of the history and risk factors.
    • Do not define typical, atypical and non-anginal chest pain differently in men and women or different ethnic groups.

Six decades have passed since the first reported invasive coronary angiogram; however, many physicians still consider detecting obstructive epicardial CAD on coronary angiography a ‘sine qua non’ for the diagnosis of angina. The detection of obstructive CAD allows evidence-based medical treatment and consideration of myocardial revascularisation. However, underlying pathophysiology is more nuanced with contributions from anatomical atherosclerotic and/or functional alterations of epicardial vessels and/or microcirculation (figure 1). ESC guidelines have revised nomenclature (‘Chronic Coronary Syndromes’) in part reflecting the importance of patients with signs and symptoms of ischaemia without obstructive coronary artery disease—INOCA. Around half of all patients with angina undergoing elective coronary angiography have no obstructive epicardial CAD. This large, heterogeneous chronic coronary syndrome is comprised of distinct vasomotor disorders including microvascular angina (MVA) and/or vasospastic angina (VSA)—the two most common underlying disorders of coronary vascular function in the INOCA population. Crucially, we stress that there are often multiple mechanisms of myocardial ischaemia occurring in various coronary compartments via different mechanisms. These frequently coexist in combination; however, an appreciation of this fact can help stratify treatment and help us understand patients with poor treatment response (eg, angina after revascularisation).

Figure 1

Reappraisal of ischaemic heart disease pathophysiology. Distinct functional and structural mechanisms can affect coronary vascular function and frequently coexist leading to myocardial ischaemia. CAD, coronary artery disease.


Share this article

To view this free access article in full, please visit the link below:


Authors: Thomas Joseph Ford, Colin Berry

Publication: Heart

Publisher: BMJ Publishing Group Ltd.

Date published: March 1st, 2020


Copyright © 2020, BMJ Publishing Group Ltd. & British Cardiovascular Society

Click to access the login or register cheese