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Introduction

Stable angina (aka Angina Pectoris) is a common presentation of Coronary Heart disease – CHD(aka Ischaemic Heart disease – IHD)

  • Stable angina, (aka ‘Angina pectoris’, and colloquially “Angina“) is a syndrome which causes exertional chest pain, relieved by either rest or the use of nitrates
  • Stable angina is a clinical syndrome rather than a disease – and represents a clinical manifestation of underlying coronary artery disease
  • It occurs when there is insufficient oxygen supply to the heart to meet demand i.e. when there is myocardial ischaemia without infarct
  • This inability typically occurs as a result of narrowing of the coronary arteries. This narrowing can be due to:
  • Angina typically presents as central or left sided chest pain, with or without radiation to the neck, arm or jaw, and is generally transient, most commonly occurring on exertion, but can also be triggered by emotion
  • Acute attacks are treated with nitrites (e.g. sublingual GTN spray)
  • It is diagnosed with a combination of history, ECG and myocardial imagining – typically an angiogram
  • Long-term management involves the use of beta-blockers, calcium-channel blockers, long-acting nitrates, aspirin and statins

It is extremely important to differentiate stable angina from ACS – acute coronary syndrome (unstable angina, NSTEMI and STEMI) – whereby there is an acute narrowing or complete occlusion of the coronary artery due to blood clot – as the treatment is very different. Acute coronary syndrome results in infarction (and death) of myocardial tissue, not just ischaemia. However, the presenting symptom – chest pain – often feels identical to that of ACS – as the mechanism of the pain is essentially the same – lack of oxygen to the heart muscle. 

Epidemiology and Aetiology

  • Prevalence of about 3%
  • This is lower than some other manifestations of cardiovascular disease – such as peripheral vascular disease – which is about 10%

The risk factors are the same as for all manifestations of cardiovascular disease:

Typical presentation

  • Central or left sided chest discomfort
    • May radiate to the jaw, arm epigastrium – like ACS pain
  • Can vary from mild to severe
  • Usually described as a “tight” or “crushing” sensation
  • Dyspnoea may or may not be present
  • Usually results from exertion
  • Symptoms relieved by rest
  • Symptoms typically of several minutes duration – shorter acting symptoms of a few seconds only are unlikely to be ischaemia related
  • Patient may get frequent symptoms (several times daily) or only rarely (months between episodes)
    • This does not necessarily correspond to the severity of the disease
  • Crescendo angina is said to occur when attacks are increasing in frequency and / or severity and is correlated to high risk of severe ACS
  • Any changes to a patient’s usual pattern of symptoms should be considered a significant risk for ACS and investigated as such

Differentiating angina and ACS

  • If the pain doesn’t resolve within 5 minutes of cessation of activity, and/or with use of GTN spray, treat as ACS
  • Angina is typically exertional
  • Suspicion of ACS should be increased if the symptoms have occurred at rest

MI causes permanent heart muscle damage (infarct), stable angina does not. They have similar symptoms, although the pain of MI is often greater than angina. Any diagnosis of sudden onset chest pain should be treated as ACS until proven otherwise (unless the pain does resolve as above and the patient already has a diagnosis of stable angina).

Causes

  • Atheroma seen in coronary artery disease – this accounts for the vast majority of cases
  • Aortic valve disease
  • Hypertrophic cardiomyopathy

Classifying causes by oxygen supply and demand

  • Oxygen demand factors – heart rate, blood pressure, left ventricular hypertrophy (more muscle to supply!), valve disease – e.g. aortic stenosis – so the heart has to work harder to pump
  • Oxygen supply – duration of diastole (needs to be long enough to allow sufficient blood to flow to the heart), coronary vasomotor tone, haemoglobin levels, oxygen saturation.

People normally experience angina as exertional chest pain that is relieved by rest.
People may also experience myocardial ischaemia as shortness of breath or without symptoms (silent ischaemia)

Other precipitating factors

  • Cold weather
  • Heavy meals
  • Intense emotion

Diagnosing Stable Angina

Diagnosing stable angina can be quite tricky. There are several aspects:

  • Ruling out other causes of chest pain – particularly ACS
  • Assessing the history as being “typical” for stable angina, with ECG
    • ECG might be normal, but changes can include:
      • Pathological Q waves
      • ST depression
      • LBBB
      • T-wave flattening or inversion
  • Confirming the diagnosis with imaging
    • Usually CT coronary angiogram (CTCA) is the first line investigation
    • Consider stress echo or myocardial perfusion scan if this is not available or appropriate
    • Depending on the severity of the disease detected, patients may be offered angiogram
    • If very high clinical suspicion you can refer to cardiology without imaging – start treatment first
    • If low clinical suspicion – consider stress test (ECG or Echo) +/- other cardiac imaging (e.g. CTCA, myocardial perfusion scan) to confirm the diagnosis before referral

Typical History

  • Chest Pain –  is ‘tight’, heavy’, or ‘gripping’.
    • The pain is usually felt behind the sternum and can radiate to the neck, jaw, arms, and sometimes back.
  • Shortness of breath (SOB)
  • Both pain and SOB brought on by exertion, and relieved by rest
  • Symptoms typically last several minutes after the precipitating event has stopped (e.g. exercise or stress)
  • Classically relieved by GTN

The likelihood of a diagnosis of angina increases when there are risk factors for cardiovascular disease present:

Investigations

Below is an outline of the investigations that may be used in the work-up of stable angina.

  • ECGwill often be normal – a normal ECG does not exclude a diagnosis of angina or ACS! If performed during an episode of angina (e.g. during an exercise tolerance test – aka stress test) then typical changes on an ECG might include:
    • ST-depression
    • Ventricular ectopic beats
    • Bundle branch abnormalities – mainly LBBB
  • CXR
    • Useful to look for other causes of chest pain (e.g. pneumonia, pneumothorax)
    • May shown signs of heart failure, which may be associated with severe coronary artery disease
  • ETT – Exercise tolerance test – aka exersize stress test. Can be ECG or echo after exercise stress.
    • Assess for symptoms and ECG changes when the heart is stressed
    • Exercise increases cardiac load and can provoke myocardial ischaemia – which manifests as chest pain, dyspnoea and ECG changes
    • Has sensitivity of about 90% but a specificity of only about 70%
    • ECG based ETT should not be used for a diagnosis of stable angina, and is more commonly used after a single acute episode of chest pain to rule out coronary artery disease
    • Stress echo is a variation of the stress test which can be used to diagnose stable angina (see below)
  • CTCA
    • Recommended by NICE is the primary diagnostic investigation
    • A type of high resolution CT scan, with contrast – injected through a peripheral cannula
    • non-invasive test
    • Typically takes about 10-15 seconds. Scan conducted whilst patient holds their breath
    • The contrast fills the coronary arteries and can indicate where they are narrowed
    • Has a very good negative predictive value for cardiovascular disease
    • Not as sensitive as coronary angiogram – (see below) – whereby the contrast is injected directly into the coronary vessels through a cardiac catheter. 
  • MPS – myocardial perfusion scan
    • An alternative to CTCA
    • Is a type of stress test – shows blood flow to different areas of the heart during exercise
    • Reduced blood flow to any given area can indicate vessel blockage in the vessel associated with that particular area of the heart
    • Does NOT directly visualise the arteries
    • It is a nuclear medicine scan – typically using technetium
    • Results are reported as a “risk stratification” – coronary artery disease, normal, or equivocal
    • If equivocal – will need other form of imaging to assess if CAD is present
  • Echocardiograph – may be considered to establish the level of left ventricular function
    • Can either be performed at rest, or as a stress test
    • Echo gives information about left ventricular function and ventricular and atrial wall motion defects
      • Wall motion defects at rest are due to previous MI
      • On stress test, stress-induced ischaemia may show similar, reversible changes
    • Stress echo is an echo performed immediately after exercise stress (i.e. within seconds). It can assess for “dynamic” (i.e. they ‘come-and-go’) contraction changes. Particularly useful in stable angina, when a resting echo may be normal, but a stress echo shows changes of ischaemia.
    • Stress echo provides similar risk stratification to MPS – i.e. it can tell if coronary artery disease is “present” or “absent” but not the location and degree of the abnormality
    • Pharmacological stress testing can be performed in individuals who cannot exercise. In this instance, medication is given to increase cardiac output – placing similar stresses on the heart as exercise.
    • Left-ventricular ejection fraction (LVEF) (at rest) is a strong predictor of long-term outcome
      • LVEF >50% – 12 year survival = 75%
      • LVEF 35-49% – 12 year survival = 55%
      • LVEF <35% – 12 year survival = 21%
  • Angiogram – is the most accurate diagnostic test for coronary artery disease (and therefore for stable angina), But it is relatively expensive, and not without risk, and not necessary for the diagnosis.
    • An invasive test – requires the insertion of a cardiac catheter
    • This gives exact information on the level of narrowing of the coronary arteries, and which vessels are affected. It is particularly useful to help determine if revascularisation is necessary. With medical treatment only (without revascularisation), 12-year survival rates are:
      • Single vessel disease – 75%
      • Two vessel disease – 59%
      • Triple vessel disease – 50%
    • Its main indication is to assess the extent of coronary artery lesions when revascularisation therapies (e.g. stenting (PCI) or bypass) are being considered. As such it is typically reserved for the most symptomatic patients, although its use is increasing.
    • Coronary artery narrowing is considered significant when the luminal diameter is reduced by >70%
    • In particular, proximal narrowing of the left main coronary artery and the left anterior descending artery is associated with a poor prognosis.
    • The preferred test when the patient already has known coronary artery disease and the clinician wants to assess the extent of the disease
  • Blood tests – for screening of risk factors – cholesterol, fasting glucose

Canadian Cardiovascular Society Angina Classification

This is sometimes used to class the severity of Angina from I-IV. It is very similar to the NYHA classification of Heart Failure

  • Class I – ‘Ordinary Activity’ (e.g. walking or climbing stairs) does not precipitate angina
  • Class II – Angina precipitated by walking upstairs, cold weather, or meals
  • Class III – marked limitation of normal physical activity
  • Class IV – Symptoms present at rest, unable to carry out many normal physical activities

Risk Stratification

The presence of angina indicates underlying coronary artery disease. The next step is to evaluate the severity of this underlying cardiac disease, for the purposes of assessing future risk of myocardial infarction – and in particular whether or not revascularisation (e.g. coronary artery stenting, or coronary artery bypass graft – CABG) is indicated. Prognostic indicators include:

  • Left ventricular function
  • Stress testing (e.g. treadmill or pharmacological stress test)
  • Coronary artery disease extent as seen on angiogram
  • Age
  • Diabetes
  • Hypertension
  • Hypercholesterolaemia
  • Heart failure

Prognosis

  • If stable angina is present, without history of MI, and with normal resting ECG and normal BP, then annual mortality is about 1.5%
  • If risk factors are present, then annual mortality greatly increases:
    • Abnormal ECG – 8.4%
    • Hypertension – 7.5%
    • Both – 12%
    • T2DM – quoted risks (above) – doubled

Management of stable Angina

This can be divided into lifestyle modifications, pharmacological interventions, and revascularisation. 

Lifestyle

  • Diet advice – plant-based whole foods diet (e.g. mediterranean diet) has been shown to improve long term outcomes
  • Smoking cessation
    • After 2 years, risk of MI is same as for those who have never smoked
  • Control hypertension
  • Treat hyperlipidaemia – start statin regardless of cholesterol levels
  • Alcohol – within safe drinking limits
    • No more than 2 standard drinks on any single day, and two days per week with no alcohol intake
  • Weight – aim for BMI <=25
  • Regular exercise – 150 minutes per week of moderate intensity exercise – reduces cardiovascular risk regardless of weight loss, by up to 30%

Pharmacological

There are two main mechanisms used to relieve the symptoms of angina:

  • Increasing blood flow to the heart muscle (by dilating coronary arteries) – e.g. wth GTN (Glycerytrinitrate)
  • Decreasing the workload on the heart (e.g. with beta-blocker or calcium channel blocker long term)

First line treatment

  • Beta-blocker (e.g. atenolol or metoprolol)
    • Proven to reduce MI and sudden death risk
    • Decreases heart rate, contractility, and cardiac output – which reduces cardiac O2 demand
    • e.g. metoprolol 25mg BD
  • Calcium channel blocker (e.g. verapamil, diltiazem)
    • These two agents are preferred due to their negative chronotropic events
    • Typically reserved for patients who are unable to tolerate beta-blockers or whose symptoms are incompletely controlled with beta-blockers
    • e.g. verapamil 120mg OD
  • Nitrates
    • Patients will also likely carry GTN spray or pills with them at all times to relieve acute episodes.
    • Nitrates cause vasodilation
    • Can cause hypotension
    • Provide quick relief – within a couple of minutes, and lasts for up to 30 minutes
    • e.g. GTN sublingual spray 400mcg – repeat every 5 minutes as required
      • GTN sublingual tablets 300mcg are also available
  • Aspirin (or another anti platelet drug – such as clopidogrel or ticagrelor)
    • Reduced the risk of thrombus formation and thus ACS
    • e.g. aspirin 100mg daily

Second line treatment

Consider adding…

  • Long acting nitrate
    • e.g. isosorbide mononitritae 30mg PO OD – up to a max of 120mg daily
    • Typically effect lasts for 4-6 hours
  • Nicorandil
  • Ivabradine
  • Ranolazine

Third line treatment

  • Consider PCI (cardiac stent, balloon angioplasty)
    • Typically both balloon angioplasty and stenting are performed simultaneously
    • The procedure carries a 1-3% mortality, and 5% risk of MI
    • There is no evidence that angioplasty (+/- stent) improves survival or reduces risk of ACS. It may however reduce symptoms of stable angina
  • CABG – Coronary arty bypass graft
    • Similar risks as PCI (above)
    • Completely eliminates symptoms in about 85% of patients
    • Does not appear to improve survival for those with class I or II disease (see above)
    • Modest improvement in survival for those with left main coronary artery disease or triple vessel disease
    • Patients with T2DM have better outcomes with CABG than PCI

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