Managing stable angina in primary care

How to manage angina and when to refer as an emergency. By Dr Vinoda Sharma and consultant cardiologist Dr Robert Henderson.

A resting ECG should be recorded
A resting ECG should be recorded

Section 1: Epidemiology and aetiology

Angina is a symptom of myocardial ischaemia, triggered by a temporary imbalance in myocardial oxygen supply and demand.

The underlying pathological process is usually atherosclerotic coronary artery disease (CAD), which remains the most important cause of premature mortality in the UK, accounting for one in four of all deaths.1 Risk factors for the development of CAD include smoking, hypercholesterolaemia, hypertension and diabetes mellitus.

It is estimated that nearly two million people in England have or have had angina. The prevalence increases with age. The condition affects 14% of men and 8% of women aged 65-74 years.1 Angina has a significant impact on quality of life, which deteriorates as symptoms worsen.

Precipitating factors
Stable angina occurs predictably with physical activity, excitement or emotional stress, but can also occur with changes in posture (decubitus angina) or can wake people from sleep (nocturnal angina). It may be more likely to occur after a heavy meal or during exposure to cold.

Other precipitants include anaemia, fever, thyrotoxicosis and the use of cocaine.

Angina associated with myocardial ischaemia on functional testing can also occur in people with normal epicardial coronaries (syndrome X).

The Canadian Cardiovascular Society classifies angina according to the intensity of activity that precipitates symptoms (table 1).

The NICE guideline, CG95,2 defines typical angina as:

  • Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms.
  • Brought on by physical exertion.
  • Relieved by rest or sublingual glyceryl trinitrate within about five minutes.

If two of these three features are present, the symptoms are considered to be atypical angina. If one or none of these features is present, the patient has non-anginal pain.

Table 1: Canadian Cardiovascular Society
classification of angina
Class 0 Asymptomatic
Class I Angina only during strenuous or prolonged physical activity
Class II  Slight limitation, with angina only during vigorous physical activity
Class III Symptoms with everyday living activities, that is, moderate limitation
Class IV  Inability to perform any activity without angina or angina at
rest, that is, severe limitation

Section 2: Making the diagnosis

When patients present with chest pain of suspected cardiac origin, it is important to exclude acute coronary syndrome (MI or unstable angina). The likelihood of acute coronary syndrome is increased in patients with:

  • Pain for more than 15 minutes.
  • New onset pain or abrupt deterioration in stable symptoms.
  • Pain with nausea and vomiting, diaphoresis, breathlessness or haemodynamic instability.

Patients with suspected acute coronary syndrome should be referred to secondary care urgently if they have chest pain, or had chest pain in the past 12 hours, and a resting 12-lead ECG is abnormal (or unavailable).

Clinicians should take a history that includes the characteristics of the pain, its location, radiation, severity, duration and frequency. Factors that provoke and relieve it, and associated symptoms, should be recorded, as should any history indicating established cardiac disease.

Physical examination is needed to identify signs of non-coronary causes of angina (for example, severe aortic stenosis, cardiomyopathy) and non-cardiac causes of chest pain. A resting 12-lead ECG should be recorded unless stable angina can be confirmed or excluded on the basis of clinical assessment alone.

Blood tests should be done to identify risk factors (blood lipids and blood sugar) and conditions which exacerbate angina, such as anaemia.

A diagnosis of stable angina is unlikely if the chest pain is continuous or prolonged, unrelated to activity, brought on by inspiration, or associated with other symptoms such as dizziness, palpitations, tingling or difficulty swallowing. The clinical assessment and the typicality of symptoms can be used to estimate the likelihood of CAD (see NICE CG95).

Individuals with typical angina on clinical assessment combined with an estimated likelihood of CAD exceeding 90% do not require further diagnostic investigation and should be managed as stable angina.

Patients with typical or atypical angina and an estimated CAD risk of 10-90% generally require further tests in secondary care.

Patients with an estimated CAD likelihood of 10-29% should be offered CT calcium scoring, if available, to determine the need for additional investigation. Patients with an estimated CAD likelihood of 30-60% should be offered functional imaging. If the estimated likelihood is 61-90%, invasive coronary angiography is generally recommended.

A diagnosis of stable angina can be confirmed when significant CAD is found during CT or invasive coronary angiography and/or reversible myocardial ischaemia is found during non-invasive functional imaging.

Section 3: Managing the condition

Patients with stable angina may benefit from lifestyle adjustments and should be advised on smoking cessation, weight loss and exercise.

Drugs are prescribed to relieve and prevent attacks of angina and to reduce cardiovascular risk (secondary prevention). Myocardial revascularisation may be appropriate in patients whose symptoms are not controlled by medication.

Left coronary arteriography shows severe stenosis in the proximal left anterior descending artery

Patients with stable angina should be offered a short-acting nitrate to treat episodes of angina and for prophylaxis before activities that provoke it.

They should be advised how to use the short-acting nitrate and warned that it may cause headache. Glyceryl trinitrate tablets may lose efficacy over time. Some patients prefer to use glyceryl trinitrate spray.

Beta-blockers or calcium-channel blockers are recommended as first-line treatment to prevent angina. Both reduce myocardial oxygen demand and prevent angina but there is no evidence that they confer a prognostic advantage in patients with stable angina.3,4 The choice of drug depends on contraindications, patient tolerance and preference.

If a single first-line drug is not effective or is not tolerated, the alternative drug class or a combination of the two drug classes can be tried. Rate-limiting calcium-channel blockers (diltiazem and verapamil) should not be combined with a beta-blocker. Dihydropyridine calcium-channel blockers (for example, amlodipine, felodipine) do not lower heart rate and can be used safely in combination with a beta-blocker.

If first-line antianginal therapy does not control the symptoms, one of the following second-line agents can be prescribed.4

- Long-acting nitrates are widely used, but evidence of efficacy in patients with stable angina is limited. Continuous treatment is limited by tolerance and may cause sympathetic activation and endothelial dysfunction.5

- Ivabradine lowers heart rate by inhibiting the pacemaker (If) current in cells of the sinoatrial node. It is effective alone or in combination with other drugs, but may cause visual disturbance.

- Nicorandil dilates systemic veins and epicardial coronary arteries. Nicorandil is an effective antianginal but its use is complicated by headache and GI ulceration.

- Ranolazine acts by inhibiting the late sodium current (INa) in ventricular myocytes and has been shown to have incremental antianginal efficacy when added to standard antianginals.

Secondary prevention
In patients with stable angina, low-dose aspirin reduces the risk of non-fatal MI and vascular events, but has not been shown to reduce the risk of fatal events. Moreover, aspirin is associated with a risk of bleeding and clinicians should balance the risks and benefits of treatment when considering its prescription.

All patients with stable angina should be offered a statin to lower cholesterol and reduce cardiovascular risk. ACE inhibitors should be continued if they are prescribed for other conditions, such as hypertension or heart failure, and may be beneficial in patients with diabetes and stable angina. NICE guidance defines optimal medical therapy (OMT) as one or two antianginals plus medication for secondary prevention of CAD.4,6

Invasive management
Patients with stable angina whose symptoms persist despite OMT should be offered invasive angiography, provided they are candidates for myocardial revascularisation.4,6

Myocardial revascularisation with percutaneous coronary intervention (PCI) or CABG improves symptoms when compared with medical therapy alone, but the effects of myocardial revascularisation on prognosis are controversial.

Treatment decisions for patients with stable angina and multivessel CAD are often complex and have a limited evidence base. Patients must be considered by a multidisciplinary team with the objective of defining the most appropriate treatment.

Section 4: Prognosis

Patients who have been diagnosed with stable angina generally have a good prognosis.

A systematic review of cohort studies of angina in primary care estimated all-cause mortality rates of 2.8-6.6% per year and cardiovascular mortality rates of 1.4-6.5% per year.7

Lower annual mortality rates have been reported in RCTs of patients with stable angina.8

Factors including older age, diabetes mellitus, hypertension, male gender and previous MI are associated with a worse prognosis in patients with stable angina.9

Section: 5 Case study

A 55-year-old male patient with a history of hypertension presented to his GP with intermittent tight pain across the upper chest.

The pain occurred with activity, but settled with rest within a few minutes. He had not experienced prolonged episodes of chest pain or chest pain at rest.

The patient's cardiovascular risk factors included smoking and hypertension. He had a BMI of 29.

He had been taking amlodipine 10mg, ramipril 10mg and bendroflumethiazide 2.5mg once daily for five years for hypertension.

The GP diagnosed typical angina and started the patient on bisoprolol 1.25mg once daily and glyceryl trinitrate spray as required, to relieve the acute episodes.

The patient's symptoms continued, so the dose of bisoprolol was increased to 2.5mg once daily. His GP referred him to the rapid access chest pain clinic (RACPC) for further assessment.

Rapid access clinic
In the RACPC, the diagnosis of typical angina was confirmed. The patient's estimated likelihood of CAD exceeded 80% (55-year-old male with typical angina symptoms with one risk factor).

The bisoprolol was increased to 5mg once daily and aspirin 75mg once daily and simvastatin 40mg were prescribed. He was advised to stop smoking and change his diet.

Invasive coronary angiography with a view to revascularisation was offered to confirm the diagnosis and because of continuing symptoms.

Coronary angiography showed a tight proximal left anterior descending artery stenosis, which was treated by implanting a drug-eluting stent.

His symptoms were relieved by the procedure and his exercise tolerance has returned to normal. He was prescribed aspirin and clopidogrel for one year to reduce the risk of stent thrombosis and he continues on simvastatin and the other antihypertensives, but is no longer on bisoprolol. He followed the lifestyle advice.

Section 6: Evidence base

Clinical trials

  • A systematic review pooled individual patient data from seven trials comparing CABG versus initial medical therapy in patients with stable angina.

    This analysis provides the best evidence that CABG improves survival in patients with stable CAD, but the trials in the review were conducted before effective secondary prevention treatments were available and the relevance to contemporary practice is therefore uncertain.10
  • A meta-analysis pooled individual patient data from 10 trials that compared initial treatment of PCI versus CABG in 7,812 patients with stable multivessel disease. Overall mortality at follow-up was no different between patients assigned to revascularisation by PCI or by CABG. In subgroup analyses, CABG conferred a survival advantage relative to PCI in patients with diabetes and aged over 65 years.11
  • The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial randomised 2,287 patients to PCI with OMT or to OMT alone. The combined endpoint of all-cause death or non-fatal MI did not differ between the two groups, but PCI with OMT reduced the prevalence of angina during follow-up compared with OMT alone.12

COURAGE has been criticised because patients may have been at low risk so less likely to gain a prognostic advantage from revascularisation. The trial does suggest that many patients who undergo PCI will not live longer as a result.

  •  The Synergy between PCI with Taxus and Cardiac Surgery (SYNTAX) trial randomised 1,800 patients with three vessel or left main stem disease to PCI or CABG. After three years there was no difference in the combined endpoint of death, stroke or MI between the groups, but subgroup analyses showed higher rates of adverse cardiovascular events and mortality in patients with complex coronary anatomy who had PCI.13

NICE guidelines

  • Chest pain of recent onset. London, NICE, 2010.
  •  The management of stable angina. London, NICE, 2011.

These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Audit your patients with stable angina and review whether they were appropriately managed.
  • Organise a cardiology conference in your CCG, to cover topics such as angina.
  • Rehearse how you would manage emergencies, such as acute coronary syndrome, in your practice.
  • Dr Vinoda Sharma, specialist registrar, and Dr Robert Henderson,consultant cardiologist, Nottingham University Hospitals

Reflect on this article and add notes to your CPD organiser on MIMS Learning


1. Fox K, Garcia MA, Ardissino D et al. Eur Heart J 2006; 27: 1341-81.

2. NICE. uk/CG95

3. Huang HL, Fox KA. Scott Med J 2012; 57: 69-75.

4. Henderson RA, O'Flynn N, Guideline Development Group. Heart 2012; 98: 500-7.

5. Gori T, Parker JD. J Am Coll Cardiol 2008; 52: 251-4.

6. NICE. uk/CG126

7. Jones M, Rait G, Falconer J et al. Fam Pract 2006; 23: 520-8.

8. Poole-Wilson PA, Lubsen J, Kirwan BA et al. Lancet 2004; 364: 849-57.

9. Hjemdahl P, Eriksson SV, Held C et al. Heart 2006; 92: 177-82.

10. Yusuf S, Zucker D, Peduzzi P et al. Lancet 1994; 344: 563-70.

11. Hlatky MA, Boothroyd DB, Bravata DM et al. Lancet 2009; 373: 1190-7.

12. Boden WE, O'Rourke RA, Teo KK et al. N Engl J Med 2007; 356: 1503-16.

13. Kappetein AP, Feldman TE, Mack MJ et al. Eur Heart J 2011; 32: 2125-34.

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