Stable angina and chronic coronary syndrome

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Stable angina is predictable myocardial ischaemia without acute plaque rupture. The syndrome is clinical, but objective testing identifies obstructive coronary disease, alternative causes and prognostically important anatomy.

Management has two parallel aims: relieve ischaemic symptoms and reduce future cardiovascular events. Antianginals improve symptoms; aspirin, lipid lowering and risk-factor treatment address events.

Microvascular or vasospastic angina remains possible when epicardial flow-limiting disease is excluded; this needs specialist phenotyping rather than a label of non-cardiac pain.

Key points

Typical angina has all three NICE features: constricting discomfort in the chest/neck/shoulders/jaw/arms, precipitation by exertion, and relief by rest or GTN within about 5 minutes; two features is atypical and zero or one is non-anginal.
For new typical or atypical stable chest pain, NICE first-line anatomical testing is 64-slice-or-above CT coronary angiography; do not use exercise ECG to diagnose or exclude angina in someone without known CAD.
Give a short-acting nitrate and a written action plan: repeat after 5 minutes; if pain remains 5 minutes after the second dose, call an ambulance.
First-line regular symptom treatment is either a beta-blocker or calcium-channel blocker; review in 2–4 weeks and titrate to the maximum tolerated dose.
If combining a beta-blocker with a calcium-channel blocker, choose a dihydropyridine such as amlodipine, felodipine or modified-release nifedipine, not verapamil or diltiazem.
Consider aspirin 75 mg daily after individual bleeding assessment, offer high-intensity statin therapy for established CVD, and treat smoking, blood pressure, diabetes, activity and diet.
Long-acting nitrate, ivabradine, nicorandil or ranolazine are NICE alternatives when both first-line classes are contraindicated or not tolerated, or selected add-ons when the other first-line class cannot be used.
Offer angiography and discuss PCI or CABG when symptoms remain uncontrolled on optimal medical therapy; do not simply add a third antianginal except while awaiting revascularisation or when revascularisation is inappropriate or declined.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Fixed epicardial atherosclerotic disease

Fixed epicardial atherosclerotic narrowing reduces vasodilator reserve, so flow may not increase adequately when myocardial oxygen demand rises.

Coronary microvascular dysfunction

Impaired regulation of small coronary vessels can limit myocardial perfusion despite no flow-limiting epicardial stenosis, producing exertional symptoms that require specialist phenotyping.

Vasospastic disease

Transient epicardial or microvascular constriction reduces coronary supply, often producing variable or rest symptoms rather than the consistently predictable pattern of fixed obstruction.

Supply-demand modifiers

Anaemia, tachyarrhythmia, uncontrolled pressure or important aortic valve disease can lower the ischaemic threshold by reducing oxygen supply or increasing cardiac workload.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Coronary supply becomes constrained
Fixed narrowing or microvascular dysfunction reduces flow reserve, while episodic epicardial or microvascular spasm can constrain supply even when baseline flow is adequate.
2
Demand rises or supply falls
Exertion or emotional stress raises heart rate, contractility and wall tension, while epicardial or microvascular spasm can reduce supply even at rest. Either can exceed the flow available through the affected circulation.
3
Reversible ischaemia develops
Affected myocardium becomes underperfused, often first in the subendocardium during demand-related ischaemia, impairing function and generating metabolites that produce chest discomfort or breathlessness.
4
The trigger settles
When workload falls or abnormal vascular tone resolves, oxygen supply and demand rebalance and symptoms settle. Stable episodes do not usually produce sustained myocyte necrosis or a dynamic troponin rise.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical pattern

Central or radiating constricting pressure reliably brought on by exertion or emotional stress and settling with rest or GTN within about 5 minutes.

Associated clues

Dyspnoea may be an anginal equivalent. Smoking, diabetes, hypertension, dyslipidaemia, established vascular disease, previous MI or revascularisation increase likelihood.

Acute coronary syndromeRed flag

Pain at rest, abrupt crescendo symptoms, episodes lasting over 15 minutes, diaphoresis, vomiting, breathlessness or haemodynamic instability require an ACS pathway.

Dangerous mimicsRed flag

Consider aortic dissection, pulmonary embolism, pneumothorax, severe aortic stenosis and hypertrophic cardiomyopathy; severe tearing pain, pulse deficit, hypoxia, syncope or a harsh murmur changes the pathway.

A normal ECG is not reassuring enough

Resting ECG can be normal in stable angina and ACS. Never use nitrate response alone to make or exclude the diagnosis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate history, examination and 12-lead ECGFirst step
Why
Classify typicality, identify ACS or an alternative cardiac diagnosis, and record baseline conduction/rhythm before rate-limiting treatment.
Interpretation and limitations
ST elevation/depression, dynamic T-wave change, pathological Q waves or instability moves the patient to an acute pathway; a normal trace does not exclude ischaemia.
02
Blood tests: FBC, U&E/eGFR, liver profile, HbA1c, fasting or non-fasting lipid profile
Why
Find anaemia or metabolic triggers, quantify risk, and establish safe prescribing baselines.
Interpretation and limitations
Correct exacerbating anaemia and use renal/hepatic function to select and dose antianginals; record pretreatment lipids before high-intensity statin.
03
CT coronary angiographyFirst line
Why
NICE first-line test for typical/atypical angina, or non-anginal pain with resting ST-T changes or Q waves.
Interpretation and limitations
Significant CAD is generally at least 70% stenosis in a major epicardial segment or at least 50% left-main stenosis; indeterminate or uncertain functional significance needs functional testing.
04
Non-invasive functional imaging
Why
Demonstrate inducible ischaemia when CT is non-diagnostic or shows CAD of uncertain significance; also used in known CAD when symptom attribution is uncertain.
Interpretation and limitations
Reversible perfusion or wall-motion abnormality supports angina and helps define ischaemic burden. Modalities include stress echo, stress CMR or myocardial perfusion SPECT.
05
Invasive coronary angiography
Why
Third-line diagnostic test when non-invasive tests are inconclusive and the result will change treatment, or when planning revascularisation for uncontrolled symptoms/prognostic anatomy.
Interpretation and limitations
Use physiology and anatomy with the patient and multidisciplinary team to choose medical therapy, PCI or CABG.
06
Echocardiography when indicated
Why
Assess LV function, valve disease or cardiomyopathy when examination, ECG, breathlessness or prior infarction suggests structural disease.
Interpretation and limitations
Reduced LVEF or severe aortic stenosis changes drug choice, prognosis and referral urgency.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute coronary syndrome

New rest pain, crescendo frequency, prolonged episodes, autonomic symptoms or dynamic ECG and troponin change indicate an acute pathway rather than stable angina.

Oesophageal reflux or spasm

Burning discomfort related to meals, regurgitation or recumbency supports an oesophageal cause, but nitrate response is non-specific and cannot safely exclude cardiac ischaemia.

Musculoskeletal chest pain

Focal pain reproducible with palpation, arm movement or trunk rotation favours a chest-wall source, although reproducibility does not completely remove cardiovascular risk.

Pulmonary embolism

Sudden pleuritic pain, unexplained dyspnoea, hypoxaemia or unilateral deep-vein signs favour embolism and require probability-led urgent assessment through an established diagnostic pathway.

Aortic stenosis or hypertrophic cardiomyopathy

Exertional pain with syncope, a characteristic systolic murmur or structural abnormalities suggests outflow obstruction, which changes risk assessment and treatment selection.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01InitialLikely stable angina while testing proceedsFirst stepPredictable stable symptoms without ACS red flags.

1Explain the diagnosis and emergency action plan; supply short-acting GTN and demonstrate use.
2Consider aspirin 75 mg once daily after allergy, bleeding and comorbidity assessment; offer atorvastatin 80 mg once daily for established CVD unless interactions, adverse-effect risk or preference justify a lower dose.
3Offer either a beta-blocker or a calcium-channel blocker, taking account of comorbidity, contraindications and preference.
4Address smoking, BP, diabetes, weight, activity and cardiac rehabilitation-style education; do not use supplements as event-prevention therapy.

02ReviewTitrate or switch antianginal therapyReview 2–4 weeks after starting or changing treatment.

1First lineAssess attack frequency, GTN use, function, pulse, BP and adverse effects; titrate the chosen first-line medicine to the maximum tolerated dose.
2First lineIf symptoms remain uncontrolled, switch to the other first-line class or combine them; with a beta-blocker use a dihydropyridine calcium-channel blocker.
3First lineIf both first-line classes are contraindicated or not tolerated, use one of long-acting nitrate, ivabradine, nicorandil or ranolazine as monotherapy; if one first-line class is inadequate and the other cannot be used, add one of these agents.
4Do not routinely add a third antianginal when symptoms are controlled on two agents.

03EscalationRevascularisation assessmentEscalationSymptoms remain uncontrolled despite optimal medical treatment, or prognostically important left-main/proximal multivessel disease is suspected.

1Offer coronary angiography and discuss the benefits, limitations and risks of continuing medical therapy, PCI and CABG.
2Base PCI versus CABG on coronary anatomy, comorbidity, procedural risk and preference; use multidisciplinary review when strategy is unclear.
3Explain that CABG may offer a survival advantage over PCI in some people with multivessel disease, especially with diabetes, age over 65 years, or complex three-vessel/left-main anatomy.
4A third antianginal is reserved for symptoms while awaiting revascularisation or when revascularisation is inappropriate or declined.

04EmergencyPain does not follow the stable patternRest/crescendo/prolonged pain, instability, or pain persisting after two nitrate doses.

1Stop exertion, sit down and take the prescribed short-acting nitrate.
2Repeat after 5 minutes; call an ambulance if pain is still present 5 minutes after the second dose.
3Use the NICE acute chest-pain/ACS pathway, including urgent ECG and troponin; do not delay transfer for diagnostic testing.

Key medicines and prescribing safety8 treatments · regimens, roles and cautions

Immediate relief and short-term prophylaxis.

Glyceryl trinitrate sublingual spray — licensed product example

400 micrograms (1 spray) under the tongue at onset; a second dose after 5 minutes under the NICE action plan. The cited SmPC permits 1–2 sprays and repeat at 5-minute intervals up to 3 sprays (1.2 mg) in 15 minutes, but the patient must call an ambulance if pain remains 5 minutes after the second dose. For prevention, 1–2 sprays 2–3 minutes before a predictable trigger.

Sit down before dosing. Avoid with PDE5 inhibitors or riociguat; caution hypotension, hypovolaemia, severe aortic stenosis and hypertrophic obstructive cardiomyopathy. Headache and dizziness are common.

First-line rate-limiting antianginal.

Bisoprolol — licensed stable-angina example

Start 5 mg by mouth once daily; usual 10 mg once daily; maximum 20 mg once daily, titrated to symptoms, pulse and BP.

Avoid unpaced second/third-degree AV block, marked bradycardia, cardiogenic shock or acute decompensated HF; use caution in asthma/COPD and peripheral vascular disease. Do not stop abruptly.

First-line alternative or the preferred calcium-channel blocker to combine with a beta-blocker.

Amlodipine — licensed chronic stable-angina example

5 mg by mouth once daily, increasing to 10 mg once daily if needed and tolerated.

Monitor oedema, flushing, headache and BP. It does not provide rapid attack relief.

Consider for secondary event prevention in stable angina.

Aspirin — NICE recommendation, licensed antiplatelet dose

75 mg by mouth once daily when the individual bleeding balance supports use.

Not universal: assess active ulcer/bleeding, aspirin hypersensitivity, interacting anticoagulants and anaemia; use an alternative antiplatelet only for a defined indication and guideline pathway.

Secondary prevention, not symptom relief.

Atorvastatin — NICE high-intensity CVD recommendation

80 mg by mouth once daily; use a lower dose when interactions, high adverse-effect risk or patient preference requires it.

Check baseline lipids, liver transaminases and interactions; investigate unexplained muscle pain or weakness. NICE secondary-prevention targets are LDL cholesterol 2.0 mmol/L or less, or non-HDL cholesterol 2.6 mmol/L or less.

Alternative/add-on when first-line therapy is unsuitable or inadequate; little effect on pulse or BP.

Ranolazine prolonged release — licensed add-on example

375 mg by mouth twice daily; after 2–4 weeks increase to 500 mg twice daily and, according to response, to a maximum 750 mg twice daily.

Contraindicated when creatinine clearance is below 30 mL/min, in moderate/severe hepatic impairment, or with potent CYP3A4 inhibitors. Check interactions and QT risk; reduce or stop for dizziness, nausea or vomiting.

Second-line alternative/add-on in selected patients.

Ivabradine — licensed antianginal example with MHRA restrictions

Start 5 mg by mouth twice daily only in sinus rhythm with resting heart rate at least 70 beats/min; maximum 7.5 mg twice daily.

Do not combine with verapamil, diltiazem or strong CYP3A4 inhibitors. Monitor for atrial fibrillation and symptomatic bradycardia; reduce if heart rate is below 50 or symptoms occur and stop if persistent. Reconsider if little/no symptom improvement after 3 months.

Second-line alternative/add-on only when first-line antianginals are insufficient or unsuitable.

Nicorandil — licensed example; MHRA second-line restriction

Usually start 10 mg by mouth twice daily (5 mg twice daily if headache-prone), commonly titrated to 20 mg twice daily; maximum 40 mg twice daily.

Stop if any skin, mucosal, ocular or gastrointestinal ulceration occurs because perforation, fistula and bleeding can follow. Avoid with PDE5 inhibitors/riociguat, hypovolaemia or acute pulmonary oedema; monitor BP and potassium, especially with renal impairment or potassium-raising drugs.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute coronary syndrome and infarction

When coronary atherosclerosis is present, plaque disruption and thrombosis can convert a predictable chronic syndrome into rest ischaemia or myocardial infarction.

Ischaemic ventricular dysfunction

Repeated or extensive ischaemia and previous silent or recognised infarction can impair ventricular function, leading to exertional breathlessness, congestion and chronic heart failure.

Arrhythmia and sudden cardiac death

Ischaemia or established myocardial scar can destabilise ventricular electrical activity, while associated atrial disease may add tachyarrhythmia and worsen symptom control.

Functional and psychological limitation

Fear of attacks and predictable exertional symptoms can restrict activity, work and social participation, promoting deconditioning and reduced quality of life even without infarction.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review symptoms, function, adherence and adverse effects 2–4 weeks after each antianginal start or dose change.
Record pulse and BP before and during beta-blocker or rate-limiting calcium-channel blocker titration; obtain ECG if bradycardia, syncope or conduction disease is suspected.
Check lipid profile and liver transaminases 2–3 months after starting or changing lipid-lowering therapy, then lipids annually once stable.
Track attack frequency and GTN use; a new rest pattern, longer episodes or declining exercise threshold requires urgent reassessment for ACS.
For ranolazine review eGFR, hepatic function, QT-prolonging/CYP3A4 interactions and treatment-related dizziness or nausea.
For ivabradine confirm sinus rhythm and resting heart rate before initiation and after dose changes; monitor for atrial fibrillation.
After revascularisation continue risk-factor treatment and reassess whether antianginals can be reduced; PCI/CABG does not remove the need for secondary prevention.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

GTN response is not diagnostic

Oesophageal spasm and other causes may improve with nitrates, while ACS may temporarily settle. Use the clinical pattern, ECG and troponin pathway.

Anatomy versus physiology

CTCA finds atherosclerotic anatomy; stress imaging shows inducible ischaemia. A moderate anatomical lesion is not automatically the cause of pain.

Combination safety

Beta-blocker plus verapamil or diltiazem can cause severe bradycardia, AV block or HF; a dihydropyridine is the safer NICE combination.

Antianginals do not all improve prognosis

Their principal purpose is symptom control. Lipid lowering, antiplatelet treatment when appropriate and risk-factor modification provide event prevention.

Think beyond obstructive CAD

Persistent typical symptoms without flow-limiting epicardial stenosis may represent vasospastic or microvascular angina and merit specialist evaluation.

11Common pitfallsFrequent interpretation and management errors.

01
Calling pain stable when it is new at rest, crescendo or prolonged.
02
Using relief with GTN or a normal resting ECG to exclude ACS.
03
Ordering exercise ECG to diagnose angina in a person without known CAD instead of CTCA.
04
Combining a beta-blocker with verapamil or diltiazem without a compelling specialist plan.
05
Escalating to three antianginals without discussing angiography/revascularisation when symptoms remain limiting.