stable angina & chronic coronary syndromes
in review
long read
11 min read
Updated 2026-08-10
Contents
stable angina & chronic coronary syndromes
Predictable exertional chest discomfort due to fixed epicardial coronary stenosis. Optimal medical therapy is non-inferior to revascularisation for most stable patients — COURAGE (2007), ISCHEMIA (2020). The role of investigation is to estimate clinical likelihood, risk-stratify, and identify the minority who benefit from revascularisation.
clinical likelihood of CAD
ESC and AHA/ACC have moved away from the Diamond-Forrester model (which substantially overestimated disease probability) to a revised “clinical likelihood” framework incorporating age, sex, symptom typicality, and risk-factor modifiers.
| Clinical likelihood | Action |
|---|---|
| very low (<5%) | defer testing — consider non-cardiac causes |
| low (5–15%) | consider CCTA or CAC (if asymptomatic) to rule out disease |
| intermediate (15–50%) | non-invasive testing indicated — CCTA or functional imaging |
| high (50–85%) | functional imaging preferred (ischaemia quantification guides management) |
| very high (>85%) | may proceed directly to ICA if symptoms refractory or high-risk features |
practical framing
Testing is most useful at intermediate likelihood — it changes management. At very low likelihood, testing generates false positives. At very high likelihood, the question shifts from “is there CAD?” to “does this lesion need revascularisation?“
baseline workup
All chest pain clinic patients, regardless of which downstream test is selected:
- resting 12-lead ECG — prior infarction, LVH, conduction disease; identifies baseline abnormalities (LBBB, paced rhythm, WPW, digoxin effect) that render exercise ECG uninterpretable
- bloods — renal function, glucose/HbA1c, lipid panel, haemoglobin (anaemia lowers anginal threshold); hs-troponin and BNP/NT-proBNP add prognostic information
- resting echocardiography — LVEF (required for all stable CAD), regional wall motion abnormalities, valvular disease (aortic stenosis, HCM as non-atherosclerotic causes); may be omitted in young patients with clear extracardiac cause
ischaemic cascade
With increasing ischaemic duration, abnormalities appear in a predictable sequence:
- perfusion abnormality (seen on myocardial perfusion imaging)
- diastolic dysfunction → systolic dysfunction (wall motion abnormalities)
- ECG changes (ST depression/elevation)
- symptoms (angina)
- myocardial necrosis (troponin release)
exam relevance
This explains why nuclear perfusion imaging is more sensitive than ECG stress testing — it detects the earliest stage of ischaemia. It also explains why “silent ischaemia” (abnormal perfusion/wall motion without symptoms) is real and clinically significant.
choosing the right test
exercise ECG
- graded exercise (Bruce protocol) with continuous ECG, HR, BP monitoring
- requires interpretable resting ECG + ability to achieve ≥5 METs
- useful for symptom reproducibility, functional capacity, haemodynamic response, arrhythmia
- interpretation: positive = horizontal/downsloping ST depression ≥1 mm; Duke Treadmill Score integrates exercise duration + symptoms + ST changes for prognosis
- limitations: modest accuracy (sensitivity ~68%, specificity ~77%); uninterpretable with LBBB, paced rhythm, LVH with ST-T changes, WPW, digoxin; non-diagnostic if target HR not reached
- RBBB is generally interpretable
- guidelines increasingly favour imaging over stand-alone exercise ECG for diagnosing ischaemia
stress imaging
Two components: stressor (exercise or pharmacologic) + imaging (echo, SPECT/PET, CMR).
Exercise preferred when feasible — provides additional prognostic data (METs, duration, BP response). Pharmacologic stress when unable to exercise or with LBBB/paced rhythm.
| Modality | Strengths | Limitations |
|---|---|---|
| stress echo | no radiation; concomitant valve/haemodynamic assessment; detects exercise-induced LVOTO, MR, pulmonary HTN | limited by poor acoustic windows (COPD, obesity) |
| SPECT MPI | widely available; well-validated prognostic data | radiation; lower accuracy than PET; attenuation artefacts (breast, diaphragm) |
| PET MPI | higher accuracy than SPECT; quantitative myocardial blood flow reserve (detects microvascular disease); fewer non-diagnostic results | limited availability; radiation |
| stress CMR | high-resolution perfusion + scar/viability characterisation; no radiation | GFR-dependent (gadolinium); claustrophobia; availability; non-MRI-conditional devices |
when to choose functional over anatomic testing
Functional imaging preferred in patients ≥65, those with known CAD and changed symptoms, and when quantifying ischaemic burden to guide revascularisation decisions. Ischaemia extent/severity directly informs whether to intensify GDMT or proceed to ICA.
CCTA
- contrast-enhanced ECG-gated CT of coronary lumen; requires rate control (beta-blockade) ± sublingual nitroglycerin
- class I first-line anatomic test for intermediate-risk patients with no known CAD
- high sensitivity and NPV → excellent rule-out; moderate specificity/PPV → may overestimate stenosis in calcified vessels
- CT-derived FFR (CT-FFR) can assess haemodynamic significance of intermediate stenoses without invasive angiography
- evidence: DISCHARGE (2022) — initial CCTA strategy in intermediate-probability patients yielded similar CV outcomes to ICA with fewer invasive procedures. Meta-analysis found CCTA reduced downstream MI vs exercise ECG/SPECT and markedly reduced need for index ICA vs direct angiography
- limitations: degraded by poor rate control, arrhythmia/ectopy, extensive calcification, large body habitus, prior stents/CABG; contraindicated with iodinated contrast allergy, renal impairment (protocol-dependent)
invasive coronary angiography (ICA)
- reference standard — reserved for:
- high clinical likelihood with refractory symptoms despite GDMT
- high event risk on non-invasive testing
- suspected high-risk anatomy (left main, proximal LAD, multivessel)
- inconclusive non-invasive testing
- to define anatomy before planned revascularisation
- enables invasive functional assessment (FFR/iFR) to determine lesion significance
- elective ICA reveals obstructive CAD in only ~38–50% of referred patients → underscores value of upstream CCTA/functional gatekeeping
ICA is not a screening test
Higher procedural risk in advanced age (>70), severe LV dysfunction, left main disease, severe valvular disease, renal/hepatic comorbidity, and bleeding disorders. Contrast-induced nephropathy risk elevated with CKD and diabetes.
coronary artery calcium (CAC) scoring
- non-contrast ECG-gated CT quantifying calcified plaque burden (Agatston score)
- primarily a primary-prevention tool — CCS recommends CAC in asymptomatic adults ≥40 at intermediate Framingham risk (10–20%) when statin decision is unclear
- CAC >0 is a formal CCS risk modifier supporting statin initiation; CAC >100 → statin indicated regardless of FRS
- may be considered in selected low-risk patients >40 with strong family history of premature ASCVD or genetic dyslipidaemia (elevated Lipoprotein(a), familial hypercholesterolaemia)
- not a diagnostic test for symptomatic patients — does not assess luminal stenosis or non-calcified plaque; ~14% of patients with flow-limiting stenosis have CAC of 0
modality selection summary
| Test | Best-suited patient | Key strength | Main limitation |
|---|---|---|---|
| exercise ECG | interpretable ECG, ≥5 METs, need functional data | cheap; functional/prognostic (Duke score) | modest accuracy; many uninterpretable ECGs |
| stress echo | valve/haemodynamic questions; avoid radiation | no radiation; versatile | acoustic windows (COPD/obesity) |
| SPECT/PET MPI | ischaemia quantification; PET for microvascular disease | high prognostic yield (PET) | radiation; vasodilator contraindications |
| stress CMR | cardiomyopathy, scar/viability assessment | tissue characterisation + perfusion | GFR, availability, device compatibility |
| CCTA | intermediate risk, no known CAD, younger patients | high NPV; detects non-obstructive plaque | overestimates calcified stenoses; contrast/rate control |
| CAC score | asymptomatic, intermediate FRS (10–20%), statin decision | reclassifies ASCVD risk | cannot exclude CAD if symptomatic |
| ICA (± FFR/iFR) | high likelihood, high-risk, refractory symptoms | definitive anatomy + enables revascularisation | invasive; procedural/contrast risk |
contraindications to stress testing
absolute contraindications to exercise stress
Mnemonic: I DO NOT STRESS
| Letter | Contraindication |
|---|---|
| I | inflammation (myocarditis, pericarditis) |
| D | dissection (aortic) |
| O | ongoing angina |
| N | no consent |
| O | ongoing MI (within 2 days) |
| T | thrombosis (acute PE/DVT) |
| S | severe AS (symptomatic) |
| T | technical issues / physical limitations |
| R | rhythm (uncontrolled haemodynamically significant arrhythmia) |
| E | endocarditis (active) |
| S | systolic dysfunction (decompensated HF) |
| S | slow (physical limitations) |
pharmacologic stress — agent-specific cautions
| Agent | Avoid in |
|---|---|
| vasodilators (adenosine, dipyridamole, regadenoson) | bronchospastic disease; high-grade AV block / sinus node disease without pacemaker; SBP <90 mmHg; active bronchospasm |
| dobutamine | uncontrolled HTN; haemodynamically significant LVOTO; severe aortic stenosis; uncontrolled arrhythmia |
- caffeine/theophylline must be held before vasodilator stress (competitive adenosine receptor antagonism → false negatives)
- reversal agent for vasodilator stress: aminophylline
- balanced triple-vessel or left main disease may produce false-negative vasodilator stress (uniform perfusion deficit)
high-risk features on non-invasive testing
These findings should prompt consideration of ICA ± revascularisation:
- Duke Treadmill Score ≤ −11
- <5 METs achieved
- ST elevation or severe ST depression ≥2 mm
- ischaemia on ≥5 leads or persisting ≥3 min into recovery
- abnormal BP response: failure to reach SBP >120, drop >10 mmHg, or drop below baseline
- ventricular arrhythmia during stress
- large or multiple perfusion defects (≥10% myocardium ischaemic on MPI)
- stress-induced LV cavity dilation or transient ischaemic dilation
- new or worsening wall motion abnormalities in ≥2 segments
management of chronic stable CAD
disease-modifying therapies (all patients)
- ASA + statin — backbone for all coronary atherosclerosis
- clopidogrel if ASA intolerant — CAPRIE (1996)
- ACEi if HTN, T2DM, LVEF <40%, or CKD
- beta-blocker if LVEF <40% (no MACE reduction if no prior MI and LVEF >50%)
- SGLT2 Inhibitors or GLP-1RA if CAD + diabetes
antianginal therapies (symptom relief)
| Class | Notes |
|---|---|
| beta-blockers | reduce HR and contractility — first-line antianginal |
| CCBs (non-DHP) | verapamil, diltiazem — caution if LVEF <40% |
| CCBs (DHP) | amlodipine — safe with reduced EF |
| nitrates | venodilate, reduce LVEDP — symptom relief only |
lifestyle and adjunctive
- smoking cessation — counselling + pharmacotherapy together more effective than either alone
- cardiac rehab (class I-A post-MI/PCI/CABG; class I-B stable CAD)
- exercise: ≥150 min/wk aerobic + 2 days/wk resistance
- vaccines: annual influenza (I-C), COVID (I-C), pneumococcal (II-a)
what NOT to recommend
Dietary supplements, alcohol for CV protection, chronic NSAIDs — all lack evidence or cause harm in CAD.
revascularisation
the evidence base for OMT-first
OMT is non-inferior to routine revascularisation for most stable CAD:
- COURAGE (2007) — PCI + OMT no better than OMT alone for death/MI
- ORBITA (2018) — PCI did not improve exercise time vs sham procedure
- ISCHEMIA (2020) — invasive strategy did not reduce death/MI vs conservative in moderate-severe ischaemia; quality-of-life benefit for angina in the invasive arm
what ISCHEMIA excluded
Left main ≥50%, LVEF <35%, unacceptable angina on GDMT, recent ACS, NYHA III–IV HF. These are the patients most likely to benefit from revascularisation — and they were not in the trial.
indications for revascularisation in stable CAD
- refractory angina despite adequate GDMT (≥2 antianginals at tolerated doses)
- high-risk anatomy: left main ≥50%, proximal LAD, multivessel disease with reduced LVEF
- large ischaemic burden on non-invasive testing (≥10% myocardium)
- haemodynamically significant lesion on FFR (≤0.80) or iFR (≤0.89)
CABG vs PCI
| Scenario | Favours CABG |
|---|---|
| left main >50% + high SYNTAX score (≥33) | survival benefit over PCI; less repeat revascularisation |
| multivessel disease + diabetes | survival benefit — particularly with LAD involvement |
| multivessel disease + LVEF ≤35% | survival benefit over PCI and over GDMT alone |
| complex multivessel CAD (high SYNTAX score) | less repeat revascularisation, lower long-term MACE |
| Scenario | PCI reasonable |
|---|---|
| left main + low SYNTAX score (<22) | similar outcomes to CABG |
| 1–2 vessel disease, no diabetes, preserved LVEF | equivalent outcomes, less invasive |
| high surgical risk / prohibitive comorbidities | preferred regardless of anatomy |
SYNTAX score
Angiographic complexity score — higher scores (≥33) reflect diffuse, calcified, bifurcation-heavy disease where CABG durability outperforms PCI. Low SYNTAX (≤22) = simpler anatomy where PCI results are comparable.
what NOT to do
- exercise stress testing with uninterpretable baseline ECG (LBBB, paced, WPW, digoxin) — add imaging
- vasodilator stress in active bronchospasm or without caffeine/theophylline washout
- CAC scoring to “rule out” CAD in symptomatic patients — CAC 0 does not exclude non-calcified stenosis
- routine ICA in low/intermediate-risk stable patients without prior non-invasive testing
- revascularisation for stable disease without a trial of GDMT (unless high-risk anatomy or refractory symptoms)
- withholding statin in established CAD regardless of baseline LDL
key trials summary
| Trial | Year | Key finding |
|---|---|---|
| CAPRIE (1996) | 1996 | clopidogrel modestly superior to ASA in atherosclerotic vascular disease |
| COURAGE (2007) | 2007 | PCI + OMT no better than OMT alone for death/MI in stable CAD |
| ORBITA (2018) | 2018 | PCI did not improve exercise time vs sham procedure in stable angina |
| ISCHEMIA (2020) | 2020 | invasive strategy did not reduce death/MI vs conservative in moderate-severe ischaemia |
| DISCHARGE (2022) | 2022 | initial CCTA strategy similar CV outcomes to ICA, fewer invasive procedures |