Exercise stress testing
Principle and modern role
- Graded exercise (Bruce protocol commonest) with continuous ECG, BP and symptom monitoring
- Principle: inc myocardial O2 demand until supply becomes limiting -> ischaemia -> ST depression, symptoms, or haemodynamic failure
- Modern role has narrowed markedly: CTCA and functional imaging have displaced it for the diagnosis of CAD. Its surviving value is functional capacity, exercise-induced arrhythmia and risk stratification**
Outputs, in order of value
1. Exercise capacity in METs - the strongest prognostic variable, stronger than the ST response
2. Haemodynamic response - BP, chronotropic response, heart rate recovery
3. Symptoms reproduced
4. ECG changes
5. Arrhythmia induced or suppressed
Diagnostic accuracy for obstructive CAD
Diagnostic accuracy for obstructive CAD
| Test | Sensitivity | Specificity |
|---|---|---|
| Exercise ECG alone | 50-70% | 70-80% |
| Stress echocardiography | 80-85% | 85-95% |
| Nuclear MPI (SPECT/PET) | 85-90% | 85-100% |
| Stress CMR | ~90% | ~85% |
| CTCA | ~95% | ~80% (highest NPV) |
- Exercise ECG is cheapest and most available, and requires no radiation or contrast
- Stress echo: limited by image quality in obesity and COPD; operator-dependent
- Nuclear: more expensive, radiation exposure; attenuation artefact (breast, diaphragm)
- Sensitivity in women is lower for exercise ECG (more false positives) - prefer imaging
Why ST depression occurs
- Demand ischaemia -> subendocardial hypoperfusion -> loss of the normal transmural repolarisation gradient
- -> horizontal or downsloping ST depression
- Coronary flow reserve is exhausted at ~70-80% stenosis -> a stenosis below this will not produce ischaemia at any workload
Bayes' theorem governs interpretation
- The test is most useful at intermediate pre-test probability
- Low pre-test probability -> a positive result is more likely false
- High pre-test probability -> a negative result does not exclude disease; go straight to anatomical or functional imaging
- Ordering an exercise ECG in a 75-year-old diabetic smoker with typical angina wastes time and may mislead
ECG criteria for a positive test
- >=1 mm horizontal or downsloping ST depression 80 ms after the J point, in 2 contiguous leads
- Upsloping ST depression is NOT diagnostic
- ST elevation in leads without Q waves = transmural ischaemia, high risk -> stop and act
- ST depression does not localise the culprit territory; ST elevation does
Markers of a high-risk (strongly positive) test
- Failure to complete stage 2 of Bruce / <5 METs
- ST depression >=2 mm, in >=5 leads, at low workload, or persisting >5 min into recovery
- Exercise-induced hypotension (fall in SBP >10 mmHg below baseline) - severe LV dysfunction or left main/3-vessel disease
- ST elevation
- Sustained VT
- Angina at low workload
- Duke treadmill score <= -11
- Duke = exercise time (min) - (5 x ST deviation in mm) - (4 x angina index) (angina index: 0 none, 1 non-limiting, 2 limiting)
- >= +5 low risk (~0.25%/yr mortality); -10 to +4 moderate; <= -11 high risk (~5%/yr)
Other prognostic markers
- Chronotropic incompetence - failure to reach 85% of age-predicted maximum HR (220 - age)
- Abnormal heart rate recovery - fall of <=12 bpm at 1 minute post-exercise (autonomic dysfunction, independent mortality predictor)
- Frequent ventricular ectopy in recovery
Reasons to stop
- Absolute: ST elevation, drop in SBP >10 mmHg with other ischaemia evidence, sustained VT, moderate-severe angina, signs of poor perfusion, patient request, technical failure
- Relative: marked ST depression, arrhythmia, fatigue, hypertensive response (>250/115), bundle branch block developing
When the ECG is uninterpretable - use imaging instead
- LBBB, ventricular paced rhythm, pre-excitation (WPW)
- >=1 mm resting ST depression, LVH with strain, digoxin
- In LBBB, use vasodilator stress (adenosine/regadenoson) MPI or dobutamine stress echo - exercise MPI gives false septal defects
Contraindications
- Absolute: ACS within 2 days, untreated life-threatening arrhythmia, symptomatic severe AS, decompensated HF, acute PE, acute aortic dissection, acute myocarditis/pericarditis
- Relative: left main stenosis, severe hypertension, HOCM with outflow obstruction, high-grade AV block, electrolyte abnormality, inability to exercise
When to use exercise ECG in 2026
A. When to use exercise ECG in 2026
- Functional capacity assessment - pre-operative, pre-transplant, HF, congenital heart disease, valvular disease
- Risk stratification in known CAD, post-revascularisation symptom assessment
- Asymptomatic severe aortic stenosis - unmask symptoms or an abnormal BP response -> triggers intervention
- Exercise-induced arrhythmia
- CPVT - bidirectional/polymorphic VT with exercise
- LQTS - failure of QT to shorten; paradoxical QT prolongation in recovery
- Rate control assessment in AF
- Exercise-induced AV block = infranodal disease -> pacing
- Asymptomatic WPW risk stratification - abrupt loss of pre-excitation at higher rates = long accessory pathway refractory period = low risk
- Exercise-induced hypertension, chronotropic incompetence (pacemaker rate response programming)
When to choose something else
B. When to choose something else
| Situation | Preferred test |
|---|---|
| Cannot exercise | Dobutamine stress echo, or vasodilator MPI/CMR |
| Uninterpretable baseline ECG | Imaging-based stress test |
| Low-intermediate probability stable chest pain | CTCA |
| Need to localise ischaemia / assess viability | MPI, stress CMR, PET |
| Known CAD with prior revascularisation | Imaging-based |
| Women, obesity, LVH | Imaging-based |
Preparation
C. Preparation
- Withhold beta blockers and rate-limiting CCBs 24-48 h if the question is ischaemia (not if the question is rate control adequacy)
- Withhold nitrates on the morning of the test
- Caffeine and theophylline for 12-24 h before adenosine/regadenoson studies (competitive antagonists - will invalidate the test)
- Nil by mouth 3-4 h, comfortable footwear, continue other medications
Acting on the result
D. Acting on the result
- High-risk test -> invasive coronary angiography
- Intermediate -> optimise medical therapy, consider anatomical imaging
- Low risk / good functional capacity -> reassure, treat risk factors
- Remember ISCHEMIA: in stable disease, revascularisation improves symptoms rather than survival - a high-risk stress test alone is not an automatic trigger for PCI in an asymptomatic patient
Related tests
- Cardiopulmonary exercise testing (CPET) - adds gas exchange; peak VO2 and VE/VCO2 slope for HF prognosis, transplant listing and dyspnoea of unclear cause
- 6-minute walk test - simpler submaximal alternative for HF and pulmonary hypertension
- Dobutamine stress echo - also used for low-flow low-gradient aortic stenosis and viability
- Exercise stress echo in valve disease - mitral stenosis gradient, exercise pulmonary hypertension
- Athlete's heart vs cardiomyopathy - exercise testing part of the assessment
- Pre-operative risk: >=4 METs (climb a flight of stairs) is the usual functional threshold
Safety
- Risk of MI or death ~1 in 10,000 tests
- Requires resuscitation facilities and trained supervision
Interpretation traps
- Upsloping ST depression is not a positive test
- Digoxin, LVH with strain and resting repolarisation change cause false positives
- False positives are far more common in women (lower disease prevalence, hormonal effects on repolarisation)
- A "negative" test in a patient who only reached 60% of predicted maximum heart rate is non-diagnostic, not negative
- Functional capacity, not the ST segment, is the dominant prognostic output - a patient who completes 12 METs has an excellent prognosis whatever the ST segment did
- ST changes in recovery only are still significant - always record 6-10 minutes of recovery
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