Stable ischaemic heart disease
Description
- Terminology has moved: "chronic coronary syndrome" (CCS), not "stable IHD"
- Emphasises that atherosclerosis is a dynamic process with stable and unstable phases, and that a patient is never truly "stable"
- Myocardial oxygen supply-demand mismatch, reproducible and predictable
Clinical presentations that all count as CCS
- Suspected CAD with stable angina or dyspnoea
- New-onset HF or LV dysfunction with suspected CAD
- Stabilised <1 year post-ACS or post-revascularisation
- >1 year after diagnosis or revascularisation
- Angina with suspected vasospastic or microvascular disease (ANOCA/INOCA)
- Asymptomatic CAD detected on screening
Angina classification
- Typical - all 3: (1) constricting chest/neck/jaw/arm discomfort, (2) provoked by exertion, (3) relieved by rest or GTN within ~5 min
- Atypical - 2 of 3 | Non-anginal - <=1 of 3
- CCS grade I-IV (Canadian Cardiovascular Society) - by the level of exertion that provokes it
Epidemiology
- Leading single cause of death in Australia; ~1 in 20 adults have CAD
- Prevalence rises steeply with age; M>F, gap narrows after menopause
- Aboriginal and Torres Strait Islander peoples: earlier onset, ~2x mortality
- Age-standardised mortality falling (~80% since the 1980s) but prevalence rising with survival
- ~50% of women with angina have no obstructive coronary disease - ANOCA/INOCA is not rare
Aetiopathogenesis
Mechanisms of ischaemia - more than one may coexist
- Obstructive epicardial stenosis - the classic; flow limitation at >~70% diameter stenosis
- Coronary microvascular dysfunction - impaired vasodilator reserve; normal angiogram
- Vasospasm (Prinzmetal) - focal or diffuse; rest/nocturnal pain, transient ST elevation
- Non-atherosclerotic - myocardial bridging, anomalous origin, arteritis, radiation, dissection
Plaque biology
- Endothelial dysfunction -> LDL retention and oxidation -> foam cells -> fatty streak
- Fibrous cap over a necrotic lipid core; smooth muscle migration
- Stable plaque = thick cap, small core (causes angina)
- Vulnerable plaque = thin cap, large lipid core, positive remodelling, macrophage-rich (causes ACS)
- *Severity of stenosis predicts symptoms; plaque composition predicts events* - the two are dissociated
Risk factors
- Modifiable - smoking, hypertension, dyslipidaemia (inc LDL, inc Lp(a)), diabetes, obesity, physical inactivity, poor diet, alcohol, psychosocial stress
- Non-modifiable - age, male sex, family history of premature CAD, ethnicity
- Under-recognised - CKD, inflammatory disease (RA, SLE, psoriasis), HIV, chest radiotherapy, pre-eclampsia and other pregnancy complications, OSA
Diagnosis
Step 1 - clinical likelihood, not a pre-test probability table
- ESC 2024 uses a risk-factor-weighted clinical likelihood model (age, sex, symptom type, plus risk factors, ECG, LV function, calcium score)
- Reclassifies many patients downward - the old Diamond-Forrester tables overestimated
- Very low likelihood (<5%): no testing
Step 2 - choose the test by the question
| Question | Test |
|---|---|
| Is there coronary disease at all? (low-intermediate likelihood) | CTCA - first-line. Excellent NPV; a normal study effectively excludes CAD |
| Is there ischaemia, and where? (higher likelihood, known CAD, planning revascularisation) | Functional imaging - stress echo, stress CMR, SPECT/PET |
| Anatomy for revascularisation | Invasive coronary angiography - clinical likelihood >85%, high-risk non-invasive findings, or refractory symptoms on optimal medical therapy |
- Exercise ECG has been demoted - use only where imaging is unavailable, or for symptom/functional/prognostic assessment
- Sensitivity ~50-70%, specificity ~70-80%; uninterpretable with LBBB, paced rhythm, pre-excitation, digoxin, resting ST change
- CTCA is inappropriate: high pre-test probability with typical angina (go straight to ICA), and asymptomatic screening
Step 3 - physiology, not just pictures
- FFR <=0.80 or iwFR <=0.89 = functionally significant
- FFR-guided PCI (FAME) beats angiography-guided PCI
- Angiographic "eyeballing" of intermediate lesions is unreliable
- If the angiogram is normal but symptoms are typical: do invasive coronary function testing
- Coronary flow reserve <2.0-2.5 or index of microcirculatory resistance >=25 -> microvascular angina
- Acetylcholine provocation -> vasospastic angina
- This is the step most often omitted, and it leaves the patient with no diagnosis
Baseline in everyone
- ECG, FBE, UEC, lipids, HbA1c, TFT, TTE (LV function, wall motion, valves)
- Resting ECG is normal in >50% of CCS
High-risk features (drive to angiography)
- LV dysfunction (EF <50%), large ischaemic burden (>10% myocardium)
- Fall in BP during exercise, early or extensive ST depression, poor exercise capacity, failure to reach 85% max HR
- Left main or proximal LAD disease, three-vessel disease
Management
- Two separate goals: (1) prevent death and MI, (2) relieve angina. Different drugs serve each.
A. Event prevention - the part that changes prognosis
- Antiplatelet - aspirin 100 mg daily lifelong (clopidogrel 75 mg if intolerant or as an alternative)
- High-intensity statin in everyone, target LDL-C <1.4 mmol/L and >=50% reduction; add ezetimibe then PCSK9 inhibitor if not reached
- ACE inhibitor if diabetes, hypertension, CKD or LV dysfunction
- SGLT2 inhibitor and/or GLP-1 receptor agonist if type 2 diabetes - independent CV benefit
- Colchicine 0.5 mg daily - Class IIa add-on for residual inflammatory risk (LoDoCo2)
- Smoking cessation is the single most effective intervention. Cardiac rehabilitation, 150 min/week exercise, Mediterranean diet, BP <130/80, influenza vaccination
- Rivaroxaban 2.5 mg bd + aspirin - consider in high ischaemic/low bleeding risk (COMPASS)
B. Symptom control - by patient phenotype, not by "first-line/second-line"
- Short-acting nitrate to all - sublingual GTN, taught for treatment and prophylaxis
- ESC 2024 abandoned the rigid beta-blocker-first hierarchy - choose by heart rate, BP and comorbidity
| Phenotype | Preferred |
|---|---|
| High heart rate | Beta blocker or non-dihydropyridine CCB (verapamil, diltiazem) |
| Low heart rate | Dihydropyridine CCB (amlodipine), long-acting nitrate |
| Low BP | Ivabradine, ranolazine, low-dose combinations |
| LV dysfunction / prior MI | Beta blocker (also prognostic here) |
| Vasospastic angina | CCB + nitrate. AVOID beta blockers - unopposed alpha worsens spasm |
| Microvascular angina | Beta blocker, ACEi, statin; ranolazine, ivabradine |
- Nitrate tolerance: build in a nitrate-free interval of 8-12 h
- Do NOT combine verapamil or diltiazem with a beta blocker - bradycardia and heart block
- Nitrates + PDE5 inhibitor = contraindicated
C. Revascularisation - for symptoms, and for prognosis in defined subsets
- The trial story:
- COURAGE - PCI relieves angina but does not improve survival over optimal medical therapy
- ORBITA (sham-controlled) - much of the symptomatic benefit of PCI is placebo; ORBITA-2 (no background antianginals) did show genuine angina relief
- ISCHEMIA - in stable moderate-severe ischaemia, an invasive strategy did not reduce death/MI; more periprocedural MI, fewer spontaneous MI, better angina
- *Conclusion: optimal medical therapy first in almost everyone; revascularise for refractory symptoms or for high-risk anatomy*
- Prognostic indications (revascularise regardless of symptoms): left main stenosis >50%, proximal LAD disease with ischaemia, multivessel disease with LV dysfunction, large ischaemic burden, last remaining patent vessel
D. PCI vs CABG
| Favours CABG | Favours PCI |
|---|---|
| Diabetes with multivessel disease (FREEDOM) | Low SYNTAX score |
| High SYNTAX score (complex, diffuse, calcified, CTO) | Isolated single-vessel or low-complexity left main |
| LV dysfunction (STICH) | High surgical risk, frailty, comorbidity |
| Three-vessel disease, need for complete revascularisation | Patient preference for less invasive |
- Left main, low-intermediate complexity: EXCEL and NOBLE support PCI as broadly equivalent; SYNTAX favoured CABG at 1 year for three-vessel/left main
- Use radial artery access and arterial grafts (LIMA to LAD in all)
- Heart Team decision for left main and multivessel disease
- DAPT after PCI in CCS: aspirin + clopidogrel for 6 months (shorter if high bleeding risk), then aspirin alone
Associations
- Peripheral arterial disease and carotid disease - polyvascular disease worsens prognosis
- Diabetes, CKD, hypertension, dyslipidaemia, obesity, OSA
- Heart failure - both HFrEF (ischaemic cardiomyopathy) and HFpEF
- AF - complicates antithrombotic decisions
- Depression and anxiety - independent predictors of events and of non-adherence
- Inflammatory disease - RA, SLE, psoriasis, IBD, HIV
- Erectile dysfunction - often precedes angina by ~3 years; a marker of endothelial disease
- Chest radiotherapy, anthracyclines, cocaine and methamphetamine use
Natural history & complications
- Annual mortality in medically treated CCS ~1-3%
- Most MIs arise from non-obstructive (<50%) plaques - which is why revascularisation of a stenosis does not abolish risk
- INOCA/ANOCA is not benign - higher event rates than the general population, and major symptom burden
Prognostic determinants (in order of weight)
1. LV function - the strongest
2. Extent and site of disease - left main > proximal LAD > three-vessel > single-vessel
3. Ischaemic burden on functional testing
4. Exercise capacity and BP fall during exercise
5. Angina class, comorbidity (CKD, diabetes), age
Monitoring
- Review symptoms, adherence and risk factors 6-12 monthly
- Repeat testing only for a change in symptoms - not routine surveillance
- Reassess LV function if symptoms change or after MI
- Recurrent angina after PCI within months = restenosis; after years = progression or graft failure
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