GC032 Chest Pain On Exertion: Ischaemic Heart Disease; Angina Pectoris
Angina pectoris is episodic chest pain or discomfort caused by transient myocardial ischemia due to an imbalance between myocardial oxygen supply and demand, typically provoked by exertion or stress and relieved by rest or nitrates.
Chest Pain on Exertion: Ischaemic Heart Disease & Angina Pectoris
The Big Idea: This lecture, delivered by Prof. Hung-Fat Tse (Chair Professor of Cardiovascular Medicine, HKU), follows a 49-year-old male smoker with exertional chest pain from oxygen supply–demand physiology through assessment, imaging, prevention, antianginal therapy, and revascularisation. It closes with vasospastic angina, the modern ANOCA/INOCA spectrum (called “cardiac syndrome X” on the slide), and congenital coronary anomalies. [1]
How it fits in the curriculum:
- This is the foundation lecture for coronary artery disease. The ACS lecture (GC 028 / WCS28) builds directly on it — same patient, a few years older, disease progressed because he didn't quit smoking [2].
- Links to: hypertension (GC 058), lipid disorders, heart failure (GC 084), sudden severe chest pain/STEMI (GC 088), cardiology interactive tutorial, clinical pharmacology of antiplatelets/anticoagulants, and CVS investigations (ECG).
Learning Objectives (inferred from slide structure and supporting tutorial):
- Understand the pathophysiology and etiologies of IHD
- Describe clinical characteristics of angina pectoris using SOCRATES
- Identify cardiovascular risk factors and their physical signs
- Outline non-invasive and invasive investigation strategies
- Describe pharmacological and non-pharmacological management of stable CAD
- Recognise vasospastic angina, ANOCA/INOCA endotypes, and high-risk congenital coronary anomalies
Core Concepts and Mechanisms
Angina pectoris is generally defined as a discomfort in the chest or adjacent areas that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. [1]
From first principles: The heart is a muscle that needs oxygen. It gets oxygen from coronary arteries. When a coronary artery is narrowed (usually by atherosclerosis), there is adequate flow at rest but inadequate flow during increased demand (exertion). The myocardium becomes ischaemic → metabolites (adenosine, lactate, bradykinin) accumulate → stimulate chemosensitive and mechanosensitive cardiac receptors → afferent signals travel via cardiac sympathetic nerves → upper 5 thoracic sympathetic ganglia → upper 5 thoracic spinal cord dorsal roots → convergence with somatic afferents from the chest wall, arm, jaw → this is why angina is "referred" to these areas. [1]
The Ischaemic Cascade (Slide 5): During effort, ischaemic events unfold in a predictable temporal sequence [1]:
- Ischaemia (seconds)
- Diastolic dysfunction
- Systolic dysfunction
- ECG changes (ST-segment depression/elevation)
- Dyspnoea
- Pain (last to appear)
On cessation of effort: pain relief → ECG normalisation → systolic recovery begins → a period of stunning may persist (minutes to possibly hours) before full recovery. [1]
Why ischaemia may be silent
Diabetes and older age are associated with less typical symptom perception. Diabetic autonomic neuropathy and altered afferent processing are the clinically useful explanations; the slide's proposed nerve-growth-factor mechanism is experimental, not a bedside diagnostic rule. Dyspnoea, fatigue, diaphoresis, nausea, dizziness, or syncope can therefore be anginal equivalents—but each remains non-specific. [1,8]
The ischaemic cascade is driven by an imbalance between myocardial oxygen supply and demand:
| Factor | Increases O₂ Demand | Decreases O₂ Supply |
|---|---|---|
| Physiological | Exercise, emotion, eating, cold environment (the "4 Es") | — |
| Pathological | Hypertension, aortic stenosis, HOCM, tachycardia, thyrotoxicosis | Coronary atherosclerosis, coronary spasm, anaemia, hypoxia, hyperviscosity |
Why does this matter clinically? A patient with a flow-limiting fixed stenosis may be comfortable at rest. Add anaemia (reduced O₂ carrying capacity) or thyrotoxicosis/tachycardia (increased demand and shorter diastole), and the same anatomy can become symptomatic. This is why haemoglobin is part of basic testing and thyroid function is checked when clinically indicated. [1]
Mechanisms of myocardial ischaemia—three overlapping pathways (Slide 7): [1]
| Mechanism | Pathway | Clinical Consequence |
|---|---|---|
| Atherosclerotic disease | Stable plaque → ↓ CFR → demand ischaemia ± angina; Vulnerable plaque → rupture → thrombosis → ACS/infarction | Stable angina or ACS |
| Vasospastic disease | Focal/transient spasm → Prinzmetal angina; Persistent spasm → MI | Variant angina or MI |
| Microvascular dysfunction | Impaired vasodilatation, increased resistance, endothelial dysfunction, and/or microvascular spasm | Causes ANOCA/INOCA and may coexist with epicardial plaque or spasm; Takotsubo syndrome is a distinct diagnosis, not simply severe microvascular angina |
These three mechanisms can overlap. [1]
The central balance is more useful than memorising a stenosis percentage:
- Demand rises with heart rate, contractility, and LV wall tension. Wall tension rises with systolic pressure and chamber volume.
- Supply depends on coronary flow, the duration of diastole, the aortic diastolic pressure–LV end-diastolic pressure gradient, collateral flow, vasomotor tone, and local autoregulation.
- Tachycardia is a double hit: it raises demand while shortening diastolic coronary perfusion time.
- The diagram's endpoints—lactate/acidosis, impaired relaxation and contraction, ST change, then pain—explain why symptoms are a late and imperfect marker of ischaemia.
The rupture illustration locates the tear at a lipid- and foam-cell-rich plaque shoulder. Exposure of thrombogenic material produces platelet activation and thrombus: a previously non-critical plaque can therefore cause ACS. The pathology panels show a spectrum—moderate narrowing, heavily calcified near-occlusion, intraplaque haemorrhage with a slit-like lumen, thrombotic occlusion, and later organisation/recanalisation. Anatomical stenosis severity and propensity to rupture are related but not identical. [1]
The older “atherophil/fibrophil” cartoon on slide 14 should be translated into modern language: macrophage/foam-cell inflammation favours a lipid-rich lesion, whereas smooth-muscle cells and extracellular matrix form a fibrous cap; both processes coexist, and inherited factors influence the response to retained apoB lipoproteins. [1]
The dominant cause is ATHEROSCLEROSIS OF CORONARY ARTERIES. [1]
| Category | Specific Causes |
|---|---|
| Atherosclerotic | The overwhelming majority |
| Primary cardiac (non-atherosclerotic) | Coronary spasm, coronary arteritis, coronary dissection, coronary artery anomalies, radiation-induced disease, myocardial bridging, aortic stenosis, HOCM, dilated cardiomyopathy, tachycardia |
| Primary non-cardiac | Anaemia, sickle cell disease, hypoxaemia, CO poisoning, hyperviscosity (polycythaemia), hyperthyroidism, phaeochromocytoma |
Substances that modify coronary risk or trigger ischaemia (Slide 18): [1]
| Substance | Key Cardiovascular Effects |
|---|---|
| Tobacco | Sympathetic activation, endothelial injury, vasoconstriction, thrombosis, and adverse lipid effects. It is a major modifiable risk factor; avoid memorising the lecture's era- and cohort-specific percentages. |
| Alcohol | Can cause hypertension, atrial arrhythmia, and cardiomyopathy. The slide's observational "J-curve" does not justify starting alcohol for cardioprotection; if a person does not drink, current guidance says not to start. [17] |
| Cocaine | Blocks dopamine/norepinephrine reuptake → ↑ sympathetic stimulation → vasoconstriction, coronary spasm → infarction. Also: procoagulant effects, tachycardias, direct cardiotoxicity. |
The lecture devotes multiple slides (slides 12–16) to this. The process in sequence:
- Endothelial injury — from risk factors (smoking, hypertension, dyslipidaemia, diabetes)
- LDL accumulation in intima → oxidised LDL provokes inflammatory response
- Monocyte recruitment → differentiate into macrophages → engulf oxidised LDL → become foam cells → form fatty streaks
- Smooth muscle cell migration from media to intima → produce collagen → fibrous cap forms over lipid/necrotic core → atheromatous plaque
- Plaque progression → stable plaque (thick cap, small core) vs. vulnerable/unstable plaque (thin cap, large lipid core) → rupture → thrombus → ACS
What the histology sequence actually shows (Slide 15): retained/modified apoB particles recruit monocytes; macrophage foam cells and extracellular lipid accumulate; smooth-muscle cells migrate and form matrix; microvessels, haemorrhage, cholesterol clefts, calcification, and cell death enlarge a necrotic core. The slide arranges these appearances as follows [1]:
| Type | Lesion | Key Features |
|---|---|---|
| — | Healthy endothelium | No intimal lesion |
| I | Intimal thickening | Initial intimal thickening |
| II | Intimal xanthoma (fatty streak) | Lipid-containing intimal lesion; may regress back to healthy endothelium |
| III | Pathological intimal thickening | Without → then with macrophage infiltration |
| IV | Fibroatheroma | Early → late necrotic core formation |
| V | Thin-cap fibroatheroma | Large necrotic core, thin fibrous cap — most vulnerable to rupture |
Accumulated LDL-C-years concept — the longer and higher the exposure, the greater the lifetime atherosclerotic burden. The plotted 200 mmol/L-years is an explanatory model, not a validated threshold at which an individual suddenly develops IHD. [1]
Slide 16 quantifies this with a possible threshold of 200 LDL-C years for ischaemic disease [1]:
- LDL-C 10.0 mmol/L → reaches threshold at age 20
- LDL-C 5.0 mmol/L → reaches threshold at age 40
- LDL-C 2.5 mmol/L → reaches threshold at age 80
This illustrates why patients with familial hypercholesterolaemia develop premature CAD and why early LDL-C lowering is critical.
Do not learn the old epidemiology as fixed constants
Slides 9–10 combine historical textbook estimates with US 2015–2018 prevalence and a selected CORONOR cohort (annual MI about 0.8%). Age, sex, prevention, case definition, and geography materially change these numbers. Learn the direction—risk rises with age and risk-factor burden—not the old universal percentages. [1]
The deck quotes several historical event rates, including a 10–20% 12-month progression figure. It also shows much lower event rates in a contemporary treated cohort. These are not interchangeable populations, and modern chronic coronary syndrome risk varies greatly with LV function, plaque burden, diabetes/CKD, prior MI, treatment, and anatomy. Use validated contemporary risk assessment rather than presenting one percentage as the prognosis for every patient. [1,8]
The past-paper item is internally inconsistent in the original note: its retained keyed answer below is B (5–10%), not C. Treat it as a recall of the local exam key, not a universal clinical estimate. [4]
Clinical Approach: The Case of CTM, M/49
The lecture is anchored around a clinical case that reappears throughout:
Presentation (Slides 2, 26):
- 49-year-old male, 3-month history of on-and-off retrosternal discomfort while walking back to office after lunch
- Constricting in character, relieved by rest
- Family Hx: Father died of CAD at age 60–65
- Social Hx: Chronic smoker, non-drinker
- No past history of cardiovascular disease [1]
Clarify the details of the pain using SOCRATES [1]
| SOCRATES | Angina Pectoris Features | Why This Matters |
|---|---|---|
| Site | Retrosternal or slightly to left, occasionally at extrathoracic sites | Cardiac pain is visceral → poorly localised; patient often uses palm/fist (Levine's sign), NOT a pointing finger |
| Onset | Gradual increase and fading away, usually 2–10 minutes | Sudden maximal-at-onset pain = think dissection/PE/pneumothorax instead |
| Character | Tightness, pressure, squeezing, heaviness, burning, aching, fullness, "heavy weight" or "band across chest" | Sharp/stabbing/knife-like pain is ATYPICAL for angina → think pleuritic/MSK |
| Radiation | Neck, throat, lower jaw, L shoulder or arm (ulnar distribution), occasionally R arm, interscapular, epigastrium or back | Due to convergence of cardiac afferents with somatic dermatomes T1–T5 |
| Associations | SOB, dizziness, syncope | These can be "angina equivalents" — important in elderly/DM |
| Time course | Worsening/improving/fluctuating | Progressive worsening → think unstable/ACS |
| Exacerbating/Relieving | 4 "E"s – Eating, Exertion, Emotion, Environment (hot/cold) vs. Rest, cessation of activity/stress, NTG | If NOT relieved by rest or NTG → think ACS or non-cardiac |
| Severity | Scale 0–10 | Important for monitoring and comparison |
| Grade | Description |
|---|---|
| 0 | Asymptomatic |
| I | Angina with strenuous exertion only |
| II | Angina with moderate exertion (slight limitation of ordinary activities) |
| III | Angina with mild exertion, e.g. 100–200m, 1 flight of stairs (great limitation) |
| IV | Angina at rest |
This slide is crucial for recognising atypical presentations:
Dyspnoea (exertional, rest, PND), non-chest locations of discomfort (neck, mandible, throat, shoulder, arm — more often left), mid-epigastric burning, nausea/vomiting (especially inferior MI with increased vagal tone), diaphoresis, excessive fatigue, dizziness and syncope. [1]
Why this matters: The 2021 past paper Q11 described a 62-year-old woman with "severe epigastric pain associated with dyspnoea on climbing stairs, subsiding after resting for 5 minutes" — the answer is IHD, not dyspepsia, because of the exertional pattern and relief with rest. [6]
The slide uses the 2019 age/sex/symptom pre-test table (a 49-year-old man with typical angina is shown as 22%) and then lists modifiers. The 2024 ESC approach replaces this with a risk-factor-weighted clinical-likelihood model: symptoms, age and sex are integrated with smoking, dyslipidaemia, hypertension, diabetes, and family history. A very low likelihood (≤5%) usually allows testing to be deferred; CCTA is preferred to rule out obstructive disease and show non-obstructive plaque in low-to-moderate likelihood, while functional imaging is useful when ischaemia and viability are the main questions. [8,9]
New, rest, or crescendo pain is not routed through a stable-angina probability table—exclude ACS first.
The majority of cases present with NORMAL physical findings. [1]
The physical exam has three goals:
| Goal | What to Look For | Clinical Significance |
|---|---|---|
| Assess risk factors | BP in both arms if indicated, adiposity, tendon xanthomas, premature corneal arcus, acanthosis nigricans, tobacco exposure, and peripheral vascular signs | Identifies modifiable risk and clues to familial dyslipidaemia/insulin resistance |
| Assess for complications | JVP distension, S3/S4, displaced apex, hepatomegaly, pulmonary/peripheral oedema (CHF); ischaemic MR; arrhythmias; carotid bruits, absent peripheral pulses (PAD) | CHF and MR are complications of IHD; PAD indicates generalised atherosclerosis |
| Assess for other causes of angina | AS (late-peaking systolic murmur, pulsus parvus et tardus), HOCM (harsh crescendo-decrescendo murmur with dynamic provocation), pulmonary hypertension (loud P2, RV heave) | These conditions cause angina by mechanisms other than coronary atherosclerosis |
In the case (Slide 28):
- BP 130/85
- Xanthelasma on bilateral upper eyelids, no tendon xanthoma
- Normal cardiovascular examination [1]
Physical Exam Pearl
The photographs show bilateral xanthelasma, corneal arcus, acanthosis nigricans, and a diagonal earlobe crease. Xanthelasma and arcus can prompt lipid assessment but are not diagnostic of familial hypercholesterolaemia; tendon xanthomas and premature arcus are more specific clues. Acanthosis suggests insulin resistance. The earlobe crease is an epidemiological association, not a diagnostic sign of CAD, and should never drive testing by itself. [1]
C. Investigations
1. Blood Tests (Slides 32–36)
| Category | Tests | Why |
|---|---|---|
| Lipid levels | LDL-C, HDL-C, triglycerides, Lipoprotein(a) | Assess dyslipidaemia — major modifiable risk factor |
| Basic evaluation | Full blood count, creatinine/eGFR, glucose/HbA1c; thyroid testing when clinically indicated | Detect anaemia, CKD, diabetes, or thyroid disease that changes diagnosis/risk/treatment |
| Selected biomarkers | hs-cTn for suspected acute myocardial injury; BNP/NT-proBNP when heart failure is suspected | Not routine screening tests for every stable-angina presentation; the slide's hs-troponin/NT-proBNP curves show prognostic association, not proof of obstructive CAD |
Lipid profile equations (Slide 33): [1]
- Friedewald equation in mg/dL: LDL-C = total cholesterol − HDL-C − (triglycerides / 5). It is an estimate and becomes unreliable with marked hypertriglyceridaemia and in some low-LDL settings; use the laboratory's validated method.
- Non-HDL-C = Total cholesterol − HDL-C (captures all atherogenic lipoproteins including VLDL, IDL, and LDL)
"The LDL-hypothesis: the lower, the better." [1]
Lipoprotein(a) — A Lecture Emphasis:
Lp(a) is an LDL-like apoB particle covalently linked to apolipoprotein(a); it is not a subtype of the LDL-C laboratory measurement. Its concentration is largely inherited and contributes to atherosclerotic and calcific-aortic-valve risk. The diagram also proposes prothrombotic effects through apo(a), but risk is continuous rather than switching on at one cut-off. [1]
The 2025 ESC/EAS update uses > 50 mg/dL (> 105 nmol/L) as a risk modifier near treatment decisions. Do not convert mg/dL to nmol/L with a fixed factor because apo(a) isoform size varies. [10]
In the case, Lp(a) 150 mg/dL is extremely high. LDL-C 4.8 mmol/L is also severe hypercholesterolaemia and should prompt assessment for secondary causes and possible familial hypercholesterolaemia. The father's event at 60 is important family history but does not meet the usual “premature CAD in a male first-degree relative < 55 years” cut-off. Xanthelasma alone is non-specific. [1,10]
Case blood results: TC 6.7, LDL-C 4.8, HDL-C 1.2, fasting glucose 5.6 mmol/L. The principal abnormalities are very high LDL-C and Lp(a); HDL-C 1.2 is not “low” for an adult man, and a single fasting glucose of 5.6 is not diabetes. [1]
2. Stress Testing (Slides 37–42)
The purpose is to expose a supply–demand mismatch and localise/quantify its consequence. The slide's broad sensitivity/specificity ranges are technology-, population-, and threshold-dependent; they should not be memorised as intrinsic constants. [1,8]
| Slide image | How to read it | Main limitation |
|---|---|---|
| Exercise ECG | Horizontal/downsloping ST depression developing with workload supports subendocardial ischaemia; exercise capacity, symptoms, BP, HR response, and arrhythmia are part of the result | Baseline LBBB, paced rhythm, marked ST abnormality, digoxin effect, and inability to exercise reduce diagnostic value. Exercise ECG is mainly useful for functional/prognostic information where imaging/CCTA is unavailable or likelihood is low. [8] |
| Stress echo | New or worsening regional wall-motion abnormality is the ischaemic signal. Contrast microbubbles can improve endocardial border definition; they are not a coronary shunt test in this context | Image quality and reader dependence; wall-motion change is later in the ischaemic cascade than perfusion abnormality |
| SPECT | A defect present on stress but not rest is reversible ischaemia; a matched fixed defect suggests scar (with artefact/viability caveats). The polar map localises the LAD/LCx/RCA territory | Ionising radiation and attenuation artefact; spatial resolution is lower than PET/CMR |
| Stress perfusion CMR | A subendocardial dark perfusion band during first-pass stress suggests inducible ischaemia. Late gadolinium enhancement is a separate sequence used to map infarct/scar | Availability, claustrophobia, device and gadolinium considerations |
Pharmacological stress agents:
- Dobutamine — β1-agonist → increases HR, contractility, O₂ demand → mimics exercise (C/I: recent MI) [7]
- Adenosine/regadenoson/dipyridamole — produce relative hyperaemia. Distal arterioles beyond a flow-limiting stenosis may already be dilated, so normal territories increase flow more and a relative perfusion defect appears. Agent-specific bronchospasm, conduction, caffeine, and hypotension cautions apply; “coronary steal” is a useful diagram but an oversimplification. [1]
3. CT Coronary Angiogram (CTCA) (Slide 43)
Non-invasive anatomical assessment of the lumen and plaque. The acquisition diagrams show retrospective gating (continuous data with more radiation), prospective triggering (data during selected phases), and high-pitch acquisition. The curved multiplanar reconstructions show calcified and non-calcified lesions matched with invasive angiography. Heavy calcium can create blooming artefact and overestimate stenosis—the mechanism behind the case discrepancy. [1]
Under the 2024 ESC pathway, CCTA is preferred in suspected CCS with low-to-moderate (> 5%–50%) clinical likelihood when image quality is expected to be adequate. It is good for excluding obstructive disease and detecting non-obstructive plaque; functional imaging is favoured when the main question is inducible ischaemia, when CCTA is uncertain/non-diagnostic, or in many patients with established CAD. [8,9]
The slide-44 pathway is historical. A current practical sequence is: [8,9]
Coronary Angiogram (Slide 48)
Indications for coronary angiography: [1]
- Unacceptable angina despite medical therapy (for consideration of revascularisation)
- Non-invasive testing results with high-risk features
- Angina or risk factors for CAD in the setting of depressed LVEF
- For diagnostic purposes when non-invasive testing results are unclear
Modern framing: ICA is appropriate when pre-/post-test likelihood and event risk are high, symptoms are severe or refractory/occur at low workload, or anatomy is needed because revascularisation is a realistic option. Intermediate lesions should be assessed physiologically (FFR/iFR) before PCI unless severity is already unequivocal. [8,9]
In the case (Slides 47–49, 78): CCTA suggested triple-vessel plaque with > 70% mid-LAD stenosis, whereas ICA showed only 30–50% lesions in LAD/LCx/RCA. Calling the latter “triple-vessel disease” can falsely imply severe obstructive disease; it is three-vessel non-obstructive/mild–moderate CAD. Calcium blooming and spatial-resolution limits can make CCTA overestimate the lumen reduction. If symptoms persisted, the next question would not automatically be PCI—it would be functional significance and possible ANOCA/INOCA. [1,8]
Management
The lecture's management section is structured around the ESC 2019 Guidelines (Slides 51–52) and concludes with the memorable ABCDE mnemonic.
- Improve prognosis (prevent MI and death)
- Relieve symptoms (improve quality of life)
1. Rule out and control aggravating conditions (non-cardiac diseases, cardiac diseases, drugs aggravating angina) 2. Smoking cessation 3. Dietary counselling for body weight and lipid control 4. Exercise prescription 5. Treat to targets: hypertension, blood lipids, diabetes [1]
The pyramid and “upper 40%” list are historical. Translate them into a sustainable Mediterranean/plant-forward pattern: vegetables, fruit, legumes, whole grains, nuts, fish and other healthy proteins; replace saturated with unsaturated fat; minimise trans fat, excess sodium, added sugar, and ultra-processed food. Do not prescribe fish-oil supplements or vitamins to prevent events. [11,17]
- Smoking: offer behavioural and pharmacological cessation support; avoid vaping as a routine first-line cessation strategy.
- Activity: reduce sitting time and build aerobic plus resistance activity; a common goal is ≥150 min/week moderate or ≥75 min/week vigorous activity, individualised for symptoms and comorbidity. Offer cardiac rehabilitation when eligible. [11]
- Weight: aim for a healthy, sustainable body composition; the slide's “optimal BMI < 21” is not a treatment target.
- Alcohol: do not encourage a non-drinker to start. If alcohol is used, keep within current low-risk limits; it is not an antianginal or lipid treatment. [17]
Pharmacological Management
| Agent | LDL-C Reduction | CVD Event Reduction Proven? | Key Notes |
|---|---|---|---|
| Statins | 18–55% | Yes | First-line; inhibit HMG-CoA reductase |
| Ezetimibe | 13–20% | Yes | Cholesterol absorption inhibitor; add-on to statin |
| PCSK9 inhibitors | 61–62% | Yes | Monoclonal antibodies (evolocumab, alirocumab); for very high risk |
| Bile-acid sequestrants | 15–30% | Yes | Older agents; GI side effects |
| Bempedoic acid | About 15–25% (context-dependent) | Yes in statin-intolerant high-risk populations | Inhibits ATP-citrate lyase; 2025 ESC/EAS supports use when statins cannot achieve the goal and selected add-on use [10] |
| Fibrates | Variable | No clear mortality benefit | Mainly for triglycerides |
| Nicotinic acid | 5–25% | No incremental ASCVD benefit on top of contemporary therapy | May lower Lp(a), but that does not make it an Lp(a)-outcome treatment |
| Icosapent ethyl | Minimal LDL effect; lowers triglycerides | Yes in selected high-/very-high-risk patients with moderately elevated triglycerides | Do not extrapolate REDUCE-IT to mixed over-the-counter fish-oil products [10,11] |
LDL-C targets (ESC Guideline):
- Very high risk (established CVD): LDL-C < 1.4 mmol/L AND > 50% reduction from baseline
- High risk: LDL-C < 1.8 mmol/L
- Moderate risk: LDL-C < 2.6 mmol/L
In the case: atorvastatin 40 mg + ezetimibe 10 mg reduced LDL-C from 4.8 to 1.4 mmol/L—about a 71% reduction, reaching the very-high-risk target boundary. Confirm adherence/tolerance and repeat lipids; with established coronary plaque and Lp(a) 150 mg/dL, residual risk remains high even when LDL-C is on target. [1,10]
Indications: [1]
- Aspirin in the absence of contraindications (first-line)
- Clopidogrel when aspirin is contraindicated
- Aspirin + P2Y12 blocker after PCI
- Rivaroxaban 2.5 mg BD added to low-dose aspirin (81–100 mg daily) for high-risk CAD/PAD patients
These lines require clinical context. Long-term single antiplatelet therapy is standard after prior MI/PCI and for significant obstructive CAD; clopidogrel 75 mg daily is now an evidence-based alternative to aspirin 75–100 mg after MI/PCI, not merely an allergy substitute. DAPT duration after PCI depends on presentation, stent/lesion complexity, bleeding risk, and any oral-anticoagulant indication. Aspirin plus vascular-dose rivaroxaban is reserved for selected patients with high ischaemic and low bleeding risk—not every stable-CAD patient. [12,13]
Why aspirin? Irreversibly inhibits COX-1 → blocks thromboxane A2 synthesis → reduces platelet aggregation → reduces thrombotic events on atherosclerotic plaques.
Side effects: GI upset (aspirin), bleeding risk.
ACE inhibitors should be prescribed in all patients with stable IHD who also have hypertension, DM, LVEF ≤ 40%, or CKD, unless contraindicated. [1] ARBs are recommended for those intolerant of ACEIs. [1]
Why? ACEIs reduce adverse cardiac remodelling, reduce afterload, have anti-atherosclerotic effects, and reduce morbidity/mortality in high-risk patients.
Side effects/monitoring: cough (ACEI), hypotension, creatinine rise, hyperkalaemia, and angioedema. Check renal function and potassium after initiation/titration. Pregnancy, previous ACEI angioedema, and haemodynamically important bilateral renal-artery stenosis (or stenosis to a solitary functioning kidney) are major cautions/contraindications. Do not combine ACEI and ARB. [1]
In uncomplicated CCS with preserved LV function and no hypertension, diabetes, CKD, or other indication, an ACEI/ARB is not automatically required solely because plaque is present. [12]
a) Beta-Blockers (Slide 62)
First-line monotherapy or in combination with CCB or nitrates to prevent or reduce frequency of angina. [1] Also indicated for systolic LV failure (EF < 40%), heart failure, prior MI, and ventricular rate control in AF. [1]
Mechanism: Block β1-receptors → ↓ heart rate, ↓ contractility, ↓ BP → ↓ myocardial O₂ demand.
Side effects: Bradycardia, syncope, hypotension, bronchospasm, impaired glucose tolerance [1] Avoid/caution: significant bradycardia, sick-sinus syndrome, higher-grade AV block without pacing, decompensated HF, and active bronchospasm. PAD, stable COPD, Raynaud phenomenon, and depression are not blanket contraindications; choose agent/dose and monitor. Pure vasospastic angina is generally treated with a CCB rather than an unopposed non-selective beta-blocker. [8,12]
Outcome trap: beta-blockers relieve angina, but long-term therapy does not improve outcomes in every person with chronic CAD. AHA/ACC does not recommend them solely for outcome improvement without MI in the past year, LVEF ≤50%, or another indication (arrhythmia, hypertension, HFrEF). [12]
Past Paper Alert — Beta-Blocker with Bradycardia
2022 Q35: A 65-year-old man with stable CAD, resting HR 50 bpm. Which first-line anti-anginal? Answer: A. Amlodipine — because beta-blockers are contraindicated with pre-existing bradycardia (HR 50), and non-dihydropyridine CCBs (diltiazem, verapamil) also slow HR. Amlodipine (dihydropyridine) does NOT significantly slow HR. [4]
b) Calcium Channel Blockers (Slides 63–64)
Three types:
- Phenylalkylamine (verapamil-like) — rate-limiting, negative inotropic
- Benzothiazepine (diltiazem-like) — rate-limiting, moderate negative inotropy
- Dihydropyridine (nifedipine/amlodipine-like) — predominantly vasodilating, may cause reflex tachycardia
| Property | Amlodipine (DHP) | Diltiazem (non-DHP) | Verapamil (non-DHP) |
|---|---|---|---|
| Heart rate | ↑/– | ↓ | ↓ |
| SA node | – | ↓ | ↓ |
| AV node | – | ↓ | ↓ |
| Contractility | ↓/– | ↓ | ↓↓ |
| Vascular dilation | ↑↑ | ↑ | ↑ |
| Coronary flow | ↑ | ↑ | ↑ |
Indications: Monotherapy (when beta-blockers contraindicated/intolerant) or combination; vasospastic angina; ventricular rate control in AF. [1] Side effects: Bradycardia (non-DHP), hypotension, peripheral oedema, headache, constipation. [1] Contraindications: AV block, sinus node dysfunction, and HF (non-DHP CCBs). [1]
Rate-slowing combination
Combining verapamil or diltiazem with a beta-blocker can cause severe bradycardia, AV block, hypotension, or worsening HF and is generally avoided unless a specialist deliberately selects and monitors it. A dihydropyridine such as amlodipine is the usual CCB partner for a beta-blocker.
c) Nitrates (Slide 65)
Mechanism: Release NO → activate guanylate cyclase → ↑ cGMP → smooth muscle relaxation → venodilatation (reduces preload) + coronary vasodilatation [1]
Short-acting nitrates: Relieve acute anginal pain; use prophylactically before exertion. [1] Long-acting nitrates: Prevent angina as monotherapy or combination. [1] Side effects: Hypotension, syncope, tachycardia, headache, facial flushing. Less common: methaemoglobinaemia. [1] Contraindications: HOCM (reduces preload → worsens dynamic LVOT obstruction), concomitant PDE-5 inhibitors (sildenafil, tadalafil, vardenafil) — catastrophic hypotension, SBP < 90 mmHg. [1]
Nitrate tolerance: Continuous use leads to reduced efficacy. Managed by providing a nitrate-free interval (usually overnight).
The lecture's “same-day” PDE-5 rule is too vague: commonly used minimum separation is 24 h after sildenafil/vardenafil and 48 h after tadalafil (longer with renal/hepatic impairment or interacting drugs). Riociguat is also contraindicated with nitrates. In obstructive HCM, severe AS, hypotension, or suspected RV infarction, nitrates require individual haemodynamic judgment rather than an automatic home dose. [12]
d) Novel Anti-Ischaemic Agents (Slides 66–68)
| Agent | Mechanism | Key Side Effects |
|---|---|---|
| Ivabradine | Selectively inhibits If current in SA node → ↓ HR without affecting contractility or BP | Phosphenes (visual flashes), bradycardia, AF |
| Ranolazine | Inhibits late inward Na⁺ current → reduces intracellular Ca²⁺ overload and improves diastolic relaxation; unlike the slide-61 label, it is not a fatty-acid oxidation inhibitor | QT prolongation, nausea, headache, dizziness, constipation; important CYP interactions; avoid significant hepatic impairment and use caution/avoidance in severe renal dysfunction |
| Trimetazidine | Shifts myocardial metabolism from fatty acid oxidation to glucose oxidation (more O₂-efficient) | Nausea, vomiting, fatigue, dizziness, myalgia. May induce/worsen Parkinsonism |
| Nicorandil | ATP-sensitive K⁺ channel opener + nitrate-like venous/epicardial dilation | Headache/hypotension and potentially severe mucocutaneous, gastrointestinal, or ocular ulceration/perforation; corticosteroids/NSAIDs may increase GI risk |
Why trimetazidine can improve symptoms: partial inhibition of long-chain 3-ketoacyl-CoA thiolase shifts substrate use towards more oxygen-efficient glucose oxidation. It is a symptom drug where licensed, not established mortality-reducing therapy, and is contraindicated in Parkinson disease/movement disorders and severe renal impairment.
First-line approach (Slide 69): [1]
- Offer a β-blocker (e.g. bisoprolol 5–10 mg daily); aim for HR 50–60 bpm
- If β-blocker contraindicated/not tolerated → rate-controlling CCB (diltiazem or verapamil)
- If rate-controlling CCB unsuitable → DHP-CCB (e.g. amlodipine)
- If symptoms persist → add a long-acting nitrate, nicorandil, ivabradine, or ranolazine
- If still inadequately controlled → refer for revascularisation
- If both β-blockers and CCBs contraindicated → monotherapy with a long-acting nitrate, nicorandil, ivabradine, or ranolazine
Clinical-situation-based algorithm (Slide 70, ESC 2019): [1]
| Clinical Situation | 1st Step | 2nd Step | 3rd Step |
|---|---|---|---|
| Standard | BB or CCB | BB + DHP-CCB | Add 2nd-line drug |
| High HR (> 80 bpm) | BB or non-DHP-CCB | BB + non-DHP-CCB | Add ivabradine |
| Low HR (< 50 bpm) | DHP-CCB | Long-acting nitrate (LAN) | DHP-CCB + LAN; then add nicorandil, ranolazine, or trimetazidine |
| LV dysfunction / HF | BB | Add LAN or ivabradine | Add another 2nd-line drug |
| Low BP | Low-dose BB or low-dose non-DHP-CCB | Add low-dose LAN | Add ivabradine, ranolazine, or trimetazidine |
The 2019 diagrams are useful phenotype maps, not rigid ladders. Current treatment is tailored to BP, heart rate/rhythm, LV function, comorbidity, mechanism (fixed obstruction versus spasm/CMD), interactions, availability, and patient preference. A beta-blocker or CCB is a usual first symptom drug; add or substitute a mechanistically complementary drug if needed. Ivabradine requires sinus rhythm and should not be combined with verapamil/diltiazem. Ranolazine or trimetazidine can be useful when HR/BP are already low. [8,12]
| Class | Mortality Benefit |
|---|---|
| Beta-blockers | Outcome benefit is established in selected settings such as HFrEF and some recent-MI patients—not all stable angina |
| Nitrates | No mortality benefit |
| CCBs | No clear mortality benefit; short-acting nifedipine alone increases reinfarction |
| Ranolazine | Symptom relief; no established mortality benefit |
| Trimetazidine | Symptom relief where licensed; the slide's short-term mortality claim should not be taught as established |
| Nicorandil | Symptom relief; no established all-cause mortality benefit |
Percutaneous Coronary Intervention (PCI):
- Balloon angioplasty + contemporary drug-eluting stent (DES). The slide's bioresorbable scaffold is historical and is not a routine default.
- Requires dual antiplatelet therapy (DAPT: aspirin + P2Y12 inhibitor) post-procedure
- Use FFR/iFR for intermediate lesions when physiology is not already established; radial access lowers access-site bleeding/vascular complications. [8,14]
Coronary Artery Bypass Grafting (CABG):
- The images show an in-situ internal thoracic artery and a free radial-artery conduit, plus CT reconstructions of bypass grafts. LIMA-to-LAD is the anchor graft; the radial artery is preferred over saphenous vein for the next important target when suitable because of better patency/outcomes. [14]
The slide's three-line “CABG preferable” rule is too absolute. Use a Heart Team for prognostically important or complex anatomy, integrating surgical risk, diabetes, LV function, anatomy/complexity, achievable completeness, frailty, life expectancy, and patient goals. [8,14]
- Significant left-main disease: CABG is the overall preferred mode in suitable low-surgical-risk patients; PCI is a guideline-supported alternative in selected low-complexity left-main anatomy (e.g. SYNTAX ≤22) when equivalent complete revascularisation is achievable.
- Complex multivessel disease, especially with diabetes: CABG generally gives better long-term outcomes and fewer repeat procedures than PCI.
- Normal LV function without significant left-main or proximal-LAD disease: revascularisation over GDMT alone has not been shown to prolong overall survival; the major indication is symptom/QoL improvement when angina persists despite tolerated therapy.
- Ischaemic cardiomyopathy/reduced LV function: CABG can confer long-term survival benefit in selected suitable patients.
Historical prognosis graphic (Slide 46): [1]
| Extent of CAD | 5-Year Survival |
|---|---|
| 1-vessel | 93% |
| 2-vessel | 88% |
| 1-vessel, > 95% proximal LAD | 83% |
| 2-vessel, > 95% proximal LAD | 79% |
| 3-vessel | 79% |
| 3-vessel, > 95% in ≥1 vessel | 73% |
| 3-vessel, 75% proximal LAD | 67% |
| 3-vessel, > 95% proximal LAD | 59% |
These survival bars come from an older medical-therapy era and must not be used as a contemporary personalised forecast. Their enduring visual lesson is that LV dysfunction plus greater anatomical jeopardy identifies higher risk; current prognosis also depends on physiology, plaque burden, comorbidities, and modern preventive therapy.
ISCHEMIA Trial (Slide 75): In selected stable patients with moderate-to-severe ischaemia, an initial invasive strategy did not significantly reduce the primary composite endpoint versus an initial conservative strategy (13.3% vs 15.5% at 5 years; adjusted HR 0.93, 95% CI 0.80–1.08; p=0.34). It improved angina most in patients who had frequent symptoms. Do not extrapolate this to groups the trial largely/exclusively did not answer—important left-main disease, severe refractory symptoms, recent ACS, or markedly reduced EF. [1,15]
Treatment: [1]
- Diet advice and smoking cessation
- Aspirin 100mg daily
- Betaloc (metoprolol) 25mg daily
- Atorvastatin 40mg + Ezetimibe 10mg daily → LDL-C dropped to 1.4 mmol/L
No revascularisation was performed because ICA showed only 30–50% lesions without a demonstrated flow-limiting target. “< 70%” is not the full decision rule: intermediate anatomy is judged with physiology (FFR/iFR) or functional imaging, while persistent symptoms with non-obstructive coronaries prompt evaluation for vasospasm/CMD. Medical therapy was appropriate. [8]
ABCDE Approach Rx for IHD: [1]
- A → Anti-platelet agents, Anti-anginal agents & ACEI/ARB, Angioplasty
- B → Beta-blocker, BP control & Bypass
- C → Cholesterol-lowering agents, Cigarette cessation & Calcium channel blockers
- D → Diabetes & Diet management
- E → Education & Exercise
Emerging Approaches: Residual Risk Framework (Slide 80)
Despite optimal evidence-based therapy, residual risk of ASCVD events persists. The lecture identifies six categories of residual risk with corresponding biomarkers and interventions [1]:
| Residual Risk | Biomarker | Potential Intervention | Key Trial Evidence |
|---|---|---|---|
| Cholesterol | LDL-C ≥ 100 mg/dL | Targeted LDL/ApoB reduction | IMPROVE-IT, FOURIER, ODYSSEY |
| Inflammatory | hs-CRP ≥ 2 mg/L | Targeted inflammation reduction | CANTOS, COLCOT, LoDoCo2 |
| Thrombotic | No simple biomarker | Targeted antithrombotic therapy | COMPASS, PEGASUS |
| Triglyceride | TG ≥ 150 mg/dL | Targeted TG reduction | REDUCE-IT |
| Lp(a) | Lp(a) ≥ 50 mg/dL | Targeted Lp(a) reduction | Planned |
| Diabetes | HbA1c; fasting glucose | SGLT2 inhibitors; GLP-1 agonists | EMPA-REG, LEADER, REWIND |
Colchicine for residual inflammatory risk (LoDoCo2): Colchicine vs placebo showed a 31% reduction in the primary composite endpoint (HR 0.69, 95% CI 0.57–0.83) and a 30% reduction in MI (HR 0.70, 95% CI 0.53–0.93), though all-cause mortality was not reduced (HR 1.21, 95% CI 0.86–1.71). [1]
This is a residual-risk framework, not a six-drug checklist. The biomarker thresholds in the slide are trial-entry or risk-modifier thresholds. Low-dose colchicine may be considered in selected chronic-CAD patients after weighing infection, gastrointestinal, renal/hepatic, drug-interaction, and mortality-signal concerns; canakinumab is not routine CCS therapy. As of the 2025 ESC/EAS lipid update, Lp(a) ≥50 mg/dL modifies risk, but no Lp(a)-specific drug had established outcome-guideline use; management intensifies all modifiable risk, particularly LDL-C. [8,10,12]
Special Entities
Occurs at rest, common after cold exposure. Cyclical in nature. ECG: episodic ST-segment elevations. Caused by coronary artery spasm ± superimposed CAD. Patients are more likely to develop ventricular arrhythmias. Rx: CCBs ± Nitrate. [1]
The angiographic sequence shows a normal-appearing vessel at baseline, marked focal narrowing after intracoronary acetylcholine, and reversal with nitroglycerin; the paired ECG demonstrates transient ST elevation during spasm. First-line prevention is a CCB; add a long-acting nitrate or nicorandil if required, and remove triggers such as smoking, cocaine/amphetamines, and vasoconstricting drugs. Avoid assuming every beta-blocker has the same effect, but non-selective beta-blockade without vasodilator activity can worsen spasm and is not the default therapy. [1,8]
ANOCA means angina with no obstructive coronary arteries; INOCA requires objective ischaemia. These are umbrella presentations, not proof of one mechanism. The slide's nested-wheel graphic correctly shows possible cardiac and non-cardiac contributors but uses the older “cardiac syndrome X” label. [8]
Important endotypes frequently overlap:
| Endotype | How it is demonstrated | Mechanism-led therapy |
|---|---|---|
| Structural CMD | Reduced CFR and/or raised IMR during adenosine testing | Risk-factor therapy; beta-blocker, CCB, ranolazine and/or ACEI according to phenotype |
| Epicardial vasospasm | Acetylcholine reproduces symptoms/ECG change with severe epicardial constriction, reversed by nitrate | CCB first-line; nitrate/nicorandil add-on |
| Microvascular spasm | Symptoms and ischaemic ECG change with acetylcholine but no ≥90% epicardial constriction | CCB-led therapy; other antianginals as needed |
| Altered pain perception/non-cardiac pain | Coronary function normal and alternative explanation found | Reassurance plus mechanism-specific non-cardiac care; selected behavioural/pain approaches |
PET/CMR can quantify myocardial blood-flow reserve, but persistent symptoms after non-obstructive CCTA/ICA despite GDMT warrant invasive coronary functional testing with FFR/iFR, CFR, IMR and acetylcholine to define the endotype. External counterpulsation or neuromodulation is reserved for carefully selected refractory cases. [8,16]
The lecture concludes with a four-step structured approach to stable angina [1]:
- Exclude ACS and non-cardiac chest pain — detailed history and PE; determine QoL impact; identify HF or valvular disease; estimate pre-test probability for CAD
- Assess objective risk markers — ECG (identify LBBB, prior infarction, LVH); consider echocardiography (LV dysfunction, valve disease); laboratory tests (renal function, DM, dyslipidaemia, hs-cTnT, NT-proBNP)
- Consider anatomical or functional testing — defer if symptoms infrequent and no high-risk findings; CTCA to detect/exclude obstructive CAD and left main/triple-vessel disease; stress testing if functional assessment desired or known CAD; invasive angiography for equivocal non-invasive results or revascularisation planning
- Manage stable angina — secondary prevention (high-potency statin, low-dose aspirin); anti-anginal therapy (β-blocker, CCB, nitrates); consider SGLT2i or GLP-1RA if diabetic; CABG if left main or triple-vessel disease with DM or LV dysfunction; titrate anti-anginals based on symptoms, HR, and BP; PCI for persistent angina impairing QoL
The illustrations show three different lesions: (1) an anomalous left coronary arising from the right sinus and passing between aorta and pulmonary artery, (2) an RCA-to-right-ventricular fistula, and (3) an acute-angle/slit-like anomalous origin on CCTA. Do not collapse all anomalies into one risk category. [1]
- High-risk AAOCA features include an interarterial/intramural proximal course, slit-like ostium, and acute take-off; resting examination and ECG may be normal.
- Coronary CT is preferred to define origin/course and ostial anatomy; stress imaging assesses inducible ischaemia.
- Exertional syncope/chest pain, ventricular arrhythmia, documented attributable ischaemia, and high-risk anatomy require congenital/sports-cardiology and surgical review. Surgery is recommended when symptoms or diagnostic ischaemia are attributable to AAOCA; selected asymptomatic anatomy may be observed after expert assessment.
- Sports advice is anatomy-, age-, symptom-, and ischaemia-specific. Blanket permanent exclusion based on an incidental benign variant is inappropriate. [18,19]
High Yield Summary
- Summary
- Chronic coronary syndromes reflect structural and/or functional epicardial or microvascular disease causing a supply–demand mismatch. Typical stable angina is reproducible pressure/tightness with exertion or another demand trigger and improves with rest or nitrate; new/rest/crescendo symptoms require ACS assessment.
- Estimate risk-factor-weighted clinical likelihood, not the old age/sex table alone. CCTA is preferred to rule out obstructive CAD and show plaque at low–moderate likelihood; functional imaging answers the ischaemia question; ICA is for high likelihood/risk, refractory low-workload symptoms, or revascularisation planning, with FFR/iFR for intermediate lesions.
- Treat two tracks together: (1) event prevention—smoking cessation, exercise/rehab, heart-healthy diet, BP/diabetes care, intensive LDL lowering, and indication-specific antithrombotic/RAAS therapy; (2) symptom relief—short-acting nitrate plus a beta-blocker or CCB tailored to HR, BP, LV function, mechanism, and comorbidity, adding alternatives as needed.
- Revascularise for refractory symptoms or prognostically important anatomy/physiology. CABG is generally preferred for suitable left-main or complex multivessel disease, especially diabetes; PCI is appropriate for selected anatomy. In normal LV function without significant left-main/proximal-LAD disease, routine revascularisation over GDMT does not prolong overall survival.
- Non-obstructive angiography is not the end of the work-up when symptoms persist: evaluate ANOCA/INOCA endotypes (structural CMD, microvascular or epicardial spasm). Variant angina is CCB-led; AAOCA risk depends on precise anatomy and attributable ischaemia.
Active Recall - Lecture Notes
[1] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (slides 1–86) [2] Senior notes: Block A - Accelerating chest pain_ Acute Coronary Syndromes.pdf (p1 — same patient reference) [3] Senior notes: Ryan Ho Cardiology.pdf (pp. 54–57, 115 — CCS grading, angina equivalents, clinical approach) [4] Past papers: 2022 Fourth Summative MCQ.pdf (Q34, Q35) [5] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (pp. 11, 13, 15, 19) [6] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Q11) [7] Senior notes: Maksim Medicine Notes.pdf (p7 — stress testing methods, pharmacological agents) [8] ESC. 2024 Guidelines for the management of chronic coronary syndromes. Eur Heart J. 2024;45:3415–3537. https://academic.oup.com/eurheartj/article/45/36/3415/7743115 [9] ESC. 2024 chronic coronary syndrome guideline update: stepwise diagnosis and test selection. https://www.escardio.org/news/news-room/congress-news/2024-esc-clinical-practice-guidelines-on-chronic-coronary-syndromes/ [10] ESC/EAS. 2025 Focused Update of the 2019 dyslipidaemia guideline. https://www.escardio.org/news/news-room/congress-news/2025-focused-update-dyslipidaemias/ [11] AHA/ACC/ACCP/ASPC/NLA/PCNA. 2023 Chronic Coronary Disease Guideline—Top Things to Know. https://professional.heart.org/en/science-news/2023-guideline-for-the-management-of-patients-with-chronic-coronary-disease/top-things-to-know [12] Virani SS, et al. 2023 Guideline for the Management of Patients With Chronic Coronary Disease. https://professional.heart.org/en/guidelines-statements/2023-ahaaccaccpaspcnlapcna-guideline-for-the-management-of-patients-withcir0000000000001168 [13] ESC. Antithrombotic changes in the 2024 CCS guideline. Eur Heart J Cardiovasc Pharmacother. 2024;10:572–575. https://academic.oup.com/ehjcvp/article/10/7/572/7759705 [14] ACC/AHA/SCAI. 2021 Coronary Revascularization Guideline—Top Things to Know. https://professional.heart.org/en/science-news/2021-acc-aha-scai-guideline-for-coronary-artery-revascularization/top-things-to-know [15] ESC. ISCHEMIA-EXTEND overview. https://esc365.escardio.org/journal/71163 [16] ESC. 2024 ANOCA/INOCA diagnosis and management recommendations. https://academic.oup.com/eurheartj/article/45/36/3415/7743115 [17] AHA. 2026 Dietary Guidance to Improve Cardiovascular Health—Top Things to Know. https://professional.heart.org/en/science-news/2026-dietary-guidance-to-improve-cardiovascular-health/top-things-to-know [18] ESC. 2020 Adult Congenital Heart Disease Guideline—anomalous coronary arteries. https://academic.oup.com/eurheartj/article/42/6/563/5898606 [19] ESC. 2020 Sports Cardiology Guideline—anomalous coronary origin and exercise. https://academic.oup.com/eurheartj/article/42/1/17/5898937
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