Cardiology
Chronic Coronary Syndrome
Also known as Stable angina · Stable ischaemic heart disease · SIHD · Stable angina pectoris · Chronic coronary disease
Chronic coronary syndrome (CCS) is the modern umbrella term replacing "stable angina" for the long-term presentations of coronary artery disease. Defined by the 2019 ESC Guidelines as the spectrum of clinical presentations driven by chronic, often predictable, myocardial ischaemia typically precipitated by exertion or emotional stress and relieved by rest or sublingual nitrates. Anatomically it is the consequence of fixed or dynamic epicardial coronary stenosis (atherosclerotic plaque with intact fibrous cap), microvascular dysfunction, or vasospasm. The classic presentation is substernal chest discomfort provoked by exertion, lasting under 10 minutes, and relieved by rest or nitroglycerin (CCS grade I-IV / Canadian Cardiovascular Society grading). Diagnosis is clinical plus exclusion of ACS (serial hs-troponin negative, no dynamic ST-T changes); risk stratification uses pre-test probability, coronary CT angiography or functional stress imaging, with invasive angiography reserved for high event risk or refractory symptoms. Management rests on four pillars: (1) disease-modifying secondary prevention (aspirin, high-intensity statin with LDL target below 1.4 mmol/L in very high risk, ACE inhibitor where indicated), (2) symptom control (beta-blocker or calcium-channel blocker first-line, nitrates for acute relief, ranolazine/ivabradine second-line), (3) lifestyle and risk-factor modification, and (4) revascularisation for prognostic left-main/multivessel disease or refractory angina despite optimal medical therapy.
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Meet the patient
A 62-year-old smoker with hypertension gets a tight central ache every time he hurries up the hill to the bus stop — it lifts within two minutes of standing still and never comes at rest. His ECG between episodes is normal. The registrar's reflex is "cardiology, stent him". The two questions that decide his next six months are the two that decide every CCS case: is this obstructive coronary disease? (pre-test probability plus a functional or CTCA test answers it), and does he need a stent or just tablets? (the COURAGE, ISCHEMIA and ORBITA evidence answers it, usually in favour of tablets).[1]
Hold those two questions and the whole topic slots into place — CCS is a supply-demand disease you manage with drugs and stents you reserve, not a plumbing emergency you reperfuse.[1]
One disease, six faces — the 2019 ESC rebrand
"Stable angina" was retired in 2019; "chronic coronary syndrome" replaced it. The 2019 ESC Guidelines (Knuuti) reframed coronary disease as a lifelong continuum a patient drifts in and out of, not a binary stable-or-unstable label — because the same patient with exertional angina today is one plaque rupture away from ACS tomorrow.[1]
CCS spans six clinical scenarios the 2019 ESC document lists, and a final-prof candidate is expected to reproduce them:[1]
Six faces of CCS (2019 ESC)
- 1. Suspected CAD with stable anginal symptoms, with or without dyspnoea
- 2. New-onset heart failure or LV dysfunction with suspected CAD (silent ischaemia included)
- 3. Stabilised after an ACS, once the acute phase has settled on guideline therapy
- 4. One year or more after revascularisation (PCI or CABG), stable or silent
- 5. Ischaemia with non-obstructive coronary arteries — INOCA
- 6. Silent ischaemia found on provocative testing
The teaching point examiners reward: CCS is not "no acute event" — it is a phase of a chronic disease that includes patients years after their stent, patients with heart failure from silent ischaemia, and the woman with INOCA whose angiogram is clean but whose microcirculation is not. The 2013 ESC stable-CAD guideline (Montalescot) was the predecessor that introduced the diamond pre-test-probability model the 2019 update built on.[7]
The therapeutic objectives fall into three, and they map onto the rest of this topic: prevent events (MI, stroke, death — the job of disease-modifying therapy), relieve symptoms (the job of anti-anginals and revascularisation), and preserve function (lifestyle, rehab, risk-factor control).[2]
The three faces of chest pain — typical, atypical, non-anginal
The history does more diagnostic work than any single test in CCS — but only if you classify the pain correctly. Three features define typical angina, and how many a patient has sets the pre-test probability: retrosternal site, provocation by exertion or emotion, and relief by rest or nitrates within minutes.[1]
| Pain type | Defining features | One-line discriminator |
|---|---|---|
| Typical angina | All three features: substernal, provoked by exertion or emotion, relieved by rest or GTN within minutes; lasts under 10 min | Reproducible exertional threshold plus relief by GTN equals a fixed stenosis until shown otherwise |
| Atypical angina | Two of the three features | Investigate — pre-test probability is intermediate |
| Non-anginal pain | One or none; sharp, pleuritic, positional, or unrelated to exertion | Look hard for a non-cardiac cause first — but exclude ACS if any red flag |
Pre-test probability of obstructive CAD is then modelled from age, sex, and symptom character (the diamond-modified model carried forward from the 2013 ESC guideline) and drives the very next test: low probability — reassure, do not test; intermediate — CTCA or functional imaging; high — go straight to invasive angiography.[7]
Everyone forgets: the classic descriptors are pressure, heaviness, tightness or squeezing — patients rarely volunteer the word "pain", and a careful historian who lets the patient describe it in their own words catches far more angina than one who ticks boxes.[1]
Up to a third of patients — women, the elderly, diabetics — never describe typical pain at all; their angina hides behind an anginal equivalent such as exertional dyspnoea, fatigue, or epigastric discomfort. Treat exertional dyspnoea in a smoking diabetic as ischaemia until you have proved it is not.[1]
The CCS grading — and the IV-equals-hospital trap
The Canadian Cardiovascular Society (CCS) grading is the bedside severity scale every angina stem expects you to quote — and it carries one trap that bites.[7]
CCS angina grading — the number rule
- CCS I — ordinary activity does NOT cause angina; only strenuous, rapid or prolonged exertion
- CCS II — slight limitation; rapid activity, cold, emotion, after meals; over one flight or 100 to 200 m on the flat
- CCS III — marked limitation; one flight of stairs or 100 to 200 m on the flat brings it on
- CCS IV — angina at REST or with any activity; unable to do anything without discomfort
The classic trap: CCS class IV means rest angina — and rest angina is unstable angina until proven otherwise, not a stable outpatient you book into a clinic in six weeks. The moment pain occurs at rest, crosses 20 minutes, accelerates over days (crescendo), or comes with dynamic ECG changes, the patient has crossed the CCS-to-ACS border and belongs on the NSTE-ACS pathway.[1]
Pathophysiology — the fixed plaque and the ischaemia cascade
The CCS plaque is the stable twin of the ACS plaque: a thick fibrous cap over a small lipid core, not a thin cap primed to rupture. Atherosclerosis begins in childhood as a fatty streak, matures over decades, and the lesion of stable angina is the end of that slow road — fixed, calcified, and predictable.[1]
Stable vs vulnerable plaque — the cap decides
- Stable (CCS) plaque — thick fibrous cap, small lipid core, heavy calcification; produces a FIXED stenosis and predictable exertional pain
- Vulnerable (ACS) plaque — thin-cap fibroatheroma, large lipid core, dense macrophages; primed to rupture or erode and occlude abruptly
- The same patient carries both — statins stabilise caps, which is why they reduce events without reopening the lumen
The ischaemia in CCS is supply-demand mismatch, not acute occlusion. Demand rises with heart rate, contractility, and wall stress during exertion; supply is fixed by the stenotic segment and a finite coronary flow reserve. As the stenosis narrows the lumen, the reserve is exhausted at lower workloads — so the angina threshold becomes reproducible ("three flights always brings it on"), which is itself the bedside marker of a fixed plaque versus vasospasm or microvascular disease.[1]
When demand outruns supply, ischaemia unfolds down a fixed cascade — and each step is one a test can catch before the patient feels pain:[4]
The ischaemia cascade — symptoms appear last
Perfusion heterogeneity
Blood flow diverges between ischaemic and normal territories — the earliest sign, detectable on myocardial perfusion imaging
Diastolic dysfunction
Ischaemic segments fail to relax — impaired filling
Regional wall-motion abnormality
Hypokinesia or akinesia on stress echo — the basis of stress echocardiography
ECG change
ST depression (subendocardial ischaemia) or, less often, ST elevation
Angina — the last symptom
Pain arrives seconds to minutes AFTER the preceding four; by the time it hurts, ischaemia is well established
Two non-obstructive mechanisms explain most "angina with clean angiograms". INOCA — ischaemia with non-obstructive coronary arteries — is microvascular dysfunction (arterioles under 500 micrometres) with exhausted flow reserve; up to half of women and a third of men referred for elective angiography have no obstructive epicardial disease. Prinzmetal (vasospastic) angina is focal or diffuse epicardial spasm, classically at rest in the early morning, with transient ST elevation.[1]
Investigations — pick the test by pre-test probability
The single most important investigation decision in CCS is NOT which test — it is whether to test at all, and that decision is set by the pre-test probability. The 2019 ESC framework routes patients by probability to avoid low-yield testing and incidental findings.[1]
Every patient first gets the baseline bundle: a 12-lead ECG (often normal between episodes, but may show a prior Q-wave infarct, LVH, or conduction disease), bloods (FBC — anaemia precipitates angina; renal function; fasting lipids including lipoprotein(a); HbA1c; thyroid function; NT-proBNP if heart-failure signs), and a chest X-ray.[1]
| Test | Sensitivity / specificity | When to use it |
|---|---|---|
| Exercise ECG (treadmill) | Sensitivity ~65-75 percent, specificity ~75-85 percent | First-line when no resting ECG abnormality and the patient can exercise; ST depression over 1 mm at low workload is high-risk |
| Stress echocardiography | Sensitivity ~80-90 percent, specificity ~80-90 percent | Better than exercise ECG when the resting ECG is abnormal (LBBB, LVH, paced) |
| Myocardial perfusion scintigraphy (MPS) | Quantifies perfusion territory and ejection fraction | When stress echo is unavailable or operator-dependent |
| Stress cardiac MRI | Perfusion, wall motion, viability, right ventricle | Preferred in younger patients and women — no radiation |
| CT coronary angiography (CTCA) | High negative predictive value; Agatston calcium score | Intermediate pre-test probability; the 2019 ESC anatomical test of choice, especially younger patients |
| Invasive coronary angiography | Gold-standard anatomy | High pre-test probability, positive or high-risk non-invasive test, or refractory symptoms |
The physiology numbers — FFR and iFR — are what turn an angiogram into a treatment decision. Anatomy alone over-reads significance; physiology tells you whether a stenosis actually matters.[1]
The two physiology thresholds that decide on a stent
A stenosis that looks ugly on angiography but has an FFR above 0.80 does not need a stent — leave it. FAME 2 is the trial: FFR-guided PCI plus optimal medical therapy cut the composite of death, MI, and urgent revascularisation versus medical therapy alone, driven almost entirely by fewer urgent revascularisations.[4]
High-risk features on any non-invasive test push a patient straight to invasive angiography regardless of probability: left main disease, severe proximal LAD, three-vessel disease with diabetes, LVEF under 50 percent with ischaemia, or a large perfusion defect.[3]
The four pillars of therapy
CCS therapy is four pillars, and the disease-modifying backbone comes first because it is what actually saves lives — the anti-anginals and the stent only make the patient comfortable.[1]
The four pillars of CCS therapy
- 1. Lifestyle — smoking cessation (the single biggest lever), Mediterranean diet, 150 min per week exercise, weight to BMI 20 to 25, alcohol under 14 units per week, cardiac rehab
- 2. Disease-modifying — aspirin 75 to 100 mg daily, atorvastatin 40 to 80 mg nocte, ACE inhibitor (ramipril 2.5 to 10 mg daily) where hypertension, diabetes, CKD or prior MI
- 3. Anti-anginal — bisoprolol first, then amlodipine, then isosorbide mononitrate, then nicorandil, ranolazine or ivabradine
- 4. Revascularisation — PCI or CABG, physiology-guided, for refractory symptoms or high-risk anatomy
CCS — the disease-modifying and anti-anginal doses
The disease-modifying detail examiners test: a high-intensity statin (atorvastatin 40 to 80 mg nocte, or rosuvastatin 20 to 40 mg nocte) for every CCS patient regardless of baseline LDL — add ezetimibe 10 mg daily if LDL-C is above 1.8 mmol/L (above 1.4 mmol/L in very high risk), and a PCSK9 inhibitor (evolocumab 140 mg subcutaneously every 2 weeks, alirocumab 75 to 150 mg every 2 weeks) if still above target.[2]
Lifestyle is not a footnote. Smoking cessation cuts mortality by 25 to 50 percent over 5 to 10 years — the single most impactful intervention in CCS, and the one most likely to be skipped in a busy clinic. Reinforce it at every visit, alongside the Mediterranean diet, 150 minutes per week of exercise, and structured cardiac rehabilitation (class I after MI and revascularisation).[2]
The anti-anginal ladder — bisoprolol first, then build
Anti-anginals relieve symptoms; they do not improve prognosis. That distinction is the whole point of the stepwise ladder — start one agent, titrate, add a second, and only escalate to a third or to revascularisation when two agents at optimal dose have failed.[7]
The anti-anginal stepwise ladder
1. Beta-blocker first-line — bisoprolol 2.5 to 10 mg daily (or metoprolol 25 to 100 mg twice daily)
Lowers rate and contractility; target resting HR 55 to 60; avoid in asthma, decompensated HF, AV block
2. Add a long-acting CCB — amlodipine 5 to 10 mg daily
Dihydropyridine, no rate effect, safe WITH a beta-blocker where BP allows
3. Add a long-acting nitrate — isosorbide mononitrate 30 to 60 mg daily
Asymmetrical dosing preserves a nitrate-free interval to prevent tolerance; sublingual GTN 0.4 mg for acute episodes and pre-exertional prophylaxis
4. Third-line add-ons — nicorandil 5 to 30 mg daily, ranolazine 375 to 500 mg twice daily, ivabradine 5 to 7.5 mg twice daily
Ivabradine only in sinus rhythm with HR above 70 despite beta-blocker; ranolazine useful in microvascular angina and diabetes
Three named traps on this ladder cost marks and harm patients:[1]
- Diltiazem or verapamil WITH a beta-blocker equals bradycardia and AV block. These are the rate-lowering non-dihydropyridine CCBs — never combine them with a beta-blocker. Amlodipine is the dihydropyridine you CAN combine safely.
- Nitrates plus a PDE5 inhibitor (sildenafil and similar agents) equals life-threatening hypotension. Nitrates are contraindicated within 24 hours of a PDE5 inhibitor — ask before you prescribe.
- Nitrate tolerance. A nitrate-free interval of 8 to 12 hours (asymmetric dosing) preserves the effect — a round-the-clock nitrate simply stops working.[7]
Revascularisation — symptoms, not survival, for most
This is the single most examinable controversy in CCS, and the four trials below are the answer to "does this patient need a stent?". For most stable patients without high-risk anatomy, optimal medical therapy is first-line, and a stent relieves symptoms rather than saving lives.[2]
| Trial | Headline finding | One-line discriminator |
|---|---|---|
| COURAGE (2007) | PCI plus OMT vs OMT alone in 2,287 stable-CAD patients — no difference in death or MI over 4.6 years; better early symptom control, narrowing over time | No survival benefit from PCI over tablets in stable CAD |
| ISCHEMIA (2020) | Initial invasive vs conservative strategy in 5,179 with moderate-severe ischaemia — no difference in death or MI over 3.2 years; better symptom control in high-angina patients | Even moderate-severe ischaemia does not mandate an invasive strategy for survival |
| ORBITA (2018) | PCI vs sham procedure in 200 with single-vessel stable angina — the placebo-controlled exercise-time benefit was smaller than believed | Part of PCI symptom benefit is a placebo effect — informed consent matters |
| FAME 2 (2014) | FFR-guided PCI plus OMT vs OMT alone in 888 — reduced the composite of death, MI, urgent revascularisation, driven by fewer urgent revascularisations | Physiology-guided PCI (FFR below 0.80) reduces events — stent the stenoses that matter |
So when DO you revascularise for prognosis rather than symptoms? The exceptions the trials left standing: left main disease, proximal LAD disease, three-vessel disease with LV dysfunction or diabetes (where FREEDOM favoured CABG over PCI), and critical anatomy with a large ischaemic burden. CABG is preferred over PCI for left main and diabetic multivessel disease; bilateral internal mammary grafts where feasible.[3]
The honest consultant line: revascularise for symptoms when two anti-anginals at optimal dose have failed and the FFR is below 0.80; revascularise for prognosis when the anatomy is high-risk. For everyone in between, intensify the medical therapy and the lifestyle work — and tell the patient honestly what ORBITA found.[4]
The subtypes that bite
CCS is an umbrella, and several faces under it demand a different pathway from "stent the fixed plaque". Name them because each changes management.[1]
The subtypes that change the pathway
- INOCA — ischaemia with non-obstructive coronary arteries; microvascular dysfunction, commoner in women; beta-blocker first-line, ranolazine, CCB or ACEI add-on; the angiogram is clean but the patient is not
- MINOCA — MI with non-obstructive coronaries (under 50 percent); plaque erosion with lysis, spasm, microvascular dysfunction, thromboembolism; myocarditis and takotsubo are mimics; cardiac MRI is diagnostic
- Prinzmetal (vasospastic) angina — rest pain, transient ST elevation, normal exercise capacity; CCB first-line and nitrates, smoking cessation; AVOID beta-blocker monotherapy (unopposed alpha vasoconstriction)
- Silent ischaemia — ST changes or perfusion defects without symptoms; diabetics, CKD, elderly, post-CABG; same prognostic weight as symptomatic ischaemia
- Post-revascularisation CCS — over 12 months after PCI or CABG; in-stent restenosis in the first year, graft disease (venous grafts degenerate after 7 to 10 years) and native progression later
- Refractory angina — CCS III or worse for over 3 months despite OMT and revascularisation; enhanced external counterpulsation, spinal cord stimulation, transmyocardial revascularisation, CTO-PCI in selected centres
The classic trap on subtypes: a woman with exertional dyspnoea, a positive stress test, and a clean angiogram does NOT have "non-cardiac pain" — she has INOCA, and the right move is anti-anginal therapy directed at the microcirculation, not reassurance and discharge.[1]
Complications — when stable disease turns
Untreated or under-treated CCS does not stay stable. It drifts towards four outcomes, and the dominant one is the event this whole topic exists to prevent.[1]
- Acute coronary syndrome — the vulnerable twin plaque ruptures; this is the event disease-modifying therapy exists to prevent, and it is why a "stable" patient who suddenly changes pattern has crossed the border.
- Heart failure — two mechanisms: acute ischaemic stunning with adverse remodelling, or chronic hibernation of viable myocardium that recovers with revascularisation.
- Arrhythmia — atrial fibrillation from atrial ischaemia and age; ventricular arrhythmia (VT or VF) from scar or LV dysfunction, driving ICD decisions.
- Functional decline — uncontrolled angina limits activity, work, and independence; depression and anxiety amplify symptoms.[2]
Chronic total occlusion of an epicardial artery beyond 3 months may develop silently, contributing to LV dysfunction or recurring angina despite medical therapy — and is increasingly amenable to specialised CTO-PCI.[2]
Annual all-cause mortality in modern CCS cohorts runs from under 1 percent in low-risk outpatients to over 5 percent with multivessel disease and LV dysfunction — which is why risk stratification (LV function, ischaemic burden, diabetes, CKD) matters more than the label "stable".[3]
How CCS patients come to harm — the preventable list
- The patient sent home with "gastritis" who was crescendo-ing into an MI — the preventable ACS.[1]
- A stent placed for a stenosis with FFR above 0.80 — bleeding and procedural risk for a lesion that did not matter.[4]
- A round-the-clock nitrate with no nitrate-free interval — tolerance, and angina back within weeks.[7]
- Diltiazem added to a beta-blocker — bradycardia and AV block on the ward.[7]
- GTN given to a patient who took sildenafil the night before — profound hypotension.[2]
- A diabetic with silent ischaemia told their normal ECG means "no heart disease" — the MI that was never investigated.[1]
- OMT abandoned the moment a stent goes in — the statin and ACE inhibitor are what prevent the next event, not the stent.[2]
Special populations — thresholds and choices change
Examiners use these heavily on NEET-PG and INICET, and each changes both the work-up and the treatment.[1]
Women. Atypical presentations dominate (dyspnoea, fatigue, epigastric discomfort over substernal pressure); pre-test probability of obstructive CAD is lower, and INOCA and microvascular angina are commoner. Stress echo or MRI beats exercise ECG; CTCA is reliable. Anti-anginal choice is similar, but ACEi or ARBs are teratogenic in pregnancy — and women still receive less aggressive secondary prevention despite higher absolute risk.[1]
Diabetes. Accelerated atherosclerosis, multivessel and silent disease, worse prognosis — a lower threshold for invasive investigation. SGLT2 inhibitors and GLP-1 receptor agonists add cardiovascular benefit beyond glycaemic control. For diabetic multivessel disease, FREEDOM favoured CABG over PCI, though modern drug-eluting stents have narrowed the gap.[3]
Chronic kidney disease. Both a risk marker and a therapeutic limit — no NSAIDs, contrast-sparing for CTCA and angiography, dose-adjusted antithrombotics, and close creatinine monitoring with ACEI or ARB. Stress MRI is preferred where available; bleeding risk is high. Joint cardiology-nephrology review for advanced CKD.[5]
The elderly and frail. Multivessel disease, prior MI, CKD, and atrial fibrillation commonly coexist; presentations are atypical (fatigue, falls, confusion). Polypharmacy and bleeding risk demand careful dose titration and a deprescribing review. Guide revascularisation by biological, not chronological, age, with shared decision-making — the 2012 ACCF/AHA stable ischaemic heart disease guideline (Fihn) still anchors these nuanced risk recommendations.[5]
Prior CABG. CTCA is hampered by metal-clip artefacts, so functional imaging is more reliable; weigh redo CABG versus PCI for graft versus native disease individually. Venous grafts degenerate after 7 to 10 years — new angina in a grafted patient is graft disease or native progression until shown otherwise.[2]
The trials that changed practice
The 2019 ESC CCS Guidelines unified the stable-CAD landscape under one umbrella and made pre-test-probability testing and FFR-guided revascularisation the defaults. The landmark trials an examiner expects you to cite, and what each changed:[1]
COURAGE (2007; NEJM)
Population: 2,287 patients with stable CAD
Key finding
No significant difference in death or MI over 4.6 years; better early symptom control with PCI, narrowing over time.
ISCHEMIA (2020; NEJM)
Population: 5,179 patients with moderate or severe ischaemia on stress testing
Key finding
No significant difference in death or MI over 3.2 years; invasive strategy better for symptom control in patients with daily or weekly angina.
FAME 2 (2014; NEJM)
Population: 888 patients with FFR 0.80 or below
Key finding
PCI reduced the composite of death, MI, and urgent revascularisation, driven primarily by fewer urgent revascularisations; mortality and MI alone did not differ.
ORBITA (2018; Lancet)
Population: 200 patients with stable angina and single-vessel disease
Key finding
At 6 weeks the placebo-controlled improvement in exercise time was smaller than previously believed; symptom scores improved more with PCI.
The 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS stable ischaemic heart disease guideline (Fihn) is the parallel North American document still referenced for nuanced risk recommendations, and the 2013 ESC stable-CAD guideline (Montalescot) was the immediate predecessor that introduced the diamond pre-test-probability model.[5][7]
Newer secondary-prevention evidence — COMPASS (low-dose rivaroxaban 2.5 mg twice daily plus aspirin) and LoDoCo2 (low-dose colchicine 0.5 mg daily) — has expanded the medical toolkit for high-risk stable CAD, on top of SGLT2-inhibitor and GLP-1-agonist benefit in diabetes.[2]
The mantra, and the mnemonic
BAINR
Beta-blocker first (bisoprolol 2.5 to 10 mg daily; target HR 55 to 60)
Add amlodipine 5 to 10 mg daily (dihydropyridine, safe with the beta-blocker)
Isosorbide mononitrate 30 to 60 mg daily — preserve a nitrate-free interval
Nicorandil, ranolazine, ivabradine — third-line add-ons
Revascularise for symptoms (refractory) or prognosis (high-risk anatomy) — FFR below 0.80
The mantra: Tablets save lives, stents relieve symptoms — revascularise the stenosis whose FFR is below 0.80 and the anatomy that is high-risk, and never call rest angina stable.[1][2]
Ward-round test — three stems, thirty seconds each
Stem 1 — the man from the top of the topic (answer)
The 62-year-old smoker with exertional central ache relieved by rest, normal ECG between episodes. His pre-test probability is intermediate. The registrar says "stent him". What do you actually do? Model: This is classic CCS. Confirm obstructive disease with an intermediate-probability test — CT coronary angiography (the 2019 ESC anatomical choice) or stress imaging. Start the disease-modifying backbone now — aspirin 75 to 100 mg daily, atorvastatin 40 to 80 mg nocte, an ACE inhibitor for his hypertension, plus smoking cessation — and a first-line anti-anginal bisoprolol 2.5 to 10 mg daily with sublingual GTN for episodes. Do NOT default to a stent: COURAGE and ISCHEMIA showed no survival benefit of PCI over optimal medical therapy in stable CAD. Reserve revascularisation for refractory symptoms or high-risk anatomy, FFR-guided (below 0.80).[2]
Stem 2 — the woman with a clean angiogram (answer)
A 58-year-old woman has exertional dyspnoea, a positive stress test, and an invasive angiogram showing no obstructive epicardial disease. The team calls it non-cardiac and plans discharge. What is the diagnosis and the right move? Model: This is INOCA — ischaemia with non-obstructive coronary arteries, driven by coronary microvascular dysfunction (and possibly vasospasm). It is NOT non-cardiac pain. The right move is anti-anginal therapy directed at supply-demand matching — a beta-blocker first-line, with ranolazine, a calcium-channel blocker, or an ACE inhibitor as add-ons — and structured risk-factor modification. Up to half of women referred for elective angiography have no obstructive epicardial disease, and dismissing them is the recurring error.[1]
Stem 3 — the patient whose pattern changed (answer)
A known CCS patient telephones: the pain that used to come after three flights now comes after one, woke him at 4am, and lasted 25 minutes. What has happened, and what do you do in the next hour? Model: This is crescendo angina with rest pain — unstable angina or NSTE-ACS until proven otherwise, not a stable-clinic follow-up. Activate the chest-pain pathway: resting ECG within 10 minutes, high-sensitivity troponin, a GRACE or HEART score, admit to coronary care, give aspirin 300 mg loading then 75 to 100 mg daily plus a P2Y12 inhibitor and an anticoagulant, anti-ischaemic therapy, and arrange early invasive angiography within 24 to 72 hours by risk. The change in pattern is the whole clue — CCS class IV (rest) means hospital.[3]
References
- [1]Knuuti J, Wijns W, Saraste A, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. European Heart Journal, 2020.PMID 31504439
- [2]Boden WE, O'Rourke RA, Teo KK, et al. (COURAGE Trial Research Group) Optimal medical therapy with or without PCI for stable coronary disease. New England Journal of Medicine, 2007.PMID 17387127
- [3]Maron DJ, Hochman JS, Reynolds HR, et al. (ISCHEMIA Investigators) Initial Invasive or Conservative Strategy for Stable Coronary Disease. New England Journal of Medicine, 2020.PMID 32227755
- [4]De Bruyne B, Fearon WF, Pijls NH, et al. (FAME 2 Trial Investigators) Fractional flow reserve-guided PCI for stable coronary artery stenosis. New England Journal of Medicine, 2014.PMID 25176289
- [5]Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients with stable ischemic heart disease. Journal of the American College of Cardiology, 2012.PMID 23182125
- [6]Al-Lamee R, Thompson D, Dehbi HM, et al. (ORBITA Investigators) Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial. Lancet, 2018.PMID 29103656
- [7]Task Force Members, Montalescot G, Sechtem U, et al. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J, 2013.PMID 23996286