Coronary Artery Disease — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Davies, 66 years old. ^[1]

Presenting complaint: Admitted 4 days ago with an acute NSTEMI. Three episodes of crushing central chest pain at rest over 24 hours, each lasting 15–20 minutes, radiating to the left arm and jaw, associated with diaphoresis and nausea. The last episode was 4 hours before presentation. No ongoing pain at the time of admission. ^[1]

Past history:

• Type 2 diabetes mellitus — 15 years (HbA1c 72 mmol/mol)
• Hypertension — 12 years
• Hyperlipidaemia
• GORD
• Current smoker — 40 pack-years
• Father had CABG at age 60 ^[1]

Current medications (pre-admission):

• Metformin 1g BD
• Gliclazide 80mg OD
• Amlodipine 10mg OD
• Atorvastatin 40mg OD
• Pantoprazole 40mg OD ^[1]

Admission findings:

• BP 150/90, HR 88 and regular, SpO₂ 97% room air, afebrile
• JVP not elevated, heart sounds normal, no murmurs, chest clear
• ECG: 1.5mm ST depression in V4–V6, no ST elevation
• hs-troponin: 25 → 520 ng/L (99th percentile 14 ng/L)
• GRACE score: 165
• HbA1c 72 mmol/mol, eGFR 42, total cholesterol 5.8, LDL 3.2, HDL 0.9, triglycerides 2.1 ^[1]

In-hospital course:

• Loaded with aspirin 300mg + ticagrelor 180mg, started on UFH and atorvastatin 80mg
• Coronary angiography at 18 hours: three-vessel disease
  • LAD: 90% proximal stenosis
  • LCx: 80% mid stenosis
  • RCA: 70% mid stenosis
  • SYNTAX score: 30
• Heart team discussion: CABG recommended (diabetic, high SYNTAX score)
• Echocardiogram: LVEF 45%, mild hypokinesia of the anterior wall
• Troponin trended down; no further chest pain ^[1]

Day 4 examination (trainee elicits):

• Conscious, alert, comfortable at rest at 45 degrees
• Sternotomy scar absent (CABG not yet done — awaiting surgery)
• Pulse 76/min regular, BP 132/78 (on bisoprolol 2.5mg and ramipril 2.5mg started post-admission)
• JVP not elevated
• Apex beat: 5th ICS, mid-clavicular line, normal character
• Heart sounds normal, no added sounds, no murmurs
• Chest clear, no peripheral oedema
• Feet: loss of light touch and vibration sense (diabetic peripheral neuropathy); no ulceration ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mr Davies is a 66-year-old retired taxi driver who was admitted four days ago with a high-risk non-ST-elevation myocardial infarction. He presented with crescendo angina at rest over 24 hours. He has a strong cardiovascular risk profile: a 15-year history of type 2 diabetes, hypertension, hyperlipidaemia, ongoing smoking, and a family history of premature coronary disease. ^[1]

Angiography confirmed three-vessel disease with a SYNTAX score of 30, and the heart team has recommended coronary artery bypass grafting. His echo shows mild left ventricular impairment with an ejection fraction of 45%. ^[1]

His main problems are:

1. Non-ST-elevation myocardial infarction with three-vessel coronary disease — CABG planned
2. Type 2 diabetes with peripheral neuropathy and suboptimal glycaemic control (HbA1c 72)
3. Stage 3a chronic kidney disease (eGFR 42) — affects drug dosing and peri-operative risk
4. Hyperlipidaemia — LDL 3.2 on presentation, far above the post-ACS target
5. Ongoing tobacco dependence (40 pack-years)
6. Polypharmacy and medication reconciliation" ^[1]

Investigation summary: ^[1]

"His angiogram demonstrates critical proximal LAD disease (90%), significant circumflex disease (80%), and moderate RCA disease (70%), with a SYNTAX score of 30 placing him in the high-complexity category. In a diabetic patient, the SYNTAX and FREEDOM trials support CABG over PCI for this anatomy ^[2]. His echocardiogram shows mild LV impairment with anterior wall hypokinesia, consistent with his NSTEMI territory. His HbA1c of 72 mmol/mol indicates poorly controlled diabetes, and his eGFR of 42 reflects stage 3a CKD, which raises his peri-operative risk and affects drug choices."

Management plan: ^[1]

1. Revascularisation:

   • CABG as recommended by the heart team — internal mammary artery to LAD, saphenous vein grafts to LCx and RCA territories.
   • Pre-operative: stop ticagrelor 24 hours before surgery; continue aspirin. Optimise glycaemic control with an insulin sliding scale peri-operatively.
   • Surgical risk assessment: calculate EuroSCORE and STS score given his diabetes, CKD, and reduced LVEF. ^[1]

2. Pharmacological — secondary prevention:

   • Aspirin 75mg lifelong + ticagrelor 90mg BD for 12 months post-ACS. After CABG, continue DAPT from the time of the index ACS event. Ticagrelor is preferred based on PLATO ^[1].
   • High-intensity statin: atorvastatin 80mg; target LDL below 1.4 mmol/L. Given his LDL of 3.2 at presentation, he will likely need ezetimibe added (IMPROVE-IT evidence) and possibly a PCSK9 inhibitor (evolocumab, per FOURIER) if the target is not met ^{[3] [4]}.
   • ACE inhibitor: ramipril, uptitrated as tolerated, for post-MI cardioprotection and renal protection in diabetes. Monitor creatinine and potassium.
   • Beta-blocker: bisoprolol, for post-MI mortality reduction and anti-anginal effect.
   • SGLT2 inhibitor: empagliflozin or dapagliflozin — for diabetes management with proven cardiovascular and renal benefit.

3. Comorbidity optimisation:

   • Diabetes: SGLT2 inhibitor addresses glycaemia and cardiovascular protection. Consider GLP-1 receptor agonist (semaglutide) for additional CV benefit. Continue metformin; review gliclazide (hypoglycaemia risk). Insulin sliding scale peri-operatively.
   • Smoking cessation: offer varenicline (most effective single pharmacotherapy) with behavioural support; this is the single most impactful secondary prevention intervention.
   • Diabetic foot surveillance: he has peripheral neuropathy; podiatry referral and education on foot care. ^[1]

4. Follow-up and rehabilitation:

   • Cardiac rehabilitation programme post-CABG.
   • Repeat echocardiogram at 3 months to reassess LVEF (may improve after revascularisation).
   • If LVEF remains ≤35% on optimal therapy at 3 months, assess for ICD primary prevention.
   • GP follow-up for cardiovascular risk factor optimisation and medication titration. ^[1]

Examiner discussion questions

Q: "Why CABG rather than PCI for this patient?" ^[1]

"Three reasons. First, his SYNTAX score of 30 places him in the high-complexity category, and the SYNTAX trial showed CABG is superior to PCI for intermediate and high SYNTAX scores, with lower rates of major adverse cardiac events driven by reduced repeat revascularisation, and long-term follow-up confirming lower mortality and MI. Second, he is diabetic — the FREEDOM trial specifically demonstrated lower mortality with CABG than PCI in diabetics with multivessel disease. Third, his proximal LAD disease and three-vessel involvement favour surgical complete revascularisation. The exception would be prohibitive surgical risk, but at 66 without severe comorbidity, his operative risk is acceptable." ^[1]

Q: "What is the significance of his ejection fraction of 45%?" ^[1]

"An LVEF of 45% represents mildly reduced systolic function — he would be classified as HFmrEF. This likely reflects ischaemic cardiomyopathy from his NSTEMI with anterior wall hypokinesia. His ejection fraction may improve after revascularisation (recovery of hibernating or stunned myocardium), so I would reassess with echocardiography at 3 months. If his LVEF remains at or below 35% despite optimal medical therapy at least 3 months post-MI, he would qualify for ICD implantation for primary prevention of sudden cardiac death, provided his functional status and life expectancy justify it." ^[1]

Q: "How long should his dual antiplatelet therapy continue?" ^[1]

"After an acute coronary syndrome, the minimum duration of dual antiplatelet therapy is 12 months, regardless of whether he received a stent or CABG — the ischaemic risk is highest in the first year. After 12 months, I would reassess: if his bleeding risk is low and he has high ischaemic risk features (diabetes, complex anatomy, prior stent thrombosis), I would consider extended DAPT or P2Y12 monotherapy. If his bleeding risk is high, I would de-escalate to aspirin monotherapy. Notably, after CABG, aspirin is the foundation and the P2Y12 inhibitor addresses the systemic atherothrombotic risk from the index ACS." ^[1]

Q: "How would you counsel him about smoking cessation?" ^[1]

"I would explain that stopping smoking is the single most effective thing he can do to reduce his risk of future heart attacks, graft failure, and death — the risk falls substantially within the first year. I would recommend a combination of pharmacotherapy and behavioural support: varenicline is the most effective single agent, or nicotine replacement therapy (patches plus short-acting forms). I would refer him to a smoking cessation programme and arrange follow-up. I would address any concerns about varenicline and mood — the evidence now supports its safety in stable cardiovascular patients. I would be supportive and non-judgmental, acknowledging that quitting is difficult but that multiple attempts are normal and each increases the chance of success." ^[1]