Coronary Artery Disease Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Davies is a 66-year-old retired taxi driver who presents with an acute non-ST-elevation myocardial infarction. Over the past 24 hours he has had three episodes of crushing central chest pain at rest, the last four hours ago, each lasting approximately 20 minutes and radiating to his left arm. ^[1]

His past history includes type 2 diabetes for 15 years, hypertension, hyperlipidaemia, and he is a current smoker with a 40-pack-year history. His current medications are metformin 1g BD, gliclazide 80mg, amlodipine 10mg, and atorvastatin 40mg. ^[1]

His ECG shows 1.5mm ST depression in V4–V6. High-sensitivity troponin has risen from 25 to 520 ng/L. His GRACE score is 165. He is haemodynamically stable with no ongoing chest pain. ^[1]

His main problems are:

1. High-risk non-ST-elevation myocardial infarction — requiring invasive strategy within 24 hours
2. Type 2 diabetes, poorly controlled (HbA1c 72) — increases complexity of revascularisation decision
3. Hyperlipidaemia on sub-target statin therapy
4. Ongoing tobacco dependence
5. Likely multivessel coronary disease requiring heart team discussion
6. Polypharmacy and medication reconciliation" ^[1]

Examiner probing questions and model answers

Q1: "What is your immediate management priority?" ^[1]

"To initiate guideline-directed acute therapy for NSTE-ACS and arrange early invasive management. I would load him with aspirin 300mg and ticagrelor 180mg — ticagrelor is my preferred P2Y12 inhibitor based on PLATO, which showed a 16% reduction in the composite of cardiovascular death, myocardial infarction, or stroke compared to clopidogrel, with a mortality benefit and no increase in major bleeding ^[1]. I would start unfractionated heparin, give atorvastatin 80mg, and arrange coronary angiography within 24 hours, as he is high-risk per GRACE. I would not give oxygen as he is not hypoxic, and I would reserve morphine for significant distress only, as it can delay antiplatelet absorption."

Q2: "Why not use prasugrel instead of ticagrelor?" ^[1]

"Prasugrel showed superior efficacy to clopidogrel in TRITON-TIMI 38, but it has two important limitations. First, it is contraindicated in patients with a prior stroke or TIA due to excess intracranial haemorrhage and net clinical harm in that subgroup. Second, it requires dose reduction in patients over 75 or under 60kg due to bleeding risk. Ticagrelor has a broader indication, demonstrated mortality benefit in PLATO, and is reversible. However, prasugrel is a reasonable alternative in a patient proceeding to PCI who has no prior stroke and favourable bleeding risk. The key point is that either is superior to clopidogrel in an invasive-strategy ACS patient." ^[1]

Q3: "Angiography shows three-vessel disease with a SYNTAX score of 34. What is your revascularisation recommendation?" ^[1]

"I would recommend coronary artery bypass grafting. The SYNTAX trial demonstrated that for patients with intermediate or high SYNTAX scores — meaning complex coronary anatomy — CABG is superior to PCI for major adverse cardiac and cerebrovascular events, driven by reduced repeat revascularisation, with long-term follow-up confirming lower mortality and myocardial infarction ^[2]. Critically, this patient is diabetic, and the FREEDOM trial specifically showed lower mortality with CABG than PCI in diabetics with multivessel disease. The exception would be if his surgical risk were prohibitive — I would calculate his EuroSCORE and STS score — but given he is 66 with no mention of severe COPD or frailty, his surgical risk is likely acceptable. I would present this to the heart team and counsel the patient that CABG offers more durable complete revascularisation, at the cost of a longer recovery and higher peri-operative stroke risk."

Q4: "He needs CABG. How do you manage his antiplatelets pre-operatively?" ^[1]

"I would continue aspirin peri-operatively, as continuation reduces graft occlusion and peri-operative MI risk without significantly increasing bleeding. I would stop ticagrelor 24 hours before surgery — its offset is rapid due to reversible binding. If he were on clopidogrel, I would stop it 5 days pre-operatively, and prasugrel 7 days. I would ensure the surgical team is aware and that he is listed promptly, as delaying CABG in an unstable ACS patient carries ongoing ischaemic risk." ^[1]

Q5: "His post-operative LDL is 1.9 mmol/L on atorvastatin 80mg. What next?" ^[1]

"The post-ACS LDL target is below 1.4 mmol/L. The principle is 'lower is better.' I would add ezetimibe 10mg daily — the IMPROVE-IT trial showed that adding ezetimibe to statin therapy post-ACS produces incremental LDL lowering and a significant reduction in cardiovascular events. If his LDL remains above target on atorvastatin 80mg plus ezetimibe, I would add a PCSK9 inhibitor: evolocumab 140mg subcutaneously fortnightly, based on the FOURIER trial, which showed a 15% reduction in major cardiovascular events and a 20% reduction in CV death, MI, or stroke in patients with established cardiovascular disease ^[4]."

Q6: "He develops a new pansystolic murmur at the apex on day 4 post-CABG. What are you concerned about?" ^[1]

"A new murmur post-CABG raises several possibilities, but the most urgent concern in a patient with recent myocardial infarction is a mechanical complication. A pansystolic murmur at the apex radiating to the axilla suggests acute mitral regurgitation from papillary muscle dysfunction or rupture — though this is more typical of an unrevascularised inferior MI. A murmur at the lower left sternal edge would suggest a ventricular septal defect. I would urgently assess him haemodynamically — checking for hypotension, pulmonary oedema, and signs of low output — and arrange an immediate bedside echocardiogram to define the mechanism and severity. If he is in cardiogenic shock, I would initiate inotropic support and involve the cardiothoracic team and interventional cardiology for possible mechanical circulatory support as a bridge to definitive repair." ^[1]