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Phys Written Answerscardiovascular

Phys Written Answers · cardiovascular

Coronary Artery Disease — Written Clinical Reasoning

DCE long-case preparation: structured written reasoning for acute coronary syndrome management, including problem-list synthesis, investigation interpretation, risk stratification, and integrated secondary prevention planning.

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Target exams

FRACP DCEMRCP Part 2

Target exams

FRACP DCEMRCP Part 2
Prompt
DCE long-case preparation: structured written reasoning for acute coronary syndrome management, including problem-list synthesis, investigation interpretation, risk stratification, and integrated secondary prevention planning.

SAQ 1 — Integrated Management of NSTEMI (20 marks, 30 minutes)

Prompt: Outline your immediate and integrated management plan for this patient, including acute pharmacotherapy, reperfusion strategy, secondary prevention, and comorbidity optimisation. Justify each decision with reference to evidence and risk stratification. [1]

Model Answer

Problem list (4 marks):

  1. High-risk non-ST-elevation myocardial infarction (NSTEMI) — GRACE 165, dynamic ST depression, troponin rise/fall
  2. Type 2 diabetes (HbA1c 72 mmol/mol) — under-optimised, high cardiovascular risk
  3. Hyperlipidaemia — on sub-target statin dose (atorvastatin 40mg, not high-intensity)
  4. Ongoing tobacco dependence (40 pack-years)
  5. Hypertension (BP 150/90 on amlodipine)
  6. Likely multivessel coronary disease — will require heart team assessment (diabetic) [1]

Immediate management — acute pharmacotherapy (6 marks): [1]

InterventionDose / detailRationale
Aspirin300 mg loading (chewed, non-enteric), then 75–100 mg dailyIrreversible COX-1 platelet inhibition; foundational antiplatelet
Ticagrelor180 mg loading, then 90 mg BDPLATO: 16% RRR vs clopidogrel in CV death/MI/stroke with mortality benefit. Preferred P2Y12 inhibitor for invasive-strategy ACS [1]
AnticoagulationUnfractionated heparin (or enoxaparin)Prevents further thrombus propagation pending angiography
High-intensity statinAtorvastatin 80 mg immediatelyTarget LDL below 1.4 mmol/L post-ACS
GTNSublingual for ongoing chest painVenodilator reduces preload and myocardial oxygen demand
OxygenOnly if SpO₂ below 90%Routine oxygen in non-hypoxic MI may worsen outcomes

Reperfusion strategy (3 marks):

  • This patient is high-risk NSTE-ACS (GRACE >140, troponin rise/fall, dynamic ST depression). He is NOT very-high-risk (no haemodynamic compromise, refractory angina, cardiac arrest, mechanical complications, or acute heart failure).
  • Indication: coronary angiography within 24 hours, with PCI to the culprit lesion if indicated.
  • If angiography reveals multivessel disease (likely given diabetes and extensive risk factors), involve the heart team for CABG vs PCI decision. As a diabetic with potential complex disease, CABG may be favoured (SYNTAX and FREEDOM evidence) [3].

Secondary prevention plan (4 marks): [1]

TherapyDetail
AntiplateletAspirin lifelong + ticagrelor for 12 months (post-ACS DAPT)
StatinAtorvastatin 80 mg; target LDL below 1.4; add ezetimibe if not at target; consider PCSK9 inhibitor (evolocumab) if still above target (FOURIER) [4]
ACE inhibitorAdd ramipril or perindopril (post-MI with diabetes; stop amlodipine or add ACEi for BP control)
Beta-blockerBisoprolol or metoprolol (post-MI; also an anti-anginal and anti-hypertensive)
SGLT2 inhibitorEmpagliflozin or dapagliflozin (diabetes + post-ACS; reduces CV death and HF hospitalisation)
Smoking cessationOffer varenicline or NRT; refer to cessation programme

Comorbidity optimisation (2 marks):

  • Diabetes: SGLT2 inhibitor addresses both glycaemic control and cardiovascular protection. Consider GLP-1 receptor agonist (semaglutide) for additional CV benefit and weight management. Continue metformin; review gliclazide (hypoglycaemia risk if adding SGLT2i).
  • Blood pressure: Target below 130/80. ACE inhibitor + beta-blocker will help; titrate as outpatient.
  • Renal function: Monitor with ACEi initiation and contrast exposure; acceptable creatinine rise up to 30%. [1]

Communication and follow-up (1 mark):

  • Cardiac rehabilitation referral for structured exercise and education.
  • Medication adherence counselling — explain that the 12-month DAPT is essential to prevent stent thrombosis.
  • Advance care planning discussion appropriate at follow-up if LV dysfunction is confirmed.
  • GP follow-up for cardiovascular risk factor optimisation. [1]

SAQ 2 — Investigation Interpretation (12 marks, 20 minutes)

Prompt: A 74-year-old woman presents with 1 hour of severe central chest pain radiating to the jaw and associated with diaphoresis. The ECG shows 2 mm ST elevation in leads II, III, and aVF, with 1 mm ST elevation in V1 and ST depression in I and aVL. Blood pressure is 100/65. Interpret the ECG, identify the culprit artery and territory, and outline the immediate management including reperfusion decisions. [1]

Model Answer

ECG interpretation (4 marks):

  • ST elevation in II, III, aVF indicates an acute inferior STEMI.
  • ST elevation in V1 in the context of inferior STEMI suggests right ventricular involvement — the culprit is a proximal right coronary artery (RCA) occlusion above the RV marginal branch.
  • ST depression in I and aVL is reciprocal change, supporting the diagnosis of true STEMI rather than a mimic.
  • Right-sided leads (V4R) should be recorded to confirm RV infarction (ST elevation in V4R is diagnostic). [1]

Culprit artery and territory (2 marks):

  • Proximal RCA occlusion causing inferior and right ventricular infarction. The RV marginal branches arise from the proximal RCA; occlusion above their origin causes RV infarction, which has important management implications. [1]

Immediate management — specific to RV infarction (4 marks):

  1. Reperfusion: This is a STEMI — activate the catheter lab for primary PCI (door-to-balloon ≤90 min). If PCI is not available within 120 minutes, fibrinolysis is indicated (no contraindications given).
  2. Avoid nitrates and diuretics: RV infarction is preload-dependent. Nitrates reduce preload and can precipitate profound hypotension. If hypotension occurs, treat with IV fluid bolus (normal saline) to maintain RV filling.
  3. Standard STEMI drug therapy: Aspirin 300 mg, ticagrelor 180 mg, heparin, atorvastatin 80 mg.
  4. Atropine for bradycardia/heart block: The RCA supplies the AV node; inferior MI commonly causes bradycardia and AV block. Atropine 0.5 mg IV for symptomatic bradycardia; temporary pacing wire if high-grade AV block with instability. [1]

Prognostic considerations (2 marks):

  • RV infarction increases in-hospital mortality compared to isolated inferior MI (due to cardiogenic shock risk).
  • Monitor in a coronary care unit for bradyarrhythmias, AV block, and hypotension.
  • Complete heart block in inferior MI is usually transient (AV node ischaemia) and resolves with reperfusion, unlike anterior MI heart block which often requires a permanent pacemaker. [1]

References

  1. [1]Wallentin L, et al. New stably transfected bioluminescent cells expressing FLAG epitope-tagged estrogen receptors to study their chromatin recruitment BMC Biotechnol, 2009.PMID 19737428
  2. [2]Yusuf S, et al. (CURE) Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation N Engl J Med, 2001.PMID 11519503
  3. [3]Serruys PW, et al. (SYNTAX) Gene expression profiles differentiating between breast cancers clinically responsive or resistant to letrozole J Clin Oncol, 2009.PMID 19224856
  4. [4]Sabatine MS, et al. (FOURIER) The BEACH-containing protein WDR81 coordinates p62 and LC3C to promote aggrephagy J Cell Biol, 2017.PMID 28404643