Heart Failure — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Wilson, 68 years old. [1]

Presenting complaint: Progressive exertional dyspnoea over 4 months, now breathless walking 50 metres on flat ground. Three-pillow orthopnoea. Wakes once nightly with breathlessness. Bilateral ankle swelling, worse by evening. Fatigue and reduced appetite. [1]

Past history:

• Anterior STEMI 2020 — primary PCI with DES to proximal LAD
• Type 2 diabetes (diagnosed 2015) — currently on metformin 1g BD and gliclazide 80mg
• Hypertension (15 years) — previously on perindopril 5mg and amlodipine 10mg (perindopril ceased 6 months ago by GP due to "cough")
• Hyperlipidaemia — atorvastatin 40mg
• Ex-smoker, 40 pack-years, ceased 2020
• Obstructive sleep apnoea — CPAP, poorly compliant [1]

Current medications:

• Metformin 1g BD
• Gliclazide 80mg OD
• Amlodipine 10mg OD
• Atorvastatin 40mg
• Aspirin 100mg OD
• Frusemide 40mg OD (started by GP 2 weeks ago) [1]

Examination findings (trainee elicits):

• Conscious, alert, comfortable at rest at 45 degrees
• Pulse 82/min, irregularly irregular (AF)
• BP 130/80
• JVP elevated 4cm above sternal angle, prominent V waves
• Apex displaced to 6th ICS, AAL, diffuse
• Parasternal heave present
• S3 gallop at apex
• Soft pansystolic murmur at apex → axilla (functional MR)
• Pansystolic murmur at LLSE, louder on inspiration (functional TR)
• Bilateral basal crackles to mid-zone
• Pitting oedema to mid-shin bilaterally
• Pulsatile liver edge 3cm below costal margin
• No ascites [1]

Investigations:

• ECG: AF, HR 82, old anterior Q waves (V1–V3), non-specific ST changes, QRS 104ms
• Echo: LVEF 28%, global hypokinesia (worse anteriorly), mild functional MR, moderate functional TR, dilated LA, RVSP 42mmHg, no pericardial effusion
• Bloods: Hb 132, WCC 7.2, Na 136, K 4.2, creatinine 145 (eGFR 48), eGFR 48, ALT 42, BNP 820
• HbA1c 68 mmol/mol
• Ferritin 85 microg/L, transferrin saturation 15%
• Troponin T 28 ng/L (chronically elevated)
• CXR: cardiomegaly (CTR 0.56), upper lobe blood diversion, bilateral pleural effusions (small), interstitial oedema [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Wilson is a 68-year-old retired builder who presents with a 4-month history of progressive exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, and bilateral ankle swelling. He has a background of ischaemic heart disease (anterior STEMI 2020, DES to LAD), type 2 diabetes, hypertension, and paroxysmal AF that now appears persistent. [1]

His main problems are:

1. Heart failure with reduced ejection fraction (LVEF 28%), NYHA III, ischaemic origin — not on any disease-modifying therapy
2. Atrial fibrillation — new persistence; requires anticoagulation and rate control
3. Iron deficiency (ferritin 85, TSAT 15%) — contributing to fatigue
4. CKD stage 3a (eGFR 48) — cardiorenal overlap
5. Suboptimally managed type 2 diabetes (HbA1c 68)
6. Poorly compliant OSA — a modifiable HF precipitant
7. Social: lives alone, at risk of medication non-adherence" [1]

Investigation summary: [1]

"His echocardiogram confirms severe HFrEF with LVEF 28%, global hypokinesia with anterior predominance consistent with his prior STEMI, and functional MR and TR reflecting ventricular dilatation. His RVSP of 42mmHg suggests mild pulmonary hypertension. The ECG shows AF with old anterior Q waves. His bloods reveal iron deficiency without anaemia (ferritin 85, TSAT 15%) and stage 3a CKD. The chronically elevated troponin is consistent with chronic myocardial injury in the setting of HFrEF." [1]

Management plan: [1]

1. GDMT — four pillars simultaneously:

   • Sacubitril/valsartan 24/26mg BID (start low — BP 130, CKD; titrate upward). No ACEi washout needed (not currently on one). Stop amlodipine (no HF benefit).
   • Bisoprolol 1.25mg OD — titrate to 10mg.
   • Spironolactone 12.5mg OD — cautious given CKD; monitor K+ at 1 week.
   • Dapagliflozin 10mg OD — dual HF and diabetes benefit, renoprotective. [1]

2. AF management:

   • Start apixaban 5mg BD (CHA₂DS₂-VASc likely 4+ given HF + diabetes + hypertension + vascular disease).
   • Rate control: beta-blocker (bisoprolol) serves dual purpose. If rate remains >110, add digoxin.
   • Consider rhythm control (cardiology referral for possible cardioversion after decongestion — AF may be contributing to decompensation). [1]

3. Iron deficiency:

   • IV ferric carboxymaltose 1000mg (FAIR-HF: improves symptoms and exercise capacity regardless of anaemia). [1]

4. Diabetes optimisation:

   • SGLT2i (dapagliflozin) addresses both HF and glycaemic control.
   • Continue metformin. Cease gliclazide once SGLT2i established (hypoglycaemia risk with dual therapy).
   • Consider GLP-1 receptor agonist (semaglutide) for residual hyperglycaemia and weight management. [1]

5. Device therapy (defer 3 months):

   • Reassess echo at 3 months on optimal GDMT.
   • If LVEF remains ≤35% → ICD primary prevention (QRS 104ms, no LBBB → no CRT indication).
   • If LVEF improves above 35% → no device needed. [1]

6. OSA:

   • Reinforce CPAP compliance — untreated OSA worsens HF through nocturnal hypertension, catecholamine surges, and pulmonary hypertension. [1]

7. Follow-up:

   • Heart failure nurse for weekly medication titration.
   • Repeat U&E at 1 week, 2 weeks, 1 month.
   • Advance care planning discussion at next visit.
   • Cardiac rehabilitation referral. [1]

Examiner discussion questions

Q: "His GP stopped perindopril due to cough. Will he tolerate ARNI?" [1]

"The cough was likely an ACEi class effect from bradykinin accumulation. ARNI inhibits neprilysin, which also increases bradykinin, so there is a theoretical risk. However, the incidence of cough with ARNI is lower than with ACEi. I would counsel the patient about the possibility of cough and monitor. If he develops angioedema — more common in Black patients — ARNI must be stopped immediately. If cough persists, I would switch to valsartan (ARB) alone, which does not cause bradykinin accumulation." [1]

Q: "What is the significance of his troponin of 28?" [1]

"In chronic HFrEF, low-grade troponin elevation is common due to ongoing myocyte injury from wall stress, subendocardial ischaemia, and neurohormonal activation. It does not necessarily indicate acute coronary syndrome. However, a rising trend or acute marked elevation would prompt investigation for type 2 MI (demand ischaemia from decompensation) or type 1 MI (plaque rupture). I would trend his troponin rather than interpreting a single value." [1]

Q: "Would you anticoagulate him?" [1]

"Yes. His CHA₂DS₂-VASc score is at least 4 (HF 1, hypertension 1, diabetes 1, vascular disease/prior MI 1, age 65–74 = 1), placing him at high stroke risk. I would start apixaban 5mg BD. His HAS-BLED should be calculated — bleeding risk factors include CKD and age. However, the net benefit of anticoagulation strongly favours treatment in this group." [1]

DCE Short Case — Cardiovascular Examination

Instruction

"Examine this patient's cardiovascular system. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Irregularly irregular pulse (atrial fibrillation)
• Elevated JVP with prominent V waves (functional TR)
• Displaced apex beat (LV dilatation in HFrEF)
• Parasternal heave (RV pressure overload / pulmonary hypertension)
• Third heart sound (elevated LVEDP — decompensated HF)
• Pansystolic murmur at apex → axilla (functional MR)
• Pansystolic murmur at LLSE louder on inspiration (functional TR)
• Bilateral basal crackles (pulmonary congestion)
• Pitting oedema (right-sided congestion)
• Pulsatile liver (severe TR) [1]

Discussion template

1. Summarise findings → "consistent with biventricular heart failure with reduced ejection fraction, complicated by atrial fibrillation and functional mitral and tricuspid regurgitation."
2. Offer differential for the murmur → "the pansystolic murmur at the apex radiating to the axilla could represent functional MR from annular dilatation, or organic mitral valve disease (rheumatic, degenerative). The murmur at the LLSE varying with respiration is consistent with functional TR."
3. Next investigation → "echocardiography to define valve structure and ventricular function."
4. Management priorities → "initiate GDMT, anticoagulate for AF, assess for device therapy." [1]