A 64-year-old man with anterior ST-segment elevation myocardial infarction (STEMI) 4 years earlier, hypertension, type 2 diabetes mellitus, and dyslipidaemia presented with persistent exertional dyspnoea despite optimally tolerated guideline-directed medical therapy (GDMT). Despite good adherence to medications and lifestyle measures, he continued to experience dyspnoea on climbing one flight of stairs and fatigue with routine activity, without orthopnoea, paroxysmal nocturnal dyspnoea, or recent heart failure hospitalisations. On examination, blood pressure was 118/72 mmHg, heart rate 70 beats/min, and oxygen saturation 98% on room air, with mild bilateral ankle oedema and no crackles. Echocardiography showed a left ventricular ejection fraction (LVEF) of 30%. Investigations revealed eGFR 72 mL/min/1.73 m², creatinine 1.0 mg/dL, potassium 4.5 mmol/L, and elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP). Electrocardiography (ECG) showed sinus rhythm with QRS 102 ms. His medications included enalapril 10 mg twice daily, bisoprolol 10 mg once daily, empagliflozin 10 mg once daily, furosemide 40 mg once daily, atorvastatin 40 mg once daily, and aspirin 75 mg once daily. A mineralocorticoid receptor antagonist (MRA) had been discontinued after recurrent hyperkalaemia despite dose adjustment. Despite this regimen, he remained symptomatic with New York Heart Association (NYHA) Class II heart failure with reduced ejection fraction (HFrEF). His blood pressure, renal function, and potassium were suitable for optimising GDMT by replacing the angiotensin-converting enzyme (ACE) inhibitor with an angiotensin receptor–neprilysin inhibitor (ARNI).¹–³