1. Case history A 57-year-old female smoker with a longstanding history of hypertension and diabetes presented to hospital with sudden onset of severe breathlessness in the absence of chest pain. Examination revealed sinus tachycardia, hypertension (blood pressure 200/120) and pulmonary oedema. Routine blood investigations and 12-h troponin measurements were normal, and a diagnosis of acute decompensated heart failure secondary to hypertensive crisis was made. She was treated with diuretics and betablockers and made a good recovery. Transthoracic echocardiography demonstrated left ventricular hypertrophy with preserved left ventricular systolic function and Grade 2 diastolic dysfunction. Renal ultrasound confirmed structurally normal kidneys with no evidence of renal artery stenosis. The patient was able to exercise to Stage 3 of a standard Bruce protocol exercise test without symptoms or electrocardiographic changes and subsequent coronary angiography demonstrated a 50% tubular stenosis of the proximal left anterior descending (LAD) artery and 60% stenoses of the mid LAD and origin of the second diagonal (D2) (Fig. 1). Consequently, moderate non-flowlimiting coronary disease was diagnosed, and the patient was discharged with appropriate medical therapy. Unfortunately, the patient re-presented on three subsequent occasions with further episodes of acute pulmonary oedema. The haemodynamic significance of the LAD disease was therefore reassessed, with additional measurements of fractional flow reserve (FFR). This revealed an FFR of 0.71 distal to the mid LAD bifurcation. The D2 and LAD/ D2 bifurcation was therefore stented resulting in a post-stent FFR of 0.85 with a pressure “jump” of 0.08 over the proximal vessel on pull-back (Fig. 2). This led to an additional stent being deployed at the site of the proximal LAD stenosis with complete restoration of flow and perfusion in the distal LAD and a post-stent FFR of 0.9 in the distal LAD. Following discharge the patient has remained well and over 18 months, there have been no further episodes of acute pulmonary oedema.