Key Clinical MessageHaemodynamically significant aortic regurgitation (AR) can be underestimated by standard echocardiography and 2D phase-contrast CMR, particularly in patients with heart rate variability. This case highlights the additive role of 4D-flow CMR in reclassifying AR severity from mild-moderate to moderate-severe. Accurate quantification is essential to identify AR as the primary driver of cardiomyopathy, explaining adverse remodelling and guiding timely aortic valve intervention to prevent irreversible myocardial fibrosis.Case DescriptionA 73-year-old female was admitted to the hospital with progressive shortness of breath. Her medical history was notable for breast cancer, treated successfully 19 years prior. She was diagnosed with acute decompensated heart failure and treated acutely with intravenous furosemide.Initial investigations revealed a significantly elevated NT-proBNP of 5772 ng/L (normal range <400). The electrocardiogram showed sinus rhythm with a narrow QRS complex. A transthoracic echocardiogram (TTE) demonstrated a dilated left ventricle (LV) with severe global systolic dysfunction (estimated ejection fraction [EF] 10–20%). The TTE also identified moderate aortic regurgitation (AR), though the aortic valve appeared morphologically normal with normal aortic dimensions. Prior to discharge, she was initiated on guideline-directed medical therapy (GDMT) including bisoprolol, ramipril, spironolactone, and dapagliflozin.To further investigate the aetiology of her non-ischaemic cardiomyopathy, an outpatient cardiac magnetic resonance (CMR) study was performed two months after her index admission. The CMR confirmed severe LV dilation (end-diastolic volume index 159 ml/m²) and severe systolic dysfunction (LVEF 26%) (Fig. 1). The right ventricle (RV) was normal in size but had impaired systolic function (RVEF 41%).AR severity analysis with standard 2D phase-contrast quantification indicated mild-to-moderate AR (regurgitant fraction [RF] 20%, regurgitant volume [RVol] 10.9 ml) (Fig. 1A – 1B). In contrast, advanced 4D-flow analysis provided a critical diagnostic revision, demonstrating moderate-to-severe AR (RF 38%, RVol 20 ml) (Fig. 1C - 1F).Furthermore, tissue characterisation provided evidence of established adverse remodelling. There was diffuse myocardial fibrosis (elevated native T1 and extracellular volume) and subtle mid-wall late gadolinium enhancement (LGE), representing the chronic sequelae of chronic volume overload.