A prospective comparative study of ischaemic heart disease and dilated cardiomyopathy in acute decompensated heart failure

Introduction Among patients with chronic heart failure, dilated cardiomyopathy (DCM) and ischaemic heart disease (IHD) predominate, but they often show different patterns of ventricular remodelling, scar burden and arrhythmic risk. These differences may influence treatment response and disease progression. However, comparative evidence across aetiologies remains heterogeneous, and clarifying these clinical profiles may help support more accurate diagnosis and guide more individualised therapeutic decisions. Purpose The purpose of this study was to compare the clinical, structural, haemodynamic and biomarker profiles of patients with acute decompensated heart failure (ADHF) according to underlying aetiology Methods We performed a prospective observational study including 167 consecutive patients hospitalised for ADHF between 2020 and 2025 at our centre. Median follow-up was 9 months (IQR 4–18). Patients were classified as either IHD or DCM. Clinical, laboratory, treatment, echocardiographic and outcomes data were systematically collected. Survival and event-free follow-up were assessed using Kaplan–Meier curves with log-rank testing. Results Of the 167 patients, 96 (57.5%) had IHD and 71 (42.5%) had DCM. Compared with DCM, IHD patients were older (76 vs 73 years), had a higher comorbidity burden (Charlson 7 vs 5) more diabetes (72.9% vs 38%) and dyslipidaemia (71.9% vs 49.3%). In contrast, DCM patients more often showed low cardiac output (18.3% vs 6.3%), greater biventricular remodelling (LV and RV dilatation) and lower LVEF (30% vs 36%). Atrial fibrillation, ventricular arrhythmias and cardiac devices were similarly distributed across groups. IHD patients also had lower diastolic blood pressure and lower haemoglobin. At discharge, CA-125 and hs-troponin T were higher in IHD, whereas NT-proBNP remained similar. Although IHD patients received beta-blockers and SGLT2 inhibitors more often before admission, post-discharge therapy converged across groups. During follow-up, rates of all-cause mortality, cardiovascular mortality and heart-failure readmissions were not significantly different. Conclusions Ischaemic and dilated cardiomyopathy were associated with different clinical, structural and biomarker profiles in ADHF, reflecting differing underlying disease mechanisms. Despite these contrasts, short-term outcomes (including all-cause mortality, cardiovascular mortality and heart-failure readmission) were comparable, and post-discharge optimisation resulted in similar implementation of guideline-directed therapies. The modestly lower haemoglobin observed in patients with IHD is likely related to their higher use of antiplatelet therapy rather than an aetiology-specific effect. Overall, these findings highlight the value of aetiology-based characterisation while suggesting that short-term prognosis may be influenced more by global disease severity and the success of therapeutic optimisation than by underlying cause alone.