Myocardial Oedema in Heart Failure with Preserved Ejection Fraction: Preliminary Findings from the NETDiamond Cohort

Heart failure with preserved ejection fraction (HFpEF) has emerged as the predominant HF phenotype worldwide, particularly in ageing populations.1 Symptomatic HFpEF typically manifests only after substantial myocardial and atrial adverse remodelling has occurred; consequently, the prognosis of HFpEF remains unfavourable despite recent therapeutic advances. Our current understanding views HFpEF as the clinical manifestation of the cumulative deleterious effects of cardiovascular (CV) risk factors on cardiac structure and function. In particular, chronic low-grade inflammation associated with prevalent CV comorbidities such as obesity, hypertension, and diabetes has emerged as a central pathogenic driver, primarily through its impact on endothelial function.2 Despite growing interest in the impact of inflammatory activation on myocardial microvascular permeability and tissue water homeostasis, the potential contribution of altered myocardial water content in HFpEF remains poorly characterized.3 A likely reason is that, unlike myocardial hypertrophy or fibrosis, interstitial fluid volume expansion is extremely challenging to identify and quantify with conventional histological or imaging tools. Routine paraffin embedding for histology requires tissue dehydration, which prevents the observation of interstitial fluid accumulation, whereas on echocardiography, oedema-driven increases in ventricular wall thickness can be easily misinterpreted as hypertrophy.