J Hypertens. 2026 Mar 6. doi: 10.1097/HJH.0000000000004283. Online ahead of print.
ABSTRACT
BACKGROUND AND AIM: Arterial hypertension is a major epidemiological risk factor for left ventricular hypertrophy (LVH) and heart failure (HF). Within this framework, the theory of hypertensive heart disease (HHD) has historically been proposed as the conceptual substrate for HF with preserved ejection fraction (HFpEF). The aim of this state-of-the-art review is to re-examine whether secondary hypertrophic remodelling due to chronic pressure overload represents an intrinsically dysfunctional myocardial state prone to HF, beyond the well recognized role of severe excess afterload as a haemodynamic precipitant of decompensation.
CONTENT AND RANGE OF EVIDENCE: This state-of-the-art review critically examines historical, experimental, imaging, histopathological, and clinical trial evidence addressing the relationship between arterial hypertension, afterload, myocardial remodelling, and HF.
SUMMARY AND MAIN POINTS: Across these domains, available evidence does not demonstrate arterial hypertension as a sufficient condition to cause HF, nor does it establish hypertensive myocardial remodelling as an intrinsic cardiomyopathy predisposed to decompensation. Clarifying this distinction has important implications for phenotyping, diagnosis, and interpretation of HF in hypertensive populations.
PMID:41801114 | DOI:10.1097/HJH.0000000000004283