Hypertensive heart disease and HFpEF:atrial functional valve regurgitation as the trigger of acute heart failure in a syndrome of exertional dyspnoea

Hypertensive heart disease (HHD) is widely regarded as the principal structural substrate underlying heart failure with preserved ejection fraction (HFpEF). Accordingly, contemporary models have largely focused on ventricular remodeling, myocardial fibrosis, microvascular abnormalities as the mechanisms linking chronic hypertension to heart failure (HF). However, current concepts increasingly recognize HFpEF as a syndrome predominantly characterized by impaired exercise tolerance and exertional dyspnea without tendency to congestion at rest, whereas the mechanisms responsible for progression to acute heart failure (AHF) remain incompletely understood. This distinction raises an important pathophysiological question: if hypertensive ventricular remodeling primarily accounts for a chronic exertional phenotype, what triggers the transition to acute congestion? We review the limitations of current epidemiological, imaging, and clinical trial data in addressing this question and discuss clinical observations suggesting that most episodes of acute heart failure with preserved or mildly reduced ejection fraction are associated with identifiable structural or haemodynamic abnormalities rather than isolated hypertensive remodeling. Based on these observations, we propose that progressive hypertensive atrial remodeling may represent an important mechanism linking stable HHD to decompensated AHF. Chronic atrial remodeling may promote atrial fibrillation and atrial functional mitral and tricuspid regurgitation. These lesions are dynamic and may become severe in patients with permanent atrial fibrillation or atrial fibrillation with a high ventricular response. When severe, they create a transient haemodynamic substrate for congestion that may partially regress following restoration of more favourable loading conditions. Rather than challenging the central role of HHD in HFpEF, this perspective extends the current pathophysiological framework by distinguishing the mechanisms responsible for chronic exertional symptoms from those precipitating AHF providing a rationale for future mechanism-oriented research.