Peak strain dispersion as a nonlinear mediator in HFpEF: Unraveling subtype-specific pathways via SHAP-augmented ensemble modeling

This study identified two distinct HFpEF subtypes with fundamentally different pathophysiological mechanisms. Cluster 0 shows prominent PSD-mediated effects through cardiorenal interactions, while Cluster 1 demonstrates weaker PSD mediation, suggesting age-related mechanisms operate through pathways less dependent on myocardial mechanical dyssynchrony. These findings support HFpEF heterogeneity and highlight PSD as a valuable biomarker for subtype-specific risk stratification and therapeutic targeting.