Evaluation of Myocardial Function and Structure in Valvular Heart Disease: What Is Needed for Risk Assessment and Therapeutic Decisions?

Abstract Valvular heart disease (VHD) is traditionally assessed through gradients, regurgitant volumes, and ejection fraction—but these valve-centric indices miss the earliest and most decisive signal: myocardial injury. Contemporary evidence shows that VHD is a myocardial disease, where outcomes are driven far more by the ventricle’s biological response than by the valve lesion itself. This state-of-the-art review redefines VHD through a myocardium-first lens, highlighting tools that expose dysfunction long before conventional thresholds fail. A focused triad—LV global longitudinal strain (LV-GLS), RV strain with RV–PA coupling, and LA reservoir strain—detects injury at its inception and sharply improves prognostic precision. Cardiac magnetic resonance adds mechanistic depth through native T1, extracellular volume, and late gadolinium enhancement, identifying diffuse and focal fibrosis that dictate timing and reversibility of remodeling. Next-generation technologies extend this paradigm: CT-derived ECV as a scalable fibrosis surrogate, molecular imaging revealing active calcification and fibro-inflammation, and AI-driven models that fuse imaging, biomarkers, and clinical variables into personalized risk trajectories. We propose a serial, multiparametric, AI-enhanced strategy centered on myocardial protection—using LV-GLS tracking, RV–PA coupling, atrial mechanics, and fibrosis imaging to intervene during the true therapeutic window. This review positions a simple but transformative concept: managing VHD means managing the myocardium. Adopting this shift is essential for preserving cardiac health—not merely correcting valve anatomy.