From morphology to function: endothelial dysfunction, inflammation, and aortic stiffness as a new paradigm in the assessment of aortic diseases

Thoracic aortic disease has traditionally been assessed using morphological parameters, primarily maximal aortic diameter. However, accumulating experimental and clinical evidence indicates that this approach is insuffi cient for individualised risk prediction. Endothelial dysfunction, chronic infl ammation, and immune activation play central roles in the pathogenesis of aortic disease, driving vascular wall remodelling and functional instability that are not captured by static imaging. Increased aortic stiffness has emerged as a clinically measurable integrator of these processes, refl ecting vascular ageing, infl ammatory burden, and impaired mechanotransduction. By affecting central hemodynamics, aortic stiffness increases left ventricular afterload, compromises diastolic coronary perfusion, and contributes to myocardial ischemia and the development of heart failure with preserved ejection fraction. Incorporating functional and biological markers alongside morphological assessment may improve risk stratifi cation and help explain the occurrence of adverse aortic and cardiovascular events in patients without advanced aortic dilatation.