Jan Verwerft

ALT Main mechanisms of calcific aortic valve disease (CAVD). Bottom: The normal valve comprises three layers, fibrosa, spongiosa, and ventricularis, containing valvular interstitial cells and covered by endothelial cells that maintain tissue homeostasis. Middle: Shear and mechanical stress disrupt the endothelial barrier, promoting lipid infiltration, oxidative stress, and inflammation. Fibrotic and osteogenic signaling drives interstitial cells toward myofibroblast-like and osteoblast-like phenotypes, causing extracellular matrix remodeling and calcification. Top: LDL and lipoprotein(a) accumulation amplifies inflammation and cell injury. Cytokines stimulate osteogenic pathways, while cell debris and procalcifying extracellular vesicles provide sites for mineral deposition. Matrix degradation impairs leaflet motion and activates mechanosensitive pathways, reinforcing a cycle of inflammation, fibrosis, and calcification.

ALT How can we diagnose HFpEF when resting evaluation is inconclusive? This case-based EACVI tutorial illustrates **CPETecho**, which combines cardiopulmonary exercise testing (CPET) with simultaneous exercise echocardiography to assess exercise capacity, ventilation, cardiac output and haemodynamic responses during exercise. The tutorial explores how CPETecho helps to: 🔹 Unmask abnormal exercise haemodynamics 🔹 Interpret pulmonary pressures in relation to cardiac output 🔹 Understand the limitations of diastolic stress testing 🔹 Distinguish cardiac, pulmonary vascular and peripheral limitations to exercise Part of the **EACVI Stress Echocardiography tutorial series**, covering a broad range of clinical applications. Many thanks to the EACVI and ESC education team for this initiative!