Calcific aortic valve disease: a consensus summary from the Alliance of Investigators on Calcific Aortic Valve Disease

Abstract

Calcific aortic valve disease (CAVD) is increasingly prevalent worldwide with significant morbidity and mortality. Therapeutic options beyond surgical valve replacement are currently limited. In 2011, the National Heart Lung and Blood Institute assembled a working group on aortic stenosis. This group identified CAVD as an actively regulated disease process in need of further study. As a result, the Alliance of Investigators on CAVD was formed to coordinate and promote CAVD research, with the goals of identifying individuals at risk, developing new therapeutic approaches, and improving diagnostic methods. The group is composed of cardiologists, geneticists, imaging specialists, and basic science researchers. This report reviews the current status of CAVD research and treatment strategies with identification of areas in need of additional investigation for optimal management of this patient population.

Keywords: aortic valve stenosis; calcification; inflammation.

Figure

Molecular, cellular, and biomechanical mechanisms in CAVD. Abbreviations: qVIC, quiescent valve interstitial cell; aVIC, activated valve interstitial cell; oVIC, osteogenic valve interstitial cell; EMT, endothelial-to-mesenchymal transition; MV, matrix vesicles. VCAM-1, vascular adhesion molecule-1; ICAM-1, intracellular adhesion molecule-1; TNF-α, tumor necrosis factor-α; RANKL, receptor activator of nuclear factor kappa-B ligand; IL1/-6, interleukin1/-6; TGF-β, transforming growth factor-β; BMP, bone morphogenic protein; Runx2, runt-related transcription factor 2; ACE, angiotensin-converting enzyme; AngI/II, angiotensinI/II; LDL, low-density lipoprotein.