Calcific aortic valve disease and cardiometabolic triggers: an explanation behind progression of aortic valvular disease and failure of medical therapy interventions.

Abstract

Calcific aortic valve disease (CAVD), a nonrheumatic stenosis of the trileaflet aortic valve, is a complex, multifaceted cardiovascular condition involving a widespread inflammatory process and an analogous atheromatous process affecting the arteries. It is currently the most encountered valvular abnormality in cardiology. Although distinctive abnormal mechanical forces are at the core propelling a responsive mechanosensitive feedback cascade, implicated in both initiation and perpetuation of CAVD; we propose a conundrum of metabolic abnormalities including hypertension, elevated fasting blood sugar, decreased high-density lipoprotein, hypertriglyceridemia, and abdominal obesity as perpetuators of this process. Furthermore, we suggest CAVD as a cardio metabolic disorder. New perspectives as well as which pathways we believe are critically involved and ideas for early intervention are discussed.