Aortic Valve Defect as an Independent Risk Factor for Endothelial Dysfunction

Endothelial dysfunction (ED) has been identified as a precursor to micro- and macroangiopathic complications and an independent risk factor for major adverse cardiac events (MACEs). Recent studies have identified a novel risk factor for ED: severe aortic stenosis (AS). Traditionally linked to other established risk factors for endothelial cell dysregulation, AS has emerged as a contributor to ED, which is supported by the improvement of endothelial function following transcatheter (TAVR) or surgical (SAVR) interventions. Furthermore, the observation of ED in patients with a dysfunctional bicuspid aortic valve (BAV) at a younger age suggests a distinct impact of AS on ED. A promising hypothesis is a hemodynamic theory suggesting that changes in the shear stress of the ascending aortic wall and peripheral vessels, along with subclinical hemolysis caused by turbulent blood flow, could lead to reduced nitric oxide (NO) bioavailability. Current hypotheses on ED have yet to consider the influence of concomitant aortic stenosis in BAV. Additionally, studies examining potential intravascular hemolysis in BAV patients or the impact of surgical treatment of this defect on endothelial function are scarce. The aim of this review is to summarize the current knowledge on the mechanisms underlying ED in patients with AS or BAV and to identify possible directions for future research.