C-type natriuretic peptide (CNP) level is reduced in AS, favoring the formation of calcified aggregates and an increased expression of bone-related transcripts and proteins (Runx2, osteonectin, osteocalcin, alkaline phospahatase).
Plasma osteoprotegerin (OPG), a cytokine from the TNF receptor family, correlates with the degree of valve calcification in AS, reflecting the activity of the tissue RANKL/RANK/OPG (receptor activator of nuclear factor κΒ ligand/RANK/osteoprotegerin) axis, and is associated with poorer outcomes in AS.
Myocardial gene expression of TNFalpha was significantly higher in patients with well compensated AS than in patients with decompensated AS (p = 0.017).
Cessation of gastrointestinal bleeding and anemia after aortic valve intervention for severe aortic stenosis may be attributed not only to recovery of HMW multimers of VWF but also to the disappearance of angiodysplasia.
Acquired loss of the largest von Willebrand factor multimers is a common hemostatic disturbance in patients with aortic valve stenosis (AS), resulting in impaired platelet adhesion and increased bleeding risk.
There has been a lot of scientific inquiry to identify biomarkers in the management of patients with aortic stenosis. von Willebrand factor activity and high molecular weight multimer level assessment has emerged as an excellent biomarker with intraoperative, point of care potential.
Therefore, we recruited N = 31 consecutive patients with severe AS and performed a high-resolution Western blot with densitometrical band quantification to characterize the von Willebrand factor (VWF) multimeric structure and reevaluate the AVWS subtype classification.
Other biomarkers such as von Willebrand factor and microRNAs are promising but further studies are needed to prove their additive value in aortic valve stenosis.
We performed a prospective analysis of periinterventional VWF parameters in 74 patients (80±7years, female in 37.5%) undergoing transfemoral TAVI for severe symptomatic aortic valve stenosis.
Von Willebrand disease-type 2A (VWD-2A) and acquired von Willebrand syndrome (AVWS) due to aortic stenosis (AS) or left ventricular assist device (LVAD) are associated with an increased proteolysis of von Willebrand factor (VWF).
CPX seems useful to identify 1) patients with a low risk of cardiac death and low risk of progression to symptoms from the aortic stenosis, and 2) patients with hemodynamic compromise who improve in functional capacity after AVR.