Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

Pro-inflammatory monocytes in patients with calcific aortic valve disease.

Abstract

There is a pressing need to elucidate the pathophysiology of calcific aortic valve disease (CAVD), because its prevalence and associated health burden is increasing and there is no pharmacological treatment option. Its risk factors and pathology show considerable overlap with atherosclerosis, in which inflammation and innate immune cells are key.1 In patients with coronary artery disease, circulating monocytes show a hyperinflammatory phenotype.2 Previous studies on monocytes in CAVD only focused on monocyte numbers and subsets,3 which is insufficient to unveil new treatment targets. We now hypothesized that monocyte activation also contributes to CAVD. We tested this in 119 patients with a tricuspid aortic valve stenosis (TAVS) and 65 healthy controls (HC)