Exploratory Analysis of the Innate Immune System in Aortic Stenosis Patients With and Without ASCVD.
The coronary story today is physiology, not grafts.
Continuous thermodilution in 51 patients with anomalous aortic origin of a coronary artery showed that the high-risk anatomic triad (intramural segment, acute take-off, slit-like ostium) produces measurably reduced hyperemic flow (179 vs 290 mL/min) and elevated microvascular resistance at rest and under stress.
Calcific aortic valve disease (CAVD) leads to aortic stenosis (AS) through inflammation and fibro-calcific remodeling. Although CAVD and atherosclerosis share features, not all patients with AS develop atherosclerotic cardiovascular disease (ASCVD), suggesting mechanistic heterogeneity. This case-control study evaluated inflammatory profiles and valvular remodeling in 128 patients with AS (59.4% with ASCVD) and 105 controls. Immune cell composition and monocyte markers were analyzed by flow cytometry, whereas cytokine production was assessed after peripheral blood mononuclear cell (PBMC) stimulation. Both AS groups had higher interleukin (IL)-6, leukocyte, monocyte, and neutrophil counts than controls, with lower monocyte human leukocyte antigen-DR isotype and higher C-C chemokine receptor (CCR)2 expression. Cytokine responses were also elevated, particularly in AS patients with ASCVD. They also showed higher IL-6 concentrations, higher proportions of classical monocytes, and lower intermediate and non-classical monocytes compared with patients without ASCVD. Overall, AS was associated with a pro-inflammatory monocyte phenotype and function, most prominently in patients with ASCVD. ClinicalTrials.gov ID: NCT04717219.
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