Aortic stenosis (AS) is a progressive valvular heart disease characterized by fibrocalcific remodeling, inflammation, and hemodynamic disturbances. Serum biomarkers may indirectly reflect these processes. Autotaxin (ATX) and lysophosphatidic acid (LPA) have been implicated in osteogenic differentiation of valvular interstitial cells, while growth differentiation factor-15 (GDF-15) reflects cellular stress and vascular changes. Thrombomodulin (TM) indicates endothelial injury and interacts with thrombin. This study aimed to evaluate biomarkers focusing on serum ATX, LPA, GDF-15, and TM levels and flow-mediated dilatation (FMD) in patients with AS. Overall, 149 patients were included in the study: 86 consecutive patients with AS hospitalized due to qualification for invasive treatment of AS and 63 controls. The clinical characteristics, echocardiographic data, FMD, and the following biomarkers—ATX, LPA, GDF-15, and TM—were included in the analysis. AS patients presented increased serum levels of ATX, GDF-15, and TM as compared to the controls. Differences in LPA levels were not statistically significant. FMD values were significantly lower in AS patients. The biomarkers mentioned above and FMD correlated with AS severity. There were no differences in both biomarkers’ serum levels and FMD regarding the hemodynamic AS phenotype. GDF-15 serum level was a risk factor for all-cause mortality and MACCE in the 12-month follow-up.

The objective of this study was to evaluate the serum biomarkers implicated in the interaction of platelets and endothelium, as well as the efficacy of antiplatelet therapy in patients with aortic stenosis (AS) and coronary artery disease (CAD). A total of 78 adult patients with CAD on aspirin therapy participated in this study, including 49 consecutive patients with AS and 29 control subjects. The analysis included the following serum biomarkers: thrombomodulin (TM), platelet factor 4 (PF4), P-selectin, and CD40L. The efficacy of antiplatelet treatment was evaluated using the VerifyNow Aspirin test (ASPI test) and P2Y12 assay test (ADP test). Patients with AS exhibited increased serum levels of TM (7.64 ± 3.5 ng/mL vs. 6.28 ± 2.1 ng/mL, p = 0.011) and PF4 (25.16; Q1: 8.3; Q3: 29.6 μg/mL vs. 12.85; Q1: 5.7; Q3: 14.5 μg/mL, p = 0.021) compared to the control group. P-selectin and CD40L levels did not differ between groups. There were no significant differences in platelet aggregation in the ASPI (474.04 ± 66.7 ARU vs. 471.31 ± 56.2 ARU; p = 0.822) or ADP (224.88 ± 46.4 PRU vs. 216.62 ± 29.6 PRU; p = 0.394) tests. Bleeding incidence did not differ significantly between groups. The coexistence of AS in patients with CAD is associated with elevated levels of the aforementioned biomarkers, which are indicative of endothelial damage and platelet activation. However, the efficacy of antiplatelet treatment was independent of the presence of AS.