Severe degenerative aortic stenosis with preserved ejection fraction does not change adipokines serum levels
Katarzyna Mizia-Stec1, Tomasz Bochenek2, Błażej Kusz1
1First Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, Katowice Poland.
Insights
Adipokine levels in aortic stenosis (AS) patients were not altered by the condition itself but were influenced by coexisting atherosclerosis. Age and E/E' index predicted adiponectin levels in AS patients.
Area of Science:
- Cardiology
- Endocrinology
- Vascular Biology
Background:
- The role of adipokines in aortic stenosis (AS) pathogenesis remains unclear.
- Investigating adipokines' relationship with clinical and echocardiographic factors in severe AS with preserved ejection fraction (EF) is crucial.
Purpose of the Study:
- To evaluate the association between serum adipokines and clinical characteristics.
- To assess the correlation between adipokines, echocardiographic indices, and vascular remodeling markers in severe AS patients with preserved EF.
Main Methods:
- Prospective enrollment of 65 severe AS patients (preserved EF) and 24 controls.
- Categorization of AS patients into paradoxical low-flow low-gradient (PLFLG AS) and normal flow high-gradient (NFHG AS) groups.
- Analysis of clinical data, vascular remodeling markers, and serum adipokines, including comparisons between AS and control groups, and between AS subgroups.
Main Results:
- No significant differences in adipokine concentrations between AS patients and controls.
- AS patients with coexisting coronary artery disease (CAD) showed decreased adiponectin and leptin levels.
- Age and E/E' index were independent predictors of adiponectin levels in the AS group.
Conclusions:
- Aortic stenosis with preserved EF does not alter the serum adipokine profile.
- Adipokine levels are influenced by atherosclerosis but not by typical cardiovascular risk factors or AS hemodynamic type.
- Findings suggest atherosclerosis, rather than AS itself, modifies adipokine levels in this patient cohort.
Background:
The role of the adipokines in the pathogenesis of aortic stenosis (AS) is not well established. The aim was to evaluate the relationship between adipokines and clinical characteristics as well as echocardiographic indices and noninvasive markers of vascular remodeling in patients with severe AS with preserved ejection fraction (EF).
Methods:
Sixty-five patients (F/M: 38/27; age: 68.3 ± 9.0 years; body mass index [BMI]: 29.6 ± 4.3 kg/m2) with severe AS with preserved EF: 33 patients with paradoxical low-flow low-gradient AS (PLFLG AS) and 32 patients with normal flow high-gradient AS (NFHG AS) were prospectively enrolled into the study. Twenty-four subjects (F/M: 14/10; age: 65.4 ± 8.7 years; BMI: 29.6 ± 4.3 kg/m2) who matched as to age, sex, BMI and coronary artery disease (CAD) constituted the control group (CG). Clinical data and markers of vascular remodeling were related to the serum adipokines.
Results:
There were no differences in the adipokines concentrations in the AS/CG. Patients with AS and coexisting CAD were characterized by decreased serum adiponectin (9.9 ± 5.5 vs. 12.7 ± 5.8 μg/mL, p = 0.040) and leptin (8.3 ± 7.8 vs. 21.6 ± 17.1 ng/mL, p < 0.001) levels compared to subjects without CAD. There were no differences in the serum adipokines concentrations between patients with PLFLG AS and NFHG AS. Systemic hypertension, diabetes, hyperlipidemia or markers of vascular remodeling did not discriminate adipokines concentrations. Multivariate regression analysis indicated that age (F = 3.02; p = 0.015) and E/E' index (F = 0.87, p = 0.032) were independent predictors of the adiponectin level in the AS group.
Conclusions:
The presence of AS with preserved EF did not change the adipokine serum profile. Adipokines levels were modified by coexisting atherosclerosis but not the typical cardiovascular risk factors or the hemodynamic type of AS.
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