First Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, Katowice Poland.
Second Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, Katowice Poland.
Cardiol J. 2019;26(5):483-492. doi: 10.5603/CJ.a2017.0135. Epub 2017 Nov 23.
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).
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.
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.
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.
脂肪因子在主动脉瓣狭窄(AS)发病机制中的作用尚不清楚。本研究旨在评估脂肪因子与临床特征以及射血分数保留的重度 AS 患者的超声心动图指数和血管重塑的无创标志物之间的关系。
前瞻性纳入 65 名患者(男/女:38/27;年龄:68.3 ± 9.0 岁;体重指数 [BMI]:29.6 ± 4.3 kg/m2),其中 33 名患者为反常低流量低梯度 AS(PLFLG AS),32 名患者为正常流量高梯度 AS(NFHG AS)。同时纳入 24 名年龄、性别、BMI 和冠心病(CAD)相匹配的受试者作为对照组(CG)。将临床数据和血管重塑标志物与血清脂肪因子相关联。
AS 患者和 CG 患者的脂肪因子浓度无差异。合并 CAD 的 AS 患者血清脂联素(9.9 ± 5.5 比 12.7 ± 5.8 μg/mL,p = 0.040)和瘦素(8.3 ± 7.8 比 21.6 ± 17.1 ng/mL,p < 0.001)水平降低。PLFLG AS 与 NFHG AS 患者的血清脂肪因子浓度无差异。高血压、糖尿病、高脂血症或血管重塑标志物均不能区分脂肪因子浓度。多变量回归分析表明,年龄(F = 3.02;p = 0.015)和 E/E'指数(F = 0.87;p = 0.032)是 AS 组脂联素水平的独立预测因子。
射血分数保留的重度 AS 并不改变血清脂肪因子谱。脂肪因子水平受共存动脉粥样硬化的影响,但不受典型心血管危险因素或 AS 的血流动力学类型的影响。