Association of Aortic Stiffness and Pressure Pulsatility With Noninvasive Estimates of Hepatic Steatosis and Fibrosis: The Framingham Heart Study.

IF 7.4 1区医学 Q1 HEMATOLOGY Arteriosclerosis, Thrombosis, and Vascular Biology Pub Date : 2024-07-01 Epub Date: 2024-05-16 DOI:10.1161/ATVBAHA.123.320553

Leroy L Cooper, Brenton R Prescott, Vanessa Xanthakis, Emelia J Benjamin, Ramachandran S Vasan, Naomi M Hamburg, Michelle T Long, Gary F Mitchell

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Abstract

Background: Arterial stiffening may contribute to the pathogenesis of metabolic dysfunction-associated steatotic liver disease. We aimed to assess relations of vascular hemodynamic measures with measures of hepatic steatosis and fibrosis in the community.

Methods: Our sample was drawn from the Framingham Offspring, New Offspring Spouse, Third Generation, Omni-1, and Omni-2 cohorts (N=3875; mean age, 56 years; 54% women). We used vibration-controlled transient elastography to assess controlled attenuation parameter and liver stiffness measurements as measures of liver steatosis and liver fibrosis, respectively. We assessed noninvasive vascular hemodynamics using arterial tonometry. We assessed cross-sectional relations of vascular hemodynamic measures with continuous and dichotomous measures of hepatic steatosis and fibrosis using multivariable linear and logistic regression.

Results: In multivariable models adjusting for cardiometabolic risk factors, higher carotid-femoral pulse wave velocity (estimated β per SD, 0.05 [95% CI, 0.01-0.09]; P=0.003), but not forward pressure wave amplitude and central pulse pressure, was associated with more liver steatosis (higher controlled attenuation parameter). Additionally, higher carotid-femoral pulse wave velocity (β=0.11 [95% CI, 0.07-0.15]; P<0.001), forward pressure wave amplitude (β=0.05 [95% CI, 0.01-0.09]; P=0.01), and central pulse pressure (β=0.05 [95% CI, 0.01-0.09]; P=0.01) were associated with more hepatic fibrosis (higher liver stiffness measurement). Associations were more prominent among men and among participants with obesity, diabetes, and metabolic syndrome (interaction P values, <0.001-0.04). Higher carotid-femoral pulse wave velocity, but not forward pressure wave amplitude and central pulse pressure, was associated with higher odds of hepatic steatosis (odds ratio, 1.16 [95% CI, 1.02-1.31]; P=0.02) and fibrosis (odds ratio, 1.40 [95% CI, 1.19-1.64]; P<0.001).

Conclusions: Elevated aortic stiffness and pressure pulsatility may contribute to hepatic steatosis and fibrosis.

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主动脉僵硬度和压力搏动性与肝脏脂肪变性和纤维化的无创估计值的关系：弗雷明汉心脏研究

背景：动脉僵化可能是代谢功能障碍相关性脂肪肝的发病机制之一。我们旨在评估血管血流动力学指标与社区肝脏脂肪变性和纤维化指标之间的关系：我们的样本来自弗雷明汉后代、新后代配偶、第三代、Omni-1 和 Omni-2 队列（N=3875；平均年龄 56 岁；54% 为女性）。我们使用振动控制瞬态弹性成像来评估受控衰减参数和肝脏硬度测量值，分别作为肝脏脂肪变性和肝脏纤维化的测量指标。我们使用动脉测压法评估了无创血管血流动力学。我们使用多变量线性回归和逻辑回归评估了血管血流动力学测量值与肝脏脂肪变性和肝纤维化的连续和二分测量值之间的横截面关系：在调整了心脏代谢风险因素的多变量模型中，较高的颈动脉-股动脉脉搏波速度（每 SD 的估计 β 值，0.05 [95% CI，0.01-0.09]；P=0.003）与较多的肝脏脂肪变性（较高的受控衰减参数）有关，但与前向压力波振幅和中心脉压无关。此外，颈动脉-股动脉脉搏波速度（β=0.11 [95% CI, 0.07-0.15]；PP=0.01）和中心脉压（β=0.05 [95% CI, 0.01-0.09]；P=0.01）越高，肝纤维化程度越高（肝脏硬度测量值越高）。男性以及患有肥胖症、糖尿病和代谢综合征（交互 P 值，P=0.02）和肝纤维化（几率比 1.40 [95% CI，1.19-1.64]；PC 结论）的参与者的相关性更为突出：主动脉僵硬度和压力搏动性升高可能会导致肝脏脂肪变性和纤维化。

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来源期刊

Arteriosclerosis, Thrombosis, and Vascular Biology 医学-外周血管病

CiteScore

15.60

自引率

2.30%

发文量

337

审稿时长

2-4 weeks

期刊介绍： The journal "Arteriosclerosis, Thrombosis, and Vascular Biology" (ATVB) is a scientific publication that focuses on the fields of vascular biology, atherosclerosis, and thrombosis. It is a peer-reviewed journal that publishes original research articles, reviews, and other scholarly content related to these areas. The journal is published by the American Heart Association (AHA) and the American Stroke Association (ASA). The journal was published bi-monthly until January 1992, after which it transitioned to a monthly publication schedule. The journal is aimed at a professional audience, including academic cardiologists, vascular biologists, physiologists, pharmacologists and hematologists.