Coronary atherosclerosis across stages of metabolic dysfunction-associated steatotic liver disease: a VCTE-CCTA study.

摘要(中文译文)

※ 中文译文由 AI 辅助生成,仅供学术参考,请以英文原文为准。

代谢功能障碍相关脂肪性肝病（MASLD）与冠状动脉疾病（CAD）具有共同的病理生理通路。然而，不同阶段的MASLD与不同冠状动脉粥样硬化表型之间的关系仍不明确。我们使用配对的振动控制瞬态弹性成像（VCTE）和冠状动脉计算机断层扫描血管造影（CCTA）评估了肝脏脂肪变性和纤维化与冠状动脉疾病结局的关联。共纳入425名在三个月内同时接受VCTE和CCTA检查的成年人。MASLD定义为受控衰减参数（CAP）≥248 dB/m，显著纤维化定义为肝脏硬度测量值（LSM）≥8 kPa。冠状动脉结局根据冠状动脉疾病报告和数据系统指南进行评估。主要结局为斑块存在；次要结局包括阻塞性狭窄、钙化斑块、高节段受累和CAD严重程度。多变量 logistic 回归模型逐步调整了人口学、生活方式和心脏代谢因素。47.3%的参与者存在MASLD。与无MASLD者相比，MASLD患者的总体斑块患病率更高（81.6% vs 60.7%，p<0.001），而两组之间的阻塞性狭窄无差异。完全调整后，MASLD与总体斑块存在的较高比值比独立相关（OR 2.22，95% CI 1.04-4.73；p=0.038）。在探索性分析中，MASLD并未增加阻塞性狭窄、钙化斑块或CAD严重程度的比值比。相比之下，LSM每增加1 kPa与阻塞性狭窄（OR 1.14，95% CI 1.00-1.30）和钙化斑块（OR 1.18，95% CI 1.04-1.34）的较高比值比相关，但与CAD的存在和严重程度无关。MASLD与冠状动脉粥样硬化斑块的存在独立相关。探索性分析进一步提示，较大的肝脏硬度可能与阻塞性狭窄和钙化斑块相关，这提高了更晚期肝病与晚期冠状动脉疾病特定特征相关的可能性。尚需在更大规模的前瞻性研究中加以证实。

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) and coronary artery disease (CAD) share common pathophysiologic pathways. However, the relationship between different stages of MASLD and distinct coronary atherosclerosis phenotypes remains unclear. We evaluated the association of hepatic steatosis and fibrosis with coronary artery disease outcomes using paired vibration-controlled transient elastography (VCTE) and coronary computed tomography angiography (CCTA). 425 adults who underwent both VCTE and CCTA within a three-month interval were included. MASLD was defined as controlled attenuation parameter (CAP) ≥248 dB/m, and significant fibrosis was defined as Liver Stiffness Measurement (LSM) ≥8 kPa. Coronary outcomes were assessed according to Coronary Artery Disease Reporting and Data System guidance. The primary outcome was plaque presence; secondary outcomes included obstructive stenosis, calcified plaque, high segment involvement, and CAD severity. Multivariable logistic regression models were progressively adjusted for demographic, lifestyle, and cardiometabolic factors. MASLD was present in 47.3% of participants. Individuals with MASLD had a higher prevalence of overall plaque than those without (81.6% vs 60.7%, p<0.001), whereas obstructive stenosis did not differ between groups. MASLD was independently associated with higher odds of overall plaque presence after full adjustment (OR 2.22, 95% CI 1.04-4.73; p=0.038). In exploratory analyses, MASLD did not increase the odds of obstructive stenosis, calcified plaque, or CAD severity. In contrast, 1 kPa increase in LSM was associated with higher odds of obstructive stenosis (OR 1.14, 95% CI 1.00-1.30) and calcified plaque (OR 1.18, 95% CI 1.04-1.34), but not CAD presence and severity. MASLD was independently associated with the presence of coronary atherosclerotic plaque. Exploratory analyses further suggested that greater liver stiffness may be associated with obstructive stenosis and calcified plaque, raising the possibility that more advanced liver disease relates to specific features of advanced coronary artery disease. Confirmation in larger prospective studies is warranted.

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