作者
马 跃,张 彦
文章摘要
代谢相关脂肪性肝病(MASLD)全球患病率约为38%,心血管疾病(CVD)为其主要死因。肝纤维化程度是心血管结局最强的独立预测因子,但尚未被现有CVD风险模型纳入。GLP-1受体激动剂与SGLT2抑制剂兼具肝脏和心血管保护作用。消化科医师应常规评估FIB-4,并主动管理MASLD患者的心血管风险。
文章关键词
代谢相关脂肪性肝病;心血管疾病;肝纤维化;胰岛素抵抗;风险评估
参考文献
[1] Ratti C,Malaguti M,Emanuele D,et al.Understanding MASLD:from molecular pathogenesis to cardiovascular risk—a concise review for the clinical cardiologist[J].Atherosclerosis,2025,409:120495.
[2] Driessen S,Francque S M,Anker S D,et al.Metabolic dysfunction-associated steatotic liver disease and the heart[J].Hepatology,2025, 82(2):487-503.
[3] Huber Y,Hofmann L,Akbari K,et al.Incidence of major cardiovascular events in patients with metabolic dysfunction-associated steatotic liver disease in the general population[J].European Journal of Heart Failure,2025,27(11):2490-2500.
[4] 杨培娟,晋明.非酒精性脂肪肝与心血管疾病共同发病机制研究进展[J].公共卫生与预防医学,2025,36(1):98-102.
[5] Bernhard J,Galli L,Speidl W S,et al.Cardiovascular risk reduction in metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis[J].Current Cardiology Reports,2025,27(1):28.
[6] Ben Dhaou C,Rom O,Orr A W.Endothelial cells at the crossroad of atherosclerosis and metabolic dysfunction-associated steatotic liver disease:a unifying target for dual treatment[J].JACC:Basic to Translational Science,2026,11(8):101624.
[7] Huang Y C,Wang C W,Huang J C,et al.FIB-4 serves as a referral index for coronary artery calcification in patients with MASLD[J]. Journal of Gastroenterology and Hepatology,2026,41(1):332-340.
[8] 倪雪桐,王若羲,张晶,杨兴华.非酒精性脂肪性肝病、代谢相关脂肪性肝病与心血管疾病关联的国内外研究进展[J].中国全科医学,2024,27(16):2033-2038.
[9] Havranek B,Loh R,Torre B,et al.Glucagon-like peptide-1 receptor agonists improve metabolic dysfunction-associated steatotic liver disease outcomes[J].Scientific Reports,2025,15(1):4947.
[10] Pham H N,Ibrahim R,Mouhaffel R,et al.SGLT2 inhibitors and cardiovascular outcomes in metabolic dysfunction-associated steatotic liver disease:a real-world retrospective cohort study[J].The American Journal of Medicine,2026,139(1):57-65.e1.
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