Review Article
Open Access

Cardiac injury induced by obstructive jaundice: A comprehensive review

Chunyang Li
Chunyang Li
School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China; School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Mingyao Chen
Mingyao Chen
School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Dedong Zhang
Dedong Zhang
Pharmacy Department, Xiamen Special Service Convalescent Center, Xiamen 361001, Fujian Province, China.
,
Tianying Xu
Tianying Xu
xutianying@smmu.edu.cn
School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Zhenmeng Wang
Zhenmeng Wang
wzm11998@163.com
Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Naval Medical University/Second Military Medical University, Shanghai 200438, China.
Address correspondence to
Article notes
Highlights
Zhenmeng Wang, Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Naval Medical University/Second Military Medical University, 225 Changhai Road, Yangpu District, Shanghai 200438, China. Tel: +86-13022130811. E-mail: wzm11998@163.com. Tianying Xu, School of Anesthesiology, Naval Medical University, 800 Xiangyin Road, Yangpu District, Shanghai 200433, China. Tel: +86-021 81872029. E-mail: xutianying@smmu.edu.cn.
Received January 7, 2024; Accepted March 13, 2025; Published March 31, 2025
  • Elevated bile acid concentrations impair myocardial structure and function by disrupting mitochondrial integrity and acting on TGR5 and FXR receptors.

  • Endotoxins contribute to cardiovascular dysfunction by exacerbating systemic inflammation, primarily via NF-κB activation and increased levels of pro-inflammatory cytokines such as TNF-α.

  • Reactive oxygen species alter cardiac electrophysiology by modulating L-type calcium channels and reversing Na+/Ca2+ exchanger activity, leading to contractile dysfunction. Excessive nitric oxide disrupts vascular tone regulation.

  • Autophagy is activated through the AMPK-mTOR-ULK1 signaling pathway, while apoptosis-driven myocardial injury is mediated by caspase activation and the Bax/Bcl-2 protein family.

  • Appropriate preoperative management, anesthetic selection, and the application of traditional Chinese medicine can alleviate cardiac injury associated with obstructive jaundice.

Review Article
Open Access
Cardiac injury induced by obstructive jaundice: A comprehensive review
Chunyang Li
Chunyang Li
School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China; School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Mingyao Chen
Mingyao Chen
School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Dedong Zhang
Dedong Zhang
Pharmacy Department, Xiamen Special Service Convalescent Center, Xiamen 361001, Fujian Province, China.
,
Tianying Xu
Tianying Xu
xutianying@smmu.edu.cn
School of Anesthesiology, Naval Medical University/Second Military Medical University, Shanghai 200433, China.
,
Zhenmeng Wang
Zhenmeng Wang
wzm11998@163.com
Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Naval Medical University/Second Military Medical University, Shanghai 200438, China.
Address correspondence to
Zhenmeng Wang, Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Naval Medical University/Second Military Medical University, 225 Changhai Road, Yangpu District, Shanghai 200438, China. Tel: +86-13022130811. E-mail: wzm11998@163.com. Tianying Xu, School of Anesthesiology, Naval Medical University, 800 Xiangyin Road, Yangpu District, Shanghai 200433, China. Tel: +86-021 81872029. E-mail: xutianying@smmu.edu.cn.
Article notes
Received January 7, 2024; Accepted March 13, 2025; Published March 31, 2025
Highlights
  • Elevated bile acid concentrations impair myocardial structure and function by disrupting mitochondrial integrity and acting on TGR5 and FXR receptors.

  • Endotoxins contribute to cardiovascular dysfunction by exacerbating systemic inflammation, primarily via NF-κB activation and increased levels of pro-inflammatory cytokines such as TNF-α.

  • Reactive oxygen species alter cardiac electrophysiology by modulating L-type calcium channels and reversing Na+/Ca2+ exchanger activity, leading to contractile dysfunction. Excessive nitric oxide disrupts vascular tone regulation.

  • Autophagy is activated through the AMPK-mTOR-ULK1 signaling pathway, while apoptosis-driven myocardial injury is mediated by caspase activation and the Bax/Bcl-2 protein family.

  • Appropriate preoperative management, anesthetic selection, and the application of traditional Chinese medicine can alleviate cardiac injury associated with obstructive jaundice.

2025 Mar;3(1):28-38
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Abstract

Obstructive jaundice can lead to systemic multi-organ complications, with the heart being one of the most critically affected organs. This review summarizes recent insights into the mechanisms of cardiac injury induced by obstructive jaundice, including bile acid toxicity, inflammatory responses, oxidative stress, nitric oxide dysregulation, endotoxemia, apoptosis, and autophagy. Currently, no specific treatment protocol exists for this condition. However, appropriate anesthetic choices, traditional Chinese herbal medicine, and optimized perioperative management have shown potential in mitigating myocardial damage. This review provides a detailed discussion of these aspects.

Keywords: Obstructive jaundice, cardiac injury, bile acids, mechanisms
Perioperative Precision Medicine

ISSN: 2957-5443

Volume 3, Issue 1

March 2025

Pages: 1-38

PDF CITE Accesses: 16
Perioperative Precision Medicine
ISSN: 2957-5443
ZENTIME PUBLISHING CORPORATION LIMITED
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