Beijing Collaborative Innovation Centre for Cardiovascular Disorders, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China; Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing 100029, China; Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China; Beijing Institute of Heart, Lung and Blood Vessel Disease, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China.
Beijing Collaborative Innovation Centre for Cardiovascular Disorders, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China; Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing 100029, China; Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China; Beijing Institute of Heart, Lung and Blood Vessel Disease, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China.
Biomed Pharmacother. 2024 Jan;170:116079. doi: 10.1016/j.biopha.2023.116079. Epub 2023 Dec 26.
Heart failure (HF) is a prevalent long-term complication of myocardial infarction (MI). The incidence of post-MI HF is high, and patients with the condition have a poor prognosis. Accurate identification of individuals at high risk for post-MI HF is crucial for implementation of a protective and ideally personalized strategy to prevent fatal events. Post-MI HF is characterized by adverse cardiac remodeling, which results from metabolic changes in response to long-term ischemia. Moreover, various risk factors, including genetics, diet, and obesity, can influence metabolic pathways in patients. This review focuses on the metabolic signatures of post-MI HF that could serve as non-invasive biomarkers for early identification in high-risk populations. We also explore how metabolism participates in the pathophysiology of post-MI HF. Furthermore, we discuss the potential of metabolites as novel targets for treatment of post-MI HF and as biomarkers for prognostic evaluation. It is expected to provide valuable suggestions for the clinical prevention and treatment of post-MI HF from a metabolic perspective.
心力衰竭（HF）是心肌梗死（MI）的一种常见长期并发症。MI 后 HF 的发生率很高，且该病症患者的预后较差。准确识别 MI 后 HF 的高危个体对于实施保护策略至关重要，理想情况下应采取个体化策略以预防致命事件。MI 后 HF 的特征为不良的心脏重构，这是由于长期缺血引起的代谢变化所致。此外，包括遗传、饮食和肥胖在内的各种危险因素可以影响患者的代谢途径。本综述重点介绍 MI 后 HF 的代谢特征，这些特征可以作为高危人群中早期识别的非侵入性生物标志物。我们还探讨了代谢如何参与 MI 后 HF 的病理生理学过程。此外，我们还讨论了代谢物作为 MI 后 HF 治疗新靶点以及预后评估生物标志物的潜力。预计从代谢角度为 MI 后 HF 的临床预防和治疗提供有价值的建议。
