在非心脏外科手术中循环心脏氨酸增加的病理生理机制:叙述性综述
Bernardo Bollen Pinto1, Gareth L Ackland2
1Division of Anaesthesiology, Department of Anaesthesiology, Pharmacology, Intensive Care and Emergency Medicine, Geneva University Hospitals, Geneva, Switzerland.
British journal of anaesthesia
|January 23, 2024
概括
在非心脏手术后心脏热素升高可能表明心肌细胞应激,而不仅仅是缺血. 了解这些多样化的机制是改善患者结果和试验设计的关键.
科学领域:
- 心脏病学 心脏病学
- 在外科手术期间的医学.
- 生物标志物 生物标志物
背景情况:
- 在非心脏手术后的患者中,有20-40%的患者出现心脏托波宁升高,这与增加的发病率和死亡率有关.
- 目前的研究经常假设缺血性心脏病是术后热素升高的主要原因.
- 驱动这些托波激素增加的精确机制在很大程度上仍未确定.
研究的目的:
- 探索非心脏手术后心脏托波宁升高的缺血以外的替代机制.
- 挑战传统的观点,即外科手术期间热血素升高仅仅表明心脏缺血.
- 突出心肌细胞应激和多因素器官损伤的作用.
主要方法:
- 审查和综合现有关于外科手术期间心脏热素的数据.
- 对心肌对系统变化的反应进行实验室研究的分析.
- 考虑一个涉及多个病理生理触发因素的"双击"模型.
主要成果:
- 心脏热素升高可能作为心肌细胞应激的非特异性标志物.
- 心肌 perfusion-contraction coupling 和冠状动脉自调节可以限制来自系统变化的缺血性损伤.
- 在这种情况下,2型缺血可能不是热素升高的主要驱动因素.
结论:
- 外科手术期间心脏热素升高可能反映了更广泛的器官损伤机制,而不仅仅是缺血.
- 一个涉及全身炎症,血液动力应变,上腺应激和自主功能障碍的"双击"模型可能会导致心肌损伤.
- 识别这些多样化的机制对于设计和解释未来的外科手术临床试验至关重要.
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