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创伤,心脏问题——创伤后心功能障碍的分子机制。

Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction.

机构信息

Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, 86081 Ulm, Germany.

Orthopaedic Trauma Institute, Department of Orthopaedic Surgery, University of California, 2550 23rd Street, San Francisco, CA 94110, USA.

出版信息

Int J Mol Sci. 2021 Jan 13;22(2):737. doi: 10.3390/ijms22020737.

DOI:10.3390/ijms22020737
PMID:33450984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7828409/
Abstract

Trauma remains a leading global cause of mortality, particularly in the young population. In the United States, approximately 30,000 patients with blunt cardiac trauma were recorded annually. Cardiac damage is a predictor for poor outcome after multiple trauma, with a poor prognosis and prolonged in-hospitalization. Systemic elevation of cardiac troponins was correlated with survival, injury severity score, and catecholamine consumption of patients after multiple trauma. The clinical features of the so-called "commotio cordis" are dysrhythmias, including ventricular fibrillation and sudden cardiac arrest as well as wall motion disorders. In trauma patients with inappropriate hypotension and inadequate response to fluid resuscitation, cardiac injury should be considered. Therefore, a combination of echocardiography (ECG) measurements, echocardiography, and systemic appearance of cardiomyocyte damage markers such as troponin appears to be an appropriate diagnostic approach to detect cardiac dysfunction after trauma. However, the mechanisms of post-traumatic cardiac dysfunction are still actively being investigated. This review aims to discuss cardiac damage following trauma, focusing on mechanisms of post-traumatic cardiac dysfunction associated with inflammation and complement activation. Herein, a causal relationship of cardiac dysfunction to traumatic brain injury, blunt chest trauma, multiple trauma, burn injury, psychosocial stress, fracture, and hemorrhagic shock are illustrated and therapeutic options are discussed.

摘要

创伤仍然是全球主要的死亡原因,尤其是在年轻人群中。在美国,每年约有 3 万名钝性心脏创伤患者被记录。心脏损伤是多发伤后预后不良的预测因素,预后差,住院时间延长。多发伤患者的心肌肌钙蛋白全身性升高与生存率、损伤严重程度评分和儿茶酚胺消耗有关。所谓“震荡性心脏损伤”的临床特征是心律失常,包括心室颤动和心搏骤停以及壁运动障碍。在低血压不适当且对液体复苏反应不足的创伤患者中,应考虑心脏损伤。因此,联合使用心电图(ECG)测量、超声心动图以及心肌细胞损伤标志物(如肌钙蛋白)的全身表现似乎是一种适当的诊断方法,可用于检测创伤后的心功能障碍。然而,创伤后心功能障碍的机制仍在积极研究中。本综述旨在讨论创伤后的心脏损伤,重点讨论与炎症和补体激活相关的创伤后心功能障碍的机制。本文阐述了心功能障碍与创伤性脑损伤、钝性胸部创伤、多发伤、烧伤、心理社会应激、骨折和失血性休克的因果关系,并讨论了治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fefa/7828409/a39d6c55ef44/ijms-22-00737-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fefa/7828409/a39d6c55ef44/ijms-22-00737-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fefa/7828409/a39d6c55ef44/ijms-22-00737-g001.jpg

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