Lukić Ivana, Mihić Damir, Varžić Silvija Canecki, Relatić Kristina Selthofer, Zibar Lada, Loinjak Domagoj, Ćurić Željka Breškić, Klobučar Lucija, Maričić Lana
Faculty of Medicine, University J. J. Strossmayer in Osijek, 31000 Osijek, Croatia.
Department of Heart and Vascular Diseases, University Hospital Centre Osijek, 31000 Osijek, Croatia.
Rev Cardiovasc Med. 2024 Jan 15;25(1):23. doi: 10.31083/j.rcm2501023. eCollection 2024 Jan.
Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced myocardial dysfunction represents reversible myocardial dysfunction which ultimately results in left ventricular dilatation or both, with consequent loss of contractility. Studies on septic cardiomyopathy report a wide range of prevalence ranging from 10% to 70%. Myocardial damage occurs as a result of weakened myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Mitochondrial dysfunction is the leading problem in the development of septic cardiomyopathy and includes oxidative phosphorylation, production of reactive oxygen radicals, reprogramming of energy metabolism, and mitophagy. Echocardiography provides several possibilities for the diagnosis of septic cardiomyopathy. Systolic and diastolic dysfunction of left ventricular is present in 50-60% of patients with sepsis. Right ventricular dysfunction is present in 50-55% of cases, while isolated right ventricular dysfunction is present in 47% of cases. Left ventricle (LV) diastolic dysfunction is very common in septic shock, and it represents an early biomarker, it has prognostic significance. Right ventricular dysfunction associated with sepsis patients with worse early prognosis. Global longitudinal stress and magnetic resonance imaging (MRI) of the heart are sufficiently sensitive methods, but at the same time MRI of the heart is difficult to access in intensive care units, especially when dealing with critically ill patients. Previous research has identified two biomarkers as a result of the integrated mitochondrial response to stress, and these are fibroblast growth factor-21 (FGF-21) and growth differentiation factor-15 (GDF-15). Both of the mentioned biomarkers can be easily quantified in serum or plasma, but they are difficult to be specific in patients with multiple comorbidities. Mitochondrial dysfunction is also associated with reduced levels of miRNA (microRNA), some research showed significance of miRNA in sepsis-induced myocardial dysfunction, but further research is needed to determine the clinical significance of these molecules in septic cardiomyopathy. Therapeutic options in the treatment of septic cardiomyopathy are not specific, and include the optimization of hemodynamic parameters and the use of antibiotic thera-pies with targeted action. Future research aims to find mechanisms of targeted action on the initial mechanisms of the development of septic cardiomyopathy.
脓毒症被定义为宿主对感染的反应失调所导致的危及生命的器官功能障碍。脓毒症诱导的心肌功能障碍表现为可逆性心肌功能障碍,最终导致左心室扩张或两者皆有,进而导致收缩力丧失。关于脓毒症性心肌病的研究报告患病率范围广泛,从10%到70%不等。心肌损伤是由于心肌循环减弱、直接心肌抑制和线粒体功能障碍所致。线粒体功能障碍是脓毒症性心肌病发展中的主要问题,包括氧化磷酸化、活性氧自由基的产生、能量代谢重编程和线粒体自噬。超声心动图为脓毒症性心肌病的诊断提供了多种可能性。脓毒症患者中50 - 60%存在左心室收缩和舒张功能障碍。50 - 55%的病例存在右心室功能障碍,而47%的病例存在孤立性右心室功能障碍。左心室舒张功能障碍在脓毒症休克中非常常见,它是一种早期生物标志物,具有预后意义。与脓毒症相关的右心室功能障碍患者早期预后较差。心脏的整体纵向应变和磁共振成像(MRI)是足够敏感的方法,但同时心脏MRI在重症监护病房难以获得,尤其是在处理危重症患者时。先前的研究已经确定了两种因线粒体对应激的综合反应而产生的生物标志物,即成纤维细胞生长因子-21(FGF-21)和生长分化因子-15(GDF-15)。上述两种生物标志物均可在血清或血浆中轻松定量,但在患有多种合并症的患者中它们难以具有特异性。线粒体功能障碍还与微小RNA(miRNA)水平降低有关,一些研究表明miRNA在脓毒症诱导的心肌功能障碍中具有重要意义,但需要进一步研究以确定这些分子在脓毒症性心肌病中的临床意义。脓毒症性心肌病治疗的选择并不特异,包括优化血流动力学参数以及使用具有靶向作用的抗生素治疗。未来的研究旨在找到针对脓毒症性心肌病发病初始机制的靶向作用机制。