脓毒症心肌病诊断及预后标志物的研究进展

doi:10.3969/j.issn.1003-9198.2024.07.024

摘要/Abstract

摘要： 脓毒症是全球面临的公共卫生问题,发病率和死亡率均较高。心脏是脓毒症众多受累靶器官中最容易累及的,其临床表现为脓毒症心肌病(septic cardiomyopathy,SC)。SC具有早期发现困难、病情进展迅速、病死率较高等特点。尽管一些生物标志物如心肌肌钙蛋白、氨基末端脑利钠肽前体等能反映心脏损伤程度,对诊断SC具有一定意义,但均缺乏特异性。近年来的研究显示,微小RNA、脂质运载蛋白、脂肪酸结合蛋白等标志物同样对反应脓毒症心肌损伤有一定诊断价值,能在一定程度上早期评估脓毒症病人心功能水平,本文主要阐述这些生物标志物近年来的研究进展以及对SC的诊断意义。

关键词: 脓毒症心肌病, 生物标志物, 诊断, 预后

中图分类号:

R 542.2

杨绍孔, 陈立文, 沈华, 张铮. 脓毒症心肌病诊断及预后标志物的研究进展[J]. 实用老年医学, 2024, 38(7): 748-752.

参考文献

[1] SINGER M, DEUTSCHMAN C S, SEYMOUR C W, et al. The third international consensus definitions for sepsis and septic shock(sepsis-3) [J]. JAMA, 2016, 315(8): 801-810.
[2] MARTIN L, DERWALL M, ZOUBI S A, et al. The septic heart: current understanding of molecular mechanisms and clinical implications [J]. Chest, 2018, 155(2):427-437.
[3] BEESLEY S J, WEBER G, SARGE T, et al. Septic cardiomyopathy [J]. Critical Care Med, 2018, 46(4):625-634.
[4] ABEREGG S K, KAUFMAN D A. Troponin in sepsis [J]. Ann Am Thorac Soc, 2019, 16(10): 1335-1336.
[5] RAHASTO P, SETIANTO B, TIMAN I S, et al. Cardiac performance by echocardiography, cardiovascular biomarker, kidney function, and venous oxygen saturation as mortality predictors of septic shock [J]. Acta Med Indones, 2019, 51(1): 47-53.
[6] KHANAM S S, SON J W, LEE J W, et al. Prognostic value of short-term follow-up bnp in hospitalized patients with heart failure [J]. BMC Cardiovasc Disord, 2017, 17(1): 215.
[7] GOETZE J P, BRUNEAU B G, RAMOS H R, et al. Cardiac natriuretic peptides [J]. Nat Rev Cardiol,2020,17(11):698-717.
[8] BHANDARI B, CUNNINGHAM J. The role of brain natriuretic peptide as a prognostic marker for sepsis [J]. Cureus, 2020,12(7):e8954.
[9] RESHMI K S, OOMMEN M S, BELGUNDI P, et al. Prognostic role of N-terminal prohormone of brain natriuretic peptide for patients in the medical intensive care unit with severe sepsis [J].Lung India, 2021,38(5):438-441.
[10] PANDOMPATAM G, KASHANI K, VALLABHAJOSYULA S. The role of natriuretic peptides in the management, outcomes and prognosis of sepsis and septic shock [J]. Rev Bras Ter Intensiva,2019,31(3):368-378.
[11] GANFORNINA M D, ÅKERSTR M B, SANCHEZ D. Editorial: functional profile of the lipocalin protein family [J]. Front Physiol, 2022,13:904702.
[12] CHARKOFTAKI G, WANG Y W, MCANDREWS M, et al. Update on the human and mouse lipocalin(LCN) gene family, including evidence the mouse mup cluster is result of an “evolutionary bloom” [J].Hum Genomics,2019,13(1):11.
[13] LU F, INOUE K, KATO J, et al. Functions and regulation of lipocalin-2 in gut-origin sepsis: a narrative review [J]. Crit Care,2019,23(1):269.
[14] WANG B, CHEN G, ZHANG J, et al. Increased neutrophil gelatinase-associated lipocalin is associated with mortality and multiple organ dysfunction syndrome in severe sepsis and septic shock [J]. Shock,2015,44(3):234-238.
[15] LIU W, GUO X, JIN L, et al. Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction [J]. Front Cardiovasc Med, 2022,9:1009726.
[16] WANG B, CHEN G, LI J, et al. Neutrophil gelatinase-associated lipocalin predicts myocardial dysfunction and mortality in severe sepsis and septic shock [J]. Int J Cardiol, 2017,227:589-594.
[17] WANG L, XIE W, LI G, et al. Lipocalin 10 as a new prognostic biomarker in sepsis-induced myocardial dysfunction and mortality: a pilot study [J]. Mediators Inflamm,2021,2021:6616270.
[18] JAIN A, SANKAR J, ANUBHUTI A, et al. Prevalence and outcome of sepsis-induced myocardial dysfunction in children with ‘sepsis' ‘with' and ‘without shock': a prospective observational study [J].Trop Pediatr,2018,64(6):501-509.
[19] HE S, LENG W, DU X. Diagnostic significance of heart-type fatty acid-binding protein as a potential biomarker to predict the mortality rate of patients with sepsis: a systematic review and meta-analysis [J]. Expert Rev Mol Diagn, 2022,22(3):379-386.
[20] CHEN F C, XU Y C, ZHANG Z C. Multi-biomarker strategy for prediction of myocardial dysfunction and mortality in sepsis [J]. Zhejiang Univ Sci, 2020, 21(7):537-548.
[21] WENG G, TIAN P, YAN X, et al. Altered function of the left ventricle and clinical significance of heart-type fatty acid-binding protein in cardiac dysfunction among patients with sepsis [J]. Exp Ther Med, 2020,20(5):58.
[22] HAN X, ZHANG S, CHEN Z, et al. Cardiac biomarkers of heart failure in chronic kidney disease [J]. Clin Chim Acta,2020,510:298-310.
[23] MANETTI A C, MAIESE A, PAOLO M, et al. Micrornas and sepsis-induced cardiac dysfunction: a systematic review [J]. Int J Mol Sci,2020,22(1):321.
[24] WANG S, WANG G, DONG L, et al. The overexpression of mir-377 aggravates sepsis-induced myocardial hypertrophy by binding to rcan2 and mediating can activity [J]. Oxid Med Cell Longev, 2022,2022:6659183.
[25] LIN Y, HU J, CHEN J, et al. Mir-155 protects against sepsis-induced cardiomyocyte apoptosis via activation of no/cgmp signaling pathway by enos [J]. Trop J Pharm Res, 2022, 21(9): 1851-1858.
[26] YU Y, OU-YANG W X, ZHANG H, et al. Mir-125b enhances autophagic flux to improve septic cardiomyopathy via targeting stat3/hmgb1 [J]. Exp Cell Res, 2021,409(2):112842.
[27] LI D, LE J, YE J, et al. Mir-361-5p inhibits the wnt axis via targeting lgr4 and promotes sepsis-induced myocardial injury [J]. Ann Clin Lab Sci,2022,52(6):927-937.
[28] PEI Y, XIE S, LI J, et al. Bone marrow-mesenchymal stem cell-derived exosomal microrna-141 targets pten and activates β-catenin to alleviate myocardial injury in septic mice [J]. Immunopharmacol Immunotoxicol,2021,43(5):584-593.
[29] HONG X, WANG J, LI S, et al. Microrna-375-3p in endothelial progenitor cells-derived extracellular vesicles relieves myocardial injury in septic rats via brd4-mediated pi3k/akt signaling pathway [J]. Int Immunopharmacol, 2021,96:107740.
[30] SUN F, YUAN W, WU H, et al. Lncrna kcnq1ot1 attenuates sepsis-induced myocardial injury via regulating mir-192-5p/xiap axis [J]. Exp Biol Med:Maywood,2020,245(7):620-630.
[31] DENG C, ZHAO L, YANG Z, et al. Targeting hmgb1 for the treatment of sepsis and sepsis-induced organ injury [J]. Acta Pharmacol Sin, 2022,43(3):520-528.
[32] CHEN R, KANG R, TANG D. The mechanism of hmgb1 secretion and release [J]. Exp Mol Med,2022,54(2):91-102.
[33] JIN Y, WANG H, LI J, et al. Exploring the beneficial role of telmisartan in sepsis-induced myocardial injury through inhibition of high-mobility group box 1 and glycogen synthase kinase-3β/nuclear factor-κb pathway [J]. Korean J Physiol Pharmacol,2020,24(4):311-317.
[34] BRUTON M, HOLLAN I, XIAO J, et al. Expression of high mobility group protein b1 in cardiac tissue of elderly patients with coronary artery disease with or without inflammatory rheumatic disease [J]. Gerontology,2017,63(4):337-349.
[35] HOMSAK E, GRUSON D. Soluble st2: a complex and diverse role in several diseases [J]. Clin Chim Acta,2020,507:75-87.
[36] JIN X L, HUANG N, SHANG H, et al. Diagnosis of chronic heart failure by the soluble suppression of tumorigenicity 2 and N-terminal pro-brain natriuretic peptide [J]. J Clin Lab Anal, 2018,32(3):e22295.
[37] XU H, TURNQUIST H R, HOFFMAN R, et al. Role of the IL-33-ST2 axis in sepsis [J].Mil Med Res,2017,4:3.
[38] MCMAKEN S, EXLINE M C, MEHTA P, et al. Thrombospondin-1 contributes to mortality in murine sepsis through effects on innate immunity [J]. PLoS One, 2011, 6(5): e19654.
[39] VAN DER WEKKEN R J, KEMPERMAN H, ROEST M, et al. Baseline thrombospondin-1 concentrations are not associated with mortality in septic patients: a single-center cohort study on the intensive care unit [J]. Intensive Care Med Exp,2017,5(1):7.
[40] XIE Y, ZHANG J, JIN W, et al.Role of thrombospondin-1 in sepsis-induced myocardial injury [J]. Mol Med Rep,2023,27(6):113.