[1]王颍骅 何奔.脓毒症型心肌病的研究进展[J].心血管病学进展,2019,(8):1150-1153.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.020]
 WANG Yinghua,HE Ben.Septic Cardiomyopathy[J].Advances in Cardiovascular Diseases,2019,(8):1150-1153.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.020]
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脓毒症型心肌病的研究进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2019年8期
页码:
1150-1153
栏目:
综述
出版日期:
2019-11-25

文章信息/Info

Title:
Septic Cardiomyopathy
作者:
王颍骅 何奔
(1.上海交通大学附属胸科医院重症监护科,上海 200030;2.上海交通大学附属胸科医院心内科,上海 200030)
Author(s):
WANG Yinghua1 HE Ben2
(1.ICU,Shanghai Chest Hospital,Shanghai Jiao Tong University,Shanghai 200030, China;2. Department of Cardiology,Shanghai Chest Hospital,Shanghai Jiao Tong University,Shanghai 200030, China)
关键词:
WANG Yinghua1 HE Ben2
Keywords:
SepsisMyocardial depressionCardiomyopathyMitochondria
DOI:
10.16806/j.cnki.issn.1004-3934.2019.08.020
摘要:
脓毒血症致心肌抑制又称为脓毒症型心肌病。18%~65%的脓毒症患者会出现心肌抑制, 死亡率为40%~70%,发病7~19d后心功能可能恢复。病因、发病机制不明,治疗也无特异性。脓毒症引起的复杂的心肌炎症反应和线粒体非稳态,最终导致心肌功能不全。脓毒症致心肌抑制成为影响脓毒症预后的重要因素。现就脓毒症型心肌病的发病机制、临床诊断和治疗进展做总结。
Abstract:
Septic cardiomyopathy is known as sepsis-induced myocardial depression.18%~65% septic patients suffered from myocardial depression and its mortality rate is 40%~70%.Heart function may recover in 7~19 days after the onset of sepsis.The etiology, pathogenesis and treatment of septic cardiomyopathy are uncertain except that sepsis leads to a complex intramyocardial inflammatory response and mitochondrial non-homeostasis,which may result in myocardial dysfunction.Since sepsis-induced myocardial depression is recognized as a major predictor of prognosis,the recent findings about pathogenesis,diagnosis and manipulation are reviewed in this article.

参考文献/References:

[1] Han SJ,Tae HL,Cho HB,et al. Risk factors and outcomes of sepsis-induced myocardial dysfunction and stress-induced cardiomyopathy in sepsis or septic shock.a comparative retrospective study[J].Medicine,2018,97:13(e0263).
[2] Prescott HC,Angus DC. Enhancing recovery from sepsis: a review[J]. JAMA,2018,319(1):62-75.
[3] Karnad DR,Saseedharan S. Myocardial dysfunction in sepsis and septic shock
[J]. Assoc Physicians India,2017,65(12):11-12.
[4]Robert RE,Ashley NS,Mark JF,et al. Pathophysiology,echocardiographic
evaluation,biomarker findings,and prognostic implications of septic cardiomyopathy:a review of the literature[J]. Crit Care,2018,22:112-126.
[5]Zhou D,Zhu Y,Ouyang MZ,et al. Knockout of Toll-like receptor 4 improves survival and cardiac function in a murine model of severe sepsis[J]. Mol Med Rep,2018,17(4):5368-5375.
[6]Unuma K,Aki T,Nagano S,et al.The down-regulation of cardiac contractile proteins underlies myocardial depression during sepsis and is mitigated by carbon monoxide [J]. Biochem Biophys Res Commun,2018,495(2):1668-1674.
[7] Elio A,Enrico F,Katia D,et al. Myocardial depression in sepsis: from pathogenesis to clinical manifestations and treatment[J]. J Crit Care,2014,29:500-511.
[8]Wang Y,Zhang L,Zhao X,et al. An experimental study of the protective effect of simvastatin on sepsis-induced myocardial depression in rats[J]. Biomed Pharmacother,2017,94:705-711.
[9]Wang X,Yu Y. MiR-146b protect against sepsis induced mice myocardial injury through inhibition of notch1[J]. J Mol Histol,2018,49(4):411-417.
[10]Ndongson-Dongmo B,Heller R,Hoyer D,et al. Phosphoinositide 3-kinase gamma controls inflammation-induced myocardial depression via sequential cAMP and iNOS signalling[J]. Cardiovasc Res,2015,108(2):243-253.
[11]Juliana MR,Ludmila RPF,Gustavo HE,et al. Exosomes from patients with septic shock convey miRNAs related to inflammation and cell cycle regulation: new signaling pathways in sepsis?[J]. Crit Care,2018,22:68-79.
[12]Stanzani G,Duchen MR,Singer M. The role of mitochondria in sepsis-induced cardiomyopathy[J]. Biochim Biophys Acta Mol Basis Dis,2019,1865(4):759-773.
[13]Jacek H.Heartfelt sepsis: microvascular injury due to genomic storm[J].Kardiol Pol,2018,76(8):1203-1216.
[14]Yang N,Shi X,Zhang B,et al. The Trend of β3-Adrenergic Receptor in the development of septic myocardial depression: a lipopolysaccharide-induced rat septic shock model[J]. Cardiology,2018,139:234-244.
[15]Yu X,Wang Y,Yang D,et al. α2A-adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation[J]. Sci Rep,2018,8:5478-5493.
[16]Li H,Xing Y,Yang D,et al. Alpha-1 adrenergic receptor agonist phenylephrine inhibits sepsis-induced cardiomyocyte apoptosis and cardiac dysfunction via activating ERK1/2 signal pathaway[J]. Shock,2019,52(1):122-133
[17]Vasques NF,Laundos TL,Cerqueira RJ,et al. MicroRNA-155 amplifies nitric oxide/cGMP signaling and impairs vascular angiotensin Ⅱ reactivity in septic shock[J]. Crit Care Med,2018,46(9):e945-e954.
[18] He C,Zhang W,Li S,et al. Edaravone improves septic cardiac function by inducing an HIF-1α/HO-1 pathway[J].Oxi Med Cell Longev,2018,2018:5216383
[19]Xu J,Lin C,Wang T,et al. Ergosterol attenuates LPS-induced myocardial injury by modulating oxidative stress and apoptosis in rats[J]. Cell Physiol Biochem,2018,48:583-592.
[20] Dagmar J,Michaela M, Jan H,et al. Cellular mechanisms of myocardial depression in porcine septic shock[J]. Front Physiol,2018,9:726.
[21] Vanasco V,Saez T,Magnani ND,et al. Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery[J]. Free Radic Biol Med,2014,77:1-9.
[22] Sánchez-Villamil JP,D’Annunzio V,Finocchietto P,et al. Cardiac-specifc overexpression of thioredoxin 1 attenuates mitochondrial and myocardial dysfunction in septic mice[J]. Int J Biochem Cell Biol,2016,81:323-324.
[23] Gonzalez AS,Elguero ME,Finocchietto P,et al. Abnormal mitochondrial fusion-fission balance contributes to the progression of experimental sepsis[J]. Free Radic Res,2014,48(7):769-783.
[24].Pan P,Wang X,Liu D. The potential mechanism of mitochondrial dysfunction in
septic cardiomyopathy[J]. J Int Med Res,2018,46(6):2157-2169.
[25] Matkovich SJ,Khiami BA,IEfimov IR,et al. Widespread down-regulation of cardiac mitochondrial and sarcomeric genes in patients with sepsis[J]. Crit Care Med,2017,45(3):407-414.
[26] Walley KR. Sepsis-induced myocardial dysfunction[J]. Curr Opin Crit Care,2018,24(4):292-299.
[27] Masson S1,Caironi P,Fanizza C,et al. Sequential N-terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponin measurements during albumin replacement in patients with severe sepsis or septic shock[J]. Crit Care Med, 2016,44(4):707-716.
[28] Sanfilippo F,Corredor C,Fletcher N,et al. Left ventricular systolic function evaluated by strain echocardiography and relationship with mortality in patients with severe sepsis or septic shock: a systematic review and meta-analysis[J]. Crit Care,2018,22:183-195.
[29] Vallabhajosyula S,Pruthi S,Shah S,et al. Basic and advanced echocardiographic evaluation of myocardial dysfunction in sepsis and septic shock[J]. Anaesth Intensive Care,2018,46(1):13-24.
[30] Liu YC.Yu MM,Shou ST,et al. Sepsis-induced cardiomyopathy:mechanisms and treatments[J]. Front Immunol,2017,8:1021.
[31] Dellinger RP,Levy MM,Rhodes A,et al. Surviving Sepsis Campaign: international
guidelines for management of severe sepsis and septic shock:2012[J]. Crit Care
Med,2013,41:580-637.
[32] Sato R,Nasu M. Time to re-think the use of dobutamine in sepsis[J]. J Intensive Care,2017,5:65.
[33] Zangrillo A,Putzu A,Monaco F,et al. Levosimendan reduces mortality in patients with severe sepsis and septic shock: a meta-analysis of randomized trials[J]. J Crit Care,2015,30(5):908-913.
[34] Duan EH,Oczkowski SJ,Belley-Cote E,et al. beta-Blockers in sepsis:protocol for a systematic review and meta-analysis of randomised control trials[J]. BMJ Open,2016,6(6):e012466.
[35] Morelli A,Ertmer C,Westphai M,et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock:a randomized clinical trial[J]. JAMA,2013,310(16):1683-1691.

备注/Memo

备注/Memo:
基金项目:国家自然科学基金重点项目(81830010) 收稿日期:2019-03-09
通讯作者:何奔,E-mail:drheben@126.com
更新日期/Last Update: 2020-01-20