Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms

Flynn, Anthony; Mani, Bhalaghuru Chokkalingam; Mather, Paul

doi:10.1007/s10741-010-9176-4

Cited by 120 publications

(88 citation statements)

References 40 publications

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“…They are initiated by a decrease in diastolic function, a status that progresses toward systolic function reduction with the worsening of sepsis (Flynn et al. 2010). In our study, the sepsis that was performed did not deteriorate cardiac function.…”

Section: Discussionmentioning

confidence: 99%

“…The up‐to‐date measurement techniques of cardiac function (echography, MRI) do not reveal important modifications of this parameter during sepsis, except a decrease in diastolic function followed by a reduction of systolic function in the sickest patients (Hunter and Doddi 2010; Flynn et al. 2010). The most evident abnormality of the cardiovascular function is a decrease in arterial pressure associated with an initial compensatory stimulation of the heart rate (Cheung et al.…”

Section: Introductionmentioning

confidence: 99%

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Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

et al. 2017

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If it is sustained for several days, sepsis can trigger severe abnormalities of cardiac function which leads to death in 50% of cases. This probably occurs through activation of toll‐like receptor‐9 by bacterial lipopolysaccharides and overproduction of proinflammatory cytokines such as TNF‐α and IL‐1β. In contrast, early sepsis is characterized by the development of tachycardia. This study aimed at determining the early changes in the cardiac function during sepsis and at finding the mechanism responsible for the observed changes. Sixty male Wistar rats were randomly assigned to two groups, the first one being made septic by cecal ligation and puncture (sepsis group) and the second one being subjected to the same surgery without cecal ligation and puncture (sham‐operated group). The cardiac function was assessed in vivo and ex vivo in standard conditions. Several parameters involved in the oxidative stress and inflammation were determined in the plasma and heart. As evidenced by the plasma level of TNF‐α and gene expression of IL‐1β and TNF‐α in the heart, inflammation was developed in the sepsis group. The cardiac function was also slightly stimulated by sepsis in the in vivo and ex vivo situations. This was associated with unchanged levels of oxidative stress, but several parameters indicated a lower cardiac production of reactive oxygen species in the septic group. In conclusion, despite the development of inflammation, early sepsis did not increase reactive oxygen species production and did not reduce myocardial function. The depressant effect of TNF‐α and IL‐1β on the cardiac function is known to occur at very high concentrations. The influence of low‐ to moderate‐grade inflammation on the myocardial mechanical behavior must thus be revisited.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

et al. 2017

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show abstract

“…In our view, sepsis-induced cardiomyopathy was also a possibility considering the patient's long septic illness preoperatively and the timing of his cardiac arrest at the end of a long surgical dissection of necrotic bowel tissue. 4 A pharmacologically mediated sympathectomy by the combination of opioids, a beta-blocker, ketamine, a volatile agent, and lidocaine may have also contributed to the mechanism. With regard to management of cardiac arrest, the patient received immediate uninterrupted resuscitation guided by ACLS protocol.…”

Section: Discussionmentioning

confidence: 99%

Cardiac arrest in the operating room requiring prolonged resuscitation

Charapov

Eipe

2012

Can J Anesth/J Can Anesth

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“…The mechanism of the altered myocardial function, at first attributed to a myocardial depressant factor (MDF) [192], began to be understood when in 1985 Parrillo [193] showed that the serum of septic humans during the acute phase may depress the contractile function of isolated myocardiocytes; this effect may be prevented, as subsequently demonstrated by Kumar, by immunoadsorption of IL-1 andF 194 Ils may cause myocardial depression both directly or through the NO produced by the induction of iNOS [195]. In the recent years the focus of the research has been turned on the upstream mediators of ILs, the TLRs, that have been shown to be main mediators of myocardial damage in sepsis models of both LPS infusion and CLP and in human sepsis [196]. Their effect as already seen is due to the release, consequent to the inflammatory reaction and to the tissue damage, of DAMP further increasing tissue injury.…”

Section: Pathophysiological Mechanismmentioning

confidence: 99%

“…Their effect as already seen is due to the release, consequent to the inflammatory reaction and to the tissue damage, of DAMP further increasing tissue injury. The main TLRs types expressed in the heart are TLR2 (recognizing lipoteichoic acid) and TLR4 (LPS receptor) but also TLR 3 and 9 are present [196]. Both TLR2 and TLR4 have been demonstrated as essential mediators of the septic myocardial damage: in mice with their genetic deficiency there was a better preservation of cardiac function and a decreased mortality [14,197,198].…”

Section: Pathophysiological Mechanismmentioning

confidence: 99%