Abstract
Sepsis is a lethal syndrome with a high incidence and a weighty economy burden. The pathophysiology of sepsis includes inflammation, immune dysfunction, and dysfunction of coagulation, while sepsis-induced cardiomyopathy (SIC), defined as a global but reversible dysfunction of both sides of the heart induced by sepsis, plays a significant role in all of the aspects above in the pathogenesis of sepsis. The complex pathogenesis of SIC involves a combination of dysregulation of inflammatory mediators, mitochondrial dysfunction, oxidative stress, disorder of calcium regulation, autonomic nervous system dysregulation, and endothelial dysfunction. The treatments for SIC include the signal pathway intervention, Chinese traditional medicine, and other specific therapy. Here, we reviewed the latest literatures on the mechanisms and treatments of SIC and hope to provide further insights to researchers and create a new road for the therapy of sepsis.
Highlights
Sepsis is a lethal syndrome induced by infection, which has a reported annual death of 200,000 in the United States [1]
With the development of tissue Doppler imaging, perfusion echocardiography myocardial, and hemodynamics monitoring [3], the definition of sepsis-induced cardiomyopathy (SIC) has been summarized as a global but reversible dysfunction of both the left and right sides of the heart, which is induced by myocardial depressants released from pathogen and host, and global ischemia after peripheral vasodilation, arterial and capillary shunting in septic distributive shock [4]
A retrospective cohort study reported that SIC developed in 13.8% of patients with sepsis and septic shock [5], which could be used as an outcome predictor in the septic patients [6]
Summary
Sepsis is a lethal syndrome induced by infection, which has a reported annual death of 200,000 in the United States [1]. The mechanisms of NO-induced SIC include vasodilatation with resulting changes in preload, afterload, and cardiac perfusion, downregulating β-adrenergic receptors [36], depression of mitochondrial respiration, and further release of pro-inflammatory cytokines [37] Another adverse effect of NO on myocardial depression is the peroxynitrite, produced by NO metabolism, which interacts with lipids, DNA, and proteins [38] and affects the function of mitochondrial permeability transition pores, with subsequent mitochondrial dysfunction [39]. It will potentially decrease the blood pressure, perform negative inotropic effects, and cause pump failure in the already depressed heart. Pathways intervention, TCM, β-adrenoreceptor antagonist, EPO, and microRNA, there is still no efficient treatment in patients with SIC
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
