Sepsis-Induced Cardiomyopathy: Mechanisms and Treatments

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.

Keywords: Chinese traditional medicine; inflammatory mediators; mechanisms; sepsis-induced cardiomyopathy; treatments.

Figure 1

The mechanisms in the sepsis-induced cardiomyopathy. (A) PAMPs and cytokines (TNF-α, IL-1, and IL-6) contribute to sepsis-induced cardiomyopathy (SIC). (B) Damage-associated molecular patterns (HMGB1, HSP, and histone) induce SIC through different mechanisms. (C) NO and NOS are involved in SIC. (D) Autonomic dysregulation play a significant role in SIC. PAMP, pathogen-associated molecular pattern. TNF-α, tumor necrosis factor-α. IL-1, interleukin-1. IL-6, interleukin-6. TLRs, toll-like receptors. NF-κB, nuclear factor-κB. LVEF, left ventricular ejection fraction. HMGB1, high mobility group protein B1. HSP, heat shock protein. ROS, reactive oxygen species. VCAM, vascular cell adhesion molecule. NO, nitric oxide. NOS, nitric oxide syntheses.