Inflammation and cardiac dysfunction during sepsis, muscular dystrophy, and myocarditis

Abstract

Inflammation plays an important role in cardiac dysfunction under different situations. Acute systemic inflammation occurring in patients with severe burns, trauma, and inflammatory diseases causes cardiac dysfunction, which is one of the leading causes of mortality in these patients. Acute sepsis decreases cardiac contractility and impairs myocardial compliance. Chronic inflammation such as that occurring in Duchenne muscular dystropshy and myocarditis may cause adverse cardiac remodeling including myocyte hypertrophy and death, fibrosis, and altered myocyte function. However, the underlying cellular and molecular mechanisms for inflammatory cardiomyopathy are still controversial probably due to multiple factors involved. Potential mechanisms include the change in circulating blood volume; a direct inhibition of myocyte contractility by cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β); abnormal nitric oxide and reactive oxygen species (ROS) signaling; mitochondrial dysfunction; abnormal excitation-contraction coupling; and reduced calcium sensitivity at the myofibrillar level and blunted β-adrenergic signaling. This review will summarize recent advances in diagnostic technology, mechanisms, and potential therapeutic strategies for inflammation-induced cardiac dysfunction.

Prognostic value of NT-proBNP levels in the acute phase of sepsis on lower long-term physical function and muscle strength in sepsis survivors

“…Potential mechanisms explaining the increased NT-proBNP levels during sepsis are still debated. The most accepted hypothesis is that cardiac insufficiency during sepsis is caused by the impact of the pro-inflammatory response and ventricular overload during aggressive fluid resuscitation therapy [15, 37]. Current literature argues that sepsis-induced cardiac dysfunction is a reversible condition driven by functional rather than structural changes, with a complete resolution within 7–10 days in survivors [24].…”

“…Usually, patients suffering from sepsis show signs of cardiac insufficiency [14]. Indeed, the destructive systemic inflammatory response and intensive resuscitation occurring during sepsis result in widespread organ overload and damage including myocardial injury [15]. Additionally, experimental studies have demonstrated that endotoxins and cytokines directly increase gene expression of BNP, explaining the higher levels of this biomarker during sepsis [16].…”

Transcriptomic study of lipopolysaccharide‑induced sepsis damage in a mouse heart model

“…Methylthioadenosine is a sepsis biomarker that is involved in the inflammatory response and is related to high rates of fever-induced host cell death ( 19 ). Several previous studies have shown that sepsis is associated with the inflammatory response in the heart ( 8 , 20 , 21 ), but the detailed molecular mechanism remains unclear. The Wnt and inflammatory response pathways were associated with T cell-specific transcription factor (TCF)/lymphoid enhancer-binding factor (LEF) ( 22 , 23 ).…”

Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-κB/p65 Expression

“…Myocardial depression is seen in approximately 50% of patients with severe sepsis, with high mortality rate as high as 70–90% 1 . A number of mechanisms have been proposed to be involved in sepsis induced myocardial dysfunction (SIMD), including bacterial toxins induced excessive production of pro-inflammatory cytokines, complement activation 2 , dysregulation of intracellular calcium transporters 3 , and mitochondrial dysfunction 4 .…”