Sepsis occurs in numerous situations and is also an arising adverse complication in vulnerable cardiovascular patients, from those with diabetes to heart failure patients supported by ventricular assist devices. Septic patients often die from cardiac failure. This effect is partially related to the binding of lipopolysaccharides to cardiac Toll-like receptors, which activates the NF-κB pathway and induces a considerable inflammation reaction. The produced pro-inflammatory cytokines favour calcium overload, mitochondrial oxidative stress, and cellular death.

Recently, we demonstrated in the rat that an ω3 fatty acid, eicosapentaenoic acid, prevents mitochondrial dysfunction induced by cecal ligation and puncture. The beneficial action occurred through decreased inflammation, reduced mitochondrial oxidative stress, and upholding of cardiac energy metabolism. Since septic shock still leads to death in a notable proportion of patients, new pharmaceutical and/or dietary treatments able to modulate inflammation, calcium overload, oxidative stress, and mitochondrial ATP production may be very useful in preventing a lethal issue.

The aim of this Special Issue is to collate research findings or review articles concerning the cardiac consequences of sepsis. This research can include both in vitro and in vivo studies.

Potential topics include but are not limited to the following:

• Cardiac consequences of sepsis in animals and humans
• The effects on inflammation, oxidative stress, fibrosis, contractile activity and cardiac failure as a result of sepsis
• Organelles (mitochondria, reticulum, other), metabolism, cell death and apoptosis in the context of sepsis
• The role of various anti-inflammatory molecules, antioxidants, anti-calcic agents, and mitochondrial protectors