Myocardial dysfunction is a common complication in patients with severe sepsis, and early recognition and aggressive supportive therapy are mandatory as mortality in patients with septic shock is still high. The pathophysiology of sepsis is a complex and dynamic process that originates from the host immune response to infection and varies according to the genetic predisposition, immune status, and comorbid conditions of the host, the type of pathogen, and the site and extent of infection. In this complex scenario, the phenomenon of myocardial depression is mediated by circulating depressant substances, including tumor necrosis factor alpha and various cytokines. In addition, myocardial depression in sepsis appears to be mediated in part through combinations of oxidative stress unbalance, mitochondrial damage, and activation of apoptotic pathways.

We invite original research and review articles focusing on interaction of cardiac inflammation, oxidative stress, and hypoxia in the setting of sepsis.

Potential topics include, but are not limited to:

• Pathophysiology of myocardial depression in the setting of sepsis
• Biomarkers of oxidative stress and inflammation in cardiac dysfunction in sepsis
• Role of myocardial apoptosis in sepsis as a key step toward myocardial dysfunction
• Role of cellular response as initiator/mediator of cardiac dysfunction in sepsis
• Microcirculatory alterations in severe sepsis
• Personalized medicine approach to heart failure in sepsis
• Postmortem cardiac findings and their interpretation