Oxidative stress and bioenergetic failure are central to the pathogenesis of sepsis-induced cardiomyopathy, representing potential targets for future therapeutic interventions.
Cardiac dysfunction may complicate the course of severe sepsis and septic shock with significant implications for patient's survival. The basic pathophysiologic mechanisms leading to septic cardiomyopathy have not been fully clarified until now. Disease-specific treatment is lacking, and care is still based on supportive modalities. Septic state causes destruction of redox balance in many cell types, cardiomyocytes included. The production of reactive oxygen and nitrogen species is increased, and natural antioxidant systems fail to counterbalance the overwhelming generation of free radicals. Reactive species interfere with many basic cell functions, mainly through destruction of protein, lipid, and nucleic acid integrity, compromising enzyme function, mitochondrial structure and performance, and intracellular signaling, all leading to cardiac contractile failure. Takotsubo cardiomyopathy may result from oxidative imbalance. This review will address the multiple aspects of cardiomyocyte bioenergetic failure in sepsis and discuss potential therapeutic interventions.
Tsolaki et al. (Sun,) studied this question.