Septic cardiomyopathy is a complex, reversible condition driven by multiple mechanisms including cardiosuppressive mediators, altered calcium homeostasis, mitochondrial dysfunction, and apoptosis.
This review highlights that sepsis-induced myocardial suppression is a multifactorial, reversible process that may act as an adaptive hibernation mechanism to maintain cardiomyocyte viability during critical illness.
Septic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression.
Flierl et al. (Thu,) conducted a review in Septic cardiomyopathy. Septic cardiomyopathy is a complex, reversible condition driven by multiple mechanisms including cardiosuppressive mediators, altered calcium homeostasis, mitochondrial dysfunction, and apoptosis.
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