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Impaired Cellular Signaling of the Adenylyl Cyclase and the Phosphoinositide Pathway in Septic Cardiomyopathy

  • Chapter
Pathophysiology of Heart Failure

Abstract

The classification of secondary cardiomyopathies is based on “myocardial damage within the scope of a systemic disease.” In view of this definition, myocardial impairment in sepsis and the multiple organ dysfunction syndrome might be reckoned as a secondary form of cardiomyopathy, as septic cardiomyopathy [1]: various infectious disease entities and myocardial virulence factors may trigger common mediator pathways. Thereby, a complex pattern of myocardial depression with different grades of severity may result, characterized on the one hand by common principles (e.g., catecholamine desensitization and the effects of tumor necrosis factor α (TNFα); see below), and on the other hand by toxin-specific and therefore infectious agent-specific pathways (e.g., inhibition of protein synthesis by P. exotoxin A; see below). In a canine model of endotoxin shock, development of myocardial dysfunction indicates a bad prognosis [2]. In patients, heart failure can be documented to a similar degree in various forms of Gram-negative and Gram-positive sepsis and also in fungal sepsis (figure 1).

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Werdan, K. et al. (1996). Impaired Cellular Signaling of the Adenylyl Cyclase and the Phosphoinositide Pathway in Septic Cardiomyopathy. In: Dhalla, N.S., Singal, P.K., Takeda, N., Beamish, R.E. (eds) Pathophysiology of Heart Failure. Developments in Cardiovascular Medicine, vol 168. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1235-2_18

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