Abstract
’septic acute myocarditis’ in the pre-antibiotic era was a purulent disease of the heart. Nowadays, non-specific pathomorphological and pathohistological alterations characterize the myocardium of patients whose hearts have failed in septic shock. For decades, septic myocardial depression in animal models was attributed to the release of cardiodepressant factors into the blood stream, while the existence of human septic myocardial depression was only unequivocally proven in the early 1980s by the group of Parrillo [1], who had examined patients in the ICU with nuclear imaging techniques. Since then, experimental and clinical evidence has accumulated arguing for a more complex alteration of the heart in sepsis than exclusive myocardial depression. The concept of a “septic cardiomyopathy” was proposed [2], which emphasizes alterations of cardiac cellular phenotype as a basis of organopathy in response to a variety of agents acting on heart cells, like bacterial toxins and endogenous cytokines, hormones, mediators, and cardiodepressant factors. Not only is impairment of complex intrinsic heart function a consequence, but regulation of cardiac function is also severely disturbed due to excessive autonomic dysfunction [3].
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Werdan, K., Oelke, A., Müller-Werdan, U. (2009). ‘Myocardial Depression’ or’ Septic Cardiomyopathy’?. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 2009. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-92276-6_18
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