Sepsis is the leading cause of death in critical ill patients in intensive care
units around the world. Cardiac dysfunction is one of the major clinical manifestations
in septic patients (about 60%), with mortality rate of approximately 80%, while septic
patients without cardiovascular impairment present mortality rates around 20%.
However, cardiac involvement as an important contributing factor to the multiple organ
dysfunction in the sepsis syndrome, has been rejected. Principal mechanisms proposed
to explain the cardiac dysfunction in sepsis originates from functional abnormalities,
not from structural changes. In spite of the evolution of septic cardiomyopathy concept,
the study of structural change as an important component in the development of
myocardial dysfunction has been omitted in sepsis. In 2007, morphological analysis of
human heart samples obtained by autopsy reported cases of severe sepsis/septic shock
condition in patients submitted a longer periods of hospitalization. Septic patients
showed structural myocardial alterations classified as "inflammatory cardiomyopathy"
probably responsible for the myocardial depression induced by sepsis. Since then,
structural changes on cardiac dysfunction in sepsis/septic shock has been object of
several studies, experimental and clinical, aiming to improve the diagnosis and
treatment of this syndrome. In this chapter, will be presented results of studies
conducted in our laboratory analyzing cellular and molecular mechanisms underlying
sepsis/septic shock, which may result in morphological alterations in the myocardium
of mice subjected to CLP-sepsis model.
Keywords: Cardiac structural changes, Dystrophin-glycoprotein complex (DGC),
Experimental sepsis model, Myocardial depression, Sepsis, Septic cardiomyopathy.
