Sepsis is defined as a life-threatening organ dysfunction caused by a
dysregulated host response to infection. Sepsis-induced myocardial dysfunction
represents reversible myocardial dysfunction which ultimately results in left
ventricular dilatation or both, with consequent loss of contractility. Studies on
septic cardiomyopathy report a wide range of prevalence ranging from 10% to
70%. Myocardial damage occurs as a result of weakened myocardial circulation,
direct myocardial depression, and mitochondrial dysfunction. Mitochondrial
dysfunction is the leading problem in the development of septic cardiomyopathy
and includes oxidative phosphorylation, production of reactive oxygen radicals,
reprogramming of energy metabolism, and mitophagy. Echocardiography provides
several possibilities for the diagnosis of septic cardiomyopathy. Systolic and
diastolic dysfunction of left ventricular is present in 50–60% of patients with
sepsis. Right ventricular dysfunction is present in 50–55% of cases, while
isolated right ventricular dysfunction is present in 47% of cases. Left
ventricle (LV) diastolic dysfunction is very common in septic shock, and it
represents an early biomarker, it has prognostic significance. Right ventricular
dysfunction associated with sepsis patients with worse early prognosis. Global
longitudinal stress and magnetic resonance imaging (MRI) of the heart are
sufficiently sensitive methods, but at the same time MRI of the heart is
difficult to access in intensive care units, especially when dealing with
critically ill patients. Previous research has identified two biomarkers as a
result of the integrated mitochondrial response to stress, and these are
fibroblast growth factor-21 (FGF-21) and growth differentiation factor-15
(GDF-15). Both of the mentioned biomarkers can be easily quantified in serum or
plasma, but they are difficult to be specific in patients with multiple
comorbidities. Mitochondrial dysfunction is also associated with reduced levels
of miRNA (microRNA), some research showed significance of miRNA in sepsis-induced
myocardial dysfunction, but further research is needed to determine the clinical
significance of these molecules in septic cardiomyopathy. Therapeutic options in
the treatment of septic cardiomyopathy are not specific, and include the
optimization of hemodynamic parameters and the use of antibiotic thera-pies with
targeted action. Future research aims to find mechanisms of targeted action on
the initial mechanisms of the development of septic cardiomyopathy.