Abstract
Inflammatory cardiomyopathy is defined as inflammation of the heart muscle associated with impaired function of the myocardium. In our region, its etiology is most often viral. Viral infection is a possible trigger of immune and autoimmune mechanisms which contributed to the damage of myocardial function. Myocarditis is considered the most common cause of dilated cardiomyopathy. Typical manifestation of this disease is heart failure, chest pain, or arrhythmias. The most important noninvasive diagnostic method is magnetic resonance imaging, but the gold standard of diagnostics is invasive examination, endomyocardial biopsy. In a significant proportion of cases with impaired left ventricular systolic function, recovery occurs spontaneously in several weeks and therefore it is appropriate to postpone critical therapeutic decisions about 3–6 months after start of the treatment. Therapy is based on standard heart failure treatment; immunosuppressive or antimicrobial treatment may be considered in some cases depending on the results of endomyocardial biopsy. If severe dysfunction of the left ventricle persists, device therapy may be needed.
Highlights
Inflammatory cardiomyopathy is defined as inflammation of the heart muscle associated with impaired function of the myocardium
Inflammatory cardiomyopathy (ICM) is defined as inflammation of the heart muscle associated with impaired function of the myocardium, which has most often the morphology of dilated cardiomyopathy
The third phase of the disease occurs after several weeks or months and may include either retreat of inflammation and improvement in left ventricle (LV) function or persistent LV dysfunction associated with development of postinflammatory dilated cardiomyopathy (DCM)
Summary
Inflammatory cardiomyopathy (ICM) is defined as inflammation of the heart muscle associated with impaired function of the myocardium, which has most often the morphology of dilated cardiomyopathy. These autoimmune reactions are based on two main mechanisms: the first is the cross-reactivity of viral epitopes and some cardiac structures (molecular mimicry phenomenon); another option is the exposure of originally intracellular structures to the immune system that occurs after the virus-induced damage of myocytes Such a situation is seen in the production of antibodies against alpha and beta myosin-heavy-chains, wherein the antibody against alpha chains is considered organ (heart) specific. The third phase of the disease occurs after several weeks or months and may include either retreat of inflammation and improvement in LV function (in 50–70% of cases, usually after removal of viruses from myocardium) or persistent LV dysfunction associated with development of postinflammatory dilated cardiomyopathy (DCM). The same was true for comparison of patients with LVEF below 45% with and without myocarditis (PVB19 presence in 33.3% versus 17.6%; p < 0.05) [5]
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