The article highlights the issue of nosological independence of ischemic cardiomyopathy – a pathological condition of the myocardium, accompanied by increase in all chambers of the heart to the degree of cardiomegaly, often with irregular thickening of its walls and the phenomena of diffuse and focal substitute fibrosis that develops in the atherosclerotic lesions of the coronary arteries, but not because of formation ventricular aneurysms, organic pathology valvular heart or presence of pathological communications. In most cases, given the pathological condition develops after myocardial infarction due to left ventricular remodeling. The term "ischemic cardiomyopathy" was proposed in 1970 by G. Burth et. al. with multiple lesions of coronary arteries, enlarged heart cavities and clinical symptoms of congestive heart failure which are similar to those in dilated cardiomyopathy. The problem of nosology repeatedly discussed in the report of WHO and in numerous publications. Ischemic cardiomyopathy was included in the WHO classification of specific cardiomyopathies and presented in ICD-10 as a form of chronic ischemic heart disease (I 25.5). In 2006, the American Heart Association proposed a scientific position on contemporary definition and classification of cardiomyopathies, according to what the term "ischemic cardiomyopathy" was excluded from the classification of cardiomyopathies as a disease of the myocardium and violation of its functions, which directly are the result of other cardiovascular disorders such as atherosclerosis of the coronary arteries, leading to myocardial ischemic injury by reducing coronary blood flow. Thus, according to the literature and own positions, the term "ischemic cardiomyopathy" is now incorrectly applied to characterize patients with coronary heart disease and severe dysfunction infarction, we must use the term "chronic heart failure of ischemic origin" (HHFIO) with the proviso that mean patients with impaired left ventricular systolic function. The severity of clinical manifestations HHFIO depends not only on their own sclerotic changes of the myocardium, but on metabolic disorders in cardiomyocytes as a result of hypoxia. It is believed that the basis of HHFIO is myocardial ischemia, which, without being the direct cause dilation of the heart, acts as a trigger factor other causal processes, possibly necrosis, fibrosis, myocardium hibernation, development of contractures myofibrils, apoptosis, which lead to fewer cardiomyocytes in unit volume of infarction and ventricular remodeling ending HHFIO. HHFIO occurs in 5-8% of patients with coronary heart disease, mostly aged 45-55 years, predominantly male (90%). The main clinical manifestation is chronic heart failure. HHFIO characterized by enlargement of the cavities of the heart, the progression of stagnation, auscultation – definition gallop and systolic murmur relative failure of the mitral valve. HHFIO diagnosis can be established in patients with coronary artery disease based on standardized criteria adopted in the world and clarified and supplemented M.M. Alshybaya et al. (2005): hemodynamically significant coronary artery disease; myocardial infarction, coronary artery bypass surgery or balloon angioplasty transluminal history; chronic heart failure functional class II or higher (NYHA); dilatation of the left ventricle (end-diastolic volume index >110ml/m2, end-systolic volume index >80 mL/m2); left ventricular ejection fraction of 35% or less; mitral regurgitation from papillary dysfunction second degree and above. In clinical practice we often have difficulty of differential diagnosis between HHFIO and dilated cardiomyopathy, in which the main clinical manifestation is progressive chronic heart failure.
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