Sydorenko R. Pathological anatomy of the heart auricles at chronic coronary artery disease.

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0410U004702

Applicant for

Specialization

  • 14.03.02 - Патологічна анатомія

14-10-2010

Specialized Academic Board

Д 64.600.01

Kharkiv National Medical University

Essay

The work covers morphofunctional aspects of heart auricle remodeling at chronic coronary artery disease (CCAD) and contains solution of an urgent problem, i.e. investigation of the structural changes in the heart auricles as morpho- (patho-) genetic components of this disease.It was determined that structural functional changes of the heart auricles were performed as a result of continuous compensation-adaptation mechanisms, namely dilatation of the cavity and wall hypertrophy, their ratio depending on the form of CCAD. Heart auricle remodeling is promoted by reorganization of their morphofunctional components with reduction of the relative volume of cardiomyocytes and increase of stoma paranchyma ratio with prevalence of connective tissue structures, the degree of them depending on the heart auricle, gender and form of CCAD. Reconstruction of the vascular component of the myocardium of the heart auricles at CCAD promotes the progress of diffuse cardiosclerosis and development of dystrophic and necrobiotic changes in the cardiomyocytes. Immunohistochemistry in the connective tissue of the endocardium and myocardium of the heart auricles demonstrates increased production of type I and III collagens with prevalence of the former. The basal membranes of the vessels are characterized by collagen I and III prevalence and decreased amount of type IV collagen. Remodeling of the heart auricles with increased dilation of the cavities is accompanied by redistribution of secretary granules in the cardiomyocytes of the heart auricles containing atrial natridiuretic peptide and reduction of their optic density suggesting exhausted synthetic activity of cardiomyocytes, which together with fibrosis of the walls of the auricles can be a factor determining the progress of heart failure at late stages of CCAD.

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