Articles
| Open Access |
DOI:
https://doi.org/10.37547/ijmscr/Volume03Issue08-04
HEART REMODELING, STATE OF HEMODYNAMICS AND STRUCTURAL AND FUNCTIONAL STATE OF MYOCARDIA IN PATIENTS WITH POST-INFARCTION HEART FAILURE
Khamraev A.N. , Bukhara State Medical Institute, Uzbekistan Abdurakhmanov M.M. , Bukhara State Medical Institute, UzbekistanAbstract
In patients with left ventricular (LV) systolic dysfunction, changes occurring in cardiomyocytes and the extracellular matrix after myocardial injury (eg, myocardial infarction or myocarditis) lead to pathological remodeling of the ventricle with dilatation, changes in geometry (the LV becomes more spherical), and impaired contractility. Next, there is a systemic response to a decrease in LV systolic function. In patients, there is an increase in the activity of pressor systems: sympathoadrenal system (SAS), renin - angiotensin - aldosterone system (RAAS), endothelin, vasopressin and cytokines systems. Activation of the renin-angiotensin-aldosterone and sympathetic nervous systems is of key importance. These neurohumoral factors not only cause peripheral vasoconstriction, sodium and fluid retention, but, consequently, an increase in the hemodynamic load on the left ventricle, but also have a direct toxic effect on the myocardium, stimulating fibrosis and apoptosis, which leads to further remodeling of the heart and disruption of its function. Clinically, all these changes are associated with the development and progression of symptoms of CHF and lead to a deterioration in the quality of life, a decrease in the physical activity of patients, decompensation of heart failure requiring hospitalization, and death as a result of both “pumping” heart failure and the appearance of life-threatening ventricular arrhythmias. The severity of clinical manifestations of diastolic CHF and the prognosis of patients is primarily determined by the severity of diastolic dysfunction [19-22] which leads to further remodeling of the heart and disruption of its function.
Keywords
sympathoadrenal system (SAS), renin - angiotensin - aldosterone system (RAAS), endothelin
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