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Occurred after acute myocardial infarction ventricular remodeling , manifested as the progressive expansion of the left ventricle and shape change , including change in ventricular volume , shape , wall thickness , myocardial structure and ultrastructure . However , the mechanism of ventricular remodeling is still not very clear . In recent years, awareness of the important role of the renin - angiotensin - aldosterone system (RAAS) in ventricular remodeling , especially aldosterone harmful effects ; myocardium also found a heart capable of synthesizing aldosterone , and in the non- infarcted myocardium aldosterone synthesis increased understanding of the phenomenon of \RALES trial and EPHESUS trials showed that , in the conventional therapy based on the use of small doses of aldosterone receptor antagonist heart failure mortality rate can be further decreased, suggesting that aldosterone receptor antagonists in heart failure patients receiving traditional treatment still benefits , but its specific mechanism of action is unclear . The study confirmed the inflammatory response after myocardial infarction , produce inflammatory cytokines , thereby regulating left ventricular tissue repair process . The application of anti-inflammatory drugs can prevent left ventricular remodeling process to a certain extent , suggesting that inflammatory response plays an important role in the promotion of left ventricular remodeling . NF-κB is a multi- regulatory function of the nuclear transcription factor , the main regulating the immune response , stress response and inflammation -related gene expression . Has confirmed that NF-κB target genes including adhesion factors, growth factors , inflammatory cytokines , chemokines . These factors on cell activation , proliferation , invasion , played a key role in chemotaxis and secretion , therefore , NF-κB and inflammatory cytokines are closely related .
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