English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Myocardial remodeling is usually accepted as a determinant of the clinical course of heart failure (HF). The distinct genome expression influences molecular, cellular, and interstitial changes and clinically manifested as changes in size, shape, and performance of heart that observed from a myocardial output. The myocardial remodeling inclined by the close investigation of hemodynamic load, neurohormonal activation, and alternative factors responsible for myocardial injuries ( et Cohn al., 2000). Ischemic injury provoked by acute myocardial infarction (MI) is typically followed by a wound repair method of the left ventricle referred to post-infarction left ventricle remodeling (LVR). Extent myocardial remodeling seen in both infarcted and non-infarcted myocardium recognized as the major determinant of the development of HF and might be a predictive factor for mortality and morbidity in patients with MI. The remodeling process contributes to hypertrophy, inflammatory response, and connective tissue changes (Vilahur et al., 2011).

Biochemical and pharmacological estimation of erythrosine in myocardial remodeling among heart failure induced by doxorubicin in rats