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

26 ischemic cardiomyopathy patients with severe LV systolic dysfunction (LVEF <35%). Reverse LV remodeling was observed in 20 (77%) of the 26 patients 21±14 months after coronary revascularization. As expected, absolute infarct mass did not change during the follow-up period in the reverse remodeling group, but relative infarct mass was significantly increased, due to reduction of myocardial mass in the segments with non-transmural infarction. athological left ventricular (LV) remodeling, defined as maladaptive LV cavity enlargement and structural change, occurs after myocardial damage, which is characterized by the combination of myocyte hypertrophy, apoptosis and interstitial fibrosis.1 Pathological LV remodeling leads to the deterioration of LV ejection fraction (LVEF) and the development of functional mitral regurgitation, contributing to further remodeling and worse prognosis in patients with heart failure (HF).1 Reduction of LV chamber volumes with an improvement in LVEF due to optimized treatment is termed “reverse remodeling”,2 which can be achieved by coronary intervention, medical treatment including angiotensin-converting enzyme inhibitors and β-blockers, cardiac resynchronization therapy and pressure unloading with LV assist device.3–5 Reverse remodeling has been also observed in a wide variety of clinical settings including viral myocarditis, postpartum cardiomyopathy, or after removal of a cytotoxic agent (Figure).6 At the molecular level, reverse remodeling can be in part explained by the calcium handling alteration, decrease in apoptosis,7 improvement of mitochondrial function,8 and reduction of the extracellular matrix remodeling promoted by matrix metalloproteinases.9

Myocardial Tissue Characterization of Left Ventricular Reverse Remodeling in Ischemic Cardiomyopathy