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

is further supported by the fact that angiotensin-convertingenzyme inhibitors and angiotensin-receptor blockers have beneficial effects in patients with hypertension, myocardial infarction, and heart failure.7–9 In the acute phase of hospital admission for AMI, activation of both the sympathetic nervous system and the RAS system has been observed; these activations subside within the first 72 h in patients without left ventricular dysfunction and overt heart failure.10 In contrast, persistent RAS activation at the time of hospital discharge is an independent predictor of cardiovascular disease death in postinfarction patients.11 However, the meaning of an elevation in plasma renin activity (PRA) on admission remains unascertained in the setting of AMI. In this issue of the Journal, Kamon et al12 report that elevated PRA on admission was independently associated I n recent decades there has been substantial improvement in the prognosis of acute myocardial infarction (AMI), mainly because of advances in the rapid restoration of coronary blood flow by percutaneous coronary intervention, as well as in secondary prevention therapies.1 However, patients with clinical complications such as cardiogenic shock, heart failure, and chronic kidney disease at the onset of AMI still have a poor prognosis. The renin-angiotensin system (RAS) is a complex system that regulates systemic functions through body salt and blood volume control.2 The RAS also exerts proliferative action at the vascular level, leading to angiogenesis and the progression of atherosclerosis3,4 thereby contributing to the development of ischemic heart disease.5 Furthermore, RAS activation is a key mechanism in cardiac remodeling in patients with AMI and of disease progression in those with ischemic and non-ischemic heart failure;5 chronic overactivation of the RAS is associated with cardiovascular adverse events.6 The occurrence of these processes in AMI Article p ????

Renin Activity as a Key Predictor of Major Adverse Cardiac Events