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

Unstable systemic hemodynamics in acute heart failure causes various detrimental effects on organs. In recent years, the heart-kidney and heart-liver interactions have been investigated under the terms “cardio-renal syndrome (CRS)” and “cardio-hepatic syndrome (CHS)”, respectively [1,2]. Each syndrome is divided into five subtypes based on the combined dysfunction of the heart and the kidney or the heart and the liver. While type 1 CRS is characterized by acute and rapid worsening of the heart leading to acute kidney injury, type 1 CHS describes the relationship between abnormal liver function tests and the the severity of acute heart failure. The main pathophysiological mechanisms of type 1 CRS and CHS are congestion and abnormal reperfusion in the heart, the kidney and the liver. Other compounding effects of type 1 CRS include neurohormonal activation, hypothalamicpituitary stress reaction, inflammation and immune cell signaling, oxidative stress and failure of counter-regulatory mechanisms [3]. Some important mechanisms of CHS have been previously described such as venous congestion, backward failure, decreased hepatic blood flow, decreased arterial saturation and sinusoidal thrombosis [4].

Case report: Cardio-renal syndrome with concomitant cardio-hepatic syndrome in a severe aortic stenosis patient