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 Tools annual

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 monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

DOI: 10.5935/abc.20190053 Nearly half of heart failure patients have preserved ejection fraction (HFPEF).1 HFPEF is traditionally attributed to an increased left ventricular end-diastolic filling pressure (Pd2), triggered by structural, metabolic and functional mechanisms. Echocardiography permits to identify HFPEF signs as diastolic dysfunction (DD),2 enlarged left atrium, and more subtle abnormalities of systolic function detected by global longitudinal strain.3,4 Right ventricular (RV) abnormalities and pulmonary hypertension are also identified by echocardiography and are frequently seen in HFPEF.5 However, there are controversies if the abnormalities seen in right cardiac chambers are a consequence of left-sided abnormalities or if they correspond to a direct effect over left and right chambers simultaneously, caused by the same mechanisms, such as diffuse subendocardial fibrosis and subclinical systolic dysfunction. In this journal, Baroncini et al.6 sought to bring more evidence to fill this knowledge gap. The authors compared two small samples of individuals with and without DD (25 subjects in each group) and found no significant changes in RV function between the groups measured by tricuspid annular plane excursion (TAPSE) or RV free wall systolic velocity (s’). The secondary analysis highlighted by the authors showed that in the subgroup with DD, the 7 individuals with a dilated left atrium presented worse RV function parameters compared to the other patients with DD (n = 18). These results could suggest that RV abnormalities would be present only in those already with a chronic increase in left atrial pressure identified by its dilatation. However, this specific finding in one subgroup is very likely to have occurred by chance. In addition to the recognized caveats of a posteriori findings, there are other reported findings that weaken the consistency of the biological plausibility of the association described. There was no significant correlation when measurements of the left atrium and right ventricle were analyzed continuously (unlike the article title), neither there was any relevant association identified in the analyzes that included the group of supposedly normal controls. Another important issue is the impossibility of the study, as performed, to adequately adjust for the intricate relationships between confounding variables. This is evident when we analyze the relationships between age, diastolic function, left atrial size and diastolic function in the study.

Let's Look Right during Diastolic Dysfunction Evaluation?