2016
DOI: 10.1111/hepr.12770
|View full text |Cite
|
Sign up to set email alerts
|

Effect of non‐alcoholic fatty liver disease on left ventricular diastolic function and geometry in the Korean general population

Abstract: The risk for LV diastolic dysfunction and remodeling proportionally increased according to the degree of NAFLD. NAFLD is significantly associated with LV functional and structural alteration.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

2
23
2
2

Year Published

2018
2018
2023
2023

Publication Types

Select...
7
3

Relationship

1
9

Authors

Journals

citations
Cited by 35 publications
(31 citation statements)
references
References 39 publications
(123 reference statements)
2
23
2
2
Order By: Relevance
“…All tests were two-sided, and p-values of less than 0.05 were considered to indicate statistical significance. We described detailed methods including statistical analyses in our previous studies [22,23].…”
Section: Statistical Analysesmentioning
confidence: 99%
“…All tests were two-sided, and p-values of less than 0.05 were considered to indicate statistical significance. We described detailed methods including statistical analyses in our previous studies [22,23].…”
Section: Statistical Analysesmentioning
confidence: 99%
“…Increased LV wall thickness and fibrosis is a marker of LV diastolic dysfunction regardless of their symptoms. Jung et al showed mild and moderate to severe NAFLD group had the higher risk of having abnormal LV relaxation compared with normal controls [21]. They showed increased odds ratios for abnormal LV [23], increased renin-angiotensinaldosterone system (RAAS) [24], and endothelial dysfunction and inflammation [11].…”
Section: Discussionmentioning
confidence: 99%
“…The presence of NAFLD was associated with higher BMI, higher left ventricular (LV) mass index, and more severe LV fibrosis [12]. Other studies showed that patients with NAFLD had increased LV wall thickness and varying degrees of subclinical LV systolic or diastolic dysfunction [21,22]. The proposed mechanisms of increased LV wall thickness include insulin resistance [23], increased activity of the renin-angiotensin-aldosterone system (RAAS) [24], and endothelial dysfunction and inflammation [11].…”
Section: Discussionmentioning
confidence: 99%