A systematic review: Burden and severity of subclinical cardiovascular disease among those with nonalcoholic fatty liver; Should we care?

Oni, Ebenezer; Agatston, Arthur S.; Blaha, Michael J.; Fialkow, Jonathan; Cury, Ricardo C.; Sposito, Andrei C.; Erbel, Raimund; Blankstein, Ron; Feldman, Ted; Al-Mallah, Mouaz; Santos, Raúl D.; Budoff, Matthew J.; Nasir, Khurram

doi:10.1016/j.atherosclerosis.2013.07.052

Cited by 317 publications

(253 citation statements)

References 82 publications

Supporting

Mentioning

222

Contrasting

Unclassified

Order By: Relevance

“…It was established that patients with histologically confirmed diagnosis of NAFLD, assessed according to the Brunt scale (Brunt of the Global Grade), had significantly higher PVPW rates (8.2 ± 1.3 m/s versus 6.9 ± 1.3 m/s, p = 0.001), greater TIMC (0.79 ± 0.18 m/s vs. 0.67 ± 0.13 m/s, p = 0.01) and lower EDVD (1.93 ± 2.11% versus a 4.8 ± 2.43%, p = 0.001) compared with patients without NAFLD [28]. The data were confirmed by the results of a systematic review of 36 studies, 16 of which had investigated the association between NAFLD and TIMC of carotid arteries, 7 -the relationship between NAFLD and calcification of carotid arteries, 7 with ED, and the rest 6 with AWS [29].…”

Section: Arterial Stiffnesssupporting

confidence: 68%

“…In recent years, NAFLD has been increasingly considered as an additional independent risk factor of CV diseases and predictor of its complications [25][26][27][28][29][30][31][32][33]. A recent study of life expectancy among patients with NAFLD after 24 years of observation found that CV diseases were the most common cause of death in 48% of patients, while diseases associated with liver damage had a lethal outcome in 7% of patients [31].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Arterial hypertension, obesity and non-alcoholic fatty liver disease: is there any connection?

Kuzmіnova

Gribenyuk

Osovska

et al. 2016

Arterial Hypertension

View full text Add to dashboard Cite

The combination of hypertension, obesity and non-alcoholic fatty liver disease occurs in medical practice very often. A number of studies have shown that non-alcoholic fatty liver disease increases the risk of cardiovascular disease independently of other predictors and manifestations of the metabolic syndrome. Current issues of research and identification of common pathogenic relationships of obesity, hypertension, and liver steatosis are investigated in the article. According to the analysed literature, it is indicated that insulin resistance and compensatory hyperinsulinaemia are considered as one of the key factors in the development of this comorbidity. The processes of chronic inflammation are increasing with the growth of adipose tissue volume. Some researchers believe that non-specific systemic inflammation combines arterial hypertension, increased body weight (especially abdominal obesity), steatosis, dyslipidaemia, atherogenesis and arteriosclerosis into a single syndrome. The role of non-alcoholic fatty liver disease in the growth of the thickness of the intima-media complex was studied. It is known that adipose tissue functions as an endocrine organ, expresses genes encoding bioactive substances, and secretes certain cytokines. A strong link between dysfunction of adipose tissue in patients with non-alcoholic fatty liver disease and in such conditions as metabolic syndrome and cardiovascular disease was demonstrated. The dysfunction of the endothelium is also advisable to consider as the connecting link between liver disease, obesity and hypertension. Despite some understanding of common pathogenic mechanisms for the development of non-alcoholic fatty liver disease and hypertension, this comorbid pathology remains the subject of much debate and a variety of studies. key words: arterial hypertension, obesity, non-alcoholic fatty liver disease, insulin resistance, dyslipidaemia, non-specific systemic inflammation, endothelial dysfunction, atherogenesis.

show abstract

Section: Arterial Stiffnesssupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Arterial hypertension, obesity and non-alcoholic fatty liver disease: is there any connection?

Kuzmіnova

Gribenyuk

Osovska

et al. 2016

Arterial Hypertension

View full text Add to dashboard Cite

show abstract

“…It represents a spectrum of liver pathology ranging from steatosis to inflammatory nonalcoholic steatohepatitis (NASH) with or without fibrosis (13). Clinically, NAFL is strongly associated with metabolic syndrome, obesity, type-2 diabetes, and dyslipidemia (2,52,53,69).…”

Section: Introductionmentioning

confidence: 99%

Glutaredoxin-1 Deficiency Causes Fatty Liver and Dyslipidemia by Inhibiting Sirtuin-1

Шао

Han

Hou

et al. 2017

Antioxidants & Redox Signaling

View full text Add to dashboard Cite

Aims: Nonalcoholic fatty liver (NAFL) is a common liver disease associated with metabolic syndrome, obesity, and diabetes that is rising in prevalence worldwide. Various molecular perturbations of key regulators and enzymes in hepatic lipid metabolism cause NAFL. However, redox regulation through glutathione (GSH) adducts in NAFL remains largely elusive. Glutaredoxin-1 (Glrx) is a small thioltransferase that removes protein GSH adducts without having direct antioxidant properties. The liver contains abundant Glrx but its metabolic function is unknown. Results: Here we report that normal diet-fed Glrx-deficient mice (Glrx -/-) spontaneously develop obesity, hyperlipidemia, and hepatic steatosis by 8 months of age. Adenoviral Glrx repletion in the liver of Glrx -/-mice corrected lipid metabolism. Glrx -/-mice exhibited decreased sirtuin-1 (SirT1) activity that leads to hyperacetylation and activation of SREBP-1 and upregulation of key hepatic enzymes involved in lipid synthesis. We found that GSH adducts inhibited SirT1 activity in Glrx -/-mice. Hepatic expression of nonoxidizable cysteine mutant SirT1 corrected hepatic lipids in Glrx -/-mice. Wild-type mice fed high-fat diet develop metabolic syndrome, diabetes, and NAFL within several months. Glrx deficiency accelerated high-fat-induced NAFL and progression to steatohepatitis, manifested by hepatic damage and inflammation. Innovation: These data suggest an essential role of hepatic Glrx in regulating SirT1, which controls protein glutathione adducts in the pathogenesis of hepatic steatosis. Conclusion: We provide a novel redox-dependent mechanism for regulation of hepatic lipid metabolism, and propose that upregulation of hepatic Glrx may be a beneficial strategy for NAFL. Antioxid. Redox Signal. 27, 313-327.

show abstract

“…6 Several evidences support the association of NAFLD/NASH and the occurrence of cardiovascular events, such as increased carotid intima-media thickness, increased coronary artery calcification, impaired flow-mediated vasodilatation and arterial stiffness independent of traditional risk factors and MetS. [7][8][9] The finding that NAFLD is associated with an increased risk of Atrial Fibrillation (AF) in people without evidence of co-existing valvular heart disease supports the assertion that NAFLD may also be an emerging risk factor for cardiac arrhythmias. 10,11 Another marker of early coronary atherosclerosis is association of NAFLD and increased Coronary Artery Calcium (CAC) score on cardiac Computed Tomography (CT).…”

Section: -4mentioning

confidence: 99%

Cardiovascular Disease and NASH

Siqueira¹,

Pereira²,

Sanyal³

2015

Liver Res Open J

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) and Non-alcoholic steatohepatitis (NASH) are associated with cardiovascular events and Metabolic Syndrome (MetS). NAFLD is considered to be a hepatic manifestation of MetS and has become an important public health issue because of its high prevalence. It is currently being considered an independent Cardiovascular disease (CVD) risk factor. In this clinical review, we will briefly review the mechanisms linking NAFLD to the complement system, endothelial dysfunction and the atherosclerosis.

show abstract

A systematic review: Burden and severity of subclinical cardiovascular disease among those with nonalcoholic fatty liver; Should we care?

Cited by 317 publications

References 82 publications

Arterial hypertension, obesity and non-alcoholic fatty liver disease: is there any connection?

Arterial hypertension, obesity and non-alcoholic fatty liver disease: is there any connection?

Glutaredoxin-1 Deficiency Causes Fatty Liver and Dyslipidemia by Inhibiting Sirtuin-1

Cardiovascular Disease and NASH

Contact Info

Product

Resources

About