The Interactions of Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases

2014 ◽  
Vol 18 (1) ◽  
pp. 233-248 ◽  
Author(s):  
Hugo Perazzo ◽  
Thierry Poynard ◽  
Jean-François Dufour
2020 ◽  
Author(s):  
Olena H. Kurinna

AbstractNonalcoholic fatty liver disease (NAFLD) bears serious economic consequences for the health care system worldwide and Ukraine, in particular. Cardiovascular diseases (CVD) are the main cause of mortality in NAFLD patients. Changes in the gut microbiota composition can be regarded as a potential mechanism of CVD in NAFLD patients.The purpose of this work was to investigate changes in major gut microbiota phylotypes, Bacteroidetes, Firmicutes and Actinobacteria with quantification of Firmicutes/Bacteroidetes in NAFLD patients with concomitant CVD.The author enrolled 120 NAFLD subjects (25 with concomitant arterial hypertension (AH) and 24 with coronary artery disease (CAD)). The gut microbiota composition was assessed by qPCR.Resultsthe author found a marked tendency towards an increase in the concentration of Bacteroidetes (by 37.11% and 21.30%, respectively) with a decrease in Firmicutes (by 7.38% and 7.77%, respectively) in both groups with comorbid CAD and AH with the identified changes not reaching a statistical significance. The author quantified a statistically significant decrease in the concentration of Actinobacteria in patients with NAFLD with concomitant CAD at 41.37% (p<0.05) as compared with those with an isolated NAFLD. In patients with concomitant AH, the content of Actinobacteria dropped by 12.35%, which was statistically insignificant.Conclusionsthe author established changes in the intestinal microbiota, namely decrease in Actinobacteria in patients with CAD, which requires further research.


Angiology ◽  
2019 ◽  
Vol 71 (1) ◽  
pp. 87-87 ◽  
Author(s):  
Çağri Yayla ◽  
Kadriye Gayretli Yayla ◽  
Mustafa Karanfil ◽  
Ahmet Göktuğ Ertem ◽  
Sefa Ünal ◽  
...  

2014 ◽  
Vol 66 (6) ◽  
pp. 574-579 ◽  
Author(s):  
Masihur Rehman Ajmal ◽  
Monika Yaccha ◽  
Mohammed Azharuddin Malik ◽  
M.U. Rabbani ◽  
Ibne Ahmad ◽  
...  

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9090
Author(s):  
Li Xiao ◽  
Tao Bai ◽  
Junchao Zeng ◽  
Rui Yang ◽  
Ling Yang

Background Non-specific ST-T segment changes are prevalent and are proven risk factors for early onset of cardiovascular diseases. They can increase all-cause mortality by 100∼200% and are candidate for early signs of cardiovascular changes. Nonalcoholic fatty liver disease (NAFLD) is prevalent worldwide and is one facet of a multisystem disease that confers substantial increases morbidity and mortality of nonalcoholic fatty liver-related cardiovascular diseases. It is unclear whether NAFLD is associated with non-specific ST-T changes warning early signs of cardiovascular changes. Therefore, we investigated this association. Methods A cross-sectional study was designed that included a sample consisting of 32,922 participants who underwent health examinations. Participants with missing information, excessive alcohol intake, viral hepatitis, chronic liver disease or established cardiovascular diseases were excluded. Electrocardiograms were used for analysis of non-specific ST-T segment changes. NAFLD was diagnosed by ultrasonographic detection of hepatic steatosis without other liver diseases. A multivariable logistic regression model was served to calculate the OR and 95% CI for non-specific ST-T segment changes. Results The prevalence of non-specific ST-T segment changes was 6.5% in participants with NAFLD, however, the prevalence of NAFLD was 42.9% in participants with non-specific ST-T segment changes. NAFLD was independently associated with non-specific ST-T segment changes (OR: 1.925, 95% CI: 1.727-2.143, P < 0.001). After adjusting for age, sex, heart rate, hypertension, body mass index, fasting glucose, total cholesterol, triglycerides, HDL-C, NAFLD remained an independent risk factor of non-specific ST-T segment changes (OR: 1.289, 95% CI: 1.122-1.480). Conclusion Non-specific ST-T segment changes were independently associated with the presence of NAFLD after adjusting for potential confounders.


2020 ◽  
Vol 126 (5) ◽  
pp. 679-704 ◽  
Author(s):  
Jingjing Cai ◽  
Xiao-Jing Zhang ◽  
Yan-Xiao Ji ◽  
Peng Zhang ◽  
Zhi-Gang She ◽  
...  

Cardiovascular diseases (CVDs) remain a leading cause of death worldwide. Among the major risk factors for CVD, obesity and diabetes mellitus have received considerable attention in terms of public policy and awareness. However, the emerging prevalence of nonalcoholic fatty liver disease (NAFLD), as the most common liver and metabolic disease and a cause of CVD, has been largely overlooked. Currently, the number of individuals with NAFLD is greater than the total number of individuals with diabetes mellitus and obesity. Epidemiological studies have established a strong correlation between NAFLD and an increased risk of CVD and CVD-associated events. Although debate continues over the causal relationship between NAFLD and CVD, many mechanistic and longitudinal studies have indicated that NAFLD is one of the major driving forces for CVD and should be recognized as an independent risk factor for CVD apart from other metabolic disorders. In this review, we summarize the clinical evidence that supports NAFLD as a risk factor for CVD epidemics and discuss major mechanistic insights regarding the acceleration of CVD in the setting of NAFLD. Finally, we address the potential treatments for NAFLD and their potential impact on CVD.


Author(s):  
Jingjing Cai ◽  
Meng Xu ◽  
Xiaojing Zhang ◽  
Hongliang Li

The physiological significance of innate immune signaling lies primarily in its role in host defense against invading pathogens. It is becoming increasingly clear that innate immune signaling also modulates the development of metabolic diseases, especially nonalcoholic fatty liver disease and cardiovascular diseases, which are characterized by chronic, low-grade inflammation due to a disarrangement of innate immune signaling. Notably, recent studies indicate that in addition to regulating canonical innate immune-mediated inflammatory responses (or immune-dependent signaling-induced responses), molecules of the innate immune system regulate pathophysiological responses in multiple organs during metabolic disturbances (termed immune-independent signaling-induced responses), including the disruption of metabolic homeostasis, tissue repair, and cell survival. In addition, emerging evidence from the study of immunometabolism indicates that the systemic metabolic status may have profound effects on cellular immune function and phenotypes through the alteration of cell-intrinsic metabolism. We summarize how the innate immune system interacts with metabolic disturbances to trigger immune-dependent and immune-independent pathogenesis in the context of nonalcoholic fatty liver disease, as representative of metabolic diseases, and cardiovascular diseases.


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