Nonalcoholic Fatty Liver Disease and Cardiovascular Disease

Przybyszewski, Eric M.; Targher, Giovanni; Roden, Michael; Corey, Kathleen E.

doi:10.1002/cld.1017

Cited by 36 publications

(36 citation statements)

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“…All subtypes of NAFLD were linked to increased CVD risk, but individuals with fibrosis and NASH have an even higher risk [ 41 ]. The pathophysiological mechanisms of NAFLD and CVD have been elegantly reviewed by Przybyszewski et al recently [ 43 ]. Although there is a lack of complete understanding of the exact causal mechanisms, it was thought that inflammation and dyslipidemia may promote atherogenesis leading to coronary heart disease [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

“…The pathophysiological mechanisms of NAFLD and CVD have been elegantly reviewed by Przybyszewski et al recently [ 43 ]. Although there is a lack of complete understanding of the exact causal mechanisms, it was thought that inflammation and dyslipidemia may promote atherogenesis leading to coronary heart disease [ 43 ]. During NAFLD progression, inflammation of visceral adipose tissue may trigger the activation of proinflammatory pathways (JNK and NF-κB) and downstream synthesis of procoagulant factors, collectively causing increased CVD risk [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

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Increased burden of cardiovascular disease in people with liver disease: unequal geographical variations, risk factors and excess years of life lost

et al. 2022

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Background People with liver disease are at increased risk of developing cardiovascular disease (CVD), however, there has yet been an investigation of incidence burden, risk, and premature mortality across a wide range of liver conditions and cardiovascular outcomes. Methods We employed population-wide electronic health records (EHRs; from 1998 to 2020) consisting of almost 4 million adults to assess regional variations in disease burden of five liver conditions, alcoholic liver disease (ALD), autoimmune liver disease, chronic hepatitis B infection (HBV), chronic hepatitis C infection (HCV) and NAFLD, in England. We analysed regional differences in incidence rates for 17 manifestations of CVD in people with or without liver disease. The associations between biomarkers and comorbidities and risk of CVD in patients with liver disease were estimated using Cox models. For each liver condition, we estimated excess years of life lost (YLL) attributable to CVD (i.e., difference in YLL between people with or without CVD). Results The age-standardised incidence rate for any liver disease was 114.5 per 100,000 person years. The highest incidence was observed in NAFLD (85.5), followed by ALD (24.7), HCV (6.0), HBV (4.1) and autoimmune liver disease (3.7). Regionally, the North West and North East regions consistently exhibited high incidence burden. Age-specific incidence rate analyses revealed that the peak incidence for liver disease of non-viral aetiology is reached in individuals aged 50–59 years. Patients with liver disease had a two-fold higher incidence burden of CVD (2634.6 per 100,000 persons) compared to individuals without liver disease (1339.7 per 100,000 persons). When comparing across liver diseases, atrial fibrillation was the most common initial CVD presentation while hypertrophic cardiomyopathy was the least common. We noted strong positive associations between body mass index and current smoking and risk of CVD. Patients who also had diabetes, hypertension, proteinuric kidney disease, chronic kidney disease, diverticular disease and gastro-oesophageal reflex disorders had a higher risk of CVD, as do patients with low albumin, raised C-reactive protein and raised International Normalized Ratio levels. All types of CVD were associated with shorter life expectancies. When evaluating excess YLLs by age of CVD onset and by liver disease type, differences in YLLs, when comparing across CVD types, were more pronounced at younger ages. Conclusions We developed a public online app (https://lailab.shinyapps.io/cvd_in_liver_disease/) to showcase results interactively. We provide a blueprint that revealed previously underappreciated clinical factors related to the risk of CVD, which differed in the magnitude of effects across liver diseases. We found significant geographical variations in the burden of liver disease and CVD, highlighting the need to devise local solutions. Targeted policies and regional initiatives addressing underserved communities might help improve equity of access to CVD screening and treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased burden of cardiovascular disease in people with liver disease: unequal geographical variations, risk factors and excess years of life lost

et al. 2022

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“…Some studies have demonstrated associations between the presence of NAFLD and worse cardiorenal outcomes in T1D patients, but these studies originate from one research group only, meriting further confirmation in other cohorts (Targher et al, 2010;Targher et al, 2012a;Targher et al, 2012b;Mantovani et al, 2016). Nevertheless, these limited set of data indicate a potential association with hepatic and cardiometabolic risks, similar to findings in T2D cohorts, which might contribute to the relative excess mortality still present in T1D cohorts (Kasper et al, 2021;Przybyszewski et al, 2021). Therefore, NAFLD must be seen as an important potential hepatic and systemic complication in T1D patients.…”

Section: Introductionmentioning

confidence: 94%

Hepatopathy Associated With Type 1 Diabetes: Distinguishing Non-alcoholic Fatty Liver Disease From Glycogenic Hepatopathy

et al. 2021

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Autoimmune destruction of pancreatic β-cells results in the permanent loss of insulin production in type 1 diabetes (T1D). The daily necessity to inject exogenous insulin to treat hyperglycemia leads to a relative portal vein insulin deficiency and potentiates hypoglycemia which can induce weight gain, while daily fluctuations of blood sugar levels affect the hepatic glycogen storage and overall metabolic control. These, among others, fundamental characteristics of T1D are associated with the development of two distinct, but in part clinically similar hepatopathies, namely non-alcoholic fatty liver disease (NAFLD) and glycogen hepatopathy (GlyH). Recent studies suggest that NAFLD may be increasingly common in T1D because more people with T1D present with overweight and/or obesity, linked to the metabolic syndrome. GlyH is a rare but underdiagnosed complication hallmarked by extremely brittle metabolic control in, often young, individuals with T1D. Both hepatopathies share clinical similarities, troubling both diagnosis and differentiation. Since NAFLD is increasingly associated with cardiovascular and chronic kidney disease, whereas GlyH is considered self-limiting, awareness and differentiation between both condition is important in clinical care. The exact pathogenesis of both hepatopathies remains obscure, hence licensed pharmaceutical therapy is lacking and general awareness amongst physicians is low. This article aims to review the factors potentially contributing to fatty liver disease or glycogen storage disruption in T1D. It ends with a proposal for clinicians to approach patients with T1D and potential hepatopathy.

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“…Despite the liver-related complication, CVD is a common cause of death among NAFLD patients [2]. However, it is important to note, while most probably all types of NAFLD are associated with elevated CVD risk, the strongest links were defined for NASH and advanced stages of fibrosis [3,4].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases

Dabravolski

Bezsonov

Baig

et al. 2021

IJMS

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The prevalence of NAFLD (non-alcoholic fatty liver disease) is a rapidly increasing problem, affecting a huge population around the globe. However, CVDs (cardiovascular diseases) are the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense LDL (low-density lipoprotein) particles, and decreased HDL-C (high-density lipoprotein cholesterol) levels, is often observed in NAFLD patients. In this review, we summarize recent genetic evidence, proving the diverse nature of metabolic pathways involved in NAFLD pathogenesis. Analysis of available genetic data suggests that the altered operation of fatty-acid β-oxidation in liver mitochondria is the key process, connecting NAFLD-mediated dyslipidemia and elevated CVD risk. In addition, we discuss several NAFLD-associated genes with documented anti-atherosclerotic or cardioprotective effects, and current pharmaceutical strategies focused on both NAFLD treatment and reduction of CVD risk.

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Nonalcoholic Fatty Liver Disease and Cardiovascular Disease

Cited by 36 publications

References 10 publications

Increased burden of cardiovascular disease in people with liver disease: unequal geographical variations, risk factors and excess years of life lost

Increased burden of cardiovascular disease in people with liver disease: unequal geographical variations, risk factors and excess years of life lost

Hepatopathy Associated With Type 1 Diabetes: Distinguishing Non-alcoholic Fatty Liver Disease From Glycogenic Hepatopathy

Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases

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