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Nonalcoholic fatty liver disease or metabolic dysfunction-associated fatty liver disease diagnoses and cardiovascular diseases: From epidemiology to drug approaches.
Dongiovanni, P, Paolini, E, Corsini, A, Sirtori, CR, Ruscica, M
European journal of clinical investigation. 2021;(7):e13519
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Abstract
BACKGROUND A consensus of experts has proposed to replace the term nonalcoholic fatty liver disease (NAFLD), whose global prevalence is 25%, with metabolic dysfunction-associated fatty liver disease (MAFLD), to describe more appropriately the liver disease related to metabolic derangements. MAFLD is closely intertwined with type 2 diabetes, obesity, dyslipidaemia, all linked to a rise in the risk of cardiovascular disease (CVDs). Since controversy still stands on whether or not NAFLD/MAFLD raises the odds of CVD, the present review aims to evaluate the impact of NAFLD/MAFLD aetiologies on CV health and the potential correction by dietary and drug approaches. RESULTS Epidemiological studies indicate that NAFLD raises risk of fatal or non-fatal CVD events. NAFLD patients have a higher prevalence of arterial plaques and stiffness, coronary calcification, and endothelial dysfunction. Although genetic and environmental factors strongly contribute to NAFLD pathogenesis, a Mendelian randomization analysis indicated that the PNPLA3 genetic variant leading to NAFLD may not be causally associated with CVD risk. Among other genetic variants related to NAFLD, TM6SF2 appears to be protective, whereas MBOAT7 may favour venous thromboembolism. CONCLUSIONS NAFLD is correlated to a higher CVD risk which may be ameliorated by dietary interventions. This is not surprising, since new criteria defining MAFLD include other metabolic risk abnormalities fuelling development of serious adverse extrahepatic outcomes, for example CVD. The present lack of a targeted pharmacological approach makes the identification of patients with liver disease at higher CVD risk (eg diabetes, hypertension, obesity or high levels of C-reactive protein) of major clinical interest.
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Emerging Pharmacotherapy to Reduce Elevated Lipoprotein(a) Plasma Levels.
Eraikhuemen, N, Lazaridis, D, Dutton, MT
American journal of cardiovascular drugs : drugs, devices, and other interventions. 2021;(3):255-265
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Lipoprotein(a) is a unique form of low-density lipoprotein. It is associated with a high incidence of premature atherosclerotic disease such as coronary artery disease, myocardial infarction, and stroke. Plasma levels of this lipoprotein and its activities are highly variable. This is because of a wide variability in the size of the apolipoprotein A moiety, which is determined by the number of repeats of cysteine-rich domains known as "kringles." Although the exact mechanism of lipoprotein(a)-induced atherogenicity is unknown, the lipoprotein has been found in the arterial walls of atherosclerotic plaques. It has been implicated in the formation of foam cells and lipid deposition in these plaques. Pharmacologic management of elevated levels of lipoprotein(a) with statins, fibrates, or bile acid sequestrants is ineffective. The newer and emerging lipid-lowering agents, such as the second-generation antisense oligonucleotides, cholesteryl ester transfer protein inhibitors, and proprotein convertase subtilisin/kexin type 9 inhibitors offer the most effective pharmacologic therapy.
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Pragmatic Analysis of Dyslipidemia Involvement in Coronary Artery Disease: A Narrative Review.
Mihăilă, RG
Current cardiology reviews. 2020;(1):36-47
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BACKGROUND Dyslipidemia is the main factor involved in the occurrence and progression of coronary artery disease. OBJECTIVE The research strategy is aimed at analyzing new data on the pathophysiology of dyslipidemia involvement in coronary artery disease, the modalities of atherogenic risk estimation and therapeutic advances. METHODS Scientific articles published in PubMed from January 2017 to February 2018 were searched using the terms "dyslipidemia" and "ischemic heart disease". RESULTS PCSK9 contributes to the increase in serum levels of low-density lipoprotein-cholesterol and lipoprotein (a). The inflammation is involved in the progression of hyperlipidemia and atherosclerosis. Hypercholesterolemia changes the global cardiac gene expression profile and is thus involved in the increase of oxidative stress, mitochondrial dysfunction, and apoptosis initiated by inflammation. Coronary artery calcifications may estimate the risk of coronary events. The cardioankle vascular index evaluates the arterial stiffness and correlates with subclinical coronary atherosclerosis. The carotid plaque score is superior to carotid intima-media thickness for risk stratification in patients with familial hypercholesterolemia and both can independently predict coronary artery disease. The lipoprotein (a) and familial hypercholesterolemia have a synergistic role in predicting the risk of early onset and severity of coronary atherosclerosis. A decrease in atherosclerotic coronary plaque progression can be achieved in patients with plasma LDL-cholesterol levels below 70 mg/dL. A highly durable RNA interference therapeutic inhibitor of PCSK9 synthesis could be a future solution. CONCLUSION The prophylaxis and treatment of coronary artery disease in a dyslipidemic patient should be based on a careful assessment of cardio-vascular risk factors and individual metabolic particularities, so it may be personalized.
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Lipotoxicity in Kidney, Heart, and Skeletal Muscle Dysfunction.
Nishi, H, Higashihara, T, Inagi, R
Nutrients. 2019;(7)
Abstract
Dyslipidemia is a common nutritional and metabolic disorder in patients with chronic kidney disease. Accumulating evidence supports the hypothesis that prolonged metabolic imbalance of lipids leads to ectopic fat distribution in the peripheral organs (lipotoxicity), including the kidney, heart, and skeletal muscle, which accelerates peripheral inflammation and afflictions. Thus, lipotoxicity may partly explain progression of renal dysfunction and even extrarenal complications, including renal anemia, heart failure, and sarcopenia. Additionally, endoplasmic reticulum stress activated by the unfolded protein response pathway plays a pivotal role in lipotoxicity by modulating the expression of key enzymes in lipid synthesis and oxidation. Here, we review the molecular mechanisms underlying lipid deposition and resultant tissue damage in the kidney, heart, and skeletal muscle, with the goal of illuminating the nutritional aspects of these pathologies.
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Lipidome Abnormalities and Cardiovascular Disease Risk in HIV Infection.
Bowman, E, Funderburg, NT
Current HIV/AIDS reports. 2019;(3):214-223
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PURPOSE OF REVIEW Human immunodeficiency virus (HIV) infection and its treatment with antiretroviral therapy (ART) are associated with lipid abnormalities that may enhance cardiovascular disease risk (CVD). RECENT FINDINGS Chronic inflammation persists in HIV+ individuals, and complex relationships exist among lipids and inflammation, as immune activation may be both a cause and a consequence of lipid abnormalities in HIV infection. Advances in mass spectrometry-based techniques now allow for detailed measurements of individual lipid species; improved lipid measurement might better evaluate CVD risk compared with the prognostic value of traditional assessments. Lipidomic analyses have begun to characterize dynamic changes in lipid composition during HIV infection and following treatment with ART, and further investigation may identify novel lipid biomarkers predictive of adverse outcomes. Developing strategies to improve management of comorbidities in the HIV+ population is important, and statin therapy and lifestyle modifications, including diet and exercise, may help to improve lipid levels and mitigate CVD risk.
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Wendan decoction for dyslipidemia: Protocol for a systematic review and meta-analysis.
Feng, W, Ye, X, Lv, H, Hou, C, Chen, Y
Medicine. 2019;(3):e14159
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BACKGROUND Dyslipidemia is one of the most popular metabolic diseases and an important risk factor for arteriosclerotic cardiovascular diseases. In China, Wendan decoction (WDD) has been widely used to treat hyperlipidemia. However, no systematic review has been found. In order to evaluate the efficacy and safety of WDD in the treatment of dyslipidemia, a meta-analysis and systematic evaluation are conducted. METHODS The randomized controlled trials (RCTs) evaluating the effectiveness and safety of WDD in the treatment of dyslipidemia will be enrolled. Data are mainly from 4 English databases (Pubmed, Embase, Cochrane Library, and Web of science) and 4 Chinese databases (Wanfang, CBM, CNKI, and VIP Database). The enrollment of RCTs is from the starting date of database establishment till December 15, 2018. Low density lipoprotein cholesterol is considered as the main outcome, while the serum concentrations of total cholesterol, triglyceride, high density lipoprotein cholesterol, apolipoprotein A, and apolipoprotein B are regarded as the secondary outcome. Safety indicators include liver enzyme, fasting blood glucose, and kidney function. The work such as selection of literature, data collection, quality evaluation of included literature, and assessment of publication bias will be conducted by 2 independent researchers. Meta-analysis will be performed by RevMan 5.0 software. RESULTS This study will provide high-quality evidence for the treatment of dyslipidemia with WDD in terms of effectiveness and safety. CONCLUSION The results of the study will help us determine whether WDD can effectively treat hyperlipidemia. PROSPERO REGISTRATION NUMBER PROSPERO CRD 42018114957.
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Current status of lipid management in acute coronary syndrome.
Fujisue, K, Tsujita, K
Journal of cardiology. 2017;(2):101-106
Abstract
The development of coronary revascularization has dramatically improved early cardiovascular outcomes in patients with acute coronary syndrome (ACS). However, patients who have experienced myocardial infarction (MI) are at high risk of recurrence of cardiovascular events compared with those who are healthy or have stable coronary artery disease. Acute coronary events induce further inflammatory responses and plaque vulnerability in either a coronary culprit or whole vessels. The majority of data have supported the importance of coronary risk management to prevent secondary events. Dyslipidemia is common and one of the therapeutic targets in patients with ACS. Statins can reduce coronary plaque burden and lower the risk of cardiovascular death, recurrent MI, stroke, and coronary revascularization in patients with ACS. Growing evidence from clinical trials and meta-analyses supports early, intensive, and continuous therapy with statins in patients with ACS. Statins are accepted worldwide as the first-line lipid-lowering therapy as guidelines recommend. However, some patients do not reach the target level of low-density lipoprotein cholesterol by statins alone or are contra-indicated for statins. Recently, several clinical trials showed the further benefit of ezetimibe combined with statins on cardiovascular outcomes and coronary plaque regression in patients with ACS. In addition, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, novel and powerful lipid-lowering agents, have been developed and used in clinical settings. In this review, we summarize the present statin therapy, and refer to ezetimibe and PCSK9 as novel or additional non-statin strategies in the management of ACS.
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The role of dyslipidemia in diabetic retinopathy.
Hammer, SS, Busik, JV
Vision research. 2017;:228-236
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Diabetic retinopathy (DR) affects over 93million people worldwide and is the number one cause of blindness among working age adults. These indicators coupled with the projected rise of patients diagnosed with diabetes, makes DR a serious and prevalent vision threating disease. Data from recent clinical trials demonstrate that in addition to the well accepted role of hyperglycemia, dyslipidemia is an important, but often overlooked factor in the development of DR. The central aim of this review article is to showcase the critical role of dyslipidemia in DR progression as well as highlight novel therapeutic solutions that take advantage of the vital roles lipid metabolism plays in DR progression.
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Practical Considerations for the Use of Subcutaneous Treatment in the Management of Dyslipidaemia.
Boccara, F, Dent, R, Ruilope, L, Valensi, P
Advances in therapy. 2017;(8):1876-1896
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Suboptimal drug adherence represents a major challenge to effective primary and secondary prevention of cardiovascular disease. While adherence is influenced by multiple considerations, polypharmacy and dosing frequency appear to be rate-limiting factors in patient satisfaction and subsequent adherence. The cardiovascular and metabolic therapeutic areas have recently benefited from a number of advances in drug therapy, in particular protease proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and incretin-based therapies, respectively. These drugs are administered subcutaneously and offer efficacious treatment options with reduced dosing frequency. Whilst patients with diabetes and diabetologists are well initiated to injectable therapies, the cardiovascular therapeutic arena has traditionally been dominated by oral agents. It is therefore important to examine the practical aspects of treating patients with these new lipid-lowering agents, to ensure they are optimally deployed in everyday clinical practice.
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Treatment of Dyslipidemias to Prevent Cardiovascular Disease in Patients with Type 2 Diabetes.
Khavandi, M, Duarte, F, Ginsberg, HN, Reyes-Soffer, G
Current cardiology reports. 2017;(1):7
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PURPOSE OF REVIEW Current preventive and treatment guidelines for type 2 diabetes have failed to decrease the incidence of comorbidities, such as dyslipidemia and ultimately heart disease. The goal of this review is to describe the physiological and metabolic lipid alterations that develop in patients with type 2 diabetes mellitus. Questions addressed include the differences in lipid and lipoprotein metabolism that characterize the dyslipidemia of insulin resistance and type 2 diabetes mellitus. We also examine the relevance of the new AHA/ADA treatment guidelines to dyslipidemic individuals. RECENT FINDINGS In this review, we provide an update on the pathophysiology of diabetic dyslipidemia, including the role of several apolipoproteins such as apoC-III. We also point to new studies and new agents for the treatment of individuals with type 2 diabetes mellitus who need lipid therapies. Type 2 diabetes mellitus causes cardiovascular disease via several pathways, including dyslipidemia characterized by increased plasma levels of apoB-lipoproteins and triglycerides, and low plasma concentrations of HDL cholesterol. Treatments to normalize the dyslipidemia and reduce the risk for cardiovascular events include the following: lifestyle and medication, particularly statins, and if necessary, ezetimibe, to significantly lower LDL cholesterol. Other treatments, more focused on triglycerides and HDL cholesterol, are less well supported by randomized clinical trials and should be used on an individual basis. Newer agents, particularly the PCSK9 inhibitors, show a great promise for even greater lowering of LDL cholesterol, but we await the results of ongoing clinical trials.