{"title":"Assessment of atherosclerosis: should coronary calcium score and intima-media thickness be replaced by ultrasound measurement of carotid plaque burden and vessel wall volume?","authors":"J David Spence","doi":"10.1097/MOL.0000000000000880","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000880","url":null,"abstract":"<p><strong>Purpose of review: </strong>To describe the uses of vessel wall volume (VWV) and measurement of carotid plaque burden, as total plaque area (TPA) and total plaque volume (TPV), and to contrast them with measurement of carotid intima-media thickness (IMT) and coronary calcium (CAC).</p><p><strong>Recent findings: </strong>Measurement of carotid plaque burden (CPB) is useful for risk stratification, research into the genetics and biology of atherosclerosis, for measuring effects of new therapies for atherosclerosis, and for treatment of high-risk patients with severe atherosclerosis. It is as predictive of risk as CAC, with important advantages. IMT is only a weak predictor of risk and changes so little over time that it is not useful for assessing effects of therapy.</p><p><strong>Summary: </strong>Measurement of CPB and VWV are far superior to measurement of carotid IMT in many ways, and should replace it. Vessel wall volume can be measured in persons with no plaque as an alternative to IMT. There are important advantages of CPB over coronary calcium; CPB should be more widely used in vascular prevention.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 3","pages":"126-132"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10259009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Triglyceride-rich lipoproteins, remnant-cholesterol, and atherosclerotic cardiovascular disease.","authors":"Om P Ganda","doi":"10.1097/MOL.0000000000000875","DOIUrl":"10.1097/MOL.0000000000000875","url":null,"abstract":"<p><strong>Purpose of review: </strong>Despite indisputable role of LDL-C lowering, a considerable residual risk for atherosclerotic cardiovascular disease (ASCVD) persists. The precise mechanism(s) underlying this phenomenon remain unclear. Triglyceride-rich lipoproteins (TRL) appear to be one of the main mediators, based on the genetic and epidemiologic data. However, whether this is caused by direct effects of Triglycerides or other components of TRL remains uncertain. The cholesterol component of TRL remnants (Rem-C) has been proposed as a more pertinent mediator of the increased risk associated with high triglycerides.</p><p><strong>Recent findings: </strong>Several long-term observational studies have shown a significant relationship between Rem-C and ASCVD events, compared with other triglyceride-related parameters. Recent trials have shown that lowering of triglyceride levels by various agents, including fibrates and omega-3 fatty acids, in statin-treated subjects, did not explain the reduction in ASCVD events. In a large clinical trial with pemafibrate, a highly selective PPAR-α agonist, in type 2 diabetes and elevated triglycerides, the reduction in triglycerides was accompanied by a significant increase in LDL-C and Apo-B levels, despite a reduction in Rem-C, and no effect on ASCVD events.</p><p><strong>Summary: </strong>Elevated Rem-C as a risk determinant, with LDL-C at goal, requires additional studies in clinical trials. Standardization and accuracy of Rem-C assays (calculated versus direct method) is also needed.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 3","pages":"105-113"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10270880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Giorgio Bedogni, Francesco Palmese, Francesco Giuseppe Foschi
{"title":"Nonalcoholic fatty liver disease: an update.","authors":"Giorgio Bedogni, Francesco Palmese, Francesco Giuseppe Foschi","doi":"10.1097/MOL.0000000000000874","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000874","url":null,"abstract":"<p><strong>Purpose of review: </strong>We discuss two recent controversial issues in the research field of fatty liver: the proposal to replace nonalcoholic fatty liver disease (NAFLD) with metabolically associated fatty liver disease (MAFLD) and the suggestion to extend to primary care the noninvasive testing for liver fibrosis that was developed for secondary care.</p><p><strong>Recent findings: </strong>There is preliminary evidence that MAFLD-only patients are at greater risk of fibrosis than NAFLD-only patients. There are a large number of false positives associated with the downshift of noninvasive testing for liver fibrosis from secondary to primary care.</p><p><strong>Summary: </strong>More studies are needed to compare the MAFLD and NAFLD operational definitions. Noninvasive testing of liver fibrosis also needs further evaluation before it can be used in primary care or in the general population.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 3","pages":"114-118"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10267445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Benjamin N Wadström, Kasper M Pedersen, Anders B Wulff, Børge G Nordestgaard
{"title":"Inflammation compared to low-density lipoprotein cholesterol: two different causes of atherosclerotic cardiovascular disease.","authors":"Benjamin N Wadström, Kasper M Pedersen, Anders B Wulff, Børge G Nordestgaard","doi":"10.1097/MOL.0000000000000867","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000867","url":null,"abstract":"<p><strong>Purpose of review: </strong>Inflammation is gaining attention as a target for prevention of atherosclerotic cardiovascular disease (ASCVD). The purpose of this review is to compare the evidence for inflammation with the evidence for low-density lipoprotein (LDL) cholesterol in ASCVD.</p><p><strong>Recent findings: </strong>Evidence from human genetic studies and randomized controlled trials implicate the inflammatory pathway from the inflammasome through interleukin (IL)-1 to IL-6 as a cause of ASCVD. Higher levels of IL-6 may lead to proportionally increased risk of ASCVD, and randomized controlled trials of IL-6 inhibitors are underway. The causal evidence for LDL cholesterol in ASCVD is overwhelming and recent important findings instead revolve around development of improved LDL cholesterol lowering therapy through RNA and DNA based therapeutics. Even though some lipid-lowering therapies lower IL-6, the IL-6 inflammatory pathway and LDL cholesterol are two separate causes of ASCVD.</p><p><strong>Summary: </strong>IL-6 mediated inflammation most likely causes ASCVD, in parallel with LDL cholesterol. However, fewer individuals in the general population are exposed to high IL-6 than high LDL cholesterol. For inflammation, future research should focus on improving efficacy and safety of anti-inflammatory therapy, and for LDL cholesterol, future research should focus on wider and more effective implementation of LDL cholesterol lowering therapy.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 3","pages":"96-104"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10269356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exosomes and lipid metabolism in metabolic and cardiovascular disorders.","authors":"Zina Zein Abdin, Apple Ziquan Geng, Mark Chandy","doi":"10.1097/MOL.0000000000000873","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000873","url":null,"abstract":"<p><strong>Purpose of review: </strong>Exosomes are lipid-bound particles that carry lipids, protein, and nucleic acid and affect cellular function. This review highlights the current knowledge on the crosstalk between exosomes and lipid metabolism and their impact on cardiometabolic disease.</p><p><strong>Recent findings: </strong>Recent studies revealed that lipids and lipid metabolizing enzymes are important for exosome biogenesis and internalization and conversely how exosomes affect lipid metabolism, secretion, and degradation. The interplay between exosomes and lipid metabolism affects disease pathophysiology. More importantly, exosomes and lipids might function as biomarkers for diagnosis and prognosis or possibly therapies.</p><p><strong>Summary: </strong>Recent advances in our understanding of exosomes and lipid metabolism have implications for our understanding of normal cellular and physiological functions as well as disease pathogenesis. Exosome and lipid metabolism have implications in novel diagnostic tests and treatments of cardiometabolic disease.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 2","pages":"82-91"},"PeriodicalIF":4.4,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9261690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Novel therapeutic opportunities for familial lecithin:cholesterol acyltransferase deficiency: promises and challenges.","authors":"Cecilia Vitali, Daniel J Rader, Marina Cuchel","doi":"10.1097/MOL.0000000000000864","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000864","url":null,"abstract":"<p><strong>Purpose of review: </strong>Genetic lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare, inherited, recessive disease, which manifests as two different syndromes: Familial LCAT deficiency (FLD) and Fish-eye disease (FED), characterized by low HDL-C and corneal opacity. FLD patients also develop anaemia and renal disease. There is currently no therapy for FLD, but novel therapeutics are at different stages of development. Here, we summarize the most recent advances and the opportunities for and barriers to the further development of such therapies.</p><p><strong>Recent findings: </strong>Recent publications highlight the heterogeneous phenotype of FLD and the uncertainty over the natural history of disease and the factors contributing to disease progression. Therapies that restore LCAT function (protein and gene replacement therapies and LCAT activators) showed promising effects on markers of LCAT activity. Although they do not restore LCAT function, HDL mimetics may slow renal disease progression.</p><p><strong>Summary: </strong>The further development of novel therapeutics requires the identification of efficacy endpoints, which include quantitative biomarkers of disease progression. Because of the heterogeneity of renal disease progression among FLD individuals, future treatments for FLD will have to be tailored based on the specific clinical characteristics of the patient. Extensive studies of the natural history and biomarkers of the disease will be required to achieve this goal.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 2","pages":"35-43"},"PeriodicalIF":4.4,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10445626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Does low-density lipoprotein fully explain atherosclerotic risk in familial hypercholesterolemia?","authors":"Shoa L Clarke","doi":"10.1097/MOL.0000000000000868","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000868","url":null,"abstract":"<p><strong>Purpose of review: </strong>Familial hypercholesterolemia (FH) is a monogenic disorder of elevated low-density lipoprotein cholesterol (LDL-C) from birth leading to increased risk for atherosclerotic cardiovascular disease. However, not all carriers of FH variants display an FH phenotype. Despite this fact, FH variants confer increased risk for atherosclerotic disease in population cohorts. An important question to consider is whether measurements of LDL-C can fully account for this risk.</p><p><strong>Recent findings: </strong>The atherosclerotic risk associated with FH variants is independent of observed adult LDL-C levels. Modeling adult longitudinal LDL-C accounts for more of this risk compared to using a single measurement. Still, even when adjusting for observed longitudinal LDL-C in adult cohorts, FH variant carriers are at increased risk for coronary artery disease. Genetic analyses, observational studies, and clinical trials all suggest that cumulative LDL-C is a critical driver of cardiovascular risk that may not be fully appreciated by routine LDL-C measurements in adulthood. As such, FH variants confer risk independent of adult LDL-C because these variants increase cumulative LDL-C exposure starting from birth.</p><p><strong>Summary: </strong>Both research and clinical practice focus on LDL-C measurements in adults, but measurements during adulthood do not reflect lifelong cumulative exposure to LDL-C. Genetic assessments may compliment clinical assessments by better identifying patients who have experienced greater longitudinal LDL-C exposure.</p>","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 2","pages":"52-58"},"PeriodicalIF":4.4,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a0/4e/colip-34-52.PMC9994798.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9309803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"DNA testing in dyslipidemia: attitudes and complexities.","authors":"Robert A Hegele","doi":"10.1097/MOL.0000000000000869","DOIUrl":"https://doi.org/10.1097/MOL.0000000000000869","url":null,"abstract":"","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"34 2","pages":"33-34"},"PeriodicalIF":4.4,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9610503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}