Current Atherosclerosis Reports最新文献

{"title":"Statin Use and Coronary Artery Calcification: a Systematic Review and Meta-analysis of Observational Studies and Randomized Controlled Trials.","authors":"Mitra Nekouei Shahraki, Soroush Mohammadi Jouabadi, Daniel Bos, Bruno H Stricker, Fariba Ahmadizar","doi":"10.1007/s11883-023-01151-w","DOIUrl":"10.1007/s11883-023-01151-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review aimed to determine the association between statin use and coronary artery calcification (CAC), as detected by computed tomography in the general population, in previously published observational studies (OSs) and randomized controlled trials (RCTs).</p><p><strong>Recent findings: </strong>A systematic search until February 2022 identified 41 relevant studies, comprising 29 OSs and 12 RCTs. We employed six meta-analysis models, stratifying studies based on design and effect metrics. For cohort studies, the pooled β of the association with CAC quantified by the Agatston score was 0.11 (95% CI = 0.05; 0.16), with an average follow-up time per person (AFTP) of 3.68 years. Cross-sectional studies indicated a pooled odds ratio of 2.11 (95% CI = 1.61; 2.78) for the presence of CAC. In RCTs, the pooled standardized mean differences (SMDs) for CAC, quantified by Agatston score or volume, over and AFTP of 1.25 years were not statistically significant (SMD =  - 0.06, 95% CI =  - 0.19; 0.06 and SMD = 0.26, 95% CI =  - 0.66; 1.19), but significantly different (p-value = 0.04). Meta-regression and subgroup analyses did not show any significant differences in pooled estimates across covariates. The effect of statins on CAC differs across study designs. OSs demonstrate associations between statin use and higher CAC scores and presence while being prone to confounding by indication. Effects from RCTs do not reach statistical significance and vary depending on the quantification method, hampering drawing conclusions. Further investigations are required to address the limitations inherent in each approach.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"769-784"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41107308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Updates in Small Interfering RNA for the Treatment of Dyslipidemias.","authors":"S Carugo,&nbsp;C R Sirtori,&nbsp;G Gelpi,&nbsp;A Corsini,&nbsp;L Tokgozoglu,&nbsp;M Ruscica","doi":"10.1007/s11883-023-01156-5","DOIUrl":"10.1007/s11883-023-01156-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Atherosclerotic cardiovascular disease (ASCVD) is still the leading cause of death worldwide. Despite excellent pharmacological approaches, clinical registries consistently show that many people with dyslipidemia do not achieve optimal management, and many of them are treated with low-intensity lipid-lowering therapies. Beyond the well-known association between low-density lipoprotein cholesterol (LDL-C) and cardiovascular prevention, the atherogenicity of lipoprotein(a) and the impact of triglyceride (TG)-rich lipoproteins cannot be overlooked. Within this landscape, the use of RNA-based therapies can help the treatment of difficult to target lipid disorders.</p><p><strong>Recent findings: </strong>The safety and efficacy of LDL-C lowering with the siRNA inclisiran has been documented in the open-label ORION-3 trial, with a follow-up of 4 years. While the outcome trial is pending, a pooled analysis of ORION-9, ORION-10, and ORION-11 has shown the potential of inclisiran to reduce composite major adverse cardiovascular events. Concerning lipoprotein(a), data of OCEAN(a)-DOSE trial with olpasiran show a dose-dependent drop in lipoprotein(a) levels with an optimal pharmacodynamic profile when administered every 12 weeks. Concerning TG lowering, although ARO-APOC3 and ARO-ANG3 are effective to lower apolipoprotein(apo)C-III and angiopoietin-like 3 (ANGPTL3) levels, these drugs are still in their infancy. In the era moving toward a personalized risk management, the use of siRNA represents a blossoming armamentarium to tackle dyslipidaemias for ASCVD risk reduction.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"805-817"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41123190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Lipid-Lowering Therapy in Post-Stroke Patients: Update and Recommendations.","authors":"E Avenatti,&nbsp;J A Carrasco-Avila,&nbsp;B Heidari,&nbsp;K Hagan,&nbsp;M Taha,&nbsp;K Nasir","doi":"10.1007/s11883-023-01159-2","DOIUrl":"10.1007/s11883-023-01159-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>Stroke is the second leading cause of death and disability-adjusted life years worldwide, and the global lifetime risk of stroke is rising. Moreover, patients with a prior stroke are at high risk of recurrent events. We aimed at reviewing the evidence supporting aggressive secondary prevention strategies for lipid-lowering treatment in this population.</p><p><strong>Recent findings: </strong>Statins are the key players in such aggressive management; however, stroke survivors remain at significant residual risk suggesting the need for both better implementation of statin use as well as additional lipid lowering therapies. Newer drugs have become available and represent important tools in the management of patients with prior ischemic stroke. The role of lipid lowering treatment in hemorrhagic stroke is more controversial, given epidemiological data linking low lipid levels with increased risk of first and recurrent events. Aggressive secondary prevention strategies, including lipid lowering treatments, have proven to mitigate the risk of recurrent events in post-stroke patients. The tools available for treating such high-risk population have expanded beyond statins, and clinicians should familiarize themselves with them.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"889-898"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50161048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Percutaneous Coronary Interventions in Women.","authors":"Golsa Joodi, Sristi Palimar, Marcella Calfon Press","doi":"10.1007/s11883-023-01150-x","DOIUrl":"10.1007/s11883-023-01150-x","url":null,"abstract":"<p><strong>Purposeof review: </strong>Cardiovascular disease is the leading cause of morbidity and mortality among women globally. Numerous studies show ongoing disparities in diagnosis, management, and outcomes of ischemic heart disease in women compared to men. We aim to review the factors contributing to sex-based differential outcomes of percutaneous coronary interventions in women.</p><p><strong>Recent findings: </strong>Hormonal influence on coronary arteries and progression of atherosclerosis in women results in distinct coronary plaque characteristics and unique pathological process such as spontaneous coronary artery dissection and myocardial infarction with non-obstructive coronary arteries. During the presentation of acute coronary syndromes, women are older and have higher burden of comorbidities, with higher short- and long-term mortality. Awareness of differences in vascular biology and unique risk factors for cardiovascular disease in women is essential for sustained improvement in cardiovascular mortality. Better representation of women in trials is crucial to address the gaps in knowledge and allow for individualized treatment approaches in women.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"829-837"},"PeriodicalIF":5.7,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhabdomyolysis or Severe Acute Hepatitis Associated with the Use of Red Yeast Rice Extracts: an Update from the Adverse Event Reporting Systems.","authors":"Maciej Banach,&nbsp;Giuseppe Danilo Norata","doi":"10.1007/s11883-023-01157-4","DOIUrl":"10.1007/s11883-023-01157-4","url":null,"abstract":"<p><strong>Purpose of review: </strong>Elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) are a major risk factor for atherosclerotic cardiovascular disease (ASCVD), and lowering LDL-C reduces the risk of cardiovascular adverse events. Among natural approaches known for their lipid-lowering properties, red yeast rice (RYR) has a cholesterol-lowering effect due to the presence of bioactive components (monacolins) that act by inhibiting the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. In August 2018, the European Food Safety Authority (EFSA) concluded in its assessment of the use of RYR (further amended in June 2022) that monacolins from RYR raise significant safety concerns when used as a food supplement at a dose of 10 mg/day. In particular, individual cases of serious adverse effects of monacolins from RYR have been reported at intakes as low as 3 mg/day. The EFSA Panel pointed out several uncertainties regarding the available data.</p><p><strong>Recent findings: </strong>We conducted an in-depth and updated analysis of the serious adverse events, with a focus on rhabdomyolysis and acute hepatitis, associated with the consumption of RYR. An analysis of the Food and Drug Administration reporting systems revealed a very small number of cases of rhabdomyolysis or severe acute hepatitis associated with RYR use. In addition, only a few case reports of these serious adverse events associated with RYR use have been published. Based on data from adverse event reporting systems and available case reports, the occurrence of rhabdomyolysis or severe acute hepatitis that could be associated with the use of RYR appears to be extremely rare compared to the occurrence with statins, which is rare to common.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"879-888"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41194148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atherosclerosis in Systemic Lupus Erythematosus.","authors":"Rachel Tobin,&nbsp;Nidhi Patel,&nbsp;Kardie Tobb,&nbsp;Brittany Weber,&nbsp;Puja K Mehta,&nbsp;Ijeoma Isiadinso","doi":"10.1007/s11883-023-01149-4","DOIUrl":"10.1007/s11883-023-01149-4","url":null,"abstract":"<p><strong>Purpose of the review: </strong>Systemic lupus erythematosus (SLE) patients are at increased risk of cardiovascular disease (CVD) compared to the general population, despite most patients being young females, who are not classically considered to be at high risk for cardiovascular disease using traditional risk assessment tools. The purpose of this review is to discuss the pathophysiology of atherosclerosis in SLE and raise awareness of the relationship between SLE and CVD.</p><p><strong>Recent findings: </strong>The increased risk of CVD in SLE patients is multifactorial, due to proatherogenic lipid profiles, immune dysregulation and inflammation, side effects of lupus treatment, and microvascular dysfunction. Conventional CV risk models often underperform in the identification of SLE patients at high risk of atherosclerosis. The use of non-invasive imaging serves as a strategy to identify patients with evidence of subclinical CVD and in the evaluation of symptomatic patients. Identification of subclinical atherosclerosis allows for aggressive management of CV risk factors. SLE patients experience an increased risk of atherosclerotic CVD, which is not solely explained by traditional CV risk factors. It is imperative that clinicians are aware of this association to implement prompt detection and treatment of atherosclerotic CVD in SLE patients.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"819-827"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41114996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms Behind NAFLD: a System Genetics Perspective.","authors":"Shirin Pourteymour,&nbsp;Christian A Drevon,&nbsp;Knut Tomas Dalen,&nbsp;Frode A Norheim","doi":"10.1007/s11883-023-01158-3","DOIUrl":"10.1007/s11883-023-01158-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>To summarize the key factors contributing to the onset and progress of nonalcoholic fatty liver disease (NAFLD) and put them in a system genetics context. We particularly focus on how genetic regulation of hepatic lipids contributes to NAFLD.</p><p><strong>Recent findings: </strong>NAFLD is characterized by excessive accumulation of fat in the liver. This can progress to steatohepatitis (inflammation and hepatocyte injury) and eventually, cirrhosis. The severity of NAFLD is determined by a combination of factors including obesity, insulin resistance, and lipotoxic lipids, along with genetic susceptibility. Numerous studies have been conducted on large human cohorts and mouse panels, to identify key determinants in the genome, transcriptome, proteome, lipidome, microbiome and different environmental conditions contributing to NAFLD. We review common factors contributing to NAFLD and put them in a systems genetics context. In particular, we describe how genetic regulation of liver lipids contributes to NAFLD. The combination of an unhealthy lifestyle and genetic predisposition increases the likelihood of accumulating lipotoxic specie lipids that may be one of the driving forces behind developing severe forms of NAFLD.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"869-878"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41108089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Do Triglyceride-Rich Lipoproteins Equal Low-Density Lipoproteins in Risk of ASCVD?","authors":"Benjamin N Wadström,&nbsp;Anders B Wulff,&nbsp;Kasper M Pedersen,&nbsp;Børge G Nordestgaard","doi":"10.1007/s11883-023-01153-8","DOIUrl":"10.1007/s11883-023-01153-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>Recent large clinical trials have failed to show that triglyceride-rich lipoprotein-lowering therapies decrease the risk of atherosclerotic cardiovascular disease (ASCVD). In this review, we reconcile these findings with evidence showing that elevated levels of triglyceride-rich lipoproteins and the cholesterol they contain, remnant cholesterol, cause ASCVD alongside low-density lipoprotein (LDL) cholesterol.</p><p><strong>Recent findings: </strong>Results from observational epidemiology, genetic epidemiology, and randomized controlled trials indicate that lowering of remnant cholesterol and LDL cholesterol decrease ASCVD risk by a similar magnitude per 1 mmol/L (39 mg/dL) lower non-high-density lipoprotein cholesterol (remnant cholesterol+LDL cholesterol). Indeed, recent guidelines for ASCVD prevention recommend the use of non-high-density lipoprotein cholesterol instead of LDL cholesterol. Current consensus is moving towards recognizing remnant cholesterol and LDL cholesterols as equals per 1 mmol/L (39 mg/dL) higher levels in the risk assessment of ASCVD; hence, triglyceride-rich lipoprotein-lowering therapies should also lower levels of non-HDL cholesterol to reduce ASCVD risk.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"795-803"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41114290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk Factors for Cardiovascular Disease: Knowledge Gained from the Hispanic Community Health Study/Study of Latinos.","authors":"Amber Pirzada,&nbsp;Jianwen Cai,&nbsp;Christina Cordero,&nbsp;Linda C Gallo,&nbsp;Carmen R Isasi,&nbsp;John Kunz,&nbsp;Bharat Thyagaragan,&nbsp;Sylvia Wassertheil-Smoller,&nbsp;Martha L Daviglus","doi":"10.1007/s11883-023-01152-9","DOIUrl":"10.1007/s11883-023-01152-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>The Hispanic Community Health Study/Study of Latinos (HCHS/SOL) has made important contributions on the prevalence of and factors associated with cardiovascular disease (CVD) risk factors among diverse Hispanic/Latino adults in the US. This article summarizes the knowledge gained thus far on major CVD risk factors from this landmark study.</p><p><strong>Recent findings: </strong>HCHS/SOL demonstrated the sizeable burdens of CVD risk in all major Hispanic/Latino groups in the US, as well as the marked variations in prevalence of hypertension, hypercholesterolemia, diabetes, obesity, and smoking by sex and background. It also identified sociodemographic, lifestyle, and sociocultural characteristics associated with risk factors. HCHS/SOL has yielded an expanding body of literature on characteristics associated with adverse CVD risk factors in this population. Long-term follow-up of this cohort will shed further light on the observed heterogeneity in CVD risk across Hispanic/Latino groups and identify specific risk/protective factors driving these variations.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"785-793"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41127309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive Modeling and Structure Analysis of Genetic Variants in Familial Hypercholesterolemia: Implications for Diagnosis and Protein Interaction Studies.","authors":"Asier Larrea-Sebal,&nbsp;Shifa Jebari-Benslaiman,&nbsp;Unai Galicia-Garcia,&nbsp;Ane San Jose-Urteaga,&nbsp;Kepa B Uribe,&nbsp;Asier Benito-Vicente,&nbsp;César Martín","doi":"10.1007/s11883-023-01154-7","DOIUrl":"10.1007/s11883-023-01154-7","url":null,"abstract":"<p><strong>Purpose of review: </strong>Familial hypercholesterolemia (FH) is a hereditary condition characterized by elevated levels of low-density lipoprotein cholesterol (LDL-C), which increases the risk of cardiovascular disease if left untreated. This review aims to discuss the role of bioinformatics tools in evaluating the pathogenicity of missense variants associated with FH. Specifically, it highlights the use of predictive models based on protein sequence, structure, evolutionary conservation, and other relevant features in identifying genetic variants within LDLR, APOB, and PCSK9 genes that contribute to FH.</p><p><strong>Recent findings: </strong>In recent years, various bioinformatics tools have emerged as valuable resources for analyzing missense variants in FH-related genes. Tools such as REVEL, Varity, and CADD use diverse computational approaches to predict the impact of genetic variants on protein function. These tools consider factors such as sequence conservation, structural alterations, and receptor binding to aid in interpreting the pathogenicity of identified missense variants. While these predictive models offer valuable insights, the accuracy of predictions can vary, especially for proteins with unique characteristics that might not be well represented in the databases used for training. This review emphasizes the significance of utilizing bioinformatics tools for assessing the pathogenicity of FH-associated missense variants. Despite their contributions, a definitive diagnosis of a genetic variant necessitates functional validation through in vitro characterization or cascade screening. This step ensures the precise identification of FH-related variants, leading to more accurate diagnoses. Integrating genetic data with reliable bioinformatics predictions and functional validation can enhance our understanding of the genetic basis of FH, enabling improved diagnosis, risk stratification, and personalized treatment for affected individuals. The comprehensive approach outlined in this review promises to advance the management of this inherited disorder, potentially leading to better health outcomes for those affected by FH.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":" ","pages":"839-859"},"PeriodicalIF":5.8,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41233101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}