Atherosclerosis plus最新文献

{"title":"Anti-atherosclerotic effects of natural compounds targeting lipid metabolism and inflammation: Focus on PPARs, LXRs, and PCSK9","authors":"Marcella Palumbo ,&nbsp;Martina Ugolotti ,&nbsp;Francesca Zimetti ,&nbsp;Maria Pia Adorni","doi":"10.1016/j.athplu.2024.12.004","DOIUrl":"10.1016/j.athplu.2024.12.004","url":null,"abstract":"<div><div>A large body of evidence has shown that modulation of the nuclear receptors peroxisome proliferator-activated receptors (PPARs), the liver X receptors (LXRs), the proprotein convertase subtilisin/kexin type 9 (PCSK9) and inflammatory processes by natural compounds has hypolipidemic and anti-atherosclerotic effects. These beneficial outcomes are certainly related to the crucial function of these targets in maintaining cholesterol homeostasis and regulating systemic inflammation. Currently, the therapeutic scenario for cardiovascular diseases (CVD) offers a plethora of widely validated and functional pharmacological treatments to improve the health status of patients. However, patients are increasingly sceptical of pharmacological treatments which are often associated with moderate to severe side effects. The aim of our review is to provide a collection of the most recent scientific evidence on the most common phytochemicals, used for centuries in the Mediterranean diet and traditional chinese medicine that act on these key regulators of cholesterol homeostasis and systemic inflammation, which could constitute important tools for CVD management.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 39-53"},"PeriodicalIF":1.4,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of NAFLD-related SNPs on the carotid atherosclerosis development; a five-year prospective observational study","authors":"Hiroaki Ikezaki ,&nbsp;Ryoko Nakashima ,&nbsp;Yuji Matsumoto ,&nbsp;Azusa Ohta ,&nbsp;Sho Yamasaki ,&nbsp;Satoshi Hiramine ,&nbsp;Koji Takayama ,&nbsp;Eiichi Ogawa ,&nbsp;Masayuki Murata ,&nbsp;Norihiro Furusyo ,&nbsp;Jun Hayashi ,&nbsp;Nobuyuki Shimono ,&nbsp;Ernst J. Schaefer","doi":"10.1016/j.athplu.2024.12.003","DOIUrl":"10.1016/j.athplu.2024.12.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>The prevalence of metabolic dysfunction associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), has become a significant public health concern with an increased atherosclerotic cardiovascular disease risk. This study investigates the impact of NAFLD-related single nucleotide polymorphisms (SNPs) on carotid atherosclerosis development in a Japanese population without diabetes, dyslipidemia, and hypertension.</div></div><div><h3>Methods</h3><div>The prospective observational study, part of the Kyushu and Okinawa Population Study (KOPS), included 945 participants (median age 55 [47, 63]) without carotid atherosclerosis, increased alcohol intake, diabetes, dyslipidemia, hypertension, or chronic hepatitis at baseline. NAFLD-related SNPs (<em>GCKR</em>, <em>NCAN</em>, <em>and PNPLA3</em>) were genotyped, and carotid intima-media thickness (cIMT) was measured using ultrasonography. Univariate and multivariate regression analyses were performed to assess the association of NAFLD-related SNPs on newly developed carotid atherosclerosis over five years.</div></div><div><h3>Results</h3><div>After five years, 125 (13.2 %) participants developed carotid atherosclerosis. The <em>NCAN</em> (rs2228603) T allele was associated with a lower incidence rate of carotid atherosclerosis (4.7 % in <em>NCAN</em> CT/TT genotype vs. 13.9 % in CC genotype; p = 0.04), and <em>NCAN</em> T allele carriers exhibited a favorable lipid profile. These associations were not altered by either recruiting area or obese. The <em>GCKR</em> T allele and <em>PNPLA3</em> C allele were associated with low carotid atherosclerosis development rates but were not significant.</div></div><div><h3>Conclusions</h3><div>Our results suggested that some NAFLD-related SNPs may influence atherosclerosis through lipid metabolism among Japanese individuals without metabolic syndrome.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 10-17"},"PeriodicalIF":1.4,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HDL-associated vitamin D binding protein levels are inversely associated with necrotic plaque burden in psoriasis","authors":"M.P. Playford ,&nbsp;H. Li ,&nbsp;A.K. Dey ,&nbsp;E.M. Florida ,&nbsp;H.L. Teague ,&nbsp;S.M. Gordon ,&nbsp;N.N. Mehta","doi":"10.1016/j.athplu.2024.12.002","DOIUrl":"10.1016/j.athplu.2024.12.002","url":null,"abstract":"<div><h3>Background and aims</h3><div>Vitamin D binding protein (DBP) serves a dual function as a vitamin D carrier and actin scavenger. Free DBP is present in high concentrations in serum, while a smaller pool is bound to lipoproteins like HDL and VLDL. The role of DBP's interaction with lipoproteins remains unclear. Given that HDL has been proposed to have both atheroprotective and anti-inflammatory properties, we sought to compare whether HDL-associated DBP and/or total serum DBP could serve as useful biomarkers for assessing disease severity in psoriasis and cardiovascular disease.</div></div><div><h3>Methods</h3><div>Psoriasis (PSO) patients (N = 83), which were part of a prospective, observational cohort and non-psoriasis (non-PSO) subjects (n = 35) underwent blood collection for HDL purification by liquid chromatography and CCTA scans to assess coronary plaque burden. Serum and HDL-bound DBP levels were measured by ELISA.</div></div><div><h3>Results</h3><div>The psoriasis cohort was middle-aged (mean ± IQR: 50 (38–59), predominantly male (n = 55, 66 %) and had moderate-to-severe skin disease [psoriasis area severity index score, PASI score, med (IQR): 9.6 (6–18.3)]. Consistent with our previous reports, PSO patients had significantly higher Framingham Risk Score (FRS), high sensitivity C-reactive protein (hs-CRP), Body Mass Index (BMI), insulin resistance (HOMA-IR) and total coronary plaque burden, driven by the rupture-prone non-calcified necrotic core. However, while the concentration of serum DBP (S-DBP) between PSO and non-PSO was unchanged (PSO: 177.80 (125.77–250.99) vs non-PSO: 177.74 (104.32–254.04), the concentration of DBP associated with HDL (HDL-DBP) was decreased in psoriatics (PSO μg/ml: 1.38 (0.64–2.75) vs non-PSO: 1.72 (1.18–3.90). Although both S-DBP and HDL-DBP levels showed inverse correlations with a measure of skin disease severity (PASI) (S-DBP, Rho = −0.022 vs HDL-DBP, Rho = −113), only HDL-DBP exhibited an inverse relationship with necrotic plaque burden [Rho −0.226, p = 0.085 vs S-DBP (0.041, p = 0.76)]. This relationship was strengthened after adjusting for traditional cardiovascular risk factors such as age and sex (β = −0.237, p = 0.045), FRS (β = −0.295, p = 0.033) and including biological treatment and HDL-cholesterol (β = −0.213, p = 0.048).</div></div><div><h3>Conclusions</h3><div>In conclusion, we found HDL-DBP levels may better capture the severity of psoriatic disease and association with cardiovascular risk factors than S-DBP.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 32-38"},"PeriodicalIF":1.4,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disparities in patterns and outcomes of dyslipidemic patients with acute coronary syndrome: A tertiary cardiac center registry","authors":"Hesham Taha ,&nbsp;Mohammad Alshehri ,&nbsp;Hossam El-Hosary ,&nbsp;Abdalla Elagha ,&nbsp;Hosam Mahrous ,&nbsp;Mirna Shaker ,&nbsp;Omar Younis ,&nbsp;Mohamed Saad","doi":"10.1016/j.athplu.2024.11.004","DOIUrl":"10.1016/j.athplu.2024.11.004","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 18-24"},"PeriodicalIF":1.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11722609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging oral therapeutic strategies for inhibiting PCSK9","authors":"Nicola Ferri ,&nbsp;Giorgia Marodin","doi":"10.1016/j.athplu.2024.11.003","DOIUrl":"10.1016/j.athplu.2024.11.003","url":null,"abstract":"<div><div>Pharmacological inhibition of Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) have been firmly established to be an effective approach to reduce low-density lipoprotein (LDL) cholesterol levels and cardiovascular events. Subcutaneous administration of monoclonal antibodies (evolocumab and alirocumab) every 2 or 4 weeks determined a 60 % reduction of LDL cholesterol levels, while the GalNac-siRNA anti PCSK9 (inclisiran) provided an effective lipid lowering activity (−50 %) after an initial subcutaneous dose, repeated after 3 months and followed by a maintenance dose every 6 months. Although these two approaches have the potentiality to bring the majority of patients at high and very-high cardiovascular risk to the appropriate LDL cholesterol targets, their cost and subcutaneous administration represent a strong limitation for their large-scale use. These problems could be overcome by the development of small chemical molecules anti PCSK9 as oral therapy for controlling hypercholesterolemia. In the present review, we summarized the pharmacological properties of oral anti PCSK9 molecules that are currently under clinical development (DC371739, CVI-LM001, and AZD0780), including the mimetic peptides enlicitide decanoate (MK-0616) and NNC0385-0434.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 25-31"},"PeriodicalIF":1.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11722601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Familial hypercholesterolemia – Targeted whole gene sequencing as a diagnostic approach","authors":"Emma Adolfsson ,&nbsp;Nils Johan Fredriksson ,&nbsp;Jon Jonasson ,&nbsp;Anna Nordenskjöld ,&nbsp;Anna Green","doi":"10.1016/j.athplu.2024.12.001","DOIUrl":"10.1016/j.athplu.2024.12.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) and other disorders with similar features are common genetic disorders that remain underdiagnosed and undertreated, due in part to the cost of screening. The aim of this study was to design and implement a whole gene targeted NGS panel for the molecular diagnosis of FH and statin intolerance with an emphasis on high quality variant calling, including copy number analysis.</div></div><div><h3>Methods</h3><div>A whole gene panel for hybridisation-based short read NGS was designed for the dominant FH-genes low density lipoprotein receptor (<em>LDLR</em>), apolipoprotein B (APOB), proproteinconvertas subtilisin/kexin type 9 (PCSK9), apolipoprotein E (APOE) and the recessive FH-genes low density lipoprotein receptor adaptor protein 1 (<em>LDLRAP1</em>), ATP binding cassette subfamily member 5/8 (ABCG5/8) and lipase A, lysosomal acid type (<em>LIPA</em>), as well as solute carrier organic anion transporter family member 1B1 (<em>SLCO1B1</em>), not an FH gene but linked to statin intolerance. Polygenetic risk score markers were also included. The panel was used for screening of a Swedish FH-study population (n = 133).</div></div><div><h3>Results</h3><div>The panel sequencing resulted in high coverage and confident variant calling of included genes. Known causal variants were found in common dominant FH-genes in 43 % of the cohort. Copy number variants were found in <em>LDLR</em> in 10 individuals and a whole gene deletion of <em>SLCO1B1</em> in one individual. In addition, coding variants in recessive genes and rare non-coding intronic and untranslated region variants were found in a large proportion of the study individuals highlighting the need for extended gene panels.</div></div><div><h3>Conclusions</h3><div>This new tool can be used for a comprehensive high-quality molecular genetic analysis according to guidelines for the diagnosis and treatment of FH.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 1-9"},"PeriodicalIF":1.4,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A cross-tissue transcriptome-wide association study identifies WDPCP as a potential susceptibility gene for coronary atherosclerosis","authors":"Xinyue Hu ,&nbsp;Guanglei Chen ,&nbsp;Xiaofang Yang ,&nbsp;Jin Cui ,&nbsp;Ning Zhang","doi":"10.1016/j.athplu.2024.11.002","DOIUrl":"10.1016/j.athplu.2024.11.002","url":null,"abstract":"<div><h3>Background</h3><div>Coronary atherosclerosis (CAS) is a complex chronic inflammatory disease with significant genetic and environmental contributions. While genome-wide association studies (GWAS) have pinpointed many risk loci, over 75 % are in non-coding regions, complicating functional analysis and understanding gene-disease mechanisms.</div></div><div><h3>Methods</h3><div>We conducted a cross-tissue transcriptome-wide association study (TWAS) using data from the GWAS Catalog (16,041 cases, 440,307 controls) and the Genotype-Tissue Expression (GTEx) v8 eQTL dataset. Initially, we used the Unified Test for Molecular Signatures (UTMOST) for analysis, followed by validation with Functional Summary-based Imputation (FUSION) and conditional and joint (COJO) analyses. Candidate genes were further refined using Multi-marker Analysis of Genomic Annotation (MAGMA). Causal relationships were assessed through Summary Data-Based Mendelian Randomization (SMR), colocalization analysis (COLOC), and Mendelian Randomization (MR). GeneMANIA was used to identify interacting genes, and Phenome-Wide Association Study (PheWAS) was employed to enhance the results.</div></div><div><h3>Results</h3><div>UTMOST identified 33 susceptibility genes for CAS. Out of these, 17 met stringent criteria in both UTMOST and FUSION analyses. Combining results from UTMOST, FUSION, and MAGMA, we identified four critical candidate genes. WDPCP was the only gene to pass SMR, COLOC, and MR analyses, confirming its causal role in CAS. GeneMANIA revealed additional interacting genes, and PheWAS validated WDPCP's role as a susceptibility gene.</div></div><div><h3>Conclusion</h3><div>WDPCP is a potential novel susceptibility gene for CAS, influencing endothelial function, lipid metabolism, and coronary artery development. This study extends GWAS findings, highlighting WDPCP's potential as a therapeutic target and its consistent expression across different tissues. Further validation studies are warranted.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 59-74"},"PeriodicalIF":1.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142742945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world data lipid profiles in one million colombian adults: The LiPAC million person study","authors":"Claudia C. Colmenares-Mejía ,&nbsp;Marcela Godoy-Corredor ,&nbsp;Esteban Morales-Mendoza ,&nbsp;Diego Alejandro Pinto-Pinzón ,&nbsp;José Medardo Rozo-Vanstrahlen ,&nbsp;Jairo Acuña-Olmos ,&nbsp;Liliana Hilarión-Gaitán ,&nbsp;María del Pilar Suarez-Ramos ,&nbsp;Diego Alberto Ruiz-Amaya ,&nbsp;Fredy Rolando Salazar-Heredia ,&nbsp;Johana Vargas-Rodríguez ,&nbsp;Mario A. Isaza-Ruget","doi":"10.1016/j.athplu.2024.11.001","DOIUrl":"10.1016/j.athplu.2024.11.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Lipid profile results are of clinical interest for assessing the presence of dyslipidemia and the risk of cardiovascular disease. This study aimed to characterize lipid profile parameters in a large adult population from different regions of Colombia.</div></div><div><h3>Methods</h3><div>Cross-sectional study. Adults with a complete lipid profile [TC, c-HDL, non-c-HDL, c-LDL, Triglycerides] from a national reference laboratory between 2018 and 2022 were included. Lipid profile levels are reported as medians and adjusted means and are also presented according to different guideline thresholds. Mixed dyslipidemia frequencies are also reported.</div></div><div><h3>Results</h3><div>1,030,195 subjects were included, with a median age of 49 years (IQR 36–61 years); 59.8 % were females. Adjusted mean value for TC was 188.1 mg/dl (CI95 % 188.0–188.2), 110.1 mg/dl (CI95 % 110.0–110.1) for c-LDL, 45.9 mg/dl (CI95 % 45.9–46.0) for c-HDL, 139.1 mg/dl (CI95 % 139.0–139.2) for non-c-HDL and 129.5 mg/dl (CI95 % 129.4–129.6) for triglycerides. The most frequent single dyslipidemia was c-HDL &lt;40 mg/dL (n = 86,725, 8.4 %), and the most common mixed dyslipidemia was TC ≥ 200 mg/dL + c-LDL &gt;130 mg/dL (n = 138,366, 17.0 %). Elevated c-LDL (≥130 mg/dL) was found in 32.4 % of the population, while c-LDL levels ≥190 mg/dL were observed in 2.0 % (n = 21,045). Triglyceride levels ≥500 mg/dL were identified in 0.3 % (n = 3103).</div></div><div><h3>Conclusion</h3><div>This large study on lipid markers from a selected sample of Colombian adults’ highlights variations in dyslipidemia by gender, age, and region. The findings emphasize the need for targeted interventions to reduce cardiovascular risk. Identifying high-risk groups is essential to improving outcomes in developing countries.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 51-58"},"PeriodicalIF":1.4,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A collaborative effort across Africa to investigate risk factors and outcomes of premature acute coronary syndrome: Protocol for the EAS Lipid Registry of Africa (LIPRA)","authors":"Ashraf Reda ,&nbsp;Alexander R.M. Lyons ,&nbsp;Alberto Zambon ,&nbsp;Ahmed Bendary ,&nbsp;Mutaz Al-Khnifsawi ,&nbsp;Habib Gamra ,&nbsp;David Marais ,&nbsp;Okechukwu S. Ogah ,&nbsp;Tigist Seleshi ,&nbsp;Ahmed A.A. Suliman ,&nbsp;Julius C. Mwita ,&nbsp;Albertino Damasceno ,&nbsp;Anastase Dzudie ,&nbsp;Atef Elbahry ,&nbsp;Elsayed Farag ,&nbsp;Chala Fekadu ,&nbsp;Lilian Mbau ,&nbsp;Mohammed Mujahed ,&nbsp;Rosemary P. Minja ,&nbsp;Bernard Samia ,&nbsp;Alexandros Tselepis","doi":"10.1016/j.athplu.2024.10.002","DOIUrl":"10.1016/j.athplu.2024.10.002","url":null,"abstract":"<div><div>Data on acute coronary syndrome (ACS) is lacking in Africa where cases of premature ACS seem to be on the rise. Africa would benefit from an epidemiological assessment of premature ACS to determine its risk factors and management in this demographic to inform guidelines and practice. The European Atherosclerosis Society recognised this urgency and formed a growing network across 11 African countries to create the Lipid Registry of Africa (EAS-LIPRA). This article is based on the EAS-LIPRA protocol and presents the aims, concept and methodological considerations, and the operations and collaborative governance structure of this project. EAS-LIPRA aims to report risk factors and outcomes of premature ACS in Africa to further understand its prevalence and management via collating and pooling multinational prospective data on premature ACS across multiple sites in Africa into a standardised registry. Data will be stratified into subgroups based on country-level income as defined by the World Bank, and within country residence of urban versus rural areas. Valid statistical procedures will be employed to compare and observe trends in the pooled data based on demographics, clinical and laboratory variables, and disparities in its management. Being the first multinational lipid registry in Africa, it is envisaged that the network will expand to other African countries and sites yet to participate, facilitate other epidemiological studies in preventive cardiology, and set a precedent for other developing countries and regions.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 46-50"},"PeriodicalIF":1.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adherence to the Healthy Nordic Food Index is associated with reduced plasma levels of inflammatory markers in patients with heterozygous familial hypercholesterolemia","authors":"Eirin B. Løvheim ,&nbsp;Kjetil Retterstøl ,&nbsp;Ingunn Narverud ,&nbsp;Martin P. Bogsrud ,&nbsp;Bente Halvorsen ,&nbsp;Thor Ueland ,&nbsp;Pål Aukrust ,&nbsp;Kirsten B. Holven","doi":"10.1016/j.athplu.2024.10.003","DOIUrl":"10.1016/j.athplu.2024.10.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) is an inherited disease associated with hypercholesterolemia, and dietary treatment is part of the treatment. We aimed to assess the dietary pattern in relation to the Healthy Nordic Food Index (HNFI) in adults with and without heterozygous FH (HeFH), and to examine the associations between dietary quality and biomarkers related to cardiovascular disease in adults with HeFH.</div></div><div><h3>Methods</h3><div>We included 205 adults (≥18 years) with HeFH who received follow-up at the Lipid Clinic in Oslo and compared them to controls (n = 228). Dietary intake was assessed using a food frequency questionnaire and dietary quality was assessed using the HNFI. Blood samples were analysed for levels of blood lipids, plasma fatty acids (FAs), and markers of inflammation and platelet activation.</div></div><div><h3>Results</h3><div>The HeFH patients (median 60 years; 50.2 % female; 25.9 % in secondary prevention) had lower intake of total and saturated fat compared to controls (32.6 energy percent (E%) vs. 34.9 E%, and 9.6 E% vs 12.0 E%, respectively; p &lt; 0.001 for both). In the HeFH patients, increasing dietary quality was associated with increased plasma levels of the n-3 polyunsaturated FAs (PUFAs) eicosapentaenoic acid and docosahexaenoic acid, and the n-6 PUFA linoleic acid, and lower plasma levels of the inflammatory cytokines Tumor Necrosis Factor and interleukin-6, and of the platelet-derived inflammatory cytokines Platelet Factor 4 and Neutrophil-Activating Peptide-2.</div></div><div><h3>Conclusion</h3><div>Norwegian patients with HeFH followed up at a Lipid Clinic eat healthier than controls. Adherence to a healthy dietary pattern is associated with higher plasma levels of n-3 and n-6 PUFA, and lower levels of inflammatory markers, including platelet markers. This may suggest that adherence to an overall healthy dietary pattern might be beneficial for HeFH patients independent of the cholesterol-lowering effect of the diet.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 38-45"},"PeriodicalIF":1.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}