Atherosclerosis最新文献

{"title":"Long-term body mass index trajectories and the risk of type 2 diabetes mellitus and atherosclerotic cardiovascular disease using healthcare data from UK Biobank participants","authors":"Anja Krüger ,&nbsp;Ko Willems van Dijk ,&nbsp;Diana van Heemst ,&nbsp;Raymond Noordam","doi":"10.1016/j.atherosclerosis.2025.119135","DOIUrl":"10.1016/j.atherosclerosis.2025.119135","url":null,"abstract":"<div><h3>Background and aims</h3><div>Most epidemiological studies ignore long-term burden, gain and variability in body weight in assessing cardiometabolic disease risk. We investigated the associations of body mass index (BMI) trajectories measured by general practitioners with incident type 2 diabetes (T2D) and coronary artery disease (CAD).</div></div><div><h3>Methods</h3><div>We used electronic healthcare data from 111,615 European-ancestry participants from UK Biobank (57.1 (SD 7.8) years, 59.6 % women) with at least three BMI measurements (median trajectory period: 14.9 [interquartile range 9.5, 20.1] years). We calculated six variables capturing different long-term aspects, including i.e. burden (long-term average, area under the curve), gain (slope) and variability (standard deviation, average of the [absolute] consecutive BMI differences). The variables were used in principal component (PC) analyses and k-means clustering. Newly-derived dimensions and subgroups were used as exposures in cox-proportional hazard models.</div></div><div><h3>Results</h3><div>The BMI-trajectory indices were captured in two PCs reflecting BMI burden and BMI gain. The BMI-burden PC associated with higher T2D (hazard ratio [95 % confidence interval] per SD higher PC: 1.57 [1.55,1.60]) and CAD (1.17 [1.15,1.19]) risks, while weak or no associations were observed with the BMI-gain PC (T2D: 1.03 [1.01,1.05]; CAD: 1.01 [0.98,1.03]). Participants with the highest BMI burden, compared to those with lowest BMI burden without significant gain, had highest T2D (6.96 [6.41,7.55]) and CAD (1.57 [1.45,1.69]) risks. Both methods to capture BMI burden, gain and variability showed superior model fit compared to a single baseline BMI assessment.</div></div><div><h3>Conclusions</h3><div>Long-term high BMI burden, irrespective of BMI gain, was a risk factor for cardiometabolic disease.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119135"},"PeriodicalIF":4.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474366","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":"Genetic association of circulating lipids and lipid-lowering drug targets with vascular calcification","authors":"Pengfei Zhang ,&nbsp;Wenting Wang ,&nbsp;Qian Xu ,&nbsp;Jing Cui ,&nbsp;Mengmeng Zhu ,&nbsp;Yiwen Li ,&nbsp;Yanfei Liu ,&nbsp;Yue Liu","doi":"10.1016/j.atherosclerosis.2025.119136","DOIUrl":"10.1016/j.atherosclerosis.2025.119136","url":null,"abstract":"<div><h3>Background and aims</h3><div>Vascular calcification (VC) significantly increases the incidence and mortality of many diseases. The causal relationships of dyslipidaemia and lipid-lowering drug use with VC severity remain unclear. This study explores the genetic causal associations of different circulating lipids and lipid-lowering drug targets with coronary artery calcification (CAC) and abdominal aortic artery calcification (AAC).</div></div><div><h3>Methods</h3><div>We obtained single-nucleotide polymorphisms (SNPs) and expression quantitative trait loci (eQTLs) associated with seven circulating lipids and 13 lipid-lowering drug targets from publicly available genome-wide association studies and eQTL databases. Causal associations were investigated by univariable, multivariable, drug-target, and summary data-based Mendelian randomization (MR) analyses. Potential mediation effects of metabolic risk factors were evaluated.</div></div><div><h3>Results</h3><div>MR analysis revealed that genetic proxies for low-density lipoprotein cholesterol (LDL-C), triglycerides (TC) and Lipoprotein (a) (Lp(a)) were causally associated with CAC severity, and apolipoprotein B (apoB) level was causally associated with AAC severity. A significant association was detected between hepatic Lipoprotein(A) (<em>LPA</em>) gene expression and CAC severity. Colocalisation analysis supported the hypothesis that the association between <em>LPA</em> expression and CAC quantity is driven by different causal variant sites within the ±1 Mb flanking region of <em>LPA</em>. Serum calcium and phosphorus had causal associations with CAC severity.</div></div><div><h3>Conclusions</h3><div>Inhibitors targeting <em>LPA</em> might represent CAC drug candidates. Moreover, T2DM, hypercalcemia, and hyperphosphatemia are positively causally associated with CAC severity, while chronic kidney disease and estimated glomerular filtration rate are not.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119136"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453701","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":"Associations of dietary fatty acids with the incidence of carotid atherosclerotic plaque components: A 6-year follow-up study with serial MRI","authors":"Luoshiyuan Zuo ,&nbsp;Maryam Kavousi ,&nbsp;Daniel Bos ,&nbsp;Trudy Voortman","doi":"10.1016/j.atherosclerosis.2025.119144","DOIUrl":"10.1016/j.atherosclerosis.2025.119144","url":null,"abstract":"<div><h3>Background and aims</h3><div>The influence of dietary fatty acids (FAs) on carotid atherosclerotic plaque components remains unknown. We aimed to assess the association of dietary saturated (SFA), mono-unsaturated (MUFA), and poly-unsaturated FAs (PUFA) with the incidence of carotid plaque components.</div></div><div><h3>Methods</h3><div>Within the population-based Rotterdam Study, 570 stroke-free participants (mean age: 68 years; 47 % women) with subclinical carotid atherosclerosis underwent two serial carotid MRI (mean scan interval: 5.9 years). Carotid calcification, lipid-rich necrotic core (LRNC) and intraplaque hemorrhage (IPH) were evaluated. Intake of dietary FAs was assessed by food-frequency questionnaires around the time of baseline MRI. We used generalized estimating equation to investigate the association between dietary FAs and new onset of carotid plaque components.</div></div><div><h3>Results</h3><div>We found that a higher PUFA intake was associated with a lower incidence of IPH (adjusted odds ratio (OR) per 5 g/d increase: 0.80 (95 % confidence interval (CI): 0.65 to 0.98)). In the substitution models, a modelled higher PUFA intake at the expense of MUFA or SFA was also associated with a lower risk of incident IPH, with adjusted ORs per 5 g/day more PUFA of 0.81 (95 % CI: 0.58 to 1.14) for replacing SFA and 0.60 (95 % CI: 0.37 to 0.97) for replacing MUFA. No associations between SFA or MUFA and the carotid plaque components were found.</div></div><div><h3>Conclusion</h3><div>Among persons with subclinical carotid plaque, dietary FA intake is a modifiable risk factor for changes in carotid plaque vulnerability. Diet with more PUFA is associated with a lower risk of IPH in carotid plaque.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119144"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591489","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":"Cardiovascular disease morbidity is associated with social deprivation in subjects with familial hypercholesterolaemia (FH): A retrospective cohort study of individuals with FH in UK primary care and the UK Simon Broome register, linked with national hospital records","authors":"B. Iyen ,&nbsp;N. Qureshi ,&nbsp;J. Kai ,&nbsp;N. Capps ,&nbsp;P.N. Durrington ,&nbsp;J. Cegla ,&nbsp;H. Soran ,&nbsp;J. Schofield ,&nbsp;H.A.W. Neil ,&nbsp;S.E. Humphries ,&nbsp;Simon Broome Familial Hyperlipidaemia Register Group","doi":"10.1016/j.atherosclerosis.2025.119142","DOIUrl":"10.1016/j.atherosclerosis.2025.119142","url":null,"abstract":"<div><h3>Background</h3><div>Social deprivation is associated with higher cardiovascular disease (CVD) morbidity and mortality. We examined whether this is also observed in people with Familial Hypercholesterolaemia (FH).</div></div><div><h3>Methods</h3><div>Subjects with FH and linked secondary care records in Hospital Episode Statistics (HES) were identified from UK Clinical Practice Research Datalink (CPRD) and the Simon Broome (SB) adult FH register. Cox proportional hazards regression estimated hazard ratios (HR) for composite CVD outcomes (first HES outcome of coronary heart disease, myocardial infarction, angina, stroke, transient ischaemic attack, peripheral vascular disease, heart failure, coronary revascularisation interventions (PCI and CABG)) in Index of Multiple Deprivation (IMD) quintiles.</div></div><div><h3>Results</h3><div>We identified 4309 patients with FH in CPRD (1988–2020) and 2956 in the SB register. Both cohorts had considerably fewer subjects in the most deprived compared to the least deprived quintile (60 % lower in CPRD and 52 % lower in SB). In CPRD, the most deprived individuals had higher unadjusted HRs for composite CVD (HR 1.71 [CI 1.22–2.40]), coronary heart disease (HR 1.63 [1.11–2.40]) and mortality (HR 1.58 [1.02–2.47]) compared to the least deprived but these became insignificant after adjusting for age, sex, smoking and alcohol consumption. In the SB register, hazard ratios for composite CVD increased with increasing deprivation quintiles and remained significant after adjustment for age, sex, smoking and alcohol consumption (adjusted HR in quintile 5 vs quintile 1 = 1.83 [1.54–2.17]).</div></div><div><h3>Conclusions</h3><div>Strikingly fewer individuals with FH are identified from lower socioeconomic groups, though the most deprived FH patients have the highest risk of CVD and mortality. In CPRD, this risk was largely explained by smoking and alcohol consumption, but not in the SB register. More effective strategies to detect FH and optimise risk factor management, are needed in lower socioeconomic groups.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119142"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143528857","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":"Effects of replacing sitting with standing and walking on cholesterol metabolism and inflammation in men and women who are overweight or obese","authors":"Willem Zwaan ,&nbsp;Bernard M.F.M. Duvivier ,&nbsp;Hans H.C.M. Savelberg,&nbsp;Herman E. Popeijus,&nbsp;Maurice C.J.M. Konings,&nbsp;Ronald P. Mensink,&nbsp;Jogchum Plat","doi":"10.1016/j.atherosclerosis.2025.119143","DOIUrl":"10.1016/j.atherosclerosis.2025.119143","url":null,"abstract":"<div><h3>Background and aims</h3><div>Reducing sedentary behaviour changes serum lipid and lipoprotein concentrations. However, detailed insights into effects on lipid and lipoprotein subclasses and functionalities, and markers of inflammation and endothelial dysfunction are lacking.</div></div><div><h3>Methods</h3><div>In this randomised cross-over study, 24 sedentary overweight/obese individuals followed two 4-day activity regimens under free-living conditions. The “Sit” regimen involved 13.5 h/day sitting, 1.4 h/day standing, and 0.7 h/day self-perceived light-intensity walking. During the “SitLess” regimen these activities lasted respectively 7.6, 4.0, and 4.3 h/day. Blood samples collected after each regimen were analysed for markers of lipid and lipoprotein metabolism, inflammation, and endothelial dysfunction.</div></div><div><h3>Results</h3><div>Compared to the Sit regimen, SitLess increased serum cholesterol concentrations in HDL (0.06 mmol/l, p = 0.002), large HDL A (0.05 mmol/l, p &lt; 0.001), medium HDL B (0.02 mmol/l, p &lt; 0.001) and small HDL C (0.09 mmol/l, p &lt; 0.001), LHDL particles concentrations (999 nmol/l, p &lt; 0.001) and HDL size (0.2 nm, p &lt; 0.001). ApoA-I, pro-ApoA-I, and HDL functionality remained unchanged. Triglyceride (−0.49 mmol/l, p &lt; 0.001), ApoB100 (−0.68 g/l, p = 0.007), and particle concentrations of LVLDL (−2.2 nmol/l, p = 0.002), SLDL (−58 nmol/l, p = 0.024) and LDL (−86 nmol/l, p = 0.006) decreased. Cholesterol concentrations in VLDL (−0.15 mmol/l, p &lt; 0.001), IDL (−0.11 mmol/l, p = 0.001) and small LDL C (−0.04 mmol/l, p &lt; 0.001) decreased, while large LDL A cholesterol (0.07 mmol/l, p = 0.031) and LDL particle size (0.1 nm, p = 0.004) increased. CRP concentrations (0.95 mg/dl, p = 0.003) rose.</div></div><div><h3>Conclusions</h3><div>Substituting sitting with standing and self-perceived light walking in free-living conditions, translates into lower CVD risk lipid and lipoprotein profiles in individuals who are overweight/obese. CRP significantly increased after the SitLess regimen.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119143"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487094","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":"Statin adherence in coronary outpatients: The relationship between a novel blood test and pharmacy registry data","authors":"Jonas Pivoriunas ,&nbsp;Ingrid Engebretsen ,&nbsp;Nils Tore Vethe ,&nbsp;Oscar Kristiansen ,&nbsp;Toril Dammen ,&nbsp;Einar Husebye ,&nbsp;Morten W. Fagerland ,&nbsp;John Munkhaugen ,&nbsp;Elise Sverre","doi":"10.1016/j.atherosclerosis.2025.119138","DOIUrl":"10.1016/j.atherosclerosis.2025.119138","url":null,"abstract":"<div><h3>Background and aims</h3><div>An accurate and feasible method to assess adherence to statin therapy is needed. We developed a novel blood test to identify reduced statin adherence and compared statin adherence determined by a single blood test to pharmacy registry data.</div></div><div><h3>Methods</h3><div>In a retrospective cohort study of patients prescribed atorvastatin or simvastatin during hospitalization for a coronary heart disease event, a single blood sample was collected median 18 months later. Patients were unaware of the forthcoming statin analyses. Statin adherence was determined by drug concentration measurements using liquid chromatography mass spectrometry and the Norwegian Prescription Database by gaps in statin dispenses.</div></div><div><h3>Results</h3><div>Out of 451 patients, 9 % (n = 39) had reduced adherence (≥2 doses omitted) determined by the blood test. Among those classified as adherent by the blood test, only 0.7 % (n = 3) had a treatment gap ≥90 days during the preceding three months, whereas 28 % (n = 115) during the entire follow-up period (median 5.9 years). Of 39 patients classified with reduced adherence by the blood test, 28 % (n = 11) had treatment gaps ≥90 days during the preceding three months, and 66 % (n = 26) during the entire study period. Patients classified with reduced adherence by the blood test, but not registry data, had numerically more coronary events prior to the index event compared to adherent patients.</div></div><div><h3>Conclusions</h3><div>In coronary outpatients, high adherence to statin treatment measured by a novel blood test aligns with adherence assessed by pharmacy registry. The blood test emerges as a promising tool for enhancing lipid management in clinical practice.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119138"},"PeriodicalIF":4.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143562637","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":"Association of guideline-directed managements of chronic kidney disease with mortality among patients with cardiovascular disease: Insight from a multi-center cohort in China","authors":"Yihang Ling ,&nbsp;Xianlin Ruan ,&nbsp;Ling Jing ,&nbsp;Yibo He ,&nbsp;Tian Chang ,&nbsp;Yong Liu ,&nbsp;Jiyan Chen","doi":"10.1016/j.atherosclerosis.2025.119133","DOIUrl":"10.1016/j.atherosclerosis.2025.119133","url":null,"abstract":"<div><h3>Background</h3><div>Chronic kidney disease (CKD) represents one of the most significant risks for death, in patients with existed cardiovascular disease (CVD). This study aimed to investigate whether the excess risk of death in these patients could be reduced or eliminated through joint intensive control of blood pressure, glucose and renin-angiotensin system inhibitors (RASi) treatment, among CVD patients with CKD.</div></div><div><h3>Method</h3><div>Overall, 6222 CVD patients with CKD and 9274 matched CVD patients who were free of CKD, hypertension and diabetes from CIN II cohort (NCT05050877), were included in the study. The association of all-cause and cardiovascular mortality with guideline-directed management was detected by Cox proportional hazards regression analysis.</div></div><div><h3>Result</h3><div>During 5.6-year median follow-up, 3076 (19.9 %) patients died and 1578 (10.2 %) for cardiovascular cause. Among patients with CKD, risk factor controls and treatment were associated with a reduction in the risk of all-cause and cardiovascular mortality. Furthermore, compared to the non-CKD patients, both risk factors within the target ranges plus RASi therapy could theoretically eliminate the excess risk of all-cause (1-year: adjusted hazard radio [aHR] = 0.79, 95 % CI: 0.39–1.63; long-term: aHR = 0.99, 95 % CI: 0.73–1.34) and cardiovascular (1-year: aHR = 1.26, 95 % CI: 0.82–1.93; long-term: aHR = 1.15, 95 % CI: 0.75–1.76) mortality associated with CKD in stage 3a patients. Similar results were observed in patients at CKD stage 3 b.</div></div><div><h3>Conclusion</h3><div>CVD Patients with early CKD who had controlled blood pressure, glucose and took RASi therapy showed no excess risk of all-cause and cardiovascular death compared to the those without CKD.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119133"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143520211","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":"A study into rare GPR146 gene variants in humans and mice","authors":"Boyan Zhang ,&nbsp;Antoine Rimbert ,&nbsp;Antoine Lainé ,&nbsp;Nicolette Huijkman ,&nbsp;Niels Kloosterhuis ,&nbsp;Marieke Smit ,&nbsp;Bart van de Sluis ,&nbsp;Jan Albert Kuivenhoven ,&nbsp;Umesh Tharehalli","doi":"10.1016/j.atherosclerosis.2025.119137","DOIUrl":"10.1016/j.atherosclerosis.2025.119137","url":null,"abstract":"<div><h3>Background and aims</h3><div>G-protein coupled receptor 146 (<em>GPR146</em>)-deficient mice exhibit a moderate 21 % reduction in plasma cholesterol. This is associated with decreased phosphorylation of ERK1/2 and reduced SREBP2 activity in the liver, which leads to lower VLDL secretion. Insight into the role of <em>GPR146</em> in humans is however limited. We therefore set out to study rare genetic variants in <em>GPR146</em> to improve our understanding of this new player in lipid metabolism.</div></div><div><h3>Methods</h3><div>We used whole genome sequencing data from UK Biobank participants to search for rare coding variants in <em>GPR146</em>. We first carried out gene-based burden tests (using SAIGE-GENE-framework) and examined the association of individual variants with plasma cholesterol levels. One of the variants (P62L) was also studied using the Global Lipids Genetics Consortium (GLGC) data set and in a knock-in mouse model.</div></div><div><h3>Results</h3><div>We found that the combination of rare genetic variants identified in <em>GPR146</em> is significantly associated with plasma cholesterol levels. Three rare variants, i.e. P62L, I129I, and A175T were individually associated with reduced plasma cholesterol. In the GLGC cohort, the P62L variant was associated with reductions in both HDL and LDL cholesterol. Follow-up experiments show lower plasma cholesterol levels in <em>GPR146</em>^P61L male and female mice (−13 %, p &lt; 0.05 and −15 %, p &lt; 0.005, respectively) when compared to controls due to a reduction in HDL cholesterol. The <em>GPR146</em>^P61L mice did not exhibit a change in VLDL secretion. In line, the ERK1/2 signalling pathway and <em>Srebp2</em> mRNA expression in liver homogenates, and the secretion of apoB by primary hepatocytes of <em>GPR146</em>^P61L and wild-type mice were unchanged.</div></div><div><h3>Conclusions</h3><div>This study shows that rare <em>GPR146</em> gene variants are associated with lower plasma cholesterol levels in humans. One of these variants, P62L is associated with reductions of HDL cholesterol and LDL cholesterol in humans while the ortholog in mice confers a loss of <em>GPR146</em> function leading to only reduced HDL cholesterol. How <em>GPR146</em> affects HDL metabolism in humans and mice remains to be resolved.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119137"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679609","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":"Differential lipid impact on mortality in patients undergoing CABG versus PCI","authors":"Xin Yuan ,&nbsp;Lihua Zhang ,&nbsp;Xi Li ,&nbsp;Kai Chen ,&nbsp;Qing Chu ,&nbsp;Liang Chen ,&nbsp;Shengshou Hu","doi":"10.1016/j.atherosclerosis.2025.119141","DOIUrl":"10.1016/j.atherosclerosis.2025.119141","url":null,"abstract":"<div><h3>Background and aims</h3><div>The impact of revascularization type, including coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI), on lipid control efficacy remains unclear. We aim to assess the associations of lipid levels with all-cause and cardiovascular mortality in patients undergoing PCI or CABG.</div></div><div><h3>Methods</h3><div>We used data from the ChinaHEART cohort and enrolled patients with a self-reported history of PCI or CABG. We employed Cox proportional hazards regression models to evaluate the associations between lipid levels and mortality.</div></div><div><h3>Results</h3><div>Our analysis included 29 003 participants, of whom 23 959 (82.6 %) undergoing PCI and 5044 (17.4 %) undergoing CABG. Over a median follow-up of 3.22 years, 1007 deaths were recorded, with 579 attributed to cardiovascular causes. Each 1 mmol/L increase in TC, LDL-C, and non-HDL-C was associated with multivariable-adjusted HRs of 1.16 (95 % CI 1.10,1.22), 1.23 (1.15,1.32) and 1.16 (1.10,1.23) for all-cause mortality, respectively. Similar results were observed in patients undergoing PCI, while no significant associations were found in patients undergoing CABG.</div></div><div><h3>Conclusions</h3><div>Elevated lipid levels are associated with all-cause and cardiovascular mortality in revascularization patients. Suboptimal lipid control appears to have a more pronounced effect on mortality in patients undergoing PCI. The effects of elevated lipid levels on mortality in CABG patients may need a longer follow-up to manifest due to the more complex nature of the grafts and the long-term adaptation process.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119141"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510642","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":"Discordance analyses comparing LDL cholesterol, Non-HDL cholesterol, and apolipoprotein B for cardiovascular risk estimation","authors":"Camilla Ditlev Lindhardt Johannesen ,&nbsp;Martin Bødtker Mortensen ,&nbsp;Børge Grønne Nordestgaard ,&nbsp;Anne Langsted","doi":"10.1016/j.atherosclerosis.2025.119139","DOIUrl":"10.1016/j.atherosclerosis.2025.119139","url":null,"abstract":"<div><div>For decades, studies have tried to identify the cholesterol marker that best reflects risk of atherosclerotic cardiovascular disease(ASCVD). Comparing low-density-lipoprotein(LDL) cholesterol, non-high-density-lipoprotein(non-HDL) cholesterol, and apolipoprotein B(apoB) as ASCVD risk markers has been challenged by high correlation between them. Thus, discordance analyses, directly addressing disagreements between the cholesterol markers, have emerged. Approaches adopted to define discordance originate in one of three methods: discordance by cut-points, discordance by percentiles, or discordance by residuals. Commonly, concordant lipid levels serve as reference examining the association between discordant lipid levels with risk of ASCVD. Importantly, concordant reference groups present heterogeneity of clinical relevance across different discordance methods as concordant low lipid levels associate with lowest ASCVD risk while concordant high lipid levels associate with highest risk. Thus, results from different discordance approaches cannot be directly compared. Moreover, discordance between cholesterol markers is more frequently seen in individuals treated with lipid-lowering medication than in individuals not treated with lipid-lowering medication. Accordingly, studies performing discordance analyses have reported inconsistent and even conflicting results. Discordance by cut-points appears the most intuitive and clinically applicable method; results from these analyses suggest that elevated LDL cholesterol, non-HDL cholesterol, or apoB levels in individuals not treated with lipid-lowering medication confer increased ASCVD risk while in individuals treated with lipid-lowering medication, elevated non-HDL cholesterol and apoB levels best indicate residual risk. Results from discordance analyses comparing LDL cholesterol, non-HDL cholesterol, and apoB in risk of ASCVD as well as complexities of discordance analyses and considerations regarding interpretations are discussed in this review.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119139"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591488","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}