Atherosclerosis plus最新文献

{"title":"Executive summary of the Hellenic Atherosclerosis Society guidelines for the diagnosis and treatment of dyslipidemias - 2023","authors":"Katsiki N ,&nbsp;Filippatos Td ,&nbsp;Vlachopoulos C ,&nbsp;Panagiotakos D ,&nbsp;Milionis H ,&nbsp;Tselepis A ,&nbsp;Garoufi A ,&nbsp;Rallidis L ,&nbsp;Richter D ,&nbsp;Nomikos T ,&nbsp;Kolovou G ,&nbsp;Kypreos K ,&nbsp;Chrysohoou C ,&nbsp;Tziomalos K ,&nbsp;Skoumas I ,&nbsp;Koutagiar I ,&nbsp;Attilakos A ,&nbsp;Papagianni M ,&nbsp;Boutari C ,&nbsp;Kotsis V ,&nbsp;Liberopoulos E","doi":"10.1016/j.athplu.2024.01.004","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.01.004","url":null,"abstract":"<div><p>Atherosclerotic cardiovascular disease (ASCVD) remains the main cause of death worldwide, and thus its prevention, early diagnosis and treatment is of paramount importance. Dyslipidemia represents a major ASCVD risk factor that should be adequately managed at different clinical settings. 2023 guidelines of the Hellenic Atherosclerosis Society focus on the assessment of ASCVD risk, laboratory evaluation of dyslipidemias, new and emerging lipid-lowering drugs, as well as diagnosis and treatment of lipid disorders in women, the elderly and in patients with familial hypercholesterolemia, acute coronary syndromes, heart failure, stroke, chronic kidney disease, diabetes, autoimmune diseases, and non-alcoholic fatty liver disease. Statin intolerance is also discussed.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 74-92"},"PeriodicalIF":1.6,"publicationDate":"2024-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266708952400004X/pdfft?md5=9461b24442f342030f6ea703f518b6fb&pid=1-s2.0-S266708952400004X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139936819","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":"Refined metabolite profiling in the collateral circulation of chronic total occlusion of coronary arteries: Insights from a metabolomics investigation","authors":"Hu Sigan,&nbsp;Li Min,&nbsp;Cheng Zengwei,&nbsp;Gao Shiyi,&nbsp;Kang Pinfang,&nbsp;Gao Dasheng","doi":"10.1016/j.athplu.2024.02.001","DOIUrl":"10.1016/j.athplu.2024.02.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>To investigate the disparities in coronary collateral circulation (CCC) and peripheral serum metabolites among patients presenting with chronic total occlusion (CTO) of the coronary arteries, a non-targeted metabolic approach was employed.</p></div><div><h3>Methods</h3><p>A cohort of 22 patients diagnosed with CTO of coronary arteries in the context of coronary heart disease (CHD) was selected for blood sample collection from CCC and peripheral arteries. The patients were categorized into two groups, namely CTO-C and CTO-P. The Waters UPLC I-Class Plus is combined with the Q Exactive high-resolution mass spectrometer for metabolite separation and detection. The acquired raw data from mass spectrometry is subsequently imported into Compound Discoverer 3.2 software for comprehensive analysis, which seamlessly integrates the BGI Metabolome Database (BMDB), mzCloud database, and ChemSpider online database. Subsequently, the identified differential metabolites were subjected to a metabolic pathway enrichment analysis, as documented in the Kyoto Encyclopedia of Genes and Genomes (KEGG) database.</p></div><div><h3>Results</h3><p>A total of 403 differential metabolites were identified in CCC and peripheral serum samples from patients with CTO of coronary arteries in CHD. Compared to the CTO-P group, the CTO-C group exhibited decreased levels of metabolites such as Testosterone, dehydroepiandrosterone (DHA), deoxyacetone, while demonstrating increased levels of metabolites including Progesterone, androstanone, <span>l</span>-threonine. The biosynthesis pathway of steroid hormones emerges as the key metabolic pathway significantly associated with differential metabolites.</p></div><div><h3>Conclusions</h3><p>Through metabolomics analysis, distinct differences in the CCC and peripheral serum metabolites have been identified among patients with CTO of coronary artery. Notably, a significant association between the steroid hormone biosynthesis pathway and CCC has been observed.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 63-73"},"PeriodicalIF":1.6,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000063/pdfft?md5=491ff531ed673039c0eb470798322705&pid=1-s2.0-S2667089524000063-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139822013","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":"Changing from lipoprotein apheresis to evolocumab treatment lowers circulating levels of arachidonic acid and oxylipins","authors":"Chaoxuan Wang ,&nbsp;Anne Kaufmann ,&nbsp;Nadja Kampschulte ,&nbsp;Ulf Elbelt ,&nbsp;Ursula Kassner ,&nbsp;Elisabeth Steinhagen-Thiessen ,&nbsp;Anne Pietzner ,&nbsp;Christoph Schmöcker ,&nbsp;Dev Datta ,&nbsp;Tiziana Sanpietro ,&nbsp;Nils Helge Schebb ,&nbsp;Karsten-H. Weylandt ,&nbsp;Nadine Rohwer","doi":"10.1016/j.athplu.2024.01.005","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.01.005","url":null,"abstract":"<div><h3>Background and aims</h3><p>Previous studies have shown that lipoprotein apheresis can modify the plasma lipidome and pro-inflammatory and pro-thrombotic lipid mediators. This has not been examined for treatment with protein convertase subtilisin/kexin type 9 inhibitors such as evolocumab, which are increasingly used instead of lipoprotein apheresis in treatment-resistant familial hypercholesterolemia. The aim of this study was to compare the effects of evolocumab treatment and lipoprotein apheresis on the fatty acid profile and on formation of lipid mediators in blood samples.</p></div><div><h3>Methods</h3><p>We analyzed blood samples from 37 patients receiving either lipoprotein apheresis or evolocumab treatment as part of a previous study. Patients were stratified according to receiving lipoprotein apheresis (n = 19) and evolocumab treatment (n = 18). Serum fatty acid analysis was performed using gas chromatography flame ionization detection and plasma oxylipin analysis was done using liquid chromatography tandem mass spectrometry.</p></div><div><h3>Results</h3><p>Changing from lipoprotein apheresis to evolocumab treatment led to lower levels of omega-6 polyunsaturated fatty acid (n-6 PUFA) including arachidonic acid, dihomo-γ-linolenic acid and linoleic acid. Moreover, several n-6 PUFA-derived oxylipins were reduced after evolocumab treatment.</p></div><div><h3>Conclusions</h3><p>Given that arachidonic acid, either directly or as a precursor, is associated with the development of inflammation and atherosclerosis, evolocumab-mediated reductions of arachidonic acid and its metabolites might have an additional beneficial effect to lower cardiovascular risk.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 55-62"},"PeriodicalIF":1.6,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000051/pdfft?md5=23f877b024fd65e2df6b11040ee4351a&pid=1-s2.0-S2667089524000051-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139748466","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":"Endothelial dysfunction and cardiovascular diseases in people living with HIV on specific highly active antiretroviral therapy regimen: A systematic review of clinical studies","authors":"Haskly Mokoena ,&nbsp;Sihle E. Mabhida ,&nbsp;Joel Choshi ,&nbsp;Phiwayinkosi V. Dludla ,&nbsp;Bongani B. Nkambule ,&nbsp;Zandile J. Mchiza ,&nbsp;Duduzile E. Ndwandwe ,&nbsp;André P. Kengne ,&nbsp;Sidney Hanser","doi":"10.1016/j.athplu.2024.01.003","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.01.003","url":null,"abstract":"<div><p>Despite the improved efficacy of highly active antiretroviral therapy (HAART) in viral suppression, emerging evidence indicates an increased burden of noncommunicable diseases in people living with HIV (PLWH). Immune activation and persistently elevated levels of inflammation have been associated with endothelial dysfunction in PLWH, likely contributing to the development of cardiovascular diseases (CVDs). Here, electronic search databases including PubMed, Google Scholar, Cochrane Library, and Science Direct were used to retrieve scientific evidence reporting on any association between markers of endothelial function and CVD-related outcomes in PLWH on HAART. Extracted data was subjected to quality assessment using the Downs and Black checklist. Most (60 %) of the results indicated the presence of endothelial dysfunction in PLWH on HAART, and this was mainly through reduced flow mediated dilation and elevated serum makers of adhesion molecules like ICAM-1, VCAM-1, and P-selectin. The summarized evidence indicates an association between persistently elevated markers of endothelial dysfunction and a pro-inflammatory state in PLWH on HAART. Only a few studies reported on improved endothelial function markers in PLWH on HAART, while limited evidence is available to prove that endothelial dysfunction is associated with CVD-risk, which could be attributed to therapeutic effects of HAART. Limited studies with relatively high quality of evidence were included in this systematic review. In conclusion, results from this review lay an important foundation for future research, even a meta-analysis, that will improve the understanding of the contributing factors to the burden of CVDs in PLWH on HAART.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 47-54"},"PeriodicalIF":1.6,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000038/pdfft?md5=e4d64fc4502624618419479fd933e822&pid=1-s2.0-S2667089524000038-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139731469","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":"Associations of carotid atherosclerosis with cognitive function and brain health: Findings from a UK tri-ethnic cohort study (Southall and Brent Revisited)","authors":"Rayan Anbar ,&nbsp;Siana Jones ,&nbsp;Nish Chaturvedi ,&nbsp;Carole Sudre ,&nbsp;Marcus Richards ,&nbsp;Salahaden R. Sultan ,&nbsp;Alun D. Hughes","doi":"10.1016/j.athplu.2024.01.002","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.01.002","url":null,"abstract":"<div><h3>Background</h3><p>Cognitive function has an important role in determining the quality of life of older adults. Cardiovascular disease (CVD) is common in older people and may compromise cognitive performance; however, the extent to which this is related to carotid atherosclerosis is unclear.</p></div><div><h3>Aim</h3><p>We investigated associations between carotid atherosclerosis and cognitive function and neuroimaging markers of brain health in a UK multi-ethnic community-based sample including older people of European, South Asian, and African-Caribbean ethnicity.</p></div><div><h3>Methods</h3><p>Carotid plaques and intima-media thickness (cIMT) were assessed using ultrasound in 985 people (mean age 73.2y, 56 % male). Associations of carotid atherosclerosis with cognitive function (memory, executive function, language and CSI-D, a global measure of cognitive state) and neuroimaging measures (total brain volume, hippocampal volume, white matter (WM) lesion volume and coalescence score) were analysed using regression analyses, with and without adjustment for potential confounders using two models: 1) adjustment for age, sex, and ethnicity; 2) model 1 plus education, physical activity category, body mass index, hypertension, diabetes, total and high density lipoprotein cholesterol, atrial fibrillation, smoking, previous CVD, alcohol consumption, and presence of chronic kidney disease.</p></div><div><h3>Results</h3><p>People with carotid plaque or higher cIMT had lower CSI-D score, poorer memory poorer executive function and higher WM lesion volume and coalescence. Language was poorer in people with plaque but was not correlated with cIMT. Associations with plaque were preserved after full adjustment (model 2) but relationships for cIMT were attenuated. Associations with other plaque characteristics were generally unconvincing after adjustment.</p></div><div><h3>Conclusions</h3><p>This multi-ethnic cohort study provides evidence that presence of carotid plaque, is associated with poorer cognitive function and brain health.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 39-46"},"PeriodicalIF":1.6,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000026/pdfft?md5=79053354001869773ddc8ebecc474ca8&pid=1-s2.0-S2667089524000026-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139718689","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":"The atorvastatin metabolite pattern in muscle tissue and blood plasma is associated with statin muscle side effects in patients with coronary heart disease; An exploratory case-control study","authors":"Trine Lauritzen ,&nbsp;John Munkhaugen ,&nbsp;Stein Bergan ,&nbsp;Kari Peersen ,&nbsp;Anja Camilla Svarstad ,&nbsp;Anders M. Andersen ,&nbsp;Jens Pahnke ,&nbsp;Einar Husebye ,&nbsp;Nils Tore Vethe","doi":"10.1016/j.athplu.2024.01.001","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.01.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>Statin-associated muscle symptoms (SAMS) is a prevalent cause of statin discontinuation. It is challenging and time-consuming for clinicians to assess whether symptoms are caused by the statin or not, and diagnostic biomarkers are requested. Atorvastatin metabolites have been associated with SAMS. We aimed to compare atorvastatin pharmacokinetics between coronary heart disease (CHD) patients with and without clinically statin intolerance and statin-dependent histopathological alterations in muscle tissue. Secondarily we aimed to assess genetic variants relevant for the observed pharmacokinetic variables.</p></div><div><h3>Methods</h3><p>Twenty-eight patients with CHD and subjective SAMS were included in the exploratory MUSE biomarker study in 2020. Participants received atorvastatin 40 mg/day for seven weeks followed by no statins for eight weeks. Muscle biopsies and blood were collected at the end of each period. Four patients were categorized as clinically intolerant to ≥3 statins prior to study start whereas four patients had signs of muscle cell damage during treatment.</p></div><div><h3>Results</h3><p>We found significantly lower levels of atorvastatin acids, and higher lactone/acid ratios in the statin intolerant, both in muscle and plasma. With optimal cut-off, the combination of 2-OH-atorvastatin acid and the 2-OH-atorvastatin lactone/acid ratio provided sensitivity, specificity, and predictive values of 100 %. Patients with variants in <em>UGT1A1</em> and <em>UGT1A3</em> had higher lactone metabolite levels than those with wild type, both in muscle and plasma.</p></div><div><h3>Conclusion</h3><p>Atorvastatin metabolites appear promising as biomarkers for the identification of clinical statin intolerance in patients with self-perceived SAMS, but the findings have to be confirmed in larger studies.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 31-38"},"PeriodicalIF":1.6,"publicationDate":"2024-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000014/pdfft?md5=ab6ad49fe798e091c4158bd231681873&pid=1-s2.0-S2667089524000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139487595","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":"Conditional deletion of Ccl2 in smooth muscle cells does not reduce early atherosclerosis in mice","authors":"Stine Gunnersen ,&nbsp;Jeong Tangkjær Shim ,&nbsp;Fan Liu ,&nbsp;Uwe J.F. Tietge ,&nbsp;Charlotte Brandt Sørensen ,&nbsp;Jacob Fog Bentzon","doi":"10.1016/j.athplu.2023.12.004","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.12.004","url":null,"abstract":"<div><h3>Background and aims</h3><p>C–C motif chemokine ligand 2 (CCL2) is a pro-inflammatory chemokine important for monocyte recruitment to the arterial wall and atherosclerotic plaques. Global knockout of <em>Ccl2</em> reduces plaque formation and macrophage content in mice, but the importance of different plaque cell types in mediating this effect has not been resolved. Smooth muscle cells (SMCs) can adopt a potentially pro-inflammatory function with expression of CCL2. The present study aimed to test the hypothesis that SMC-secreted CCL2 is involved in early atherogenesis in mice.</p></div><div><h3>Methods</h3><p>SMC-restricted Cre recombinase was activated at 6 weeks of age in mice with homozygous floxed or wildtype <em>Ccl2</em> alleles. Separate experiments in mice lacking the Cre recombinase transgene were conducted to control for genetic background effects. Hypercholesterolemia and atherosclerosis were induced by a tail vein injection of recombinant adeno-associated virus (rAAV) encoding proprotein convertase subtilisin/kexin type 9 (PCSK9) and a high-fat diet for 12 weeks.</p></div><div><h3>Results</h3><p>Unexpectedly, mice with SMC-specific <em>Ccl2</em> deletion developed higher levels of plasma cholesterol and larger atherosclerotic plaques with more macrophages compared with wild-type littermates. When total cholesterol levels were incorporated into the statistical analysis, none of the effects on plaque development between groups remained significant. Importantly, changes in plasma cholesterol and atherosclerosis remained in mice lacking Cre recombinase indicating that they were not caused by SMC-specific CCL2 deletion but by effects of the floxed allele or passenger genes.</p></div><div><h3>Conclusions</h3><p>SMC-specific deficiency of <em>Ccl2</em> does not significantly affect early plaque development in hypercholesterolemic mice.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 12-20"},"PeriodicalIF":1.6,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000512/pdfft?md5=7d5a4c8de844186df973dac21adc4df3&pid=1-s2.0-S2667089523000512-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139099837","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":"Plasma lipids in Pseudoxanthoma Elasticum (PXE) patients: A comparative study with population-based reference values and Non-PXE controls","authors":"Iris M. Harmsen ,&nbsp;Frank L.J. Visseren ,&nbsp;Madeleine Kok ,&nbsp;Pim A. de Jong ,&nbsp;Wilko Spiering","doi":"10.1016/j.athplu.2023.12.003","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.12.003","url":null,"abstract":"<div><h3>Background and aims</h3><p>– Pseudoxanthoma elasticum (PXE) is a rare genetic disease caused by pathogenic mutations in the ABCC6 gene, resulting in low values of inorganic pyrophosphate (PPi). While low PPi is thought to contribute to arterial calcification, it remains unclear whether this fully explains premature calcification in PXE. It has been hypothesized that the ABCC6 gene could be related to dyslipidemia, which could contribute to vascular calcification seen in PXE. The aim of this study is to evaluate the relation between PXE and plasma lipid concentrations in a large cohort of PXE patients compared with reference values for the general population and compared with non-PXE controls.</p></div><div><h3>Methods</h3><p>– The plasma concentrations of total cholesterol, HDL-cholesterol, tiglycerides, and LDL-cholesterol of 312 PXE patients were compared to age- and sex-matched modeled data of the general Dutch population. Differences in median lipid levels were compared with Mann-Whitney-U test. Secondly, plasma lipid concentrations of 44 PXE patients were compared to 44 not-genetically related relatives (spouses or friends), with linear models adjusted for age, sex and BMI.</p></div><div><h3>Results</h3><p>– Total cholesterol in PXE patients was 5.6 [IQR 4.6–6.4] mmol/L versus 5.3 [IQR 4.7–6.0] mmol/L (p &lt; 0.01) in the general population; triglycerides were 1.1 [IQR 0.9–1.7] mmol/L versus 1.0 [0.7–1.4] mmol/L (p &lt; 0.01); HDL-c was 1.4 [IQR 1.2–1.7] mmol/L versus 1.5 [IQR 1.2–1.8] mmol/L (p = 0.03) and LDL-c was 3.3 [IQR 2.7–4.1] mmol/L versus 3.2 [IQR 2.7–3.8] mmol/L (p = 0.01). In the patient control analysis with 44 pairs and age, sex and BMI adjusted, comparison with the non-PXE controls only triglycerides were significantly different (mean difference: 0.38 (0.13–0.63)).</p></div><div><h3>Conclusion</h3><p>–The lipid profiles of PXE patients are marginally different from the general population or compared to a matched control group, but the differences are unlikely to be clinically relevant<strong>.</strong> It is therefore unlikely that plasma lipids contribute to the premature vascular calcifications in PXE patients.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 5-11"},"PeriodicalIF":1.6,"publicationDate":"2023-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000500/pdfft?md5=f246b1ef66cc5f76a4507f16cab4fd8a&pid=1-s2.0-S2667089523000500-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138839661","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":"Acute myocardial infarction preferentially alters low-abundant, long-chain unsaturated phospholipid and sphingolipid species in plasma high-density lipoprotein subpopulations","authors":"Maharajah Ponnaiah ,&nbsp;Emile Zakiev ,&nbsp;Marie Lhomme ,&nbsp;Fabiana Rached ,&nbsp;Laurent Camont ,&nbsp;Carlos V. Serrano Jr. ,&nbsp;Raul D. Santos ,&nbsp;M. John Chapman ,&nbsp;Alexander Orekhov ,&nbsp;Anatol Kontush","doi":"10.1016/j.athplu.2023.12.001","DOIUrl":"10.1016/j.athplu.2023.12.001","url":null,"abstract":"<div><h3>Aim</h3><p>High-density lipoprotein (HDL) particles in ST-segment elevation myocardial infarction (STEMI) are deficient in their anti-atherogenic function. Molecular determinants of such deficiency remain obscure.</p></div><div><h3>Methods</h3><p>Five major HDL subpopulations were isolated using density-gradient ultracentrifugation from STEMI patients (n = 12) and healthy age- and sex-matched controls (n = 12), and 160 species of phosphatidylcholine, lysophosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylglycerol, phosphatidylserine, phosphatidic acid, sphingomyelin and ceramide were quantified by LC-MS/MS.</p></div><div><h3>Results</h3><p>Multiple minor species of proinflammatory phosphatidic acid and lysophosphatidylcholine were enriched by 1.7–27.2-fold throughout the majority of HDL subpopulations in STEMI. In contrast, minor phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, phosphatidylethanolamine, sphingomyelin and ceramide species were typically depleted up to 3-fold in STEMI vs. control HDLs, while abundances of their major species did not differ between the groups. Intermediate-to-long-chain phosphatidylcholine, phosphatidylinositol and phosphatidylglycerol species were more affected by STEMI than their short-chain counterparts, resulting in positive correlations between their fold decrease and the carbon chain length. Additionally, fold decreases in the abundances of multiple lipid species were positively correlated with the double bond number in their carbon chains. Finally, abundances of several phospholipid and ceramide species were positively correlated with cholesterol efflux capacity and antioxidative activity of HDL subpopulations, both reduced in STEMI vs controls. KEGG pathway analysis tied these species to altered glycerophospholipid and linoleic acid metabolism.</p></div><div><h3>Conclusions</h3><p>Minor unsaturated intermediate-to-long-chain phospholipid and sphingolipid species in HDL subpopulations are most affected by STEMI, reflecting alterations in glycerophospholipid and linoleic acid metabolism with the accumulation of proinflammatory lysolipids and maintenance of homeostasis of major phospholipid species.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 21-30"},"PeriodicalIF":1.6,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000482/pdfft?md5=d1c9c5b6eb0e82b02af9dfadd2e5c21a&pid=1-s2.0-S2667089523000482-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139023406","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":"CTCA in children with severe heterozygous familial hypercholesterolaemia: Screening for subclinical atherosclerosis","authors":"M. Doortje Reijman ,&nbsp;Sibbeliene E. van den Bosch ,&nbsp;D. Meeike Kusters ,&nbsp;Willemijn E. Corpeleijn ,&nbsp;Barbara A. Hutten ,&nbsp;Irene M. Kuipers ,&nbsp;R. Nils Planken ,&nbsp;Albert Wiegman","doi":"10.1016/j.athplu.2023.12.002","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.12.002","url":null,"abstract":"<div><p>Familial hypercholesterolemia (FH) is one of the most common genetically inherited disorders in the world. Children with severe heterozygous FH (HeFH), i.e. untreated low-density lipoprotein cholesterol (LDL-C) levels above the 90th percentile for age and sex among FH mutation carriers, can have LDL-C levels that overlap levels of children with homozygous FH (HoFH), but treatment regimen and cardiovascular follow-up to prevent cardiovascular disease are less intensive in children with severe HeFH. In children with HoFH, subclinical atherosclerosis can already be present using computed tomography coronary angiography (CTCA). The question remains whether this is also the case in children with severe HeFH who have a high exposure to elevated LDL-C levels from birth onwards as well. We calculated the cumulative LDL-C exposure (CE_total [mmol]) in four children with severe HeFH and performed computed tomography coronary angiography (CTCA). These children, aged 13, 14, 15 and 18 years, had CE_total of 71.3, 97.8, 103.6 and 136.1 mmol, respectively. None of them showed abnormalities on cardiovascular imaging, despite high LDL-C exposure. The results of this study, do not give us an indication to recommend performing CTCA routinely in children with severe HeFH.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"55 ","pages":"Pages 1-4"},"PeriodicalIF":1.6,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000494/pdfft?md5=9f0a311f58a088f3bd203e52bb9938bc&pid=1-s2.0-S2667089523000494-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713407","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}