Journal of clinical lipidology最新文献

{"title":"Lipoprotein subfractions and carotid plaque: NMR analysis of triglyceride-rich vs LDL particle size concentrations (ELSA-Brasil study)","authors":"William R. Tebar PhD ,&nbsp;Vandrize Meneghini PhD ,&nbsp;Alessandra C. Goulart MD, PhD ,&nbsp;Itamar S. Santos MD, PhD ,&nbsp;Raul D. Santos MD, PhD ,&nbsp;Marcio S. Bittencourt MD, MPH, PhD ,&nbsp;Giuliano Generoso MD, PhD ,&nbsp;Alexandre C. Pereira MD, PhD ,&nbsp;Michael J. Blaha MD, PhD ,&nbsp;Steven R. Jones MD, PhD ,&nbsp;Peter P. Toth MD, PhD ,&nbsp;Paulo A. Lotufo MD, DPH ,&nbsp;Isabela M. Bensenor MD, PhD","doi":"10.1016/j.jacl.2025.02.015","DOIUrl":"10.1016/j.jacl.2025.02.015","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>This study analyzed the cross-sectional association of elevated concentrations of low-density lipoprotein particles (LDLp) and triglyceride-rich lipoprotein particles (TRLp) with carotid artery plaque (CAP) in the ELSA-Brasil cohort.</div></div><div><h3>METHODS</h3><div>Data from 3801 participants (median age: 50.0 years [IQR 44.0-57.0], 54.3% women) with no prior history of cardiovascular disease nor use of lipid-lowering medications were analyzed. CAP was assessed by ultrasonography, while nuclear magnetic resonance (NMR) spectroscopy was used to measure LDLp and TRLp concentrations according to size. Poisson regression models characterized the association of elevated lipid concentrations (≥1 SD above the mean) with CAP, adjusted for sociodemographic variables, cardiovascular risk factors, and for the concentration of high-density lipoprotein particles (HDLp), LDLp, and TRLp.</div></div><div><h3>RESULTS</h3><div>The frequency of CAP was 33.9% (<em>n</em> = 1,287). Elevated concentrations of total TRLp (prevalence ratio [PR]:1.05 [95% CI:1.01-1.10]) and small-sized TRLp (PR:1.23 [95% CI:1.11-1.36]) were associated with CAP, but lost significance after adjustment for LDLp. Elevated LDLp concentration was associated with CAP in total (PR:1.10 [95% CI:1.05-1.15]) and in all the different sizes (large [PR:1.09], medium [PR:1.11] and small [PR:1.09]), regardless of TRLp. When both LDLp and TRLp were simultaneously included in a dedicated model, only LDLp remained associated with CAP (PR:1.11 [95% CI: 1.06-1.16]). By particle size, elevated small TRLp and elevated LDLp in all sizes were associated with CAP even when mutually adjusted.</div></div><div><h3>CONCLUSION</h3><div>The elevated concentration of small TRLp seems to portend an incremental residual likelihood of prevalent CAP beyond LDLp, whereas the association of LDLp with CAP remained consistent beyond classical risk factors and NMR-assessed HDLp and TRLp concentration.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages 498-508"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Familial chylomicronemia syndrome caused by 2 genetic variants in the APOA5 gene: Severe hypertriglyceridemia that complicates pregnancy","authors":"Johnayro Gutiérrez MD ,&nbsp;Pablo Castaño MD ,&nbsp;Gregorio Fariña Msc ,&nbsp;Gabriela Berg PhD ,&nbsp;Jubby Marcela Gálvez MD ,&nbsp;Juan Patricio Nogueira MD, PhD","doi":"10.1016/j.jacl.2024.12.020","DOIUrl":"10.1016/j.jacl.2024.12.020","url":null,"abstract":"<div><div>A case of a 29-year-old female patient with a history of a single episode of hypertriglyceridemia-induced pancreatitis 4 years prior is reported. She had been treated with fibrates until 2 months before conception and required hospitalization at 33 weeks of gestation due to severe hypertriglyceridemia (6690 mg/dL) and gestational diabetes. Upon hospital admission, there was no evidence of pancreatitis. A comprehensive treatment approach was initiated, combining a low-fat diet, fibrates, omega-3 fatty acids (2 g/d), and continuous insulin infusion. This regimen resulted in a significant reduction of triglyceride levels to 960 mg/dL. The pregnancy progressed to full term without any maternal-fetal complications.</div><div>Genetic analysis revealed 2 compound heterozygous mutations in the <em>APOA5</em> gene, which encodes apolipoprotein AV. Notably, these specific mutations have not been previously reported as causative factors for familial chylomicronemia syndrome (FCS). The diagnosis of FCS was confirmed by the patient's markedly reduced lipoprotein lipase activity of 3.2%.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages 701-706"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triglyceride-rich lipoprotein sphingolipids are altered in primary hypertension: A pilot case-control study","authors":"Fazil M. Alidjan MD ,&nbsp;Sandra den Hoedt MSc ,&nbsp;Mardin Rashid MD ,&nbsp;Leonie C. van der Zee-van Vark BSc ,&nbsp;Gardi J. Voortman BSc ,&nbsp;Kristien Y. Dorst-Lagerwerf BSc ,&nbsp;Christina Christoffersen MD, PhD ,&nbsp;Melvin Lafeber MD, PhD ,&nbsp;Jeanine E. Roeters van Lennep MD, PhD ,&nbsp;Adrie J.M. Verhoeven PhD ,&nbsp;Edith C.H. Friesema PhD ,&nbsp;Monique T. Mulder PhD","doi":"10.1016/j.jacl.2025.03.014","DOIUrl":"10.1016/j.jacl.2025.03.014","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Sphingolipids modulate vascular function and alterations in plasma sphingolipid profiles have been associated with hypertension. Plasma sphingolipids, such as ceramides (Cer) and sphingosine-1-phosphate (S1P), are predominantly carried by lipoproteins.</div></div><div><h3>OBJECTIVE</h3><div>We compared sphingolipid profiles in plasma and isolated lipoproteins of patients with primary hypertension with those of normotensive controls.</div></div><div><h3>METHODS</h3><div>Blood was obtained from 19 patients with hypertension and 19 age- and sex-matched normotensive controls. S1P and the 7 most abundant Cer were quantified by liquid chromatography-tandem mass spectrometry in plasma and in lipoproteins.</div></div><div><h3>RESULTS</h3><div>Total plasma Cer were significantly higher in patients with hypertension compared to controls (14.3 ± 1.0 vs 11.9 ± 0.7 µM; <em>P</em> = .047), while there were no differences in plasma S1P levels (1.8 ± 0.1 vs 2.1 ± 0.1 µM; <em>P</em> = .128). Total Cer carried by patient triglyceride-rich lipoproteins (TRL; ie, predominantly very low-density lipoproteins) were also significantly higher (1.33 ± 0.15 vs 0.58 ± 0.10 µM; <em>P</em> = .001), which held for all Cer tested. Systolic blood pressure positively correlated with plasma levels of Cer(d18:1/20:0), and Cer(d18:1/24:1), and diastolic blood pressure positively correlated with total Cer, Cer(d18:1/18:0), Cer(d18:1/20:0) and Cer(d18:1/24:0). Relative to plasma Cer(d18:1/24:0), levels of Cer(d18:1/18:0), Cer(d18:1/20:0), and Cer(d18:1/24:1) were significantly higher in patients with hypertension than in controls.</div></div><div><h3>CONCLUSION</h3><div>Patients with hypertension display higher plasma Cer levels than normotensive controls, which is mainly explained by elevated concentrations in TRLs. Cer levels positively correlate with systolic and diastolic blood pressure, and ratios of Cer relative to Cer(d18:1/24:0) suggest an increased cardiovascular risk.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages 468-476"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative cardiovascular outcomes of statin monotherapy versus statin plus ezetimibe combination therapy in patients with atherosclerotic cardiovasc","authors":"M Kenan Rahima MD,&nbsp;Fernando Faxas MD,&nbsp;Kayode Oguniyi MD,&nbsp;Muayad Alzamara MD,&nbsp;Godbless Ajenaghughrure MD","doi":"10.1016/j.jacl.2025.04.024","DOIUrl":"10.1016/j.jacl.2025.04.024","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>The optimal lipid-lowering strategy for patients with atherosclerotic cardiovascular disease (ASCVD) remains debated. While statins are the cornerstone of therapy, the additional benefit of ezetimibe in real-world settings needs further investigation.</div></div><div><h3>Objective/Purpose</h3><div>To compare the clinical outcomes of patients with atherosclerotic cardiovascular disease (ASCVD) who were treated with statin monotherapy versus those treated with statin plus ezetimibe combination therapy in a real-world setting.</div></div><div><h3>Methods</h3><div>Using the TriNetX global federated health research network comprising 104 healthcare organizations, we conducted a retrospective cohort study comparing patients on statin monotherapy (n=119,338) versus statin plus ezetimibe (n=119,338) after propensity score matching. All patients had established ASCVD and LDL-C ≥ 70 mg/dL. The primary outcomes included death, cardiovascular events, and neurological outcomes over a 5-year follow-up period.</div></div><div><h3>Results</h3><div>After propensity score matching, baseline characteristics including hypertension (85.4% vs 85.3%), diabetes (46.3% vs 46.3%), and prior myocardial infarction (29.8% vs 29.6%) were well-balanced between groups. The statin plus ezetimibe group showed significantly lower risk across multiple outcomes compared to statin monotherapy: all-cause mortality (HR 1.445, 95% CI 1.412-1.480), dementia (HR 1.498, 95% CI 1.447-1.550), cardiac arrest (HR 1.332, 95% CI 1.263-1.404), and stroke (HR 1.253, 95% CI 1.202-1.306). More modest risk reductions were observed for atrial fibrillation (HR 1.132, 95% CI 1.110-1.154) and heart failure (HR 1.075, 95% CI 1.059-1.091), while ventricular tachycardia showed no significant difference between groups (HR 1.035, 95% CI 0.999-1.072).</div></div><div><h3>Conclusions</h3><div>In this large real-world study of ASCVD patients, combination therapy with statin plus ezetimibe was associated with significantly lower risks of mortality and major cardiovascular outcomes compared to statin monotherapy. These findings support the increased use of combination therapy in high-risk patients with ASCVD</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e17"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physician-reported reasons for not intensifying lipid-lowering therapy in patients with recent myocardial infarction","authors":"Benjamin Richter MD,&nbsp;Scott Hessen MD,&nbsp;Laney Jones PharmD,&nbsp;Dean Karalis MD","doi":"10.1016/j.jacl.2025.04.005","DOIUrl":"10.1016/j.jacl.2025.04.005","url":null,"abstract":"<div><h3>Funding</h3><div>This study was funded by Amgen.</div></div><div><h3>Background/Synopsis</h3><div>Clinical practice evidence indicates that patients with high risk of a secondary event after a recent myocardial infarction (MI) often do not receive guideline-recommended lipid-lowering therapy (LLT), leaving them at unnecessary cardiovascular risk. We implemented a quality initiative to evaluate and improve LLT prescribing according to the 2018 AHA/ACC/Multisociety guidelines that recommend LDL-C lower than 70 mg/dL for patients with very high ASCVD risk.</div></div><div><h3>Objective/Purpose</h3><div>This study assessed the reasons cardiologists selected for not following AHA/ACC/Multisociety LLT guidelines for patients with recent MI when alerted to best practice recommendations at the point of care.</div></div><div><h3>Methods</h3><div>From August 2020 to February 2021, our practice group (96 cardiologists, 35 locations) implemented a ‘hard stop’ best practice alert in the electronic health records (EHR) of patients with MI history within 12 months and elevated LDL-C (70 mg/dL or greater) or no LDL-C values within 6 months of the index visit. If the patient had no LDL-C within 6 months, clinicians were prompted to order an LDL-C test and schedule a follow-up visit. If LDL-C was current and elevated, clinicians received stepwise prompts to prescribe guideline-recommended LLT (high-intensity statin, ezetimibe, and PCSK9i) or provide a reason for not doing so. Reasons for not intensifying LLT were summarized by the type of intensification recommended.</div></div><div><h3>Results</h3><div>In 42% (244/587) of patients for whom the best practice alert was triggered, treatment was not intensified. In 53/244 (22%) of these patients, treatment was not intensified because the LDL-C was not current, and the physician was prompted to order an LDL-C test. LLT intensification was not followed in 86 patients when high-intensity statin was recommended, 16 patients when ezetimibe was recommended, and 142 patients when PCSK9i was recommended. The most common reasons physicians gave (Figure) for not adding high-intensity statins were intolerance (n=62/86, 72%) and patient refusal (n=14/86, 16%); the most common reasons for not adding ezetimibe were past intolerance (n=8/16, 50%) and no current LDL-C available (n=5/16, 31%); and the most common reasons for not adding PCSK9i were no current LDL-C available (n=42/142, 30%) and patient refusal (n=31/142, 22%).</div></div><div><h3>Conclusions</h3><div>For patients with an MI in the last 12 months, opportunities to intensify LLT and monitor LDL-C were frequently missed. In addition to a ‘hard-stop’ best practice alert in the EHR, additional strategies need to be explored to overcome common reasons for not intensifying LLT, including addressing adverse events/intolerance and better routine monitoring of LDL-C.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e2-e3"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipoprotein apheresis to address residual risk in recurrent atherosclerotic events","authors":"Anish Adhikari MB ChB,&nbsp;Eugenia Gianos MD,&nbsp;Caleb Wutawunashe MD,&nbsp;Guy Mintz MD,&nbsp;Mahima Mangla DO","doi":"10.1016/j.jacl.2025.04.052","DOIUrl":"10.1016/j.jacl.2025.04.052","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Optimal medical therapy may be insufficient in attenuating cardiovascular risk in individuals with elevated Lipoprotein(a) (Lp(a)). Lipoprotein apheresis can play a role in such cases.</div></div><div><h3>Objective/Purpose</h3><div>To describe a unique case of accelerated atherosclerosis refractory to aggressive LDL-C lowering.</div></div><div><h3>Methods</h3><div>Medical record review.</div></div><div><h3>Results</h3><div>A 66-year-old male, non-smoker, with controlled type 2 diabetes mellitus, familial hypercholesterolemia (FH), peripheral vascular disease, and recurrent acute coronary syndrome (ACS) presented to our lipid clinic. His mother had severe hyperlipidemia. Baseline lipid panel from 40 years prior showed a total cholesterol of 330 mg/dL and LDL-C of 220 mg/dL. He took rosuvastatin and ezetimibe for over 20 years. His first ACS event five years prior required a left anterior descending artery (LAD) stent. At this time, icosapent ethyl was added and his lipid profile was controlled with apolipoprotein B of 60 mg/dL. However, months later, he required carotid endarterectomy for severe carotid stenosis. Two years later, another LAD stent was placed for new disease in the setting of an LDL-C of 54 mg/dL. After this event, PCSK9 inhibitor was prescribed but denied by insurance. One year later, repeat lipid panel showed: LDL-C 37 mg/dL, apolipoprotein B 66 mg/dL, Lp(a) 297 nmol/L, and hs-CRP 2.6mg/L. PCSK9 inhibitor was denied again so bempedoic acid was added. Lipid apheresis was recommended but denied by insurance. The following year, he had severe two-vessel coronary disease including in-stent restenosis of a prior LAD stent, necessitating coronary artery bypass graft. Two days after surgery, evolocumab was approved and initiated. However, one month later, he required a stent to his bypass graft. Eventually he received insurance approval for lipoprotein apheresis and had significant LDL-C and Lp(a) reduction.</div><div>This case demonstrates that despite optimal lipid and anti-platelet therapy, risk factor control, and invasive treatment, recurrent ACS and plaque progression ensued. This was likely mediated by high Lp(a). Lipoprotein apheresis is the only FDA approved treatment for elevated Lp(a), now with an approved FDA indication for Lp(a) ≥ 60 mg/dL or ≥ 130 nmol/L with coronary or peripheral artery disease, noting a cardiovascular event reduction greater than 75% in such patients. Phase 3 trials are ongoing for Lp(a) lowering agents which will inform future treatment.</div></div><div><h3>Conclusions</h3><div>Patients with FH, elevated Lp(a) and hs-CRP represent an ultra high-risk profile for aggressive atherosclerosis. For our patient, delays in PCSK9 inhibitor and apheresis initiation likely influenced disease progression. Lipoprotein apheresis has demonstrated a reduction in cardiovascular events.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e37-e38"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of serum lipoprotein(a) and progression of structural heart disease: Insights from CARDIA study","authors":"Rishi Parikh MPH,&nbsp;Donald Jones MD,&nbsp;John Wilkins MD,&nbsp;Alan Go MD,&nbsp;Norrina Allen PhD,&nbsp;Catherine Shields BS,&nbsp;Mirasol Apostol-Largeteau MPH,&nbsp;Sascha Goonewardena MD,&nbsp;Venkatesh Murthy MD,&nbsp;David Jacobs PhD,&nbsp;Daniel Duprez MD,&nbsp;So Yi PhD,&nbsp;Joao Lima MD,&nbsp;Ankeet Bhatt MD,&nbsp;Zara Butte MD","doi":"10.1016/j.jacl.2025.04.029","DOIUrl":"10.1016/j.jacl.2025.04.029","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background/Synopsis&lt;/h3&gt;&lt;div&gt;Lipoprotein (a) [Lp(a)] is an atherothrombotic and inflammatory lipoprotein associated with atherosclerosis and arterial stiffness, which may contribute to heart failure (HF). Few studies have focused on its role in HF progression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Objective/Purpose&lt;/h3&gt;&lt;div&gt;This study assessed the association between Lp(a) measured in young adulthood and HF stages over 25 years in the Coronary Artery Risk Development in Young Adults Study (CARDIA) study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;We identified CARDIA study participants with Lp(a) measurements at Year 7 (ages 25-37). Lp(a) was categorized as normal (&lt; 75 nmol/L), intermediately elevated (75-124 nmol/L), or significantly elevated (&gt; 124 nmol/L), aligned with NLA guidelines. HF stages at Year 5 and Year 30 were defined according to the 2013 AHA/ACC guidelines: stage 0, without risk factors; stage A, HF risk factors; stage B, asymptomatic cardiac structural or functional abnormalities; and stage C/D, symptomatic or end-stage HF. Among those with available data to classify HF stage at Year 5, we evaluated the cross-sectional association between Lp(a) and HF stage. Among those with available HF stages at both Year 5 and Year 30, we evaluated the association between Lp(a) and the change in HF stage from Year 5 to Year 30 (&lt;em&gt;i.e.,&lt;/em&gt; no increase, increase by 1 stage, increase by 2 or more stages) using ordinal logistic regression. All models were stratified by race (Black vs White). Base models adjusted for age and sex, with additional adjustment for HF risk factors (SBP, diabetes, smoking status, total &amp; LDL cholesterol, lipid-lowering medication use).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We identified 3501 CARDIA participants with both Lp(a) at Year 7 and HF stage at Year 5. 2275 (65%) had normal Lp(a), 584 (16.7%) had intermediately elevated, and 642 (18.3%) had significantly elevated Lp(a) (Figure). At Y5, intermediately elevated Lpa was not associated with higher HF stage in Black (odds ratio [OR]: 1.14, 95% confidence interval [CI]: 0.9, 1.45) or White (OR: 1.10, 95% CI: 0.77, 1.58) participants (interaction p=0.58). Significantly elevated Lp(a) was also not associated with HF stage, and point estimates were slightly but not significantly stronger in White (OR: 1.27, 95% CI: 0.91, 1.78) than in Black (OR: 1.03, 95% CI: 0.82, 1.31) participants. Point estimates for White participants were attenuated after further adjustment for cardiovascular risk factors. Among 2140 participants with available HF stages at both Y5 and Y30, intermediate and significantly elevated serum Lp(a) were not associated with progression of HF stages from Y5 to Y30 in Black (intermediately elevated: 1.02, 95% CI: 0.76, 1.37, significantly elevated: 1.07, 95% CI: 0.81, 1.42) or White (intermediately elevated: 0.96, 95% CI: 0.68, 1.37, significantly elevated: 0.86, 95% CI: 0.6, 1.22) participants (interaction p=0.23).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Lp(","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e22"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipoprotein(a) screening for cardiac allograft vasculopathy among heart transplant recipients","authors":"Deepasree Bangaru-Raju MD,&nbsp;Dhivyashree Bangaru-Raju MD,&nbsp;Vi Nguyen PharmD,&nbsp;Shamim Khosrowjerdi BS,&nbsp;Sotirios Tsimikas MD,&nbsp;Jose Benjamin Cruz Rodriguez MD,&nbsp;Antoinette Birs MD,&nbsp;Andrew Kao MD","doi":"10.1016/j.jacl.2025.04.032","DOIUrl":"10.1016/j.jacl.2025.04.032","url":null,"abstract":"<div><h3>Background/Synopsis</h3><div>Lipoprotein(a) [Lp(a)] is a well-established inheritable risk factor of atherosclerotic cardiovascular disease (ASCVD) for which the National Lipid Association (NLA) recommends Lp(a) screening once in all adults. Heart transplant (HTx) recipients develop both cardiac allograft vasculopathy (CAV) hallmarked by a chronic but progressive coronary intimal thickening as well as atherosclerosis. While traditional ASCVD risk factors such as hypertension, diabetes, hyperlipidemia are stringently optimized among transplant recipients, the impact of Lp(a) on CAV development remains unknown.</div></div><div><h3>Objective/Purpose</h3><div>Elevated Lp(a), defined as level &gt; 50mg/dL, has been shown to confer development of ASCVD. The complex pathophysiology of early CAV is a result of both donor and recipients baseline risk factors, and post-transplant factors. This study aims to investigate the association of Lp(a) and early CAV development in HTx recipients.</div></div><div><h3>Methods</h3><div>A single-center, retrospective study analyzed 88 HTx recipients between 2015 to 2024 with measured Lp(a) and at least one post-HTx coronary angiogram with highly sensitive intravascular ultrasound (IVUS). The primary endpoint was CAV quantified by maximal intimal thickness (MIT) of 1mm and 1.5mm. Cox proportional hazard models were used to evaluate the association of elevated Lp(a) with MIT. The model was adjusted for key covariates: treated cytomegalovirus, rejection, LDL-cholesterol, high intensity statin use, donor ischemic time, BMI, and sex.</div></div><div><h3>Results</h3><div>A total of 24 (27.3%) of HTx recipients had an elevated Lp(a) &gt; 50 mg/dL; median Lp(a) was 17.5 [7.0, 34.0] and 91.5 [68.8, 128.5] mg/dL, respectively. Median follow-up time post HTx was 2.12 years [1.17, 4.04]. Baseline lipid profile and characteristics were similar between groups, Table 1. In univariate analysis, Lp(a) &gt; 50 mg/dL was not associated with MIT 1.5mm development (HR 1.9, 95% CI 0.49-7.60, p = 0.35), nor in multivariate analysis, (HR 2.36, 95% CI 0.45-12.4, p = 0.30; overall model p = 0.03). LDL-C &gt; 100 mg/dL was highly correlated with CAV outcomes (HR 4.7, p = 0.02).</div></div><div><h3>Conclusions</h3><div>Elevated Lp(a) was not associated with an increased risk for the early development of CAV as determined by IVUS. As elevated Lp(a) has been associated with increased long-term risk of angiographic disease, additional study is required to understand how cumulative exposure to elevated Lp(a) may contribute to this process. The complex relationship between Lp(a), the immune response to HTx, and CAV warrants further investigation.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Page e24"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary results of a multifaceted intervention to improve guideline-directed lipid-lowering therapy in patients with recent MI","authors":"Ning Rosenthal MD,&nbsp;Laney Jones PharmD,&nbsp;Cezary Wojcik MD,&nbsp;Ran Jin MD,&nbsp;Zachary Johnson BS,&nbsp;Leslie Carabuena MS,&nbsp;Edna Kavuma MPH,&nbsp;Rachel Mackey PhD","doi":"10.1016/j.jacl.2025.04.022","DOIUrl":"10.1016/j.jacl.2025.04.022","url":null,"abstract":"<div><h3>Funding</h3><div>This research (the LOGAN-CV study)was sponsored by Amgen Inc.</div></div><div><h3>Background/Synopsis</h3><div>Most patients with atherosclerotic cardiovascular disease (ASCVD) do not achieve guideline-recommended LDL-C &lt; 70 mg/dL. Effective interventions are urgently needed to reduce risk of recurrent CV events. Within the Premier, Inc. hospital network, we conducted a multicenter single-arm interventional study (LOGAN-CV) to improve lipid management in high-risk, post-myocardial infarction (MI) patients.</div></div><div><h3>Objective/Purpose</h3><div>To evaluate whether a 1-year multifaceted intervention improves lipid-lowering therapy (LLT) intensification and LDL-C control in statin-treated adults who had an MI in the past year and had uncontrolled LDL-C.</div></div><div><h3>Methods</h3><div>Clinicians with patients who met inclusion criteria (age ≥ 21, acute MI, statin treatment, LDL-C ≥ 70 mg/dL) during the year prior to start of the intervention were recruited from 7 sites. Clinician-focused interventions included custom cholesterol guideline and LLT education modules and a personalized dashboard of LDL-C and LLT-related patient metrics. Index date is the end of clinician education and baseline is 12 months before the index. This preliminary analysis includes the 2 sites that have completed the 1-year intervention.</div></div><div><h3>Results</h3><div>The 2 completed sites had 15 clinicians and 126 patients. Mean patient age was 65.7 years (SD=13.4), 56% were women, 63% white, 29% black, 36% had diabetes, 41% had obesity, and 54% had hypertension (Table). Patients’ most recent MI occurred a mean of 4.5 months (SD=3.1) prior to index, with 31% receiving PCI, 7.1% receiving CABG, and 62% medical management only. At index, majority of patients were prescribed moderate- (25%) or high-intensity (73%) statin. Ezetimibe was prescribed in 13% (n=17) of patients in combination with moderate- (n=3) or high- (n=14) intensity statin. During the 1-year intervention, 10% of patients had 1 recurrent MI and 21% had 2 recurrent MIs. LLT intensification occurred in 17% of patients (8.7% statin intensification, 4.8% ezetimibe addition, 3.2% PCSK9i mAb addition) (Figure). Only 64% (n=80) patients had LDL-C tests ordered. Median (Q1, Q3) LDL-C decreased from 90 (78, 110) mg/dL at index (n=126) to 71 (54, 94) mg/dL at month 12 of follow up (n=79), and 40/126 (32%) patients reached LDL-C control (&lt;70 mg/dl) in an average of 5.4 (SD=3.2) months, and 16% reached LDL-C &lt;55 mg/dL in an average of 6.3 (SD=3.2) months.</div></div><div><h3>Conclusions</h3><div>During a 1-year, multifaceted intervention to improve lipid management in patients with recent MI and uncontrolled LDL-C, 32% of patients reached the guideline-recommended LDL-C of &lt; 70 mg/dL. Additional efforts to this intervention are needed to improve LDL-C testing and LDL-C control in these high-risk patients to prevent recurrent events.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e15-e16"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144166974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of serum omega-6 polyunsaturated fatty acids with apolipoprotein B and atherogenic lipoprotein lipids","authors":"Carol Kirkpatrick PhD,&nbsp;Meredith Wilcox MPH,&nbsp;Liana Guarneiri PhD,&nbsp;Peter Attia MD,&nbsp;David Allison PhD,&nbsp;Kevin Maki PhD","doi":"10.1016/j.jacl.2025.04.086","DOIUrl":"10.1016/j.jacl.2025.04.086","url":null,"abstract":"<div><h3>Funding</h3><div>The Indiana University Foundation funded this research.</div></div><div><h3>Background/Synopsis</h3><div>Observational evidence supports associations between higher intakes of omega-6 polyunsaturated fatty acids (PUFAs) and reduced risk for atherosclerotic cardiovascular disease. Serum levels of total omega-6 PUFAs and linoleic acid (LA), the predominant dietary omega-6 PUFA, correlate with dietary LA intake.</div></div><div><h3>Objective/Purpose</h3><div>Aegis was a prospective cohort study that investigated immunological and other biomarker changes after incident severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This cross-sectional analysis of baseline data from the Aegis cohort examined the relationships between serum omega-6 PUFA (total and LA) levels and selected biomarkers of cardiovascular risk, including apolipoprotein B (apoB) and lipoprotein lipid concentrations.</div></div><div><h3>Methods</h3><div>Baseline fasting serum levels of omega-6 PUFAs, apoB, low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides were assessed. Multivariate linear models were used to assess biomarker levels across quintile categories of serum fatty acids with body mass index (BMI), age, and sex as covariates.</div></div><div><h3>Results</h3><div>Analyses included 1894 participants for whom relevant biomarker data were available (65% female, mean age: 50 y, mean BMI: 29.0 kg/m², 62% Non-Hispanic White, 11% Black/African American, 7% Hispanic/Latino, 10% Asian, 10% mixed/other). The 20^th and 80^th percentiles for omega-6 PUFAs as a percentage of total circulating fatty acids were 38.5% and 42.8%, respectively, and for LA were 31.3% and 36.4%, respectively. Least squares geometric means (LSGMs) in mg/dL for serum omega-6 PUFA level quintile (Q)1 and Q5, respectively, were: apoB, 101 and 90.1 (P &lt; 0.001); LDL-C, 107 and 100 (P = 0.069); non-HDL-C, 140 and 117 (P &lt; 0.001); and triglycerides, 184 and 69.0 (P &lt; 0.001). LSGMs for serum LA level Q1 and Q5, respectively, were: apoB, 90.5 and 105; LDL-C, 93.8 and 118; non-HDL-C, 122 and 138; and triglycerides, 151 and 89.1 (all P &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>A higher serum total omega-6 PUFA level was linked to a more favorable lipid profile, with lower concentrations of apoB, non-HDL-C, and triglycerides. However, a higher serum LA concentration was associated with a lower triglyceride concentration but higher apoB, LDL-C, and non-HDL-C concentrations, highlighting potential differential relationships for specific omega-6 PUFAs.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"19 3","pages":"Pages e62-e63"},"PeriodicalIF":3.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}