Journal of clinical lipidology最新文献

{"title":"Corrigendum to \"The prognostic value of high-density lipoprotein cholesterol in patients with decompensated cirrhosis: a propensity score matching analysis,\" (Journal of Clinical Lipidology [2022] 16, 325-334].","authors":"Binxin Cui, Gaoyue Guo, Yangyang Hui, Xiaoyu Wang, Wentian Liu, Chao Sun","doi":"10.1016/j.jacl.2026.09.011","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.011","url":null,"abstract":"","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110393","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":"Pharmacokinetic evidence of an abiraterone-rosuvastatin drug interaction resulting in rhabdomyolysis and acute kidney injury.","authors":"Erik Dove, Samson Peter, Hannah Lusk, Kara Lynch","doi":"10.1016/j.jacl.2026.09.025","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.025","url":null,"abstract":"<p><p>Statins are among the most common causes of medication-associated rhabdomyolysis. Abiraterone, an oral androgen biosynthesis inhibitor, has been reported to increase the risk of statin-associated muscle toxicity through inhibition of hepatic transporters involved in statin disposition, potentially increasing systemic statin exposure. Despite this proposed mechanism, direct pharmacokinetic evidence of this interaction in patients experiencing this adverse event has not previously been reported. We report a case of rhabdomyolysis complicated by acute kidney injury (AKI) in a patient on long-term rosuvastatin therapy following initiation of abiraterone for the treatment of prostate cancer. Quantitative plasma analysis using liquid chromatography-mass spectrometry demonstrated a rosuvastatin concentration substantially higher than concentrations observed with therapeutic dosing and consistent with previously reported toxic concentrations. This case provides pharmacokinetic support for a clinically significant abiraterone-rosuvastatin drug interaction and underscores the importance of medication review, early recognition of muscle toxicity, and consideration of alternative lipid-lowering strategies to preserve atherosclerotic cardiovascular disease (ASCVD) risk reduction in patients being treated with abiraterone. To our knowledge, this is the first reported case demonstrating markedly elevated plasma rosuvastatin concentrations in the setting of abiraterone-associated rhabdomyolysis.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216177","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":"NST-1024 for the treatment of very high triglycerides: A placebo-controlled, randomized, double-blind, 28-day clinical trial.","authors":"John Jp Kastelein, Tore Skjæret, Sophie Jeannin, Robin Beyusen, David A Fraser, Kevin C Maki","doi":"10.1016/j.jacl.2026.09.016","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.016","url":null,"abstract":"<p><strong>Background: </strong>NST-1024 is a semisynthetic eicosapentaenoic acid (EPA) derivative developed with the aim of achieving more potent triglyceride (TG) lowering effects as compared to unmodified EPA in conjunction with improved glycemic control.</p><p><strong>Objective: </strong>To evaluate the efficacy and safety of oral NST-1024 400 mg twice daily in patients with severe hypertriglyceridemia (sHTG) in a phase 2 proof-of-concept study.</p><p><strong>Methods: </strong>After a 2 to 4-week run-in period, men and women with TG levels ≥500 mg/dL and ≤ 2000 mg/dL were randomized to double-blind treatment with placebo or NST-1024 for 4 weeks. The primary endpoint was the % change from baseline in TGs at 4 weeks.</p><p><strong>Results: </strong>The evaluable population for efficacy analysis comprised 44 participants (NST-1024 [n = 23], placebo [n = 21]). At baseline, median TG (interquartile limits) levels were 730 (599-862) and 723 (611-863) mg/dL in the NST-1024 and placebo groups, respectively, and the median % changes after 4 weeks of treatment were -35.9% and -9.1%, respectively, a placebo-corrected change of -31.8% (P = .01). Treatment with NST-1024 significantly increased high-density lipoprotein cholesterol vs placebo (P = .04) with no significant difference between groups for non-high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, or apolipoprotein B. Fasting plasma glucose (least square [LS] mean difference -22 mg/dL, P = .01) and C-peptide (LS mean difference -398 pmol/L, P < .01) were both significantly reduced in NST-1024 treated patients vs placebo. NST-1024 was generally well tolerated.</p><p><strong>Conclusion: </strong>Treatment with oral NST-1024 400 mg twice daily significantly reduced TGs in patients with sHTG in conjunction with improvements in glycemic control. This trial was registered at www.</p><p><strong>Clinicaltrials: </strong>gov as NCT05889156.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110347","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":"To test or not to test: Indications and actionability in lipid genetics.","authors":"Robert A Hegele","doi":"10.1016/j.jacl.2026.09.023","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.023","url":null,"abstract":"","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182200","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":"Implementing genetics-based cascade testing for familial hypercholesterolemia in Colombia: Results from a pilot study and implications for national screening strategies.","authors":"Darwin Abril-León, Greizy López, Nancy Gelvez, Luisa Fernanda Gómez Navarro, Lenin Maldonado, Luz Mery Bernal, Martha L Tamayo","doi":"10.1016/j.jacl.2026.09.022","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.022","url":null,"abstract":"<p><strong>Background: </strong>Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder mainly caused by pathogenic variants in the LDLR gene, leading to elevated low-density lipoprotein cholesterol levels and an increased risk of premature cardiovascular disease. In Colombia, FH remains largely underdiagnosed because of the absence of systematic screening programs and structured cascade screening strategies.</p><p><strong>Objective: </strong>To evaluate the applicability of a genetic cascade screening strategy in Colombian families carrying pathogenic variants in LDLR in order to identify new cases and describe genotype-phenotype correlations.</p><p><strong>Methods: </strong>A descriptive pilot study was conducted in 5 families of index cases with a previous clinical and molecular diagnosis of FH. Cases were analyzed by Sanger sequencing targeting the previously identified variants c.11G>A (p.Trp4*), c.1246C>T (p.Arg416Trp), and c.1187-1_1187delinsTA. Clinical classification was performed using the Dutch Lipid Clinic Network (DLCN) score.</p><p><strong>Results: </strong>Twenty-five individuals from 5 families were evaluated, including 5 index cases and 20 relatives. Molecular testing confirmed FH in 12 of 20 relatives (60%) newly identified as carriers through cascade screening. Carriers of the same pathogenic variant tended to exhibit similar clinical and biochemical characteristics, suggesting a relatively homogeneous phenotype within individual families.</p><p><strong>Conclusion: </strong>This pilot study supports the feasibility and diagnostic utility of genetic cascade screening for FH in Colombian families. The identification of 12 previously undiagnosed carriers among 20 relatives (60%), including relatives with low DLCN scores, highlights the limitations of relying solely on clinical criteria and underscores the value of molecular diagnosis as part of a family-based detection strategy.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182140","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) identifies premature coronary artery disease in patients with low LDL-cholesterol: A large multicenter cohort study.","authors":"Yahya Bawahab, Vlad C Vasile","doi":"10.1016/j.jacl.2026.09.021","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.021","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] is a genetically determined, causal risk factor for atherosclerotic cardiovascular disease. Whether elevated Lp(a) is associated with premature coronary artery disease (pCAD) in young and middle-aged adults with low levels of low-density lipoprotein cholesterol (LDL-C) remains poorly characterized in real-world practice.</p><p><strong>Objective: </strong>To assess the association between elevated Lp(a) (≥50 mg/dL) and incident pCAD after comprehensive lipid adjustment, including among patients with LDL-C <100 mg/dL.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study across 3 Mayo Clinic sites of adults without prior CAD (males 18-50 years; females 18-60 years) who underwent Lp(a) testing (enrollment 2000-2020; follow-up through 2024). The exposure was Lp(a) ≥50 mg/dL; the outcome was incident pCAD. Multivariable Cox models were adjusted for LDL-C, high-density lipoprotein cholesterol, triglycerides, and standard risk factors, with competing-risk, multiple-imputation, and prespecified sensitivity analyses, including patients with LDL-C <100 mg/dL.</p><p><strong>Results: </strong>Among 35,622 patients (55.9% female; median age 46 years), 459 (1.3%) developed pCAD over a median of 6.0 years (incidence rate 1.85 per 1000 person-years; 95% CI, 1.69-2.03). Elevated Lp(a) was independently associated with pCAD (adjusted hazard ratio [HR] 1.40; 95% CI 1.12-1.74; P = .003), with a log-linear dose-response. The association did not weaken when LDL-C was low: among 10,949 patients with LDL-C <100 mg/dL, elevated Lp(a) carried a 67% higher adjusted risk (HR 1.67; 95% CI 1.15-2.43; P = .007). The Lp(a) × LDL-C interaction was nonsignificant (P = .571), indicating the effect was undiminished rather than amplified by low LDL-C.</p><p><strong>Conclusion: </strong>In young and middle-aged adults with low LDL-C, elevated Lp(a) is significantly associated with premature coronary risk that is not captured by conventional lipid panels. These real-world data support Lp(a) measurement at a younger age as a tool for individual risk reclassification, identifying patients who carry occult residual atherogenic risk and may benefit from emerging Lp(a)-targeted therapies.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182153","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":"Reduced LDL receptor expression and LDL uptake in lymphoblastoid cells from a patient with cholesteryl ester storage disease.","authors":"Maëlle Jan, Marie-Nathalie Lebel, Olivier Bluteau, Alain Carrié, Jean-François Perregaux, Soumeya Bekri, Jean-Pierre Rabès, Antonio Gallo, Mathilde Varret","doi":"10.1016/j.jacl.2026.09.018","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.018","url":null,"abstract":"<p><strong>Background: </strong>Lysosomal acid lipase deficiency (LAL-D) is characterized by severe dyslipidemia, including elevated low-density lipoprotein (LDL) cholesterol, despite activation of sterol-responsive pathways.</p><p><strong>Objective: </strong>We investigated whether altered receptor-mediated LDL catabolism may contribute to this phenotype.</p><p><strong>Methods: </strong>Epstein-Barr virus (EBV)-transformed lymphoblastoid cells from a patient with cholesteryl ester storage disease (CESD) homozygous for the LIPA Exon 8 Splice-Junction Mutation were compared with cells from heterozygous carriers, heterozygous familial hypercholesterolemia patients, and controls. LAL activity was measured using a fluorometric assay. LDL receptor (LDLR) surface expression and LDL internalization were assessed by flow cytometry.</p><p><strong>Results: </strong>CESD cells displayed markedly reduced LAL activity together with modest but significant reductions in LDLR surface expression and LDL internalization. Under low-serum conditions, LDLR gene expression was also significantly lower in CESD cells than in controls.</p><p><strong>Conclusion: </strong>These findings suggest that impaired LDLR-mediated LDL uptake may contribute to dyslipidemia in LAL-D, alongside previously reported alterations in lipoprotein production. Confirmation in additional patients and disease-relevant cellular models is required.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193867","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":"Real-world threshold-based eligibility for emerging lipoprotein(a)-targeted therapies in chronic and acute coronary syndrome.","authors":"Eva Steinacher, Johannes Bernhard, Felix Wollmann, Victoria Radl, Ulrike Baumer, Patrick Haider, Felix Hofer, Niema Kazem, Max Lenz, Rayyan Hemetsberger, Christian Hengstenberg, Alexander Niessner, Konstantin A Krychtiuk, Lorenz Koller, Walter S Speidl","doi":"10.1016/j.jacl.2026.09.017","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.017","url":null,"abstract":"<p><strong>Background: </strong>Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease. Phase 3 programs are evaluating Lp(a)-lowering therapies using high entry thresholds; however, the real-world prevalence of trial-aligned Lp(a) thresholds in secondary prevention remains uncertain.</p><p><strong>Objective: </strong>To assess the prevalence of trial-aligned Lp(a) thresholds, national apheresis criteria, and the prognostic impact of elevated Lp(a) in a contemporary percutaneous coronary intervention (PCI) cohort.</p><p><strong>Methods: </strong>Patients undergoing PCI at a tertiary center with Lp(a) reported in nmol/L were analyzed. The proportion meeting trial-aligned thresholds (≥150, ≥175, ≥200 nmol/L) and the European Society of Cardiology/European Atherosclerosis Society risk-enhancing threshold (≥105 nmol/L) was estimated. National apheresis criteria were applied. 5-year major adverse cardiovascular events (MACE) and target lesion failure (TLF) were assessed.</p><p><strong>Results: </strong>Among 5942 patients with PCI, 25.2% had Lp(a) ≥105 nmol/L, with progressively smaller proportions meeting higher thresholds: 18.4% ≥150 nmol/L, 14.8% ≥175 nmol/L, 11.6% ≥200 nmol/L. Lp(a) concentrations were similar in chronic and acute coronary syndrome (CCS and ACS) (CCS, median 28.0 [IQR 9.0-118.5] vs ACS, 25.0 [IQR 9.0-96.5] nmol/L; P = .117). 1.8% to 6.1% met national apheresis criteria. Over 5 years, higher Lp(a) was independently associated with risk of MACE (adjusted hazard ratio [HR] per 1 SD 1.06 [95% CI 1.01-1.12]; P = .015) and TLF (adjusted HR per 1 SD 1.05 [95% CI 1.00-1.10]; P = .044).</p><p><strong>Conclusion: </strong>Elevated Lp(a) was highly prevalent and independently predicted adverse 5-year outcomes in a contemporary PCI cohort. While a substantial proportion met trial-aligned Lp(a) thresholds for emerging therapies, few fulfilled apheresis criteria. Systematic Lp(a) testing may improve risk stratification and identify patients meeting trial-aligned Lp(a) thresholds for emerging therapies.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182185","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): Particle vs mass and prevalent cardiovascular disease in the cardiovascular risk in Young Finns study population.","authors":"Olli Raitakari, Matias Knuuti, Anna Linko-Parvinen, Katja Pahkala, Suvi Rovio, Noora Kartiosuo, Sini Stenbacka, Irina Lisinen, Britt-Marie Loo, Terho Lehtimäki, Mika Kähönen, Claudia Lamina, Florian Kronenberg, Markus Juonala, Jorma S A Viikari, Juha Mykkänen","doi":"10.1016/j.jacl.2026.09.019","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.019","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] can be reported as mass (mg/dL) or particle concentration (nmol/L). Because Lp(a) acts at the particle level, molar concentration may better reflect biologically relevant exposure.</p><p><strong>Objective: </strong>To compare molar- and mass-based Lp(a) in relation to cardiovascular outcomes, risk classification, LPA genetic variation, and apo(a) isoform phenotype in the Young Finns Study.</p><p><strong>Methods: </strong>Molar Lp(a) was measured using a traceable Roche Tina-quant Gen.2 assay and mass using a nontraceable Thermo Fisher assay. Associations with cardiovascular outcomes and aortic valve stenosis were assessed by logistic regression in adults aged ≥40 years (N = 3898). Agreement was assessed using Bland-Altman analysis and guideline-based risk reclassification. Associations with LPA genetic risk score and apo(a) isoform phenotype were assessed using Spearman correlation.</p><p><strong>Results: </strong>Both metrics showed similar associations across cardiovascular outcomes, with significant associations for coronary artery disease (CAD) and aortic valve stenosis. In fully adjusted CAD models, the odds ratio for the highest vs lowest quintile was 1.55 for molar and 1.67 for mass. Agreement between guideline-based risk categories was 95.6%. Molar assigned 2.9% of individuals to a higher risk category than mass, vs 1.5% in the opposite direction. The molar-to-mass ratio was associated with LPA score and apo(a) isoform size, with greater attenuation after adjustment for molar than mass.</p><p><strong>Conclusion: </strong>Molar and mass showed comparable associations with cardiovascular outcomes. However, molar reporting aligned more closely with the genetic and structural determinants of Lp(a) and more often assigned individuals to higher guideline-based risk categories, supporting continued standardization toward particle-based reporting.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193754","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) management simplified: The National Lipid Association lipid simplified series.","authors":"Marlys L Koschinsky, Christie M Ballantyne","doi":"10.1016/j.jacl.2026.09.013","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.09.013","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] is a unique apolipoprotein B-containing lipoprotein, similar to low-density lipoproteins. Plasma concentrations of Lp(a) are largely genetically determined. High Lp(a) levels are recognized as a causal and independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and are an important contributor to residual ASCVD risk. International guidelines reflect the importance of measuring Lp(a) at least once in all adults as an important component of ASCVD risk assessment and management.</p><p><strong>Objective: </strong>This document aims to summarize the guidelines recommending universal measurement of Lp(a), including the associated risk thresholds that can be used to identify individuals with higher ASCVD risk based on their plasma Lp(a) concentrations. Additionally, direction on managing patients with high Lp(a) is provided, as well as information on therapies in development to lower Lp(a).</p><p><strong>Methods: </strong>The most recent statements and updates from international societies were reviewed for guidance on Lp(a) measurement and management, with particular attention to the 2026 American College of Cardiology/American Heart Association multisociety guideline on the management of dyslipidemia. Information on pharmaceutical agents that are in late stages of development for targeted lowering of Lp(a) is also summarized.</p><p><strong>Results: </strong>The synthesis of existing information on how to manage patients with elevated Lp(a) reinforces the importance of measurement of Lp(a) in all adults at least once in their lifetime and provides direction on when repeated measurement may be warranted. In the absence of available drugs to specifically and effectively lower Lp(a), management of modifiable risk factors is encouraged. Furthermore, the large contribution of genetics to the determination of Lp(a) levels underscores the importance of cascade screening of family members to identify at-risk individuals.</p><p><strong>Conclusion: </strong>There is broad recognition of the importance of measuring Lp(a) at least once in all adults, owing to the recognized role of elevated Lp(a) as an important ASCVD risk enhancer. At present, this information is useful in risk stratification and can guide optimal management of ASCVD risk in patients. However, the potential for new Lp(a) lowering therapies to specifically and substantially reduce Lp(a) levels underscores the importance of Lp(a) measurement in all adults.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182203","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}