Journal of clinical lipidology最新文献

{"title":"Familial hypercholesterolemia cascade testing: Insights from the Dutch Program.","authors":"Bram M Weijs, Dennis Boor, Willemijn Corpeleijn, Sibbeliene E van den Bosch, Linda Zuurbier, G Kees Hovingh, Barbara A Hutten, Laurens F Reeskamp, Erik S G Stroes, Willemijn A M Schonck","doi":"10.1016/j.jacl.2026.08.027","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.027","url":null,"abstract":"<p><strong>Background and objective: </strong>Familial hypercholesterolemia (FH) is a prevalent genetic disorder causing lifelong elevated LDL-cholesterol and premature cardiovascular disease. After the Dutch national FH testing program ended in 2014, the Landelijk Expertisecentrum Familiaire Hypercholesterolemie (LEEFH) foundation continued testing with an 80% reduction in funding and a leaner model. This study evaluates the first 10 years of FH testing via LEEFH as a model for global FH testing initiatives.</p><p><strong>Methods: </strong>Cross-sectional study of retrospective data from the Dutch FH cascade testing program (LEEFH, 2014-2024). Outcomes included the number of individuals tested, diagnostic yield, relatives identified per index patient, temporal trends, and referral patterns. Geographic coverage was assessed by mapping testing data to postal codes and comparing detected cases with estimated FH prevalence.</p><p><strong>Results: </strong>31,487 individuals underwent genetic FH-testing. Annual testing increased from 1416 in 2014 to 4356 in 2024, while the annual yield of cascade testing increased from 165 to 541 FH-positive relatives. Diagnostic yield among index patients declined from 20.9% (236/1128) in 2014 10.0% (304/3044) in 2024 (P < .001), while yield among relatives remained close to 50% (56.9%-48.7%, P = .013). Cascade testing efficiency improved, from 0.69 to 1.78 FH-positive relatives per index case. The proportion of individuals aged <18 years identified through cascade testing was 41.4% in 2014 and 48.1% in 2024 (P = .138; P for trend = .006).</p><p><strong>Conclusion: </strong>The LEEFH cascade testing program effectively detects new FH cases through family cascade testing, with substantial public health impact. Updated insights into outcomes and efficiency may guide international FH testing efforts.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001952","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) across coronary plaque phenotypes from high-risk to layered plaque: An OCT analysis from the RELACS registry\".","authors":"Vincenzo Acerbo, Arturo Cesaro, Flavio Giuseppe Biccirè, Alexis F Guédon, Vincenzo De Sio, Antonio Capolongo, Matteo Conte, Silvio Coletta, Vincenzo Diana, Elisabetta Moscarella, Felice Gragnano, Italo Porto, Rocco Vergallo, Francesco Prati, Paolo Calabrò","doi":"10.1016/j.jacl.2026.08.021","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.021","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] is a causal risk factor for coronary artery disease, but its relationship with coronary plaque morphology assessed by optical coherence tomography (OCT) remains incompletely characterized.</p><p><strong>Objective: </strong>To investigate the association between circulating Lp(a) levels and OCT-defined coronary plaque phenotypes using a comprehensive segment-level approach.</p><p><strong>Methods: </strong>In this prospective single-center study (RELACS registry; NCT05496790), consecutive patients undergoing intracoronary OCT with available Lp(a) measurements were included. Coronary vessels were divided into 3 mm segments and analyzed for plaque characteristics. Lp(a) was primarily modeled as a continuous variable to assess its association with OCT-defined plaque phenotypes, including high-risk, layered, and fibrous plaques. High-risk plaque was defined as the presence of ≥2 criteria between lipid-rich plaque, thin-cap fibroatheroma (TCFA), and macrophages. Mixed-effects logistic regression models were used to account for within-patient clustering.</p><p><strong>Results: </strong>A total of 952 coronary segments from 50 patients were analyzed. Increasing Lp(a) levels were significantly associated with multiple features of plaque vulnerability, including TCFA, lipid-rich plaques, macrophages, and microchannels. In the multivariate mixed-effects analysis, higher Lp(a) levels were independently associated with a greater likelihood of high-risk plaque (odds ratios [OR] 1.31, 95% CI 1.16-1.48; P < .001) and layered plaques (OR 1.15, 95% CI 1.02-1.29; P = .024), whereas an inverse association was observed with fibrous plaques (OR 0.84, 95% CI 0.70-1.00; P = .047).</p><p><strong>Conclusion: </strong>Increasing Lp(a) levels were associated with OCT-defined coronary plaque phenotypes related to vulnerability and instability, including high-risk and layered plaques. Given the limited patient-level sample size, these findings should be considered exploratory and hypothesis-generating.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169539","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":"Uncovering dysbetalipoproteinemia in a patient initially diagnosed with familial hypercholesterolemia: The role of whole exome sequencing and longitudinal follow-up in diagnostic precision and care.","authors":"Sharon L T Pek, Sanjaya U Dissanayake, Hoe M Chen, E Shyong Tai, Subramaniam Tavintharan","doi":"10.1016/j.jacl.2026.08.028","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.028","url":null,"abstract":"<p><p>We report an 18-year-old woman with severe dysbetalipoproteinemia and apolipoprotein E (ApoE) deficiency. Laboratory evaluations showed total cholesterol level: 11.76 mmol/L (454.8 mg/dL); triglyceride (TG) level: 2.90 mmol/L (256.9 mg/dL), and a low-density lipoprotein cholesterol level: 8.18 mmol/L (316.3 mg/dL). Lipoprotein electrophoresis revealed elevated very-low-density lipoprotein (VLDL) cholesterol and VLDL TGs of 5.69 mmol/L (220 mg/dL) and 1.73 mmol/L (153 mg/dL), respectively. She had severe xanthomatosis, which cleared after lipid-lowering but recurred when medications were stopped. Her lipids markedly improved and remained at cholesterol targets on both atorvastatin 40 mg and ezetimibe 10 mg a day. Whole exome sequencing showed 2 novel APOE variants, c.43 + 3delA and c.754G>T, p.(Glu252Ter), with corresponding very-low levels of plasma apolipoprotein E. Familial segregation revealed that the proband carried monogenic biallelic variants in APOE and first-degree relatives heterozygous for the APOE variants. This case report highlights an unusual form of dysbetalipoproteinemia with severe ApoE deficiency associated with early onset of clinical manifestations, elevated remnant cholesterol, and a favorable therapeutic response to a combination of statins and ezetimibe.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110350","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":"Management of complex lipid disorders in a community lipid clinic setting: Implementing a multidisciplinary model.","authors":"Michael I Miyamoto, Carol Ko, Shih-Ting Chiu, Grace S Miyamoto, Christine Coy, Sainaz Mumtaz, Arthur H Loussararian, Fatima El-Haj-Ibrahim, Sandra M Brown","doi":"10.1016/j.jacl.2026.08.022","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.022","url":null,"abstract":"<p><strong>Background: </strong>Large treatment gaps exist in the management of lipid disorders, and many high-risk patients have factors that complicate management efforts. While lipid clinics exist within academic medical centers, most of these patients are cared for in community settings.</p><p><strong>Objective: </strong>To report our experience and results managing challenging and complex lipid disorders in a community-based lipid clinic.</p><p><strong>Methods: </strong>We established a specialized lipid clinic in a community medical setting, with a focus on patients with management challenges and/or suspicion of a genetic lipid disorder, employing a multidisciplinary approach to optimize patient outcomes, emphasizing appropriate medical therapies and lipid genetic testing in selected patients. Retrospective electronic health record data were collected to analyze patient characteristics, treatment patterns, and lipid results.</p><p><strong>Results: </strong>Over the period 2022 through 2024, 183 patients were seen (mean 63 years, 62% female). The challenging nature of the patient population was highlighted by high rates of statin intolerance (50%), no lipid medical therapy at baseline (50%), and comorbidities (atherosclerotic cardiovascular disease [ASCVD], diabetes, and/or hypertension-61%). Despite this, over a mean follow-up of 9.4 ± 7.3 months, we observed a mean low-density lipoprotein cholesterol decrease of 49 mg/dL (-24.5%, P < .001), along with significant decreases in total cholesterol and triglycerides. Pathogenic dyslipidemia genetic variants were discovered in 21 patients (of 105 tested). Significant lipid improvements in the whole cohort, as well as multiple subgroups, were associated with greater utilization of combination therapies.</p><p><strong>Conclusion: </strong>Patients with complex lipid disorders can be successfully managed within a specialized lipid clinic in community medical settings. Applying such a multidisciplinary model outside of traditional academic medical centers offers the potential to raise the level of lipid management and ASCVD prevention more broadly in larger populations.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990075","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":"Current challenges in diagnosing homozygous familial hypercholesterolemia: Insights from the historical evolution of diagnostic criteria.","authors":"Daniel Gaudet, Richard Godin, Robert S Rosenson, Gerald F Watts","doi":"10.1016/j.jacl.2026.08.024","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.024","url":null,"abstract":"<p><strong>Background: </strong>Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by dysfunctional low-density lipoprotein receptors (LDLR) and markedly elevated low-density lipoprotein cholesterol (LDL-C) from birth. Cumulative exposure to elevated LDL-C results in premature atherosclerotic cardiovascular disease (ASCVD) and death, but early effective treatment can restore near-normal life expectancy. Unfortunately, HoFH is severely underdiagnosed and undertreated, perhaps because of a lack of awareness and confusion around diagnostic criteria.</p><p><strong>Sources of material: </strong>This historical narrative reviews the evolution of HoFH diagnosis, drawing on key milestones in the field.</p><p><strong>Abstract of findings: </strong>The HoFH diagnostic journey began in 1939 when Müller linked xanthomas, elevated cholesterol, and coronary heart disease with a dominant inheritance pattern. From here to the 1970s, diagnosis was focused on phenotypic observation. The genetic era (1970s to 2000s) began with a series of studies linking 2 identical pathogenic mutations in LDLR to HoFH. The 1990s to early 2000s saw the emergence of numerous clinical criteria and scoring systems, driven by availability and sensitivity issues around genetic testing. Today's contemporary guidelines recommend that a diagnosis should be made based on a combination of clinical criteria, including LDL-C, physical manifestations, and family history; genetic testing is not required for diagnosis.</p><p><strong>Conclusion: </strong>As the diagnosis of HoFH continues to evolve, future diagnostic criteria should place less emphasis on genetics and greater emphasis on modern clinical applications. These changes will help ensure that all individuals with HoFH have access to the most appropriate therapies to reduce their risk of premature ASCVD and death resulting from prolonged exposure to elevated LDL-C levels.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149061409","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":"Predictors of aortic stenosis in homozygous familial hypercholesterolemia: A study from the Canadian HoFH registry.","authors":"Martine Paquette, Armen Erzingatzian, Isabelle Ruel, Zobaida Al-Baldawi, Leslie Brown, Mark H Sherman, Nathalie Laflamme, Jean Bergeron, Patrick Couture, Diane Brisson, Miriam Larouche, Daniel Gaudet, Lubomira Cermakova, Darryl Wan, Nathaniel Moulson, Gordon A Francis, G B John Mancini, Brooke A Kennedy, Robert A Hegele, Gary F Lewis, Brian W McCrindle, Barbara Cifra, Thomas Ransom, Ruth McPherson, Jacques Genest, Liam R Brunham, Iulia Iatan, Alexis Baass","doi":"10.1016/j.jacl.2026.08.023","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.023","url":null,"abstract":"<p><strong>Background: </strong>Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disease of low-density lipoprotein cholesterol (LDL-C) metabolism. This disease is associated with a major risk of both atherosclerotic cardiovascular disease and aortic stenosis (AS). The predictors of AS in this population are not well established.</p><p><strong>Objective: </strong>To investigate the univariable and multivariable predictors of AS in patients from the Canadian HoFH registry.</p><p><strong>Methods: </strong>Individuals from the Canadian HoFH registry were included in this retrospective longitudinal study. Clinical data were obtained from the treating physicians using a standardized questionnaire. Cox proportional hazards models were used to investigate the predictors of AS. The observed lifetime risk of AS was calculated using Kaplan-Meier estimates.</p><p><strong>Results: </strong>Among the 67 patients with HoFH, 25 (37%) developed AS. The mean age at baseline was 22 ± 17 years and women represented 57% of the cohort. The independent predictors of AS were the baseline LDL-C (hazard ratio [HR] 1.22 [1.09-1.35], P = .0003) as well as the presence of at least 1 null genetic variant (HR 3.73 [1.41-9.86], P = .008). Having a baseline LDL-C value above 13 mmol/L was associated with an observed lifelong risk of developing AS approaching 100% within this cohort, whereas having a value below this threshold was associated with a risk of 27% (P = .0002).</p><p><strong>Conclusion: </strong>This is the first systematic evaluation within a national HoFH registry to report the univariable and multivariable predictors of AS in patients with HoFH. An external validation of our results in an international cohort of HoFH is warranted.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990127","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) and subclinical atherosclerosis.","authors":"Apurva Khedagi, Yusi Gong, Gourisree Dharmavaram, Harpreet S Bhatia","doi":"10.1016/j.jacl.2026.08.025","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.025","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease.</p><p><strong>Sources of material: </strong>Literature review.</p><p><strong>Abstract of findings: </strong>A large body of evidence has established the association between Lp(a) and subclinical atherosclerosis. In particular, Lp(a) is associated with coronary artery calcium (CAC), coronary artery plaque identified by coronary computed tomography angiography (CCTA), and carotid artery plaque. Lp(a) is more strongly associated with noncalcified coronary artery plaque than calcified plaque. In addition, CAC scoring has demonstrated utility for risk stratification among individuals with elevated Lp(a). The role of CCTA and carotid imaging to risk-stratify individuals with elevated Lp(a) in a primary prevention setting remains to be established.</p><p><strong>Conclusions: </strong>Lp(a) is associated with subclinical atherosclerosis, and imaging for subclinical atherosclerosis is useful for risk-stratifying individuals with elevated Lp(a).</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944805","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) variability in high cardiovascular risk individuals with hypertriglyceridemia and controlled LDL-C on statin therapy in REDUCE-IT.","authors":"Michael Szarek, Deepak L Bhatt, Michael Miller, Eliot A Brinton, Jean-Claude Tardif, Christie M Ballantyne, Steven B Ketchum, Armando Lira Pineda, Ph Gabriel Steg, Terry A Jacobson, R Preston Mason","doi":"10.1016/j.jacl.2026.08.020","DOIUrl":"https://doi.org/10.1016/j.jacl.2026.08.020","url":null,"abstract":"<p><strong>Background: </strong>Although repeated testing of lipoprotein(a) [Lp(a)] is generally not recommended because of the genetically determined nature of concentrations, reports of significant intraindividual variability in serial assessments have challenged the single lifetime measurement framework.</p><p><strong>Objective: </strong>To determine sources of Lp(a) variability among individuals with elevated triglyceride levels and well-controlled low-density lipoprotein cholesterol (LDL-C).</p><p><strong>Methods: </strong>Using Lp(a) assessments at baseline, month 12, and month 24 from participants in the Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial (REDUCE-IT), we identified characteristics that could support repeated testing.</p><p><strong>Results: </strong>Among 386 participants with baseline Lp(a) 50 to <70 mg/dL, 140 (36.3%) had at least 1 subsequent assessment ≥70 mg/dL, whereas among 630 participants with baseline Lp(a) ≥70 mg/dL, 133 (21.1%) had at least 1 subsequent assessment <70 mg/dL. Baseline Lp(a), sex (female vs male), race, and several other characteristics were related to variability.</p><p><strong>Conclusion: </strong>Among individuals at high cardiovascular risk with hypertriglyceridemia and controlled LDL-C on statin therapy, considerable variability was observed over 24 months. These findings suggest multiple assessments may be warranted for Lp(a)-related risk stratification and, potentially, eligibility for Lp(a)-targeted treatments, particularly among individuals with relatively high concentrations or certain demographic and clinical characteristics.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982909","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":"Effectiveness, safety, and treatment persistence of bempedoic acid in a Spanish real-world cohort","authors":"David León-Jiménez MD,&nbsp;Sergio Martínez-Hervás MD, PhD,&nbsp;Nagore Lois-Martínez MD,&nbsp;Carlos Jericó-Alba MD,&nbsp;María Jesús Martínez-Soriano MD,&nbsp;Meritxell Royuela-Juncadella MD,&nbsp;Anabel Franco-Moreno MD,&nbsp;Gemma Rodríguez-Carnero MD,&nbsp;José F. Varona MD, PhD,&nbsp;Alberto Muela-Molinero MD, PhD,&nbsp;Rocío García-Alonso MD,&nbsp;Jesús Castiella-Herrero MD,&nbsp;Miguel Cainzos-Achirica MD, PhD,&nbsp;Analía Ramos MD,&nbsp;Gema Gutiérrez-Lara MD,&nbsp;José Pablo Miramontes-González MD, PhD,&nbsp;Paula Luque-Linero MD,&nbsp;Miguel Ángel Vázquez-Ronda MD,&nbsp;Ana Torres-Do-Rego MD,&nbsp;Pablo González-Bustos MD,&nbsp;Carlos Puig-Jové MD, PhD","doi":"10.1016/j.jacl.2026.07.033","DOIUrl":"10.1016/j.jacl.2026.07.033","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>Bempedoic acid (BA) is an oral adenosine triphosphate-citrate lyase inhibitor that reduces low-density lipoprotein cholesterol (LDL-C) and is particularly relevant in patients with statin intolerance. However, real-world evidence on its effectiveness and safety remains limited.</div></div><div><h3>OBJECTIVE</h3><div>To assess the effectiveness, safety, and treatment persistence of BA in a multicenter Spanish real-world cohort.</div></div><div><h3>METHODS</h3><div>This retrospective observational study included 814 patients treated with BA across 21 vascular risk units in Spain. Lipid and laboratory parameters were evaluated at baseline and after 3 months. Generalized mixed models were used to estimate adjusted marginal means and treatment effects.</div></div><div><h3>RESULTS</h3><div>BA significantly reduced total cholesterol (207.4-167.8 mg/dL; −19.1%) and LDL-C (121.3-86.5 mg/dL; −28.8%) (both <em>P</em> &lt; 0.001). Smaller reductions were observed for high-density lipoprotein cholesterol (−3.9%) and triglycerides (−2.4%), while high-sensitivity C-reactive protein decreased nonsignificantly (−13.7%; <em>P</em> = 0.102). Uric acid increased (+11.4%; <em>P</em> &lt; 0.001). LDL-C reduction was consistent across subgroups, with greater absolute reductions in patients with statin intolerance (−43.2 vs −26.7 mg/dL; <em>P</em> for interaction = 0.046). Concomitant ezetimibe use was associated with numerically greater LDL-C reduction without significant interaction. Patients receiving proprotein convertase subtilisin/kexin type 9 inhibitors or inclisiran achieved lower LDL-C levels and greater reductions. The discontinuation rate was 4.18%, mainly because of gastrointestinal symptoms and myalgias.</div></div><div><h3>CONCLUSION</h3><div>In routine clinical practice, BA is an effective and generally well-tolerated lipid-lowering therapy, particularly in patients with statin intolerance or requiring combination treatment. These findings support its use as an effective lipid-lowering option in patients with statin intolerance or requiring combination therapy.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 9","pages":"Pages 1933-1945"},"PeriodicalIF":6.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712650","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 lipoprotein(a) with renal and cardiac outcomes in chronic kidney disease: a nationwide cohort study","authors":"Fan Luo MD,&nbsp;Xian Shao MD,&nbsp;Yuxin Lin MD,&nbsp;Mingzhen Pang MD,&nbsp;Shiyu Zhou MS,&nbsp;Ruixuan Chen MD,&nbsp;Caoxiang She MD,&nbsp;Bianxiang Hu MD, PhD,&nbsp;Xin Xu MD, PhD,&nbsp;Sheng Nie MD, PhD","doi":"10.1016/j.jacl.2026.06.027","DOIUrl":"10.1016/j.jacl.2026.06.027","url":null,"abstract":"<div><h3>BACKGROUND</h3><div>The role of lipoprotein(a) [Lp(a)] in chronic kidney disease (CKD) remains incompletely defined.</div></div><div><h3>OBJECTIVE</h3><div>This study aimed to investigate the association of Lp(a) with renal and cardiac outcomes in CKD.</div></div><div><h3>METHODS</h3><div>Patients with CKD were identified from the China Renal Data System, a joint initiative of the National Clinical Research Center for Kidney Disease and the China Center for Disease Control and Prevention. The primary outcome was a composite of CKD progression (kidney failure, &gt;40% estimated glomerular filtration rate [eGFR] decline, or kidney replacement therapy). The secondary outcome was cardiovascular (CV) mortality.</div></div><div><h3>RESULTS</h3><div>Among 27,037 and 52,895 participants assessed for renal and cardiac outcomes, 4608 (12.4%) and 4768 (9.0%) experienced the renal and cardiac outcome, respectively, over a median follow-up of 24 and 47 months. Positive and linear relationships were observed between log-Lp(a) and CKD progression and between Lp(a) and CV mortality. Lp(a) ≥30 mg/dL was associated with an elevated risk of CKD progression (adjusted hazard ratio [aHR], 1.13, 95%CI, 1.06, 1.21) and CV mortality (aHR, 1.14, 95%CI, 1.08, 1.22); these associations persisted after adjusting for time-varying covariates and were evident in individuals with low LDL-C levels. High Lp(a) levels were associated with both increased risk of end-stage kidney disease and faster decline in eGFR. Incorporating Lp(a) into the established prediction models enhances predictive performance and risk stratification capability for renal and cardiac outcomes.</div></div><div><h3>CONCLUSION</h3><div>Elevated Lp(a) may potentially serve as a target for kidney and CV protection. It is recommended that future interventional studies be conducted in this high-risk population.</div></div>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":"20 9","pages":"Pages 1954-1964"},"PeriodicalIF":6.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148549374","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}