Journal of clinical lipidology最新文献

{"title":"Exploring the correlation between triglyceride levels and atherosclerotic cardiovascular disease prevalence in adults with familial hypercholesterolemia: Insights from a cross-sectional analysis in the HELLAS-FH registry.","authors":"Panagiotis Anagnostis, Christos V Rizos, George Liamis, Loukianos Rallidis, Ioannis Skoumas, Genovefa Kolovou, Konstantinos Tziomalos, Emmanouil Skalidis, Anastasia Garoufi, Vasileios Kotsis, Michalis Doumas, George Sfikas, Vaia Lambadiari, Georgia Anastasiou, Ermioni Petkou, Estela Kiouri, Κonstantinos A Papathanasiou, Ioanna Dima, Vana Kolovou, Evangelos Zacharis, Christina Antza, Chrysoula Boutari, Charalambos Koumaras, Amalia Boufidou, Haralampos Milionis, Evangelos Liberopoulos","doi":"10.1016/j.jacl.2024.12.017","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.017","url":null,"abstract":"<p><strong>Background: </strong>High triglyceride (TG) levels are associated with increased atherosclerotic cardiovascular disease (ASCVD) risk in the general population. Yet, the role of TG in familial hypercholesterolemia (FH) remains understudied. This research aims to evaluate the link between TG levels and ASCVD prevalence in adult patients with FH.</p><p><strong>Methods: </strong>This cross-sectional analysis, derived from the Hellenic Familial Hypercholesterolemia Registry (HELLAS-FH), involves categorizing patients into tertiles based on their TG concentrations.</p><p><strong>Results: </strong>In our study of 1772 adults with heterozygous FH (HeFH), aged 51 ± 15 years at registration and diagnosed at 44 ± 16 years, TG concentrations in the 1st (80 mg/dL), 2nd (124 mg/dL), and 3rd (200 mg/dL) tertiles revealed varying ASCVD prevalence (18.0%, 28.5% and 28.5%, respectively). Adjusted for ASCVD risk factors, TGs ≥116 mg/dL were linked to higher ASCVD risk than levels <116 mg/dL (OR: 1.37, 95% CI 1.05-1.80, P = .02).</p><p><strong>Conclusions: </strong>A notable association with ASCVD is evident in FH patients, even at relatively low TG levels, starting from 116 mg/dL (1.31 mmol/L).</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074742","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":"Lipid-lowering efficacy of obicetrapib: A comprehensive systematic review and meta-analysis.","authors":"Walter Masson, Leandro Barbagelata, Martin Lobo, Juan Patricio Nogueira, Yehuda Handelsman","doi":"10.1016/j.jacl.2024.12.016","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.016","url":null,"abstract":"<p><strong>Background: </strong>Obicetrapib is a next-generation, oral, selective cholesteryl ester transfer protein inhibitor known to significantly affect atherogenic lipoproteins, including low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), non-high-density lipoprotein cholesterol (Non-HDL-C), and lipoprotein(a) [Lp(a)].</p><p><strong>Objective: </strong>To evaluate the lipid-lowering efficacy of obicetrapib based on available evidence.</p><p><strong>Methods: </strong>This systematic review was drafted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A comprehensive literature search was conducted to identify randomized clinical trials assessing the lipid-lowering effects of obicetrapib compared to placebo. Fixed- and random-effects models were used.</p><p><strong>Results: </strong>Five randomized clinical trials (n = 288 patients) were included in this analysis. Patients treated with obicetrapib exhibited significantly greater reductions in LDL-C (mean difference [MD]: 41.4% [95% CI: 45.7 to -37.1]; I²: 6%), ApoB (MD: 26.5% [95% CI: 31.3 to -21.6]; I²: 45%) and Non-HDL-C (MD: 34.5% [95% CI: 37.0 to -31.6]; I²: 80%) compared to those receiving a placebo. Additionally, HDL-C levels were significantly higher in the obicetrapib group (MD: 157.4% [95% CI: 142.2 to 172.6]; I²: 69%). While triglyceride levels did not differ significantly between the 2 groups, Lp(a) levels were notably reduced with obicetrapib treatment (MD: 39.5% [95% CI: 54.6 to -24.3]; I²: 67%).</p><p><strong>Conclusion: </strong>Obicetrapib is associated with significant reductions in key atherogenic lipoproteins, including LDL-C, ApoB, Non-HDL-C and Lp(a). Further investigation is needed to assess its impact on cardiovascular risk.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074741","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":"Differential effects of volanesorsen on apoC-III, triglycerides and pancreatitis in familial chylomicronemia syndrome diagnosed by genetic or non-genetic criteria.","authors":"Sotirios Tsimikas, Henry N Ginsberg, Veronica J Alexander, Ewa Karwatowska-Prokopczuk, Andy Dibble, Lu Li, Joseph L Witztum, Robert A Hegele","doi":"10.1016/j.jacl.2024.12.018","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.018","url":null,"abstract":"<p><strong>Background: </strong>Familial chylomicronemia syndrome (FCS) is diagnosed by genetic or non-genetic criteria.</p><p><strong>Objective: </strong>To assess responses to treatment of apolipoprotein (apo)C-III, triglycerides, and pancreatitis events in patients with FCS-based diagnostic methods.</p><p><strong>Methods: </strong>APPROACH enrolled 66 patients with FCS randomized to volanesorsen or placebo for 12 months. In 50 participants, genetic confirmation of FCS was based on the presence of pathogenic bi-allelic variants in LPL, APOC2, APOA5, GPIHBP1, or LMF1 genes. In 16 participants without a genetic diagnosis, FCS was diagnosed using clinical criteria and post-heparin lipoprotein lipase activity ≤20 % of normal. Plasma levels of apoC-III, triglycerides and related variables were measured at 3, 6 and 12 months.</p><p><strong>Results: </strong>No significant differences were present in mean apoC-III reductions with volanesorsen at 3, 6 or 12 months in patients with FCS diagnosed either genetically or non-genetically. In contrast, the triglyceride reductions were statistically less robust in patients with genetic diagnosis at each timepoint, with mean (95 % confidence interval) percent reduction in triglycerides of -68.7 % (-78.7, -58.6) vs. -84.0 % (-99.4, -68.6), p = 0.014 at Month 3; -58.2 % (-78.1, -38.2) vs. -84.5 % (-122.4, -46.7), p = 0.009 at Month 6; and -35.6 % (-57.7, -13.4) vs. -69.0 % (-105.0, -33.1), p = 0.005 at Month 12. Patients with a genetic diagnosis had significantly lower response rates for achieved triglycerides <500 mg/dL, <750 mg/dL, <880 mg/dL and <1000 mg/dL than patients with a non-genetic diagnosis. All 5 episodes of acute pancreatitis occurred in patients with a genetic diagnosis.</p><p><strong>Conclusions: </strong>For a similar reduction in apoC-III in response to volanesorsen, triglyceride reduction is attenuated in patients with genetically versus non-genetically diagnosed FCS.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028337","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":"Effect of empagliflozin on plasma lipids and lipoproteins in type 2 diabetes and heart failure - Empire HF and SIMPLE.","authors":"Frida Emanuelsson, Jesper Jensen, Massar Omar, Mikkel Jürgens, Caroline Kistorp, Niels H Brandt-Jacobsen, Jacob Eifer Møller, Morten Schou, Louise Ellegaard Bechmann, Emil List Larsen, Børge G Nordestgaard, Marianne Benn","doi":"10.1016/j.jacl.2024.12.015","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.015","url":null,"abstract":"<p><strong>Objective: </strong>Beyond glucose-lowering, sodium-glucose co-transporter 2 (SGLT2) inhibitors have cardioprotective effects with unclear mechanisms. We examined changes in an extensive panel of plasma lipids, lipoproteins, and apolipoproteins and whether these changes were independent of weight loss, hemoglobin A1c, and hematocrit in patients treated with empagliflozin versus placebo to better understand the observed cardioprotective effects.</p><p><strong>Methods: </strong>Post-hoc analyses of two double-blind, placebo-controlled trials, the Empire HF trial including 190 patients with heart failure and reduced ejection fraction and the SIMPLE trial including 90 patients with type 2 diabetes randomized to, respectively, 10 mg and 25 mg empagliflozin daily or placebo for 12 weeks.</p><p><strong>Results: </strong>In studies combined, empagliflozin reduced age and sex adjusted body weight by 1.40 kg (SEM: 0.10; p < 0.001) and hemoglobin A1c by 2.71 mmol/mol (SEM: 0.24; p < 0.001); and increased hematocrit by 1.9% (SEM: 0.12; p < 0.001) compared to placebo. No mean changes were seen in concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, small dense LDL cholesterol, very low-density lipoprotein cholesterol, triglyceride rich lipoprotein cholesterol, non-high-density lipoprotein (non-HDL) cholesterol, apolipoprotein B, lipoprotein(a), HDL cholesterol, and triglycerides adjusted for body weight, hemoglobin A1c, and hematocrit with empagliflozin compared to placebo.</p><p><strong>Conclusion: </strong>Empagliflozin treatment reduced body weight and hemoglobin A1c; and increased hematocrit. No changes were seen in concentrations of lipids and lipoproteins with empagliflozin compared to placebo. This suggests that the cardioprotective effects of SGLT2 inhibitors are independent of lipid and lipoprotein concentrations.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023627","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":"Non-fasting triglyceride screening in volunteer blood donors: A pilot program.","authors":"Caroline Abe, Emily Decicco, Stephen Eason, Frances Compton, Merlyn Sayers, Sukh Makhnoon, Michelle L Xing, Chao Xing, Amit Khera, Zahid Ahmad","doi":"10.1016/j.jacl.2024.12.013","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.013","url":null,"abstract":"<p><p>This pilot study explores the feasibility of large-scale non-fasting triglyceride level screening at blood donation centers. Hypertriglyceridemia is a risk factor for cardiovascular disease and acute pancreatitis. Triglyceride levels were measured in 10,176 blood donors at Carter BloodCare North Texas and found 39.2% with moderate and 2.4% with severe hypertriglyceridemia. Predictors of elevated triglycerides included age, male gender, blood pressure, and body mass index, with increased odds in Hispanic and Asian individuals compared to White individuals. Survey results from 50 donors with severe hypertriglyceridemia showed 69% had positive intent to seek medical care. The study highlights the potential of blood donation centers to serve as platforms for public health screening, and scaling low-cost, non-fasting triglyceride screening is feasible. This approach provides an opportunity for early intervention and disease prevention.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039017","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":"A novel variant in the ABCA1 gene for Tangier Disease with diffuse histiocytosis of bone marrow.","authors":"Ana Rita Ramalho, Sónia Moreira, Lina C Ramos, José Pereira de Moura","doi":"10.1016/j.jacl.2024.12.008","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.008","url":null,"abstract":"<p><p>Tangier disease is an extremely rare autosomal recessive monogenic disorder caused by mutations in the ATP binding cassette transporter A1 gene (ABCA1). It is characterized by severe deficiency or absence of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-1 (ApoA1), with highly variable clinical presentations depending on cholesterol accumulation in macrophages across different tissues. We report a case of a 47-year-old man with very low HDL-C and very high triglyceride levels, initially attributed to the patient's metabolic syndrome, alcohol abuse, and splenomegaly. He had pancytopenia and splenomegaly for over fourteen years and developed premature myocardial infarction during his diagnostic workup. Suspecting of Tangier disease, we sequenced the ABCA1 gene, which revealed a homozygous new variant c.164A>G p (His5Arg) in the exon 4. Given the limited number of published cases, there are no reliable data on genotype-phenotype correlations in Tangier disease, highlighting the importance of reporting new variants and associated clinical features.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039030","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":"Exploring the impact of insurance switching on the cost-effectiveness of population genetic screening for familial hypercholesterolemia to US payers.","authors":"Lauren E Hendy, Lisa P Spees, Casey Tak, Delesha M Carpenter, Kathleen C Thomas, Megan C Roberts","doi":"10.1016/j.jacl.2024.12.003","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.003","url":null,"abstract":"<p><strong>Background: </strong>Widespread familial hypercholesterolemia screening requires a large upfront economic investment, but the health benefits and cost savings of cardiovascular disease prevention directed by screening occur over many years.</p><p><strong>Objective: </strong>We evaluated the cost-effectiveness of population genetic screening for familial hypercholesterolemia compared to cascade testing to US payers while accounting for patient insurance switching between commercial and Medicare insurance.</p><p><strong>Methods: </strong>We developed a hybrid decision-tree Markov model to assess genetic screening in 20-year-old adults over a lifetime horizon in which cohort members transitioned between commercial payers representing three commercial plans and Medicare. Health state and coverage transition probabilities, utilities, and event costs were primarily sourced from published literature. We estimated incremental cost-effectiveness ratios per quality-adjusted life year gained and conducted probabilistic and one-way sensitivity analyses to explore parameters.</p><p><strong>Results: </strong>Population genetic screening cost an additional $1,024,126, $495,909, and $479,170 per quality-adjusted life year gained for the high, medium, and low benefit commercial payers. Medicare experienced both cost savings and greater quality-adjusted life years in its members under population genetic screening.</p><p><strong>Conclusions: </strong>Insurance switching substantially affects the cost-effectiveness of population genetic screening for familial hypercholesterolemia to US payers. Future research examining screening and treatments for other rare diseases that require high investment early in life for downstream health benefits should consider the impact of insurance switching in the US.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039012","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":"Novel 327bp Alu element insertion in LDLR exon 17 causes alternative splicing and familial hypercholesterolemia.","authors":"Mohamed Imran, Divya Agarwal, Kriti Menon, Vinod Scaria, Sridhar Sivasubbu","doi":"10.1016/j.jacl.2024.11.006","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.11.006","url":null,"abstract":"<p><strong>Background: </strong>Homozygous familial hypercholesterolemia (HoFH) is a severe form of familial hypercholesterolemia (FH), characterized by high low-density lipoprotein cholesterol (LDL-C) levels and increased coronary artery disease risk. This study reports a novel Alu insertion in the LDLR gene in a consanguineous Indian family, causing FH.</p><p><strong>Objective: </strong>To identify and characterize the mutation causing HoFH in a proband and their family members.</p><p><strong>Methods: </strong>Clinical exome sequencing was conducted on the proband with subsequent bioinformatic analysis of single nucleotide variants, loss-of-function variants, structural variants, and mobile element insertions (MEI). Polymerase chain reaction (PCR) amplification and Sanger sequencing of exon 17 of the LDLR gene were performed to elucidate the sequence and length of the Alu insertion. Additionally, RNA analysis of the proband identified splice site events.</p><p><strong>Results: </strong>Bioinformatic analysis revealed a small sequence duplication followed by an Alu element insertion. PCR amplification and Sanger sequencing uncovered a 17 base pair (bp) duplication at the breakpoint, a \"T\" base insertion, followed by a 309 bp Alu Yb8 insertion. This led to a 70 bp deletion at the beginning of exon 17 due to alternative splicing, resulting in a frameshift and extended protein truncation. The proband and siblings were homozygous for the mutation, while the parents and two other family members were heterozygous.</p><p><strong>Conclusion: </strong>Our study uncovers a novel AluYb8 element insertion in the LDLR gene, highlighting the need for MEI detection in genetic screening for FH. Reanalyzing FH cohorts for MEIs could significantly improve diagnostic accuracy and enhance our understanding of FH genetics.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023641","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":"From the editors: Upcoming treatments for familial chylomicronemia syndrome: Agents that inhibit production of apolipoprotein CIII.","authors":"P Barton Duell, Kevin C Maki","doi":"10.1016/j.jacl.2024.12.001","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.12.001","url":null,"abstract":"","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824232","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":"Variation in lipoprotein(a) response to potent lipid lowering: The role of apolipoprotein (a) isoform size.","authors":"Adedoyin Akinlonu, Michael B Boffa, Chen Lyu, Judy Zhong, Manila Jindal, Maja Fadzan, Michael S Garshick, Arthur Schwartzbard, Howard S Weintraub, Cindy Bredefeld, Jonathan D Newman, Edward A Fisher, Marlys L Koschinsky, Ira J Goldberg, Jeffrey S Berger","doi":"10.1016/j.jacl.2024.11.008","DOIUrl":"https://doi.org/10.1016/j.jacl.2024.11.008","url":null,"abstract":"<p><strong>Background: </strong>Lipoprotein(a) [Lp(a)] is a driver of residual cardiovascular risk. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) decrease Lp(a) with significant heterogeneity in response. We investigated contributors to the heterogeneous response.</p><p><strong>Methods: </strong>CHOlesterol Reduction and Residual Risk in Diabetes (CHORD) was a prospective study examining lipid lowering in participants with a low-density lipoprotein cholesterol (LDL-C) >100 mg/dL with and without diabetes (DM) on lipid lowering therapy (LLT) for 30-days with evolocumab 140 mg every 14 days combined with either atorvastatin 80 mg or ezetimibe 10 mg daily. Lp(a) level was measured by immunoturbidometry, and the apolipoprotein (a) [apo(a)] isoform size was measured by denaturing agarose gel electrophoresis and western blotting. We examined the change in Lp(a) levels from baseline to 30 days.</p><p><strong>Results: </strong>Among 150 participants (mean age 50 years, 58% female, 50% non-White, 17% Hispanic, 50% DM), median (interquartile range) Lp(a) was 27.5 (8-75) mg/dL at baseline and 23 (3-68) mg/dL at 30 days, leading to a 10% (0-36) median reduction (P < 0.001). Among 73 (49%) participants with Lp(a) ≥30 mg/dL at baseline, there was a 15% (3-25) median reduction in Lp(a) (P < 0.001). While baseline Lp(a) level was not correlated with change in Lp(a) (r = 0.04, P = 0.59), apo(a) size directly correlated with Lp(a) reduction (P < 0.001). After adjustment for age, sex, race/ethnicity, DM, and type of LLT, apo(a) size remained positively associated with a reduction in Lp(a) (Beta 0.95, 95% confidence interval, 0.93-0.97, P < 0.001).</p><p><strong>Conclusion: </strong>Our data demonstrate variation in Lp(a) reduction with potent LLT. Change in Lp(a) was strongly associated with apo(a) isoform size.</p>","PeriodicalId":15392,"journal":{"name":"Journal of clinical lipidology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006224","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}