Genetics and causality 300 items
The LPA gene, the kringle IV type 2 copy-number variation, the SNPs that modify it, and the Mendelian randomisation studies (Clarke, Kamstrup, Burgess, Emdin, Björnson) that made Lp(a) a causal risk factor rather than a marker.
Studies
- The 2022 EAS consensus statement on Lp(a) in ASCVD and aortic stenosis (Kronenberg, Mora, Stroes et al., EHJ 2022)
- Pelacarsen (AKCEA-APO(a)-LRx) lowers Lp(a) by up to 80 percent in patients with cardiovascular disease: the phase 2 trial (Tsimikas et al., NEJM 2020)
- LPA is the genome-wide signal for aortic valve calcification and stenosis (Thanassoulis et al., NEJM 2013)
- LPA variants raise Lp(a) and coronary risk: the PROCARDIS gene-chip study (Clarke et al., NEJM 2009)
- Genetically elevated Lp(a) causes myocardial infarction: the Copenhagen Mendelian randomisation (Kamstrup et al., JAMA 2009)
- Design and rationale of Lp(a)HORIZON, the first Lp(a) outcomes trial: pelacarsen in 8,323 patients (Cho, Nicholls, Nordestgaard et al., Am Heart J 2025)
- Baseline and on-statin Lp(a) predict events in statin trials: patient-level meta-analysis (Willeit et al., Lancet 2018)
- How much Lp(a) lowering equals 1 mmol/L of LDL-C? The Mendelian randomisation answer (Burgess et al., JAMA Cardiol 2018)
- IONIS-APO(a)Rx and the GalNAc-conjugated APO(a)-LRx: two dose-ranging trials (Viney et al., Lancet 2016)
- Elevated Lp(a) and risk of aortic valve stenosis in the general population (Kamstrup et al., JACC 2014)
- Lp(a) as a cardiovascular risk factor: the first EAS consensus panel (Nordestgaard et al., EHJ 2010)
- The apo(a) gene accounts for more than 90 percent of the variation in plasma Lp(a) (Boerwinkle et al., JCI 1992)
- Apo(a) is homologous to plasminogen: the cDNA sequence (McLean et al., Nature 1987)
- Lp(a) is about six times more atherogenic than LDL per particle: apoB-based Mendelian randomisation (Björnson et al., JACC 2024)
- Lepodisiran phase 1: a single 608 mg dose keeps Lp(a) 94 percent down at day 337 (Nissen et al., JAMA 2023)
- Olpasiran, a GalNAc-conjugated siRNA against LPA: preclinical development and phase 1 (Koren et al., Nat Med 2022)
- Lp(a) molar concentration, not apo(a) size, drives cardiovascular risk; loss of Lp(a) raises diabetes risk: deCODE (Gudbjartsson et al., JACC 2019)
- How much Lp(a) lowering for a clinically relevant CHD reduction? The Lp(a)-GWAS-Consortium estimate (Lamina and Kronenberg, JAMA Cardiol 2019)
- The phenotypic consequences of genetically lowered Lp(a) (Emdin et al., JACC 2016)
- Lipoprotein apheresis cuts event rates in Lp(a) hyperlipoproteinaemia with progressive disease (Leebmann et al., Circulation 2013)
- Berg describes the Lp system, the first report of lipoprotein(a) (1963)
- First-degree relatives of people with elevated Lp(a) have more MACE: Swedish registry cohort (Kindborg et al., EHJ 2026)
- Aspirin benefits older adults with Lp(a)-raising genotypes in primary prevention: ASPREE (Lacaze et al., JACC 2022)
- Statin therapy increases Lp(a) levels: subject-level meta-analysis of six trials (Tsimikas et al., EHJ 2020)
- High Lp(a) and high risk of cardiovascular and all-cause mortality (Langsted et al., EHJ 2019)
- Elevated Lp(a) and risk of ischaemic stroke, observational and genetic (Langsted et al., JACC 2019)
- NLA scientific statement: use of Lp(a) in clinical practice, a biomarker whose time has come (Wilson et al., J Clin Lipidol 2019)
- A test in context: Lp(a) diagnosis, prognosis, controversies and emerging therapies (Tsimikas, JACC 2017)
- Lp(a) as a cause of cardiovascular disease: epidemiology, genetics and biology (Nordestgaard and Langsted, J Lipid Res 2016)
- Five years of lipoprotein apheresis for Lp(a)-associated disease: the German prospective follow-up (Roeseler et al., ATVB 2016)
- Low Lp(a) and large apo(a) isoforms are causally linked to type 2 diabetes (Kamstrup and Nordestgaard, Lancet Diabetes Endocrinol 2013)
- Lipoprotein(a): resurrected by genetics (Kronenberg and Utermann, J Intern Med 2013)
- The mysteries of lipoprotein(a) (Utermann, Science 1989)
- Lp(a) genetics beyond the kringle IV repeat (Coassin and Kronenberg, Atherosclerosis 2022)
- Genetically elevated Lp(a) shortens parental lifespan and health span (Arsenault et al., JAMA Netw Open 2020)
- HEART UK consensus statement on Lp(a): a call to action (Cegla et al., Atherosclerosis 2019)
- Whole-genome sequencing of Lp(a) in European and African ancestries (Zekavat et al., Nat Commun 2018)
- NHLBI working group recommendations to reduce Lp(a)-mediated risk of CVD and aortic stenosis (Tsimikas et al., JACC 2018)
- LPA variants, apo(a) isoforms and events differ by ethnicity: the Dallas Heart Study (Lee et al., Circulation 2017)
- Elevated Lp(a) and LPA risk genotypes raise the risk of heart failure (Kamstrup and Nordestgaard, JACC Heart Fail 2016)
- Lp(a)-lowering therapies: a promising future (Zhang, Navar, Tokgozoglu, EHJ 2026)
- Lp(a) as a pharmacological target: premises, promises and prospects (Greco et al., Circulation 2025)
- An Lp(a)-linked proteomic signature predicts cardiovascular disease beyond Lp(a) alone in young adults, CARDIA study of 3,920 with UK Biobank replication (J Clin Invest 2026)
- Lp(a) causally affects coronary disease and HbA1c but not diabetes risk, UK Biobank phenome-wide MR of 425,677 (JACC Adv 2026)
- Lowering Lp(a) and IL-6 signalling together additively cuts coronary disease risk, Mendelian randomisation of 408,687 (Eur J Prev Cardiol 2026)
- Genetic Lp(a) raises large-artery stroke risk 23% but not small vessel stroke, Mendelian randomisation of 343,681 (J Am Heart Assoc 2026)
- Proteomic screen of 48,859 UK Biobank participants finds ITIH3 and CBLN4 as a non-heritable Lp(a) axis linked to atherosclerotic events (medRxiv preprint 2025)
- Genetically elevated Lp(a) dysregulates vascular redox signalling via eNOS uncoupling and predicts cardiac mortality in advanced coronary disease (Arterioscler Thromb Vasc Biol 2026)
- Mendelian randomization confirms Lp(a) causally raises risk of five cardiovascular diseases, and finds aspirin lowers Lp(a) by 5.4% per SD of salicylic acid (Rev Cardiovasc Med 2025)
- A new genomic method predicting Lp(a) from exome data flags high-risk individuals better than prior tools, especially outside European ancestry, 76,147-person study finds (JACC Basic Transl Sci 2025)
- Lp(a)'s causal effect on MI and large-artery stroke matches across East Asian and European ancestry, Mendelian randomization study finds (Circulation 2025)
- A genome-scale CRISPR screen identifies the LDL receptor, not a disputed alternative, as the key hepatocyte gateway for Lp(a) uptake (Atherosclerosis 2025)
- Factorial Mendelian randomisation in 385 917 UK Biobank participants finds Lp(a) lowering benefits add to, not multiply, LDL-C and lifestyle effects (Int J Epidemiol 2025)
- Lp(a)'s heart attack risk is not explained by prothrombotic mechanisms, 410,177-person UK Biobank genetic study finds, and Lp(a) shows no link to venous thromboembolism at all (Eur J Intern Med 2025)
- Genetically predicted Lp(a) tracks coronary plaque severity independent of LDL-C in nearly 23,000 Million Veteran Program participants (Eur J Prev Cardiol 2025)
- REFERCHOL study of 2,979 heterozygous FH patients finds extreme Lp(a) confers cardiovascular risk equivalent to secondary prevention (J Clin Lipidol 2025)
- Low Lp(a) tracking with worse liver disease in cross-sectional studies is reverse causality, UK Biobank and genetic analysis of 270,004 people reveals (Clin Gastroenterol Hepatol 2025)
- German Chronic Kidney Disease study finds each 10 mg/dL rise in Lp(a) independently raises cardiovascular risk in 5,043 CKD patients (J Intern Med 2024)
- A Lancet review by Nordestgaard and Langsted finds one in five people carry high-risk Lp(a), as five lowering drugs achieve 65-98% reductions in trials (Lancet 2024)
- Very low Lp(a) raises new-onset diabetes and fatty liver risk in UK Biobank, but Mendelian randomisation finds no causal link (Atheroscler Plus 2024)
- In 68,748 subjects, correcting LDL-C for its Lp(a) cholesterol content adds nothing at the population level, but Lp(a) mass changes what apoB and LDL-C mean for individual risk (J Am Coll Cardiol 2024)
- High Lp(a) triples peripheral artery disease and doubles abdominal aortic aneurysm risk, confirmed genetically, in 108,146 Danes (J Am Coll Cardiol 2023)
- Cascade screening yields elevated Lp(a) in 47% of first-degree relatives, a 7.4-fold higher odds than unrelated individuals, in 52,418 UK Biobank participants (JAMA Cardiol 2023)
- Genetically higher Lp(a) raises atrial fibrillation risk in Europeans but not in a Chinese cohort, a Mendelian randomisation meta-analysis of 2.1 million participants (Curr Probl Cardiol 2024)
- Lp(a) drives progressive carotid wall thickening in children with familial hypercholesterolaemia followed 20 years into adulthood, a Dutch cohort of 200 (Lancet Diabetes Endocrinol 2023)
- Lp(a) predicts faster aortic valve stenosis progression and higher mortality, confirmed genetically via two LPA variants, in a meta-analysis of 163,139 subjects (Cardiovasc Res 2023)
- Median Lp(a) ranges from 12 to 41 nmol/L across Hispanic/Latino backgrounds in the US, tracking genetic ancestry, in 16,117 HCHS/SOL participants (JAMA Cardiol 2023)
- Lp(a) of 180 mg/dL carries the same heart attack risk as genetically diagnosed familial hypercholesterolaemia, in 69,644 Danes followed 42 years (J Am Coll Cardiol 2022)
- Lp(a) causally raises atrial fibrillation risk largely independent of atherosclerosis, a Mendelian randomisation study of 435,579 UK Biobank participants (J Am Coll Cardiol 2022)
- Lp(a) causally drives both mitral and aortic valve calcification, mediating 31% of its effect on aortic stenosis, in 97,890 Copenhagen participants (Atherosclerosis 2022)
- A newly discovered LPA splicing variant lowers Lp(a) by 13.6 mg/dL and cuts coronary disease risk by 9%, found in 4,673 Germans and validated in 440,234 UK Biobank participants (J Am Coll Cardiol 2021)
- Low Lp(a) shows no safety signal for cancer or infection risk, reassuring news as lowering drugs advance, an analysis of 109,440 Danes (Eur Heart J 2021)
- Measured Lp(a) and a 43-variant genetic risk score predict cardiovascular disease equally well, but adding either only modestly improves standard risk scores, in 374,099 UK Biobank participants (JAMA Cardiol 2021)
- APOH, encoding beta2-glycoprotein I, emerges as a new genetic locus for Lp(a) levels, a GWAS of 293,274 UK Biobank participants (Arterioscler Thromb Vasc Biol 2021)
- Familial hypercholesterolaemia does not cause elevated Lp(a); instead, high Lp(a) makes FH more likely to be diagnosed, an analysis of 37,877 people (J Am Coll Cardiol 2020)
- Niacin-laropiprant lowers Lp(a) by just 18% in patients with the highest baseline Lp(a) and small isoforms, an HPS2-THRIVE substudy of 3978 patients (Circ Genom Precis Med 2018)
- LPA gene variants triple Lp(a) levels, and the highest Lp(a) quartile raises heart attack risk by 49% in chronic kidney disease, the CRIC Study of 3744 patients (Arterioscler Thromb Vasc Biol 2017)
- Lp(a) and its gene variants predict coronary disease severity but not mortality once heart disease is established, a study of 3313 LURIC patients validated in over 106 000 (Lancet Diabetes Endocrinol 2017)
- 48 gene variants and a rare SNP with an odds ratio of 1.73 for CAD found in the largest Lp(a) genome-wide study yet, a meta-analysis of 13,781 people (J Lipid Res 2017)
- Both smaller apo(a) isoform size and higher Lp(a) concentration independently cause coronary heart disease, a Mendelian randomisation study of over 184 000 people (Lancet Diabetes Endocrinol 2017)
- APOE genotype e4/e4 carriers have 65% higher Lp(a) than e2/e2 carriers, an analysis of 431 239 patients (Arterioscler Thromb Vasc Biol 2017)
- Ideal cardiovascular health cuts the excess risk from high Lp(a) by two-thirds, the EPIC-Norfolk study of 14,051 adults (Atherosclerosis 2017)
- A PCSK9 loss-of-function mutation lowers Lp(a) and reduces aortic valve stenosis risk, a Danish study of 103 083 people (J Clin Endocrinol Metab 2016)
- High Lp(a) predicts death from infection in younger dialysis patients with diabetes, the 4D Study post hoc analysis of 1255 patients (Nephrol Dial Transplant 2016)
- A common LPA null allele carried by 3% of people lowers Lp(a) and cuts coronary disease risk, the PROCARDIS study of 4073 CAD cases and 4225 controls (Arterioscler Thromb Vasc Biol 2014)
- Lp(a) above 30 mg/dL triples the risk of death or heart attack after bypass surgery, a Russian study of 356 patients followed 15 years (Atherosclerosis 2014)
- Pro-inflammatory IL-1 genotype raises coronary disease risk from oxidized phospholipids seven-fold in younger patients, a study of 499 patients (J Am Coll Cardiol 2014)
- Extreme Lp(a) or its gene variants correctly reclassify up to 23% of heart attack risk predictions, a Danish study of 8720 people (J Am Coll Cardiol 2013)
- Lp(a) genetically drives atherosclerotic narrowing but not venous blood clots, a Mendelian randomisation study of 41,231 people (Arterioscler Thromb Vasc Biol 2012)
- The first antisense drug targeting apo(a) cuts Lp(a) by up to 25% and oxidized phospholipids by up to 92.5% in mice, a foundational study (J Am Coll Cardiol 2011)
- Lp(a) doubles coronary disease risk in men but not women, with apo(a) isoform size adding no predictive value, the Framingham Offspring Study (J Lipid Res 2011)
- A genome-wide study finds at least 6 genes beyond LPA that independently affect Lp(a) levels, a study of 386 people (J Lipid Res 2009)
- An apo(a) gene variant doubles cardiovascular risk in women, but aspirin cuts that risk more than two-fold, the Women's Health Study of 25,131 participants (Atherosclerosis 2009)
- Extreme Lp(a) predicts a 3- to 4-fold higher heart attack risk, with absolute 10-year risk up to 35% in high-risk men, the Copenhagen City Heart Study of 9330 people (Circulation 2008)
- A specific LPA gene haplotype raises heart attack risk in women independent of Lp(a) level, a German study of 834 MI patients and 1548 controls (Circulation 2003)
- Lp(a) and a 43-variant genetic risk score predict sudden cardiac death in older men with high triglycerides, UK Biobank cohort of 323,666 (Mayo Clin Proc 2026)
- Lp(a) is causally linked to aortic aneurysm risk by Mendelian randomisation, UK Biobank cohort of 312,332 (J Clin Lipidol 2026)
- Genetic evidence suggests Lp(a) lowering is unlikely to raise pregnancy-complication risk, Mendelian randomisation preprint (medRxiv 2026)
- IL-6 receptor signalling and Lp(a) independently lower cardiovascular risk, Mendelian randomisation study (JACC Basic Transl Sci 2026)
- Cholesterol content per Lp(a) particle rises with larger apo(a) isoform size, direct-assay study of 94 (J Lipid Res 2026)
- Lp(a) concentration and fewer KIV-2 repeats each independently predict MI risk in China, INTERHEART China study of 4,479 (Lipids Health Dis 2026)
- Lp(a) reduction explains only a small part of IL-6 inhibition's cardiovascular benefit, Mendelian randomisation study (Atherosclerosis 2026)
- Children with parental heart disease have Lp(a) 7-10 mg/dL higher, meta-analysis of fifty-one pediatric studies (Postgrad Med 2026)
- Linear and Nonlinear Associations Between Lipoprotein(a) and the Risks of Atherosclerotic Cardiovascular Disease
- Global Lp(a) standardization nears reality with a mass-spectrometry reference method, review (Clin Chem Lab Med 2026)
- Lp(a) causally raises abdominal aortic aneurysm risk, UK Biobank analysis of 1,026 cases (JACC Basic Transl Sci 2026)
- Genetic evidence suggests fatty liver damage lowers Lp(a), not the reverse, while combined high Lp(a) and liver stiffness sharpen carotid plaque risk (Cardiovasc Diabetol 2025)
- Lp(a) concentrations vary more than 100-fold by ancestry, yet the relative ASCVD risk per unit is universal, review of ancestral variation finds (Curr Atheroscler Rep 2025)
- Lp(a) and LDL-C synergistically raise MI risk, amplified by polygenic risk score, UK Biobank cohort of 346,751 (Am J Cardiol 2026)
- Lp(a) above 50 mg/dL nearly doubles calcific aortic valve disease risk, and lab work shows it disrupts TGF-beta signalling to trigger valve cell transition, meta-analysis and mechanistic study finds (Eur J Med Res 2025)
- Measured Lp(a) molar concentration outperforms LPA genetic variants for predicting coronary disease severity in 3,779 Han Chinese patients (Lipids Health Dis 2025)
- Elevated Lp(a) doubles cardiovascular risk in familial hypercholesterolaemia but not in familial combined hyperlipidaemia, where diabetes dominates instead, 909-patient study finds (Nutr Metab Cardiovasc Dis 2025)
- Mendelian randomization finds Lp(a) causally raises depression risk, while depression and bipolar disorder causally lower Lp(a), a bidirectional relationship (J Affect Disord 2025)
- Systematic review of 153,192 participants confirms a dose-dependent Lp(a)-aortic valve disease link, strongest above 50 mg/dL (Front Cardiovasc Med 2025)
- Lp(a) predicts coronary artery disease regardless of family history in 4,512 Japanese patients (J Lipid Atheroscler 2025)
- Apo(a) isoform size, not baseline Lp(a), explains why PCSK9 inhibitor combination therapy lowers Lp(a) unevenly (CHORD study, J Clin Lipidol 2025)
- A new nanopore sequencing method resolves the notoriously complex LPA KIV-2 repeat region with near-ddPCR accuracy across five ancestries (Genome Med 2024)
- UK Biobank observational and Mendelian randomisation analyses find Lp(a) raises abdominal aortic aneurysm risk independent of ApoB (medRxiv 2024)
- Kamstrup and colleagues quantify Lp(a) as a causal risk factor for peripheral artery disease and abdominal aortic aneurysm using CGPS and UK Biobank data (Curr Opin Cardiol 2024)
- Mendelian randomisation finds genetically higher insulin causally lowers Lp(a), helping explain why low Lp(a) tracks with diabetes risk (Cardiovasc Diabetol 2024)
- Systematic review of 49,871 individuals suggests aspirin lowers cardiovascular risk in primary prevention patients with elevated Lp(a) (Curr Probl Cardiol 2024)
- Smoking, high Lp(a) and heavy cumulative LDL-C exposure together push coronary disease risk to 85.7% in heterozygous FH (J Atheroscler Thromb 2025)
- A Polynesian-specific SLC22A3 gene variant lowers Lp(a) independent of apo(a) isoform size in 302 Māori and Pacific men (Biosci Rep 2024)
- Bidirectional Mendelian randomisation confirms Lp(a) causally raises chronic kidney disease risk, not the reverse (Ren Fail 2024)
- Review by Koschinsky, Rosenson and colleagues explains why Lp(a) runs up to threefold higher across racial groups and 5-10% higher in women (J Am Heart Assoc 2024)
- Genome-scale CRISPR screen resolves a long-standing controversy: the LDL receptor, not a dedicated protein, is the main gateway for Lp(a) uptake (bioRxiv 2024)
- Elevated Lp(a) plus a family history of coronary disease nearly doubles MACE risk in 6,056 chronic coronary syndrome patients (J Atheroscler Thromb 2024)
- Nordestgaard-led study of 15 Danish lipid clinics finds elevated Lp(a) explains 27% of clinical familial hypercholesterolaemia diagnoses (J Clin Endocrinol Metab 2024)
- Mendelian randomisation finds no causal link between Lp(a) and type 2 diabetes despite an inverse observational correlation, in 563,420 participants (Arch Med Sci 2024)
- Lp(a) is not elevated in familial hypercholesterolaemia and is metabolically independent of LDL-C, in 256 FH patients and 272 controls (CJC Open 2024)
- Elevated Lp(a) is already present by age 5 and remains largely unmodifiable by lifestyle or lipid drugs, a review by a leading Lp(a) assay expert (Crit Rev Clin Lab Sci 2023)
- One in five people of European ancestry has elevated Lp(a), and new RNA drugs can lower it more than 95%, a review by three leading Lp(a) researchers (Pharmacol Res 2023)
- Nissen and Laffin call Lp(a) an overlooked risk factor affecting 20-30% of the world's population, as pharmacotherapies advance (Trends Cardiovasc Med 2024)
- Correcting LDL-C for genetically estimated Lp(a) reclassifies up to 9% of suspected FH patients as unlikely FH, in 1,504 Dutch referrals (Atherosclerosis 2023)
- PCSK9 inhibition Lp(a)-lowering effect explains under 4% of its coronary disease benefit, a Mendelian randomisation study of 310,020 UK Biobank participants (Atherosclerosis 2022)
- Lp(a) stays remarkably stable over 25 years, but people from eastern Finland run 20% higher levels than western Finns, the Young Finns Study (Atherosclerosis 2022)
- A common LPA gene variant only raises Lp(a) and coronary disease risk in the 96% of people who do not also carry a specific splicing mutation, a genetic study of 184,283 people (Atherosclerosis 2022)
- Lp(a) rises 22-43% from childhood to adulthood depending on lipid-lowering treatment, with 70% intra-individual variation, in 2,740 Dutch children (Atherosclerosis 2022)
- Cascade testing for FH finds a new case of elevated Lp(a) for every 2.1-2.4 relatives tested, a review proposing a combined FH-Lp(a) care model (Front Genet 2022)
- Cascade testing for both FH and elevated Lp(a) uncovers a new case of either every 1.5-2.1 relatives tested, in 162 family members (Atherosclerosis 2022)
- Lp(a) is linked to more vulnerable carotid plaque features, with sex-specific patterns, in the Dutch PARISK study of 182 patients (Atherosclerosis 2021)
- Pelacarsen lowers Lp(a) equally regardless of LPA genotype or apo(a) isoform size, a pooled analysis of 455 patients across 4 trials (Atherosclerosis 2021)
- Effect of C-Reactive Protein on Lipoprotein(a)-Associated Cardiovascular Risk in Optimally Treated Patients With High-Risk Vascular Disease: A Prespecified Secondary Analysis of the ACCELERATE Trial
- Elevated Lp(a) and family history combine for a 43% higher cardiovascular risk than either alone, in 12,149 ARIC participants (J Am Coll Cardiol 2020)
- Lp(a) matches LDL as a cause of heart attacks but outweighs it for mortality risk, a head-to-head comparison in about 100,000 Danes (Curr Opin Lipidol 2020)
- Starting statins raises Lp(a) only in patients with the low molecular weight apo(a) phenotype, a study of 81 patients (Atherosclerosis 2019)
- Four Lp(a)-associated gene variants predict more severe coronary disease in 1403 Han Chinese patients, a genome-wide association study (J Lipid Res 2019)
- An estimated 5 million people with familial hypercholesterolaemia worldwide have Lp(a) high enough to double aortic valve calcification risk, a review (Atherosclerosis 2019)
- Lp(a) concentration, not apo(a) isoform size, predicts angiographic coronary disease severity in 263 men (Atherosclerosis 2018)
- Finns have about 50% lower Lp(a) than Central Europeans, with known genetic variants explaining 71.8% of the gap, a study of 12,284 participants (Arterioscler Thromb Vasc Biol 2018)
- Elevated Lp(a) and LDL together predict the most severe coronary lesions in young patients with premature coronary disease, a study of 147 patients (J Clin Lipidol 2018)
- Lp(a) predicts early-onset cardiovascular disease in families better than LDL cholesterol, a study of 129 children with familial hypercholesterolaemia (J Clin Lipidol 2018)
- Inflammatory IL-1 genotype doubles the cardiovascular risk from high Lp(a), the Ioannina Study of 603 patients (J Clin Lipidol 2018)
- Lp(a) predicts carotid artery thickening only in HIV-infected young women, the Women's Interagency HIV Study of 250 participants (Arterioscler Thromb Vasc Biol 2017)
- Lp(a) and familial hypercholesterolaemia together predict early, severe coronary disease, a Chinese angiography cohort of 8050 patients (Atherosclerosis 2017)
- Homozygous autosomal dominant hypercholesterolaemia doubles Lp(a) levels compared to heterozygous carriers, a Dutch study of 119 individuals (J Clin Lipidol 2017)
- PCSK9 and Lp(a) levels independently predict coronary calcium buildup in statin-treated FH patients, a study of 161 patients (Atherosclerosis 2016)
- Mendelian randomisation applied to Lp(a) two decades ago proved causality for cardiovascular disease, aortic stenosis and diabetes, a review of Lp(a) genetics (Cardiovasc Drugs Ther 2016)
- The CHARGE consortium's discovery that LPA variants cause aortic valve calcification affects over 2.5 million North Americans, a review by the discovering author (J Lipid Res 2016)
- Lp(a) oxidized phospholipids boost HDL production machinery by up to 3-fold in liver cells, a mechanistic study (J Lipid Res 2015)
- Tocilizumab blocks IL-6 to lower Lp(a) via a specific LPA gene promoter site, but TNF-alpha inhibition does not, a mechanistic study (J Lipid Res 2015)
- Scavenger receptor SR-BI is identified as a novel Lp(a) clearance receptor, a mechanistic study across transgenic and knockout mice (J Lipid Res 2013)
- HIV disease control raises apo(a) levels tied to atherogenic small isoforms, a study of 139 white and 168 Black HIV-positive patients (Arterioscler Thromb Vasc Biol 2013)
- Lp(a) assembles inside the cell from newly made LDL and apo(a), a stable-isotope kinetic study of 9 healthy people (Atherosclerosis 2012)
- Lp(a) above 25 mg/dL affects 30% of Caucasians and up to 70% of Black people, a rationale for developing targeted Lp(a) therapies (J Am Coll Cardiol 2012)
- In people with type 2 diabetes, genetically high Lp(a) does not raise cardiovascular risk, unlike in the general population, a GWAS of 2308 diabetic patients (Eur Heart J 2012)
- Lp(a) triples atherosclerotic plaque area in uremic mice, a transgenic mouse study of kidney disease and Lp(a) (J Lipid Res 2010)
- Lp(a) more than triples ischemic stroke risk in the elderly, a Greek case-control study of 163 stroke patients and 166 controls (Atherosclerosis 2006)
- The liver clears Lp(a) mainly via apo(a) itself, not the LDL receptor, taking up 34.6% of the dose in 24 hours, a mouse study (J Lipid Res 2005)
- Despite 2-3 times higher Lp(a), Black adults show no link between Lp(a) and coronary calcium, the Dallas Heart Study of 761 Black and 527 white adults (Circulation 2005)
- A new mouse model reaches Lp(a) levels of 700 mg/dL, over 20 times the human risk threshold, revealing oxidized phospholipids unique to Lp(a) (J Lipid Res 2005)
- Swapping four lysines for serines in apoB impairs Lp(a) assembly in transgenic mice, a structural mechanistic study (J Lipid Res 2004)
- About half of Lp(a) apoB comes from pre-existing LDL, not fresh liver secretion, a kinetic study of 7 people (Atherosclerosis 2001)
- Lp(a) ability to bind lysine varies because LDL and fibronectin mask its binding site, not because of the particle itself, a mechanistic study (J Lipid Res 2000)
- Rabbits lacking a functional LDL receptor accumulate over 4 times more Lp(a), a transgenic animal study (J Lipid Res 2000)
- Homozygous familial hypercholesterolaemia nearly doubles Lp(a) compared to heterozygotes, showing a clear LDL receptor gene-dose effect, a study of 69 family members (Arterioscler Thromb Vasc Biol 2000)
- Lp(a) is not clinically linked to atrial fibrillation, meta-analysis of 16 observational and 7 Mendelian randomisation studies (J Clin Lipidol 2026)
- LPA gene variants explain 28% of Lp(a) variability but not coronary anatomy in chronic coronary syndrome, 390-patient study (J Clin Lipidol 2026)
- Aspirin shows no clear cardiovascular benefit in elevated Lp(a) or high-risk LPA genotypes, meta-analysis of 6 studies (Eur J Prev Cardiol 2026)
- Clinical risk factors cannot distinguish FH from elevated Lp(a), 378-patient lipid clinic study argues for universal genetic and Lp(a) testing (J Clin Lipidol 2026)
- Aspirin shows no overall MACE benefit in elevated Lp(a) but a signal in rs3798220 carriers, meta-analysis of seven studies (Am J Cardiovasc Drugs 2026)
- Cutting saturated fat reshapes the Lp(a) lipidome in African Americans, randomised trial of 166 (J Lipid Res 2026)
- Lipoprotein(a) levels in children with hypercholesterolemia
- Sequencing advances resolve LPA genetic architecture across ancestries, but the Lp(a) receptor stays elusive, review (Curr Opin Lipidol 2026)
- Structural model separates functional LPA gene variants from bystanders shaping Lp(a) and CAD risk, review (Prog Lipid Res 2026)
- LPA risk alleles rs3798220 and rs10455872 raise coronary disease odds up to 75%, meta-analysis of 55,647 (Am J Med Sci 2026)
- From kringle IV type 2 copy number to arterial wall: the mechanistic biology of Lp(a) reviewed (Eur J Clin Invest 2026)
- The LPA +121 G>A variant protects against venous thromboembolism, but Lp(a) protein level itself does not predict it, case-control study finds (Biochem Biophys Rep 2025)
- A critical review examines how Middle Eastern genetic diversity and high consanguinity rates may uniquely shape Lp(a) distribution, a data-scarce region (JACC Asia 2025)
- Over a quarter of suspected FH patients at a lipid clinic have high-risk Lp(a), which tracks with coronary disease but not carotid plaques, 220-patient study finds (Clin Cardiol 2025)
- Neither Lp(a) concentration nor apo(a) isoform size predicts new-onset diabetes in prediabetic adults, IT-DIAB study of 303 finds, challenging a general-population signal (Diabetes Metab 2025)
- Mendelian randomisation finds no causal link between Lp(a) and nine immune-mediated inflammatory diseases (Sci Rep 2025)
- Elevated Lp(a) predicts worse graft occlusion and MACE after CABG, review argues for routine perioperative Lp(a) measurement (Ann Thorac Surg 2025)
- Cutting dietary saturated fat raises Lp(a) by 24% in African Americans, more so with smaller apo(a) isoforms (Nutrients 2025)
- Carrying the CYP2C19 AA genotype alongside elevated Lp(a) raises the odds of poor stroke recovery more than 15-fold (Am J Transl Res 2025)
- Corneal arcus and thick Achilles tendons flag elevated Lp(a) and higher MACE risk in 484 patients with familial hypercholesterolaemia (J Clin Lipidol 2025)
- A single dose of lipid-nanoparticle-delivered TALEN mRNA cuts Lp(a) by over 80% for at least five weeks in transgenic mice (Mol Ther 2025)
- Review traces how Lp(a) shifts from newborn to menopause and argues women carry equal or greater Lp(a)-related cardiovascular risk than men (Am J Prev Cardiol 2024)
- A new short-read caller for the KIV-2 repeat region correlates with Lp(a) protein levels and reveals distinct ancestry-specific copy-number distributions (BMC Med Genomics 2024)
- Hegele group finds Lp(a) is paradoxically halved in patients with severe hypertriglyceridaemia (J Int Med Res 2024)
- Amsterdam UMC review finds cascade screening for elevated Lp(a) needs as few as 1.3 relatives tested per new case found (Curr Opin Lipidol 2024)
- Familial hypercholesterolaemia, not familial hypobetalipoproteinaemia, is linked to higher Lp(a) in a study of 1,153 subjects with genetically extreme LDL (Nutr Metab Cardiovasc Dis 2025)
- An LPA genetic risk score explaining 45% of Lp(a) variation predicts calcific aortic valve disease but adds little once coronary status is known (Eur J Prev Cardiol 2024)
- Quantifying LPA KIV-2 repeat number by qPCR better predicts 5-year MACE than measured Lp(a) alone, particularly in women (Rev Cardiovasc Med 2024)
- In a 10-week RCT, sugar-sweetened beverages lowered Lp(a) by 13% in overweight adults, independent of apo(a) size (J Lipid Res 2024)
- Girls with genetic FH have 45% higher baseline Lp(a) than boys, a sex gap that persists over nearly nine years of follow-up (Atheroscler Plus 2024)
- Genotype-based RCT finds both plant-based omega-3 and omega-6 oils lower Lp(a) by 7-10%, regardless of FADS1 genotype (Atherosclerosis 2024)
- HER(a) study finds 59.4% of first-degree relatives of high-Lp(a) ACS patients also have elevated Lp(a) (J Clin Med 2024)
- Meta-analysis of seven Mendelian randomisation studies confirms Lp(a) causally raises heart failure risk (Curr Probl Cardiol 2024)
- Kronenberg traces how genetic studies, absent good animal models, first proved Lp(a) causal in the early 1990s (Curr Atheroscler Rep 2024)
- Mendelian randomisation using 290,497 UK Biobank participants finds no causal link between Lp(a) and arterial stiffness (Eur J Clin Invest 2024)
- Lp(a) evidence in children lags far behind adults, but early testing could still guide family-based cardiovascular prevention, a review (Biomedicines 2023)
- Lp(a) is linked to mitral valve calcification but shows mixed results for mitral dysfunction, a systematic review pooling over 1 million individuals across 8 studies (Nutr Metab Cardiovasc Dis 2023)
- Lp(a) is higher in Black populations and in women, but a lack of standardised assays and cutoffs still limits clinical use, a review (Best Pract Res Clin Endocrinol Metab 2023)
- Smaller apo(a) isoforms raise Lp(a) mainly by boosting production, and ancestry strengthens this link, in a kinetic study of 32 individuals (J Lipid Res 2023)
- Lp(a) is higher in children with homozygous familial hypercholesterolaemia than heterozygous FH or unaffected children, a Dutch cross-sectional study of 232 children (J Clin Lipidol 2023)
- About 20% of people have elevated Lp(a) above 50 mg/dL, and a meaningful share also have familial hypercholesterolaemia, a review of this dual risk (Metabolites 2022)
- A new isoform-independent Lp(a) ELISA matches the gold-standard assay and mass spectrometry with over 97% correlation (J Lipid Res 2022)
- Lp(a) levels are driven mainly by how much the liver makes, not how fast it clears, redirecting drug development toward blocking production, a review (Curr Opin Lipidol 2022)
- Black individuals have the highest Lp(a) levels of any ethnicity studied, followed by South Asians, complicating a single universal risk threshold, a review (Atherosclerosis 2022)
- Up to 1 billion people worldwide may have high-risk Lp(a) levels, a genetic epidemiology review spanning heart attacks to lifespan (Atherosclerosis 2022)
- Children with FH and Lp(a) above 30 mg/dL are nearly twice as likely to have family history of premature cardiovascular disease, LIPIGEN paediatric data on 653 children (Atherosclerosis 2022)
- The receptor sortilin boosts apo(a) secretion from liver cells and promotes Lp(a) uptake, but rare SORT1 mutations amplify only the secretion effect (J Lipid Res 2022)
- Familial hypercholesterolaemia doubles cardiovascular risk when Lp(a) is also elevated, making cascade screening a key opportunity to catch both, a review (Curr Atheroscler Rep 2022)
- ApoE2 carriers have lower Lp(a), with APOE the second most important gene after LPA in determining Lp(a) levels, a mechanistic review (Curr Atheroscler Rep 2022)
- Up to a quarter of familial hypercholesterolaemia diagnoses are actually driven by high Lp(a), not LDL cholesterol itself, a review argues for updating diagnostic criteria (Curr Atheroscler Rep 2022)
- Lp(a) is highest in APOB-dependent familial hypercholesterolaemia, 36.5 mg/dL, versus 21.9 mg/dL in the LDLR-dependent form, a Spanish study of 2,419 people (Atherosclerosis 2022)
- Genetics explains 80-90% of Lp(a) variation, up to 1000-fold between people, and antisense drugs can cut it 80% as the HORIZON trial nears, a review (Curr Atheroscler Rep 2021)
- Lp(a) elevation above 50 mg/dL may be the most common monogenic lipid disorder, affecting over 1.4 billion people worldwide, a review (Curr Atheroscler Rep 2021)
- High Lp(a) affects 10-20% of the population and up to 1 billion people worldwide, tripling risk of aortic stenosis and peripheral artery disease, a review (Clin Chem 2021)
- The Effect of PCSK9 (Proprotein Convertase Subtilisin/Kexin Type 9) Inhibition on the Risk of Venous Thromboembolism
- Lipoprotein apheresis lowers macrophage cholesterol-loading capacity alongside Lp(a), an Italian case-control study of 34 patients with two novel LPA variants (J Clin Lipidol 2020)
- Elevated Lp(a) affects 30-50% of familial hypercholesterolaemia patients, compounding their inherited cardiovascular risk, a review of emerging RNA-based therapy (J Intern Med 2020)
- Lp(a) causally drives calcific aortic valve stenosis and predicts faster disease progression, a systematic review of 21 studies (Prog Cardiovasc Dis 2020)
- Elevated Lp(a) affects 25% of South Asians and doubles to triples their coronary disease risk, a review of malignant CAD in young Indians (Indian Heart J 2019)
- Lp(a) correlates with PCSK9 levels only in patients with the low molecular weight apo(a) phenotype, a study of 205 patients with suspected familial hypercholesterolaemia (Atherosclerosis 2018)
- Lp(a) varies up to 1000-fold between individuals, and 1 in 4 has levels that raise cardiovascular risk, a review asking if Lp(a) is ready for clinical use (Cardiol Clin 2018)
- Lp(a)-lowering therapies cut levels by 25-30% in familial hypercholesterolaemia, though clinical benefit is unproven, a review (Curr Pharm Des 2018)
- Elevated Lp(a) above 50 mg/dL affects 1 in 5 people worldwide, a review of modern genomic insights into Lp(a) (Curr Opin Lipidol 2017)
- Lp(a) ranges from under 0.1 to over 100 mg/mL between individuals, and is higher in women, a review of its evolutionary origins and genetic determinants (Curr Med Chem 2017)
- Lp(a) was discovered in 1963 and its size heterogeneity explained decades later by Gerd Utermann, a historical appraisal (J Lipid Res 2017)
- Lp(a) LPA gene copy number variation remains only partly understood despite its strong coronary disease link, a review of Lp(a) structure and genetics (J Lipid Res 2016)
- Elevated Lp(a) above 30 mg/dL affects 20-30% of the global population, a review of emerging Lp(a)-lowering therapies (Curr Opin Endocrinol Diabetes Obes 2016)
- Mouse and rabbit Lp(a) models fall short since animals naturally express under 20 mg/dL and only one of over 40 human apo(a) isoforms, a review (Cardiovasc Drugs Ther 2016)
- A key European Lp(a) risk variant found in up to 11.6% of Asians has no effect on Lp(a) or isoform size there, a multi-population genetic study (Atherosclerosis 2015)
- India lacks its own Lp(a) threshold, using a 20 mg/dL cutoff versus 30 mg/dL for Caucasians, a review of Lp(a) as a unique risk factor for coronary disease (Indian J Clin Biochem 2016)
- Lp(a) fully expresses by age 2, but guidelines only recommend testing children after stroke, a review of Lp(a) in pediatrics (J Clin Lipidol 2015)
- Lp(a) and apoB are more closely linked in African-Americans than Caucasians, a study of 336 Caucasians and 224 African-Americans (Atherosclerosis 2014)
- A rapid qPCR method replaces laborious electrophoresis for counting Lp(a) gene repeats, a methods study (J Lipid Res 2009)
- Eating fish and a specific LPA gene variant together lower Lp(a) levels, an Italian study of 647 people (Atherosclerosis 2007)
- Apo(a) protein size ranges from 300 to 800 kDa, driving Lp(a) extreme variability, a review of this elusive risk factor (Arterioscler Thromb Vasc Biol 2004)
- No single gene explains why African Americans have higher Lp(a), a genetic linkage study across three populations (J Lipid Res 2003)
- Distribution of Lipoprotein(a) concentrations in children and young people with Familial Hypercholesterolemia (FH) compared to those without FH: A systematic review and narrative synthesis
- Common vitamin and supplement use does not shift Lp(a) over time, UK Biobank analysis of 12,109 (Lipids Health Dis 2026)
- From Phenotype to Genotype and Beyond: Insights into Familial Hypercholesterolemia and Familial Hypertriglyceridemia
- Improved diagnosis of familial hypercholesterolemia by correcting LDL-C for lipoprotein(a) in a German cohort
- Polygenic risk scores and Lp(a) extend genetic risk stratification beyond monogenic hypercholesterolaemia, review (Genes Basel 2026)
- Lipoprotein(a) and premature myocardial infarction: Mechanistic insights and implications for PCI-era residual risk
- Molecular Mechanisms and Therapeutic Targets of RNA-Based and Traditional Lipid-Lowering Agents in Residual Cardiovascular Risk: A Scoping Review of Key Directions Towards Future Perspectives
- Prevalence of Lipoprotein(a) Testing in Patients With Atherosclerotic Cardiovascular Disease Within a Large Australian Cardiology Network
- Lp(a) is unrelated to body composition, unlike HDL-C and triglycerides, high-risk cohort of 207 (Adv Med Sci 2026)
- PCSK9 gain-of-function gene variants show no measurable effect on lipids or arterial wall properties in statin-treated post-MI patients with severely elevated Lp(a) (Sci Rep 2025)
- Children with Prader-Willi syndrome have markedly higher Lp(a) and hs-CRP than controls, with the deletion genetic subtype most affected, 32-patient study finds (J Endocr Soc 2025)
- Twenty-year follow-up of Dutch familial hypercholesterolaemia cohort finds no link between Lp(a) and arterial stiffness (J Clin Med 2025)
- A nine-miRNA signature links high Lp(a) to coronary calcification through inflammation and lipid pathways in 24 SAFEHEART FH patients (Comput Struct Biotechnol J 2025)
- Digital droplet PCR outperforms quantitative PCR for measuring the LPA KIV2 repeat that drives Lp(a) variability (J Clin Lab Anal 2024)
- Lipoprotein(a) correlates with DNA damage in heterozygous familial hypercholesterolaemia, with an ASCVD-relevant cut-off of 23.45 nmol/L (Sci Rep 2024)
- An Lp(a) gene haplotype (rs10455872-rs3798220) is linked to higher inflammation and antifibrinolytic markers after myocardial infarction (Int J Mol Sci 2024)
- A practical clinical guide to Lp(a), genetics, real-world risk-factor interactions, and emerging metabolic targets for lowering it (Prog Cardiovasc Dis 2023)
- Is Lp(a) a real risk multiplier in familial hypercholesterolaemia, or just along for the ride? A review calls for direct drug-based proof (Curr Opin Lipidol 2022)
- Lower Lp(a) predicts new-onset diabetes, but whether the link is truly causal remains muddled by conflicting Mendelian randomisation studies, a review (Atherosclerosis 2022)
- Whether Lp(a)-raising gene variants add predictive value beyond Lp(a) concentration itself remains controversial, a review of a decade of advances (Pharmacol Res 2021)
- Black populations of Sub-Saharan descent have higher Lp(a) than Whites, yet remain underrepresented in Lp(a) research, a review (Curr Opin Lipidol 2021)
- Genotyping for Lp(a)-raising variants adds little beyond simply measuring Lp(a) itself, a review of contemporary genetics and clinical use (Curr Opin Cardiol 2021)
- Low Lp(a) predicts new-onset diabetes, yet high Lp(a) still raises cardiovascular risk in people who already have it, a review of causes and consequences (Curr Opin Endocrinol Diabetes Obes 2021)
- Elevated Lp(a) drives residual cardiovascular risk even at optimal LDL-C, but proof that lowering it helps still awaits trial data, a review (J Cardiovasc Med 2021)
- People of African descent have the highest Lp(a) levels of any ethnicity, yet standardisation gaps hinder screening across diverse populations, a review (Cardiol Ther 2020)
- Mendelian randomisation confirms Lp(a) drives coronary disease, aortic stenosis, stroke and heart failure regardless of LDL control, a review revisiting two decades of evidence (Circ J 2020)
- Lp(a) risk is independent of every other lipid marker, but treatment options remain scarce, a residual-risk update (Am J Cardiol 2020)
- Lp(a) is a proven causal cardiovascular risk factor but still lacks a specific therapy or standardised test, a review (J Clin Med 2019)
- The 2018 cholesterol guideline recognizes elevated Lp(a) as a risk enhancer for statin therapy, a review of Lp(a) as a causal cardiovascular risk factor (Indian Heart J 2019)
- Lp(a) is cleared by five distinct receptor families, but none are yet clear drug targets, a review of Lp(a) catabolism (Pathology 2019)
- Kidney disease raises Lp(a) mainly in patients with large apo(a) isoforms or heavy protein loss, a review of Lp(a) in chronic kidney disease (J Lipid Res 2018)
- Lp(a) re-emerges as a major cardiology focus more than 50 years after its discovery, a review for preventive cardiology (Prog Lipid Res 2017)
- Lp(a) assembly and clearance mechanisms remain unresolved since its 1963 discovery, a review of Lp(a) metabolism (J Lipid Res 2017)
- Lp(a) has modest predictive value for cardiovascular and cerebrovascular outcomes, a review of evidence-based questions still unanswered (Crit Rev Clin Lab Sci 2016)
- Lp(a) is higher in familial hypercholesterolaemia patients who develop early heart disease than those who don't, a Norwegian comparison study (Atherosclerosis 2011)
- Genetic studies support Lp(a) as a cause of ischemic heart disease, though no outcome trial has ever tested lowering it, a review (Atherosclerosis 2010)
- No correlation between apo(a) isoform size and Lp(a) concentration in 43 acute coronary syndrome patients with Lp(a) above 50 mg/dL (Clin Investig Arterioscler 2026)
- The LPA rs10455872 genotype does not predict childhood obesity itself, but tracks with insulin, CRP and vitamin B12 differences within obese children, exploratory study finds (Diagnostics (Basel) 2025)
- The rs3798220-C LPA variant tracks with higher Lp(a) and more early myocardial infarction in a 251-patient case-control study (Diagnostics 2025)
- Monozygotic twins with homozygous FH and Lp(a) above 270 nmol/L develop nearly identical coronary disease at the same age, the first such case report (Turk Kardiyol Dern Ars 2020)
- LPA may be an unprocessed pseudogene duplicated from the plasminogen gene, a hypothesis for apo(a) functionless structure and Lp(a) pathology (Cureus 2018)
- Distribution of Lipoprotein(a) Levels and Clinical Associations in a Lebanese Adult Population: A Retrospective Observational Study
- Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target
- Association of lipoprotein(a), oxidized phospholipids and apolipoprotein B100 in acute ischemic stroke cohort
- Genetic Prediction of Circulating Lipoprotein(a) Levels in Diverse Populations
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