Aortic stenosis 132 items
Lp(a) as a causal factor in calcific aortic valve disease: the LPA GWAS signal, the Copenhagen cohorts, PET and CT progression studies, and the prospect of Lp(a) lowering as the first medical therapy for the valve.
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)
- 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)
- 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)
- ALPACAR: zerlasiran lowers time-averaged Lp(a) by more than 80 percent over 36 weeks in ASCVD (Nissen et al., JAMA 2024)
- Lepodisiran phase 1: a single 608 mg dose keeps Lp(a) 94 percent down at day 337 (Nissen et al., JAMA 2023)
- Muvalaplin, the first oral inhibitor of Lp(a) formation: phase 1 (Nicholls et al., JAMA 2023)
- Lp(a) and oxidised phospholipids drive valve calcification activity and progression in aortic stenosis (Zheng et al., JACC 2019)
- First antisense drug against apo(a) in humans: ISIS-APO(a)Rx phase 1 (Tsimikas et al., Lancet 2015)
- Lp(a) drives ASCVD, MI and aortic stenosis risk independent of C-reactive protein: Copenhagen (Thomas et al., EHJ 2023)
- APOLLO: single ascending doses of SLN360 (zerlasiran) lower Lp(a) by up to 98 percent (Nissen et al., JAMA 2022)
- Oxidised phospholipids as a unifying theory for Lp(a) in ASCVD and aortic valve disease (Boffa and Koschinsky, Nat Rev Cardiol 2019)
- A test in context: Lp(a) diagnosis, prognosis, controversies and emerging therapies (Tsimikas, JACC 2017)
- IL-6 modifies Lp(a)-associated coronary risk but not aortic stenosis risk: UK Biobank (JAMA Cardiol 2026)
- Regular aspirin use and lower incidence of aortic valve calcium and severe stenosis in people with high Lp(a): MESA (Razavi et al., EHJ 2026)
- Zerlasiran single and multiple doses in ASCVD patients: Lp(a) down 90 percent at 201 days after two doses (Nissen et al., JAMA 2024)
- Lp(a) is associated with the onset but not the progression of aortic valve calcification: the Rotterdam Study (Kaiser et al., EHJ 2022)
- HEART UK consensus statement on Lp(a): a call to action (Cegla et al., Atherosclerosis 2019)
- Lp(a)-lowering therapies: a promising future (Zhang, Navar, Tokgozoglu, EHJ 2026)
- New antisense and RNA interference drugs may lower Lp(a) by up to 90%, a JCL Roundtable expert discussion on the emerging risk factor (J Clin Lipidol 2018)
- Adding Lp(a) to ApoB improves aortic-stenosis risk prediction, especially in men, UK Biobank cohort of 365,771 (Eur J Prev Cardiol 2026)
- Lp(a) of 125 nmol/L or above raises valve replacement risk 58% in calcific aortic valve stenosis, UK Biobank study of 1,962 finds (J Am Heart Assoc 2025)
- Lp(a) above 100 mg/dL nearly doubles risk of severe degenerative aortic stenosis, but not bicuspid or rheumatic disease, in 44,742 patients (JACC Asia 2024)
- JAMA Cardiology meta-analysis of 710 patients finds top-tertile Lp(a) drives 41-57% faster echocardiographic progression of aortic stenosis (JAMA Cardiol 2024)
- MESA study of 6,792 participants over 16.7 years finds a zero aortic valve calcium score beats Lp(a) or LDL-C for ruling out future severe aortic stenosis (Circ Cardiovasc Imaging 2024)
- MFSD5 identified as a receptor mediating lipoprotein(a) uptake and calcification in heart valve cells, with variants linked to aortic stenosis (Circulation 2024)
- 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)
- Extreme Lp(a) and extreme body weight together carry a 3.5-fold risk of calcific aortic valve disease, in 69,988 Danes (J Am Coll Cardiol 2022)
- Lp(a) above 175 nmol/L explains 3% of population cardiovascular disease burden, and lowering it 80% could cut CHD risk by 24%, an analysis of 413,734 UK Biobank participants (Eur J Prev 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)
- Familial hypercholesterolaemia patients face nearly 4-fold higher risk of needing aortic valve replacement, driven partly by elevated Lp(a), in 5,022 SAFEHEART participants (Eur Heart J 2021)
- Higher Lp(a) linearly predicts faster aortic valve stenosis progression, especially in younger patients, an ASTRONOMER trial secondary analysis of 220 patients (JAMA Cardiol 2018)
- 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)
- Elevated Lp(a) and oxidized phospholipids predict faster aortic stenosis progression and need for valve replacement, an ASTRONOMER substudy of 220 patients (J Am Coll Cardiol 2015)
- Autotaxin carried by Lp(a) drives aortic valve mineralization, raising valve autotaxin activity by 60% in diseased valves, a mechanistic study (Circulation 2015)
- Elevated Lp(a) raises restenosis risk 3-fold after PCI, meta-analysis of twenty-six studies (J Clin Med 2026)
- Elevated Lp(a) is linked to mitral annular calcification but not regurgitation, propensity-matched study of 66,292 pairs (J Clin Lipidol 2026)
- Elevated Lp(a) independently predicts stenotic bioprosthetic valve degeneration, cohort of 174 (Eur Heart J Cardiovasc Imaging 2026)
- Time-weighted Lp(a) outpredicts single-measurement Lp(a) for calcific aortic valve disease, cohort of 5,156 (Lipids Health Dis 2026)
- Lp(a) as a shared driver of atherosclerosis, aortic stenosis and abdominal aortic aneurysm, with lowering therapies now in outcomes trials (Annu Rev Med 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)
- Lp(a)'s coronary risk is amplified in patients with high cholesterol or triglycerides, but not for aortic stenosis or stroke, UK Biobank study of 127,958 finds (Am J Prev Cardiol 2025)
- Only 1 in 4 aortic stenosis patients has high Lp(a), limiting how many could benefit from future Lp(a)-lowering therapies, 162-patient Canadian valve clinic study finds (JACC Adv 2025)
- Mass-based and molar-based Lp(a) immunoassays are interchangeable, near-identically predicting coronary and aortic valve calcification, Rotterdam Study of 5,129 finds (Am Heart J 2025)
- Elevated Lp(a) predicts both higher mortality and faster bioprosthetic valve degeneration after TAVR in 601 patients (J Clin Lipidol 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)
- High lipoprotein(a) predicts bioprosthetic aortic valve degeneration in 210 patients (Heart 2024)
- Olpasiran and pelacarsen cut Lp(a) by 85-90%, with phase 3 outcome trials testing whether this prevents aortic stenosis progression (Int J Mol 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)
- Aortic valve calcification is strongly linked to elevated Lp(a), a meta-analysis pooling 446,179 patients across 7 studies (Curr Probl Cardiol 2023)
- Lp(a) above the 90th percentile nearly doubles aortic valve stenosis incidence over 14 years, in 23,298 routinely tested Swedes (Atherosclerosis 2022)
- Lp(a) above 50 mg/dL, but not 30 mg/dL, is significantly linked to calcific aortic valve disease, a meta-analysis of 52,931 participants across 8 studies (Front Cardiovasc Med 2022)
- Lp(a) predicts aortic valve calcium in Whites and Blacks but not South Asians, despite South Asians having higher Lp(a) than Whites, in MASALA and MESA (Atherosclerosis 2020)
- About one-third of aortic stenosis cases are linked to high Lp(a) and oxidized phospholipids, a review of emerging Lp(a)-targeted therapies (Circ 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) drives calcium deposition and oxidative stress in human aortic valve cells more than LDL does, a mechanistic study (Atherosclerosis 2018)
- High Lp(a) predicts aortic valve surgery only in patients who also have coronary artery disease, a Swedish study of 336 surgical cases (J Am Heart Assoc 2017)
- Different Lp(a) assay methods perform similarly for predicting valve and coronary disease, but only in white participants, a MESA study of 4679 adults (Clin Chem 2017)
- Statins may worsen aortic stenosis by raising Lp(a) and oxidized phospholipids, a review of Lp(a)-targeted therapy in calcific aortic valve disease (Curr Opin Cardiol 2016)
- The standard 30 mg/dL Lp(a) cutoff predicts aortic valve calcification in white and Black adults, but not Hispanics or Chinese, the MESA study of 4678 adults (Arterioscler Thromb Vasc Biol 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)
- ISIS-APO(a)Rx cuts Lp(a) by up to 89% in a phase 1 trial, the first drug specifically designed to lower Lp(a), a review of antisense inhibition of apo(a) (J Lipid Res 2016)
- High Lp(a) combined with chronic Chlamydia infection may worsen aortic valve stenosis, a Swedish study of 101 patients (Eur Heart J 2003)
- Lp(a) drives worse outcomes after PCI and progression of aortic stenosis before TAVI, review for interventional cardiologists (J Clin Med 2026)
- Lp(a)-lowering agents could become the first pharmacological therapy for aortic valve stenosis, review argues (J Clin Med 2025)
- Chronic lipoprotein apheresis progresses aortic valve stenosis at a similar rate whether or not Lp(a) is elevated, 47-patient follow-up finds (Endocrine 2025)
- A Cleveland Clinic Journal of Medicine primer distills what clinicians need to know about Lp(a) risk, screening and emerging therapies (Cleve Clin J Med 2025)
- Lp(a) above 26.65 nmol/L predicts new-onset aortic valve calcification in coronary artery disease patients, 208-patient study finds (BMC Cardiovasc Disord 2025)
- From kringle IV type 2 copy number to arterial wall: the mechanistic biology of Lp(a) reviewed (Eur J Clin Invest 2026)
- A clinical practice review of Lp(a) risk stratification and the emerging lowering agents (Eur J Clin Invest 2026)
- Lp(a) shows no association with valve calcium burden or mortality in 454 TAVR patients (Clin Res Cardiol 2025)
- High Lp(a) plus high hs-CRP together confer a 4.74-fold risk of subclinical valve leaflet thickening after TAVR (J Am Heart Assoc 2024)
- Comparing 503 TAVI patients against 25,343 controls finds only a mild Lp(a) elevation in severe aortic stenosis, driven by men (JACC Adv 2024)
- 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)
- Lp(a) is rarely tested before cardiac rehab despite high prevalence, German registry of 3,393 (Clin Res Cardiol 2026)
- International guidelines now support a once-in-a-lifetime Lp(a) measurement in every adult, first phase 3 outcome trial results due in 2025 (Curr Opin Cardiol 2024)
- Lp(a) risk rises above 30 mg/dL, with the accepted 50 mg/dL threshold, and levels can range beyond 1000 mg/dL, a pathophysiology and treatment review (Int J Environ Res Public Health 2023)
- New ASO and siRNA drugs cut Lp(a) by up to 98%, far beyond what existing lipid-lowering therapies achieve, a review argues we are not yet ready to treat Lp(a) (Curr Atheroscler Rep 2023)
- Lp(a) is a causal risk factor for calcific aortic valve disease via oxidised phospholipids, though whether lowering it slows progression remains unproven, a review (Curr Opin Clin Nutr Metab Care 2024)
- Beyond statins and PCSK9 inhibitors, several non-lipid drug classes also alter Lp(a) levels, a review through January 2023 (Pharmaceuticals 2023)
- Lp(a) promotes aortic valve calcification via a 'three hit' mechanism, lipid deposition, inflammation and autotaxin transport, a review of emerging RNA treatments (J Cardiovasc Dev Dis 2023)
- The LPA gene IL-6 response elements make Lp(a) an inflammatory driver, not just a lipid particle, at levels above 125 nmol/L, 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)
- 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)
- 1.4 billion people worldwide have elevated Lp(a), and siRNA drugs dosed just 3-4 times a year could finally treat it, a review (Cardiovasc Res 2022)
- Severe aortic stenosis patients have 35% higher Lp(a) and more lysis-prone fibrin clots, linking Lp(a) to a prothrombotic phenotype in 138 patients (Atherosclerosis 2022)
- About 1 in 5 people has Lp(a) above 50 mg/dL, and it raises cardiovascular risk even with LDL cholesterol below 70 mg/dL, a review (J Cardiovasc Pharmacol 2022)
- LPA shares up to 70% of its sequence with plasminogen, explaining Lp(a) triple threat of atherosclerosis, thrombosis and inflammation, a review (Biomolecules 2022)
- 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)
- Aortic stenosis affects 2% of people over 65, and Lp(a) drives its progression through oxidised-phospholipid-triggered valve calcification, a review (Trends Cardiovasc Med 2021)
- An Exploratory Analysis of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibition and Aortic Stenosis in the FOURIER Trial
- Antisense apo(a) and apoB inhibitors could cut Lp(a) by up to 80%, a review of Lp(a)-lowering strategies for coronary disease (Drugs 2020)
- Lp(a) above 50 mg/dL raises cardiovascular risk, above 180 mg/dL matches familial hypercholesterolaemia, a review 57 years after Lp(a) discovery (Prog Cardiovasc Dis 2020)
- Lp(a) causally drives calcific aortic valve stenosis and predicts faster disease progression, a systematic review of 21 studies (Prog Cardiovasc Dis 2020)
- Lp(a) triggers a cascade from valve damage to calcification via autotaxin and NF-kB, a review of aortic valve stenosis mechanisms (Biomolecules 2019)
- 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)
- 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)
- Oxidised phospholipids and autotaxin link Lp(a) to aortic valve calcification, mechanistic review (Int J Mol Sci 2026)
- Lp(a) does not predict bioprosthetic aortic valve degeneration, unlike native valve disease, cohort of 389 (Clin Res Cardiol 2026)
- High Lp(a) may worsen long-term survival after TAVI despite similar 12-month MACCE, prospective cohort of 82 (Pol Arch Intern Med 2026)
- In severe aortic stenosis, Lp(a) does not track with valve calcium and shows only a modest, male-specific link to fibrosis, CT and cytokine study finds (J Transl Med 2025)
- A practical review positions Lp(a) as predictive of aortic stenosis onset, progression, and even bioprosthetic valve durability (Nutr Metab Cardiovasc Dis 2025)
- Higher Lp(a) drives earlier onset and faster pressure-gradient progression in calcific aortic stenosis, review finds, with RNA-based agents the emerging therapeutic hope (Am J Med 2025)
- Review argues Lp(a) is an under-recognised, modifiable driver of aortic stenosis progression as targeted drugs emerge (Int J Cardiol Heart Vasc 2024)
- A cardiac surgeon's perspective argues Lp(a) testing should refine risk assessment after aortic valve replacement and heart transplantation (Int J Cardiol Cardiovasc Risk Prev 2024)
- Review explains how Lp(a) drives both atherosclerosis and aortic valve calcification through shared inflammatory and antifibrinolytic mechanisms (Cureus 2024)
- As Lp(a)-lowering drugs approach outcome trials, aortic stenosis joins atherosclerosis as a key target, a review from synthesis to therapy (Int J Mol Sci 2022)
- Mechanistic, epidemiologic and genetic evidence converges on Lp(a) as a causal driver of both atherosclerosis and aortic stenosis, a review of emerging therapies (J Clin Med 2022)
- From Kare Berg 1963 discovery to today targeted drugs, a practising clinician guide to Lp(a) (J Clin Med 2022)
- Oxidised phospholipids bound to apo(a) kringle IV-10 domain may explain why Lp(a) is such a potent risk factor at far lower concentrations than LDL, a review (Atherosclerosis 2022)
- Lp(a) drives calcific aortic valve disease through four distinct mechanistic routes, but no clinical trial has yet targeted it directly, a review (Front Cell Dev Biol 2022)
- Genetic studies now confirm Lp(a) causally drives aortic valve stenosis, but no approved therapy yet lowers it, a review of imaging and emerging targets (Nutr Metab Cardiovasc Dis 2022)
- Lp(a)-carried oxidised phospholipids drive valve calcification through pro-osteogenic signalling, a review of the current landscape in calcific aortic valve disease (Curr Opin Cardiol 2021)
- As Lp(a)-lowering drugs enter outcome trials, should everyone be screened? A review by a leading cardiologist weighs the case (Curr Cardiol Rep 2021)
- PCSK9 inhibitors are the only current lipid drugs that both lower Lp(a) and reduce cardiovascular events, while niacin and CETP inhibitors fall short, a review (Vasc Health Risk Manag 2021)
- 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)
- Apo(a)-targeted drugs can lower Lp(a) by up to 90%, a review of Lp(a) mechanisms in atherosclerosis and aortic stenosis (Hellenic J Cardiol 2020)
- Emerging apo(a)-targeted therapies could transform Lp(a) management, a review of Lp(a)'s role in preventive cardiology (Curr Opin Cardiol 2019)
- Lp(a) clinical utility remains undefined despite mounting evidence for its causal role in atherosclerosis and aortic valve disease, a review of remaining questions (Curr Opin Lipidol 2018)
- The Lp(a) hypothesis awaits its first clinical trial test, unlike the LDL hypothesis, a review of Lp(a) and cardiovascular disease (Front Biosci (Landmark Ed) 2018)
- Lp(a)-lowering therapies remain limited despite proven links to residual cardiovascular risk, aortic stenosis and peripheral arterial disease, a review (Curr Treat Options Cardiovasc Med 2017)
- Lp(a) at the crossroads: review of emerging strategies to cut residual cardiovascular risk (Curr Atheroscler Rep 2026)
- Investigational agents cut Lp(a) by 80% to 100%, pharmacotherapy review (Am J Health Syst Pharm 2026)
- A bibliometric map of Lp(a) research finds inflammation, aortic valve stenosis and postmenopausal hormone changes as the dominant themes (Front Public Health 2022)
- Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target
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