Atherosclerosis

La epidemiologia, genética respaldan que TRL-RC es un factor causal y modificable del riesgo de evento Debiéramos.priorizar agentes que reducen tanto la RC como la apoB e incluir a pacientes con niveles marcadamente elevados de TRL-RC @EASCongress2026 atherosclerosis-journal.com/article/S0021-…

A new era in atherothrombosis 🚀 Prof. Lina Badimon’s @ATHjournal review explores how lipids, inflammation and thrombosis are reshaping ASCVD care. More tomorrow at #EASCongress2026 🕣 08:30 | Anitschkow Hall 🔗 atherosclerosis-journal.com/article/S0021-… #MyEAS2026 @EASCongress @society_eas

Los conocimientos sobre ✅progresión aterosclerosis ✅interacción factores de riesgo vascular y lpared vascular ✅disfunción endotelial ✅depósito lípidos ✅respuestas inmunitarias innatas, adaptativa ✅linflamación sistémica Revision👇👇 atherosclerosis-journal.com/article/S0021-… #SEACongress2026

Remnant cholesterol: no longer just a biomarker?Following Prof. Rosenson’s #EASCongress2026 plenary, this @ATHjournal review makes the case for RC as a causal, modifiable contributor to residual ASCVD risk 🔗atherosclerosis-journal.com/article/S0021-… #MyEAS2026 @EASCongress @society_eas

El ejercicio reduce la inflamación y ralentiza la acumulación de placa ✅Recupera lesion cardíaca después de IAM ✅Reduce el riesgo de ictus ✅Transforma el manejo de la insuficiencia ✅Mantiene el equilibrio inmunológico e inflamatorio #EAScongress2026 atherosclerosis-journal.com/article/S0021-…

CHIP, loss of Y chrom, inflammation, ath: a lot to discuss❗️ In @ATHjournal, Ramos-Neble reviews hematopoietic somatic mutations in ASCVD. Perfect reading ahead of SaaG session on CAD genetics & clonal hematopoiesis at #EASCongress2026 🔗 atherosclerosis-journal.com/article/S0021-… #MyEAS2026

How do genetics and modifiable risk interact in ath❓ Prof. Heribert Schunkert addresses this in a 🆕 @ATHjournal review, and will discuss it tonight during the Anitschkow Lecture at #EASCongress2026. 🕡 18:45–19:30 📍 Anitschkow Hall 🔗 atherosclerosis-journal.com/inpress #MyEAS2026

Inflammation in ASCVD: measurable, targetable, clinically actionable 🌟 A timely #EASCongress2026 read in @ATHjournal, where Prof. Ridker revisits key lessons from his 2025 Anitschkow Lecture: hsCRP, residual inflammatory risk, CANTOS and IL-6 inhibition 🔗atherosclerosis-journal.com/article/S0021-…

👉Just published in Atherosclerosis — a true milestone for the global lipid community. 🌍🫀 ☝️The new EAS Consensus Statement on lipid clinics brings together experts from 55 countries and more than 500 lipid clinics to provide practical guidance on harmonization, organization, staffing, education, patient pathways, and funding of lipid services worldwide. 📌 Why it matters: • Establishes a global framework for lipid clinic development • Promotes equitable access to high-quality lipid care • Supports earlier diagnosis and better management of inherited and complex lipid disorders • Strengthens prevention of ASCVD on a worldwide scale • Highlights the importance of education, registries, and multidisciplinary care ☝️A fantastic initiative by the European Atherosclerosis Society Lipid Clinic Network and all contributing authors. Proud to have participated in this important international effort. ☝️A must-read for anyone involved in preventive cardiology, lipidology, cardiovascular prevention, and healthcare policy. 🔓🔗 atherosclerosis-journal.com/article/S0021-… @society_eas @ATHjournal @BNordestgaard @ProfKausikRay

What is good for the 🫀 may also be good for the 🧠 In @ATHjournal, Prof. Ruth Frikke-Schmidt reviews the links btw ath and dementia, w/ a focus on causality and prevention Catch her lecture 🔜 at #EASCongress2026 🕤 09:36–09:58 🔗 atherosclerosis-journal.com/article/S0021-… #MyEAS2026 @society_eas

What if one of the most powerful CV tools is also one of the simplest❓ In @ATHjournal, Prof. Hendrik B. Sager and colleagues review exercise as medicine for cardiovascular health. Catch his lecture 🔜 at #EASCongress2026 🕘 09:14–09:36 🔗 atherosclerosis-journal.com/article/S0021-… #MyEAS2026

#EASCongress2026 starts today, and some of the science will move from the stage to the page. During the @EASCongress, @ATHjournal will publish reviews by selected presenters on 🗝️ topics discussed in 🇬🇷. Keep an 👁️ on 👇 atherosclerosis-journal.com/inpress ... and spread the word! #MyEAS2026

Excited to share our editorial in Atherosclerosis on a common question in ACS care...how do we look beyond the culprit lesion and think about what remains untreated? 🫀 Special thanks to @ATHjournal @cardiac_md @CMartinezLicha sciencedirect.com/science/articl…

Exogenous PCSK9 can be internalized by Smooth Muscle Cell, likely a major resource for arterial wall in vivo LRP1-mediated Compete with oxLDL Mathilde Varret lab @ATHjournal 2026 atherosclerosis-journal.com/article/S0021-…

Proud and truly delighted to share that the results of our research-The ANFIBIO Study- have been published in @ATHjournal Thanks to everyone involved @IRBLleida_Info @harnaulleida @IISAragon @idisbaib Also to @secardiologia @cuidarcorazon for supporting this project through a competitive research grant. Coronary macrovascular and microvascular involvement and their association with distinct circulating microRNA patterns: The ANFIBIO Study atherosclerosis-journal.com/article/S0021-…

New publication in @ATHjournal . Proud to collaborate with colleagues from Latin America and Europe on this review addressing the safety of very low LDL-C levels. Current evidence supports intensive LDL-C lowering without major safety concerns in high-risk patients. @society_eas

🙌 Our last manuscript is out. 👉“Safety of Very Low LDL-Cholesterol: Ten Common Concerns, Misconceptions, and Evidence-Based Clarifications” 📍Very low LDL-C levels continue to generate debate, fear, and misinformation in clinical practice. 📍In this review, we critically examined 10 of the most frequent concerns related to intensive LDL-C lowering: — Cognitive decline — Hemorrhagic stroke — Cancer — Cataracts — Hormonal dysfunction — Diabetes risk — Muscle symptoms — Older adults — Sex differences — Overall cardiovascular benefit 📍The key message is clear: RCTs, meta-analyses, and genetic evidence consistently support the safety profile of very low achieved LDL-C levels in appropriately selected high-risk patients. 📍Some adverse effects are real — particularly statin-associated dysglycemia and muscle symptoms — but their absolute risk is generally modest compared with the magnitude of ASCVD risk reduction. 📍Therapeutic inertia and misinformation remain major barriers in preventive cardiology. Evidence-based communication matters. 📍Lower LDL-C. Earlier. Longer. Safer than many still believe. ☝️Proud to collaborate with outstanding colleagues from Latin America, Europe, and beyond in this international effort. 🔗 doi.org/10.1016/j.athe… @society_eas @ATHjournal

👆 Inflammation ≠ Lp(a): Parallel Paths to ASCVD 📍 Mendelian randomization study assessing IL-6 signaling inhibition, Lp(a), and ASCVD risk 👉 IL-6 inhibition → modest reduction in Lp(a) (~–3 mg/dL) 👉 Clear reduction in ASCVD risk across outcomes (CAD, stroke, carotid plaque) 👉 Key point: Lp(a) explains only a small fraction of this benefit (~1–5%) 👉 Even in high Lp(a) genetic carriers, mediation remains limited (up to ~15%) 👉 Stronger IL-6 → Lp(a) effect in these carriers, but no greater clinical benefit 👉 Most cardiovascular benefit driven by Lp(a)-independent inflammatory pathways 👉 No evidence that elevated Lp(a) modifies IL-6–ASCVD risk reduction 📍 Clinical implication: 👉 IL-6 pathway ≠ Lp(a) pathway 👉 They are independent and complementary targets Translation: lowering inflammation won’t meaningfully replace Lp(a)-lowering strategies 📍 Bottom line: 👉 IL-6 and Lp(a) are independent, complementary targets 👉 Lowering one won’t replace treating the other 🔗 Open Access atherosclerosis-journal.com/article/S0021-… @society_eas @ATHjournal

Lipoprotein(a), interleukin-6 and cardiovascular risk in a primary prevention setting ☝️New data from UK Biobank (n=34,092): In primary prevention, the cardiovascular risk associated with elevated Lp(a) was significantly influenced by IL-6, a key upstream inflammatory cytokine. 1️⃣ Higher Lp(a) increased MACE risk only when IL-6 was elevated (HR 1.17; 95% CI 1.07–1.28), while no significant association was seen when IL-6 was below median levels. 2️⃣ Inflammation appears to amplify Lp(a) pathogenicity, supporting the concept that not all elevated Lp(a) carries the same biological risk burden. 3️⃣ hs-CRP did not show the same modifying effect, suggesting IL-6 may be a more informative biomarker than conventional inflammatory markers for Lp(a)-related risk stratification. 4️⃣ Clinical implication: Future Lp(a)-lowering therapies may yield greatest benefit in individuals with concomitant elevated IL-6, enabling more precise preventive targeting. 👉 Elevated Lp(a) appears to confer its greatest cardiovascular hazard in the presence of heightened IL-6–mediated inflammation, supporting a biologically integrated model in which inherited atherothrombotic burden and residual inflammatory risk act synergistically @ATHjournal @society_eas 🔗 doi.org/10.1016/j.athe…

👉The secretory PCSK family in cardiovascular disease and beyond 👉PCSK9 & PCSK7: from atherosclerosis to oncology 📍PCSK9 = more than LDL-C → ↓LDLR → ↑LDL-C (classical role) → also drives vascular inflammation and plaque instability • Immune modulation (the oncology bridge) → PCSK9 promotes degradation of MHC-I → ↓ antigen presentation → ↓ CD8+ T-cell activation → facilitates tumor immune escape 📍PCSK7: complementary effects → ↑ apoB/VLDL secretion → atherogenic burden → in T-cells: modulates immune checkpoint proteins → impacts cytotoxic activity • Oncology signals (preclinical but consistent) → PCSK9 inhibition → ↑ intratumoral CD8+ T-cells → ↓ tumor growth and metastasis → enhances response to immunotherapy ☝️Dual targeting = synergy → PCSK9 (circulation + tumor interface) → PCSK7 (T-cell intrinsic regulation) → combined inhibition → >90% reduction in metastasis in models • Conceptual shift From lipid biology → immunometabolic regulation of cancer 👉Bottom line: PCSK9 helps tumors hide. PCSK7 weakens the attack. 🔗 atherosclerosis-journal.com/article/S0021-… @society_eas @ATHjournal @nationallipid