RSanchezEndo

✅Adición de inhibidores de PCSK9 a la terapia con inhibidores de SGLT2 ➡️Provoca una remodelación de las subespecies de LDL y de la composición lipídica, con implicaciones mecanicistas para la protección vascular en la diabetes tipo 2. atherosclerosis-journal.com/article/S0021-…

👉 Update on familial hypercholesterolemia: An expert clinical consensus from the National Lipid Association 👆 FH is common (≈1:311) and systematically underdiagnosed → the real problem is not rarity, it’s detection 👆 Driven by lifelong LDL-C exposure, not a single value → risk = LDL-C × time 👆 Genetics help, but phenotype rules → treat based on LDL-C burden, not just mutations 📍 Diagnosis LDL-C ≥190 mg/dL (adults) → think FH, but confirm clinically Genetic testing = useful for cascade screening, not mandatory Always exclude secondary causes before labeling 📍 Screening Universal pediatric screening (9–11 yrs) is not optional—it’s delayed prevention Cascade screening = highest yield strategy (and still underused) 📍 Risk Standard risk calculators? Useless in FH → they underestimate risk Risk depends on: Lifetime LDL exposure Lp(a) Family history Timing of treatment 📍 Treatment (no shortcuts) Lifelong, early, aggressive Targets: <55 mg/dL (secondary prevention) <70 mg/dL (primary prevention) Start with: High-intensity statin, ezetimibe, PCSK9i / others as needed ≥50% LDL reduction is the floor, not the goal 📍 Take-home FH is not a lipid disorder. It’s a time-dependent vascular disease. Diagnose early, treat hard, treat forever. 🔗 🔓 Open Access #fig0010" target="_blank" rel="nofollow noopener">lipidjournal.com/article/S1933-… @nationallipid @LipidJournal @society_eas

In an open-label, randomized trial in @NEJM, researchers compared an intensive LDL goal (<55 mg/dl) with a conventional one (<70 mg/dl) among patients with stable cardiovascular disease.

¿Las enfermedades autoinmunes ocultan un factor de riesgo cardiovascular frecuentemente ignorado? Una reciente revisión sistemática revela el papel crucial de la Lipoproteína(a) en estos pacientes. 🧵👇🏻 doi.org/10.1016/j.jacl… @GEAS_SEMI_ @gt_rcv @GAELPaArg @drpablocorral @MaximaMendez15 @anymzcs @joraltron @alavallecobo @maciejbanach @alejoromanmd @gonzaeperez @LipidoSeen

2026 AACE Diabetes Algorithm — the comorbidities-first approach is a game changer for T2D management. No longer just “lower the A1C.” We now select therapy based on complications & comorbidities first, independent of glycemic targets. ▸ Heart Failure → SGLT2i (+ GLP-1 RA / GIP/GLP-1 RA) ▸ CKD → SGLT2i (+ GLP-1 RA) ▸ ASCVD / High Risk → GLP-1 RA (+ SGLT2i) ▸ Stroke/TIA → GLP-1 RA or Pioglitazone ▸ MASLD → GLP-1 RA / GIP/GLP-1 RA or Pioglitazone Key pearl: A1C >9%? Start ≥2 agents. Severe hyperglycemia → consider basal insulin early. Don’t let titration lag cost your patient. Bottom line: treat the whole patient, not just the glucose. 💊 #Diabetes #T2D #Endocrinology #AACE2026 #MedEd #ClinicalPearls

🧂 Excess aldosterone doesn’t just raise blood pressure — it drives fibrosis, endothelial dysfunction, oxidative stress & immune activation across the heart, kidney, and vasculature. The downstream consequences: ❤️ Heart failure ⚡ Atrial fibrillation 🩺 Hypertension & atherosclerosis 🫘 CKD Steroidal MRAs (spironolactone, eplerenone) can block this — so why are they underused? 🚧 Barriers to treatment: ▪️ Adverse effects in risk groups ▪️ Optimism bias: “nothing will happen” ▪️ Loss aversion: perceived side effects outweigh proven benefit ▪️ General inertia & decision fatigue We have the drug. We need the will to prescribe it. #Aldosterone #MRA #HeartFailure #Cardiology #CardioTwitter

Coronary artery calcium scoring in 2026: strengths, limitations, and optimized clinical use frontiersin.org/journals/radio… via @SABOURETCardio et al

🧠 ESTENOSIS CAROTÍDEA ASINTOMÁTICA: ¿Cuándo revascularizar en 2026? 1️⃣ El riesgo de ictus ipsilateral en estenosis ≥70% bajo terapia médica intensiva es ~1.5%/año (CREST-2, NEJM 2026) — mayor de lo estimado por estudios observacionales previos (0.5–1.0%/año). 2️⃣ CREST-2 (n=2485): Stenting redujo el evento primario vs. terapia médica sola (2.8 vs. 6.0%; NNT=31). CEA no alcanzó significancia estadística (3.7 vs. 5.3%). Ambas técnicas mostraron tasas perioperatorias similares (~1.3–1.5%). 3️⃣ La revascularización en estenosis 70–99% asintomática se sugiere SOLO si: expectativa de vida ≥5 años + riesgo perioperatorio de ACV/muerte <1.5% (umbral actualizado post-CREST-2). Estenosis 50–69%: terapia médica intensiva sin intervención. 4️⃣ Marcadores de alto riesgo que individualizan la decisión: émbolos silentes en TCD, infarto silente ipsilateral en neuroimagen, hemorragia intraplaca en RM (HR 7.9), placa ecolucentе, área negra yuxtacanal >10mm² (stroke rate 5%/año). 5️⃣ La terapia médica intensiva es la base universal: estatinas (LDL <70mg/dL), antiagregación, control PA <130mmHg, cesación tabáquica y actividad física. Sin esto, ninguna revascularización optimiza su beneficio real. 🏥 Clínica Ricardo Palma — Centro Avanzado de Stroke | Lima, Perú ✍🏽 Dr. Manuel A. Moquillaza Valle | Neurólogo Vascular e Intervencionista | CMP 54060 / RNE 25595 #IctusIsquémico #EstenisisCarotídea #NeurologíaVascular #CREST2 #StrokePrevention

💬 Editorial: Statin guidelines and patient preferences for #ASCVD prevention often misalign, supporting the need for clearer risk communication and shared decision-making in clinical practice. ja.ma/4ckSECM

➡️El xantelasma se asocia con mayor incidencia a corto y largo plazo de MACCE, por sus siglas en inglés) a 10 años ✅Es un marcador clínico para la estratificación del riesgo vascular y el manejo preventivo sciencedirect.com/science/articl…

🫀🔥 LDL is controlled. Statins are optimized.
And yet… patients still have events. This study addresses one of the most important unanswered questions in cardiology: 👉 What really drives residual cardiovascular risk? 📊 In >9,400 statin-treated patients with LDL <70 mg/dL undergoing PCI: Patients were stratified by: Triglycerides (TG ≥150 mg/dL) Inflammation (hs-CRP ≥2 mg/L) 💡 The result is striking: 👉 Inflammation—not triglycerides—drives risk Residual inflammatory risk → ~1.8x higher MACE Combined TG + inflammation → ~1.9x higher MACE Residual TG risk alone → NO significant increase ⚠️ And what’s driving this? 👉 Mostly all-cause mortality Not subtle. Not marginal. 👉 Clinically meaningful. 🧠 Let’s be clear: We’ve spent decades optimizing: ✔ LDL ✔ Lipid profiles ✔ Cholesterol targets But this study shows: 👉 You can win the lipid battle… and still lose the war 🔥 Because atherosclerosis is not just lipid-driven. 👉 It’s an inflammatory disease 🎯 Clinical implication Risk stratification cannot stop at LDL. We need to integrate: hs-CRP Inflammatory burden Systemic biology 🚀 Paradigm shift From: ❌ “How low is LDL?” ➡️ to ✅ “How active is the disease?” 🧠 Bottom line Lowering LDL is necessary. 👉 But it is NOT sufficient. If inflammation persists: 👉 Risk persists. ⚡ The future of prevention? Not just lipid control. 👉 Inflammation-guided precision cardiology.

APOLIPOPROTEÍNAS: abecedario del riesgo cardiovascular 🧪De la A a la F, implicación en diferentes procesos cardio-vasculo- metabólico-trombo-inflmamatorios 🧪Marcadores que pueden mejorar la estratificación de riesgo cardiovascular 🧪ApoA1/ApoB y dislipemia aterogénica #CardioED

En pacientes con evidencia de aterosclerosis sin antecedentes de eventos cardiovasculares en la práctica clínica, el tratamiento con anticuerpos monoclonales inhibidores de PCSK9 se asoció con menores tasas de eventos isquémicos y mortalidad academic.oup.com/eurheartj/adva…

New in #EJPC: ✅ In statin-treated patients with well-controlled LDL-C undergoing percutaneous coronary intervention, residual inflammatory risk (alone or in combination with residual triglyceride risk) is associated with a higher incidence of MACE. 📕 ow.ly/C3Zg50YLyg7 #EJPC @EJPCEiC @AboyansV @SilCastelletti @PTBuketAkinci @PeroneFrancesco @SMosteoru @TimKambic #cvprev

New ACC/AHA Lipid Guidelines 2026 — Practice-Changing Insights:At a glance.. 📌 Core Philosophy “Lower LDL-C, earlier and for longer → better lifetime ASCVD reduction.” 🔬 1. Start Early – Think Lifetime Risk Lipid screening should begin at ≥19 years, with repeat every 5 years or earlier in high-risk individuals. Statin therapy can be initiated as early as 30 years if LDL-C ≥160 mg/dL, strong family history, or high 30-year risk—even if 10-year risk is low. 🎙️Key shift: Move from “10-year risk” to lifetime cumulative exposure model 🧮 2. PREVENT Risk Calculator Replaces PCE New AHA PREVENT tool improves ASCVD risk prediction and starts risk estimation from age 30. Includes 30-year risk estimation, crucial for younger patients. 📊 3. Recalibrated Risk Categories Low: <3% Borderline: 3–5% Intermediate: 5–10% High: ≥10% 👉 Clinical implication: Statins now justified at lower thresholds (≥5%) 🎯 4. LDL-C Targets Are Back <100 mg/dL → Low/intermediate risk <70 mg/dL → High risk <55 mg/dL → Established ASCVD 👉 Shift: From % reduction → absolute target-driven therapy 🧬 5. Universal Lp(a) Testing One-time Lp(a) measurement for ALL patients is now recommended. ≥125 nmol/L → ↑ ASCVD risk ≥250 nmol/L → ~2× risk ≥430 nmol/L → ~4× risk 👉 Intensify LDL lowering even if Lp(a) cannot yet be directly treated 🧪 6. ApoB & CAC — Precision Risk Tools ApoB reflects total atherogenic particle burden and helps detect residual risk. CAC score acts as “tiebreaker” in borderline/intermediate risk. ⚠️ 7. Expanded Risk Enhancers Now includes: PCOS, early menopause, adverse pregnancy outcomes South Asian and Filipino ethnicity CKM syndrome, inflammation markers 👉 Clinical message: Take detailed reproductive & ethnic history seriously 🩺 8. Special Populations – Stronger Statin Mandate All patients (40–75 yrs) with: CKD stage 3–4 HIV infection → Should receive statins irrespective of LDL-C 🍔 9. Triglycerides – Lifestyle First Statins remain foundational even in hypertriglyceridemia. Refer to dietitians if TG ≥150–1000 mg/dL with CKM features. 💊 10. Supplements – Clear Negative Recommendation Non-prescription supplements (e.g., fish oil) are NOT recommended for ASCVD risk reduction due to lack of benefit. 🔥 CME INDIA Take-Home Messages Atherosclerosis begins early → intervene early LDL exposure = cumulative toxin → duration matters as much as level Lp(a) is now a universal risk marker, not optional Risk assessment is shifting from short-term to lifetime biology Precision lipidology = LDL-C + ApoB + Lp(a) + CAC 🏷️ “From numbers to lifetime exposure: Lipidology has entered the era of precision prevention.” jamanetwork.com/journals/jama/…

🧬 Conclusiones clave sobre la Lp(a) por el Dr José López Miranda #recardio26 @preventiva_SEC 1️⃣ Es 6 veces más aterogénica que el LDL. 2️⃣ El 90% está determinada genéticamente. 3️⃣ Su síntesis es hepática y depende casi exclusivamente de la tasa de producción. 4️⃣ Trastorno lipídico muy prevalente en la población general: • >50 mg/dL → 20% • >100 mg/dL → 5-8% • >180-200 mg/dL → 1% 5️⃣ Síndrome de Hiper Lp(a): • Afecta al 1% de la población • Riesgo cardiovascular igual que la Hipercolesterolemia Familiar • Doble de prevalente que la HF

🚨🫀 We could prevent >350,000 deaths per year in the US from coronary disease… and we’re not. Let that sink in. This paper lays out a bold—but realistic—vision: 👉 By 2050, the majority of deaths from atherosclerotic coronary artery disease (ACAD) could be prevented. 💡 And the shocking part? We don’t need futuristic therapies. We already have: ✔ Blood pressure control ✔ Lipid-lowering therapies ✔ Smoking cessation ✔ Basic preventive care 👉 The problem is not knowledge. 👉 It’s implementation. 📊 Today’s reality: ✔️ Millions with uncontrolled hypertension ✔️ Massive underuse of statins ✔️ Many patients having their first MI without any preventive therapy 👉 This is not a science failure. 👉 It’s a system failure. 🧠 But here’s where it gets interesting… The paper proposes a paradigm shift: ❌ From treating late-stage disease (ischemia, events) ➡️ to ✅ Treating atherosclerosis as a lifelong process Starting: ✔️ Early ✔️ Before symptoms ✔️ Before stenosis 🔥 This aligns perfectly with what imaging is showing us: 👉 Disease starts early 👉 Progresses silently 👉 Becomes visible only when it’s already advanced ⚠️ The uncomfortable truth: We’ve built a system optimized for: ✔️ Procedures ✔️ Acute care ✔️ Late-stage intervention Not for: 👉 Prevention at scale 🚀 The real opportunity Combine: ✔️ Early detection (imaging, risk profiling) ✔️ Aggressive prevention ✔️ System-level implementation 🧠 Final thought We don’t need to discover how to prevent coronary disease. 👉 We already know how. The real question is: Why aren’t we doing it?

👉Antes y despues de iPCSK9 👉Más allá de la barrera del precio atherosclerosis-journal.com/article/S0021-… ➡️Una interesante revisión⬅️

➡️➡️➡️El embarazo es una de las primeras pruebas de esfuerzo de la mujer⬅️⬅️⬅️ ✅Diabetes gestacional, trastornos hipertensivos y otras complicaciones obstétricas no son antecedentes personales cualquiera en riesgo vascular ➡️Tener en cuenta en todas las estrategias de prevención

¿El HDL-C alto es siempre sinónimo de "colesterol bueno" y protección cardiovascular? Una revisión reciente de Parini y Pedrelli (2026) desmiente este mito y redefine nuestra interpretación clínica. 👇 DOI:10.1097/MOL.0000000000001041 @anymzcs @drpablocorral @MaximaMendez15 @society_eas @gt_rcv @LipidoSeen @preventiva_SEC @maciejbanach @BrezanSimonMD @PuigJove @SABOURETCardio