@ARAA1981

DIOS, LA PATRIA, LA ETICA SOCIAL, YA BASTA DE TANTO EXCREMENTO MENTAL. QUIERE A TU PROJIMO

en el monte topochero
Joined January 2012
IMPUNIDAD CERO retweeted
Editorial @Nature this week calls out lack of real world data for AI medical algorithms nature.com/articles/d41586-0…
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This systematic review and meta-analysis suggests that LDL-C-lowering therapies may offer a greater benefit in preventing first-time MI compared with recurrent MI 📖 doi.org/10.1093/eurjpc/zwaf3… @escardio @AboyansV @SilCastelletti @PeroneFrancesco @PTBuketAkinci @SMosteoru @TimKambic
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IMPUNIDAD CERO retweeted
Original Article: Prevalence of Silent Atherosclerosis across Adult Life (REACT trial) nej.md/46gp1hP #ESCCongress | @escardio
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IMPUNIDAD CERO retweeted
Replying to @dadstrengthday
Except CAC is less likely to be positive in folks < 40 years of age unless they have very abnormal risk factors. In the younger group, Carotid ultrasound looking for plaque would be a better choice. And data from the recently published REACT trial shows plaque shows up a bit more frequently in carotids before coronaries
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IMPUNIDAD CERO retweeted
الروابط الجديدة لموقع sci-hub لتحميل الابحاث العلمية المدفوعة مجاناً 👇👇 1- sci-hub.ee 2- sci-hub.xin 3- sci-hub.ai 4- sci-hub.st 5- sci-hub.se 6- sci-hub.do
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IMPUNIDAD CERO retweeted
We have a new paper today that links Lp(a) with triglycerides in patients with moderate hypertriglyceridemia (TG 150-500). Using our new methods we developed @UCSDCardiology Lp(a) becomes TG- and cholesterol-enriched. ApoC-III inhibition reduced Lp(a)-TG and Lp(a)-C by ~60–70% without lowering Lp(a) particle number, revealing pharmacologically modifiable Lp(a) heterogeneity. We now need to see how Lp(a)-C and Lp(a)-TG correlate with CV outcomes. sciencedirect.com/science/ar…
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IMPUNIDAD CERO retweeted
Replying to @codiguillos
El venezolano como siempre no ve lo que tiene enfrente, es envidioso, inventor, y pura cizaña. A muchos ha ayudado este sistema y claro la mentalidad de poca cosa y pobreza que metió Chávez en la cabeza de todos. No creen que pueda haber una persona que haya hecho esto.
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IMPUNIDAD CERO retweeted
🧵 In patients with severe asymptomatic #carotid artery stenosis, carotid revascularization with carotid artery stenting or carotid endarterectomy plus intensive medical management did not improve cognition vs intensive medical management alone over up to 4 years. These findings indicate that cognitive benefit should not be presented as an expected outcome when discussing treatment options for this population. ja.ma/4xwkzH9
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IMPUNIDAD CERO retweeted
👉This new Mendelian randomization study, including more than 425,000 participants from the UK Biobank, provides important insights into the specific causal effects of Lp(a) and its implications for future Lp(a)-lowering therapies. ☝️Top 5 Take-Home Messages 1️⃣ Lp(a) exerts a direct causal effect on coronary artery disease (CAD), independent of LDL-C. This reinforces that Lp(a) is not simply another LDL particle, but an independent driver of atherosclerosis. 2️⃣ Among 1,456 phenotypes analyzed, only CAD and HbA1c showed direct causal effects of Lp(a). Most other associations appear to be indirect or mediated through other pathways, highlighting the remarkable specificity of Lp(a). 3️⃣ Very low genetically determined Lp(a) levels were not associated with a higher risk of type 2 diabetes. These findings provide reassuring evidence for the long-term safety of profound Lp(a)-lowering therapies currently under development. 4️⃣ The optimal Lp(a) threshold for myocardial infarction risk discrimination was ~86 nmol/L in Europeans and ~93 nmol/L in Africans, suggesting that clinically relevant risk may begin at lower levels than the current 125 nmol/L cutoffs adopted by many guidelines. 5️⃣ The study supports treating LDL-C and Lp(a) as complementary but distinct cardiovascular risk factors. Even with optimal LDL-C control, elevated Lp(a) remains a causal contributor to coronary disease, emphasizing the need for dedicated Lp(a)-lowering strategies. ☝️Bottom line: Lp(a) appears to have a highly specific causal role in coronary atherosclerosis, independent of LDL-C, while concerns about diabetes risk from very low Lp(a) levels are not supported by this large Mendelian randomization analysis. 🔓🔗 jacc.org/doi/10.1016/j.jacad… @society_eas @nationallipid @JACCJournals
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#CorCal #ESCCongress #CVPrev 🫀5,772 primary prevention pts (52% women) → CAC-guided vs PCE-guided statin therapy ➡️At 4.2 yrs: MACE 2.7% vs 2.7% HR 0.99 (95% CI 0.71–1.38)- no diff ➡️Noninferiority NOT met due to low event rates but CAC recommended fewer statins with better adherence: 62% CAC 🆚23% PCE So, Risk Scores 🆚 #CAC? What’s the best choice?
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IMPUNIDAD CERO retweeted
🚨 Your cardiologist targets an LDL below 70 and calls it good control. A new randomized trial just proved that number is too high. Ez-PAVE randomized 3,048 heart attack survivors to a target below 55 versus below 70, and the lower target cut nonfatal MI by 54%. "But the data says otherwise." And no, this is not another drug trial pretending to answer a target question. I am a cardiologist. I have hundreds of patients on high-intensity statins, ezetimibe, and PCSK9 inhibitors. I have spent years watching patients get told their LDL of 68 is "controlled." Ez-PAVE proves that framing is wrong. 🩺 Here is what the science actually says. For years we had PROVE-IT, TNT, IMPROVE-IT, and FOURIER. Great trials. Wrong question. They tested drugs added to other drugs. None of them randomized patients to an actual LDL target. Ez-PAVE did. 💓 EZ-PAVE (statin, ezetimibe, PCSK9 inhibitor combinations): 3,048 high-risk ASCVD patients in South Korea, randomized to below-55 versus below-70 mg/dL targets, followed a median of 3.0 years. 🔬 The numbers: Median achieved LDL: 56 mg/dL versus 66 mg/dL. Primary endpoint: 6.6% versus 9.7%. HR 0.67, 95% CI 0.52 to 0.86, P=0.002. 33% relative risk reduction. 3.1 percentage point absolute risk reduction. Nonfatal MI: 1.7% versus 8%. A 54% relative reduction. That matters because a 10 mg/dL difference in achieved LDL, nothing more, produced that separation. ⚠️ The safety question everyone asks: New-onset diabetes was lower in the intensive group, 6% versus 16.1%. Kidney function was better in the intensive group, not worse. Creatinine elevation 2% versus 2.7%, P=0.004. No increase in muscle symptoms, cancer, or liver enzymes. Going lower did not cost these patients anything. It protected them. 🔸 One subgroup showed a numerically worse HR of 1.22 in women. The confidence interval crossed 1.0, 0.66 to 2.28, and only 638 women were enrolled. This trial was not powered for sex-specific analysis. That is a statistical artifact, not a safety signal. Do not let anyone tell you otherwise. ❌ Only 60.8% of the intensive group even reached below-55, in a research setting with motivated investigators watching every visit. ❌ In real-world practice, fewer than 25% of eligible patients reach below-55. Fewer than 10% are on ezetimibe. About 1% are on a PCSK9 inhibitor. The gap between what works and what we actually do is enormous. ❤️ Bottom line: An LDL of 70 is not a finish line. It is a compromise we settled for before we had the trial to prove we could do better. This is one randomized trial of 3,048 patients, but it directly answers the target question that four prior landmark trials never asked. Get your LDL checked. If you have known heart disease and your number is above 55, ask your doctor about escalating therapy. Statin. Ezetimibe. PCSK9 inhibitor if needed. A patient who pushes LDL from 68 to 56 mg/dL can meaningfully lower their MI risk within 3 years. That is the difference between a second heart attack and a normal life. The question is no longer whether lower is better. The question is why your LDL still is not below 55. #Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #LDL #Statins #PCSK9 #ApoB #PreventiveCardiology #LifestyleMedicine
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IMPUNIDAD CERO retweeted
👉Precision genome editing for lipid lowering: a new therapeutic paradigm? 🧬 Human genetics provides the blueprint: protective loss-of-function variants validate PCSK9 and ANGPTL3 as targets ✂️ The field is evolving from conventional CRISPR-Cas9 toward more precise base and prime editing 🎯 Beyond PCSK9 and ANGPTL3, APOC3, LPA, APOB and LDLR expand the therapeutic landscape 💉 LNP-based hepatic delivery opens the possibility of sustained one-and-done lipid lowering ⚠️ Permanence is both the strength and the challenge: off-target effects, irreversibility and long-term safety remain critical 🤔The ultimate question: Can a single intervention replace decades of lipid-lowering pharmacotherapy? 🔗 sciencedirect.com/science/ar… @society_eas
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Echocardiography is the key tool for the diagnosis and evaluation of valve disease. Explore our Valve Disease Resources web page! bit.ly/3XTzvx2 The resources page features: ❤️ Guidelines ❤️ Lectures ❤️ Cases ❤️ Articles ❤️ Videos
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IMPUNIDAD CERO retweeted
Among >94,000 patients with #moderate AS: 🔹 Nearly 2 in 5 did not undergo follow-up echocardiography within 2 years 🔹 Among those with follow-up, 1 in 3 progressed to severe AS Read more in @CircAHA 👇🏻 ahajournals.org/doi/full/10.…
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IMPUNIDAD CERO retweeted
Here is our @JACCJournals paper on Lp(a) vs OxPL in same model in pre-existing mild-mod aortic stenosis. Each are independent predictors of progression, but in same model, @OxPL_apoB is a significant predictor but Lp(a) is not. This type of work over for 2 decades allowed us to understand not all Lp(a) particles are similar @EricTopol @hsbhatia ncbi.nlm.nih.gov/pubmed/3954…
Thank you @EricTopol for highlighting our ESC presentation!🙏🏻
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IMPUNIDAD CERO retweeted
Tiene razón en el diseño: Lp(a)HORIZON randomizó un grifo y dejó el de ApoB fijo en los dos brazos, así que ese resultado negativo no dice nada sobre el modelo de partículas en su conjunto. Pero el desagüe no es un solo caño: hay una salida segura, el receptor de LDL (LDLR), que recicla la partícula en el hígado, y una salida patológica, los receptores scavenger de macrófagos y del endotelio (como LOX-1), que solo entran a tallar cuando la partícula ya llegó modificada, y no la reciclan, la atrapan. Por cuál sale cada partícula depende de cuánto tiempo lleva circulando y en qué estado químico llega, y eso no lo fija solo la genética, lo fija el ambiente metabólico: glucemia, inflamación, tabaco, uremia, sueño, entrenamiento. Al modelo clásico no le falta un dato, le falta una pata: cuenta partículas y mira el subendotelio, pero nunca mide el ambiente que las va modificando mientras circulan. Cuanto más tiempo circula una partícula, más se modifica (glicación, oxidación, carbamilación) hasta que el LDLR deja de reconocerla y termina saliendo por la vía scavenger, que no recicla, inflama: activa LOX-1, sube PCSK9, baja el LDLR disponible para el resto de las partículas, un circuito que se retroalimenta. Por eso diálisis, con ApoB normal, tiene 10 a 20 veces más riesgo cardiovascular y las estatinas no bajan eventos ahí: el LDLR funciona bien, el problema es que el ligando ya llegó dañado por la uremia y sale por la otra puerta. Marco completo, hipótesis con predicciones falsables: doi.org/10.3389/fcvm.2026.18… Fair point on design: Lp(a)HORIZON randomized one faucet while ApoB stayed fixed in both arms, so a null there says nothing about the particle model as a whole. But the drain isn't one pipe: there's a safe exit, the LDL receptor (LDLR), which recycles the particle in the liver, and a pathological exit, scavenger receptors on macrophages and the endothelium (like LOX-1), which only kick in once the particle is already modified, and don't recycle it, they trap it. Which exit a particle takes depends on how long it's been circulating and what chemical state it's in when it gets there, and that's not set by genetics alone, it's set by the metabolic environment: glucose control, inflammation, smoking, uremia, sleep, training load. The classic model isn't missing a data point, it's missing a leg: it counts particles and looks at the subendothelium, but never measures the environment modifying them while they circulate. The longer a particle circulates, the more it gets modified (glycation, oxidation, carbamylation) until the LDLR stops recognizing it and it exits through the scavenger route instead, which doesn't recycle, it inflames: activates LOX-1, upregulates PCSK9, lowers the LDLR available for every other particle still circulating, a feedback loop. That's why dialysis patients, with normal ApoB, carry 10 to 20x the cardiovascular risk, and statins don't reduce events there: the LDLR works fine, the ligand already arrived damaged by uremia and exits through the other door. Full framework, hypothesis with falsifiable predictions: doi.org/10.3389/fcvm.2026.18…
So why are all keto zealots crawling from under their rocks declaring "lipid hypothesis is dead!" after the Lp(a) HORIZON readout? Let's find out. Both arms of Lp(a)HORIZON were on optimized lipid-lowering therapy. The trial randomized one thing on top of that, and the thing it randomized was Lp(a). Classic conflation. An exposure held constant in both groups is an exposure the trial cannot speak to. What it asked was whether stripping Lp(a) out adds anything once the rest of the particle burden is already being treated, across 8,323 patients with established disease. On the primary endpoint the answer was no. That is a finding about Lp(a), and about pelacarsen, and about nothing else. The design says as much itself. All 8,323 entered with Lp(a) at or above 70 mg/dL, and the trial was powered on a Mendelian randomization estimate that an absolute reduction of 70 to 90 mg/dL would be needed to buy what 1 mmol/L of LDL-C lowering buys. The benchmark written into the protocol is the particle model. It was built on that model rather than against it. For all 8,323 of those patients, Novartis and Ionis released no event rates, no hazard ratios and no p-values. Anyone explaining why it missed is explaining something the sponsors have not published. The question people are now calling "open" has 26 randomized trials and 170,000 participants behind it, and the genetics underneath that. None of it moved on Wednesday. @ProfDFrancis, is that how a trialist reads a null on a second exposure? Your own ApoB sat outside the randomization entirely. It remains the number to ask for by name, and where you cannot get it, total cholesterol minus HDL-C gives you non-HDL-C from the panel you already hold. Never give up. Never surrender.
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IMPUNIDAD CERO retweeted
Since the 2015 American Heart Association Scientific Statement, the incidence of infective endocarditis (IE) has continued to rise with major shifts in epidemiology, including increasing injection drug use–associated IE related to the opioid epidemic, an aging population with complex comorbidities, and expanding use of cardiovascular implantable devices and prosthetic materials. More here > professional.heart.org/en/sc…
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IMPUNIDAD CERO retweeted
In view of all the Lp(a) interest, I thought it is a good timed to again explain and make less confusing Lp(a) and LDL metrics using my graphics. There is tremendous misuse of various particle metrics. Once again - LDL refers to a specific lipoprotein - THERE IS NO LAB TEST CALLLED LDL, Enlarge the graphic to study the subtleties. @nationallipid @foundationofnla @society_eas @ASPCardio @escardio @atherosociety @TheEndoSociety @FamilyHeartFdn @fhpatienteurope #cholesterol
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