Ruben Sanchez

En personas con sobrepeso y enfermedad renal crónica, el aGLP1 semaglutide ↓6mmHg sistólica, efecto esperado por la natriuresis/diuresis, y su relación con ↓1 litro de agua extracelular. No asociado a pérdida de peso CJASN 2026 10.2215/CJN.0000001051

🟥 #Guerrero | La Organización Campesina de la Sierra del Sur (OCSS), de la comunidad de Tepetixtla, municipio de Coyuca de Benítez, señaló que el gobierno federal mantiene la narrativa de que los recientes ataques con explosivos a poblados indígenas de Chilapa de Álvarez, que provocaron el desplazamiento de familias, se debe a disputas entre grupos criminales y no al intento de mineras extranjeras para apropiarse del territorio y sus recursos naturales. Lee más aquí 👇 jornada.com.mx/noticia/2026/0…

Por cada deceso reportado originalmente hubo dos más. Entre 2020 y 2023 en México murieron aproximadamente 900 mil personas por COVID-19.

🔱Documento de consenso ESC @escardio 2026 sobre las Complicaciones Mecánicas del IAM. 🫀💥 🟥Rotura de pared libre ventricular, pseudoaneurisma ventricular y rotura del músculo papilar. Aunque hoy ocurren en <1% de los IAM gracias a la reperfusión temprana, siguen siendo complicaciones devastadoras, con mortalidad intrahospitalaria de 30–40%. ⚠️📈☠️ 🔺️Rotura de pared libre ventricular (RPLV): suele aparecer entre las primeras 24–48 h, aunque clásicamente se describía a los 5–7 días post-IAM. Puede manifestarse con dolor torácico, disnea, choque cardiogénico, taponamiento o paro cardíaco. Factores de riesgo: presentación tardía, IAM extenso, sexo femenino, edad avanzada e hipertensión. 🔺️Pseudoaneurisma ventricular Es una ruptura contenida por pericardio o trombo, con alto riesgo de ruptura franca. Su incidencia actual es 0.1–0.3%. Suele localizarse en pared inferior o posterolateral y puede debutar semanas o meses después del IAM. El riesgo de ruptura espontánea puede alcanzar 30–45%. Datos clásicos: cuello estrecho (relación cuello/fondo <0.5) y flujo turbulento Doppler. El riesgo de ruptura espontánea puede alcanzar 30–45%. 📜🆓️⤵️ doi.org/10.1093/eurhea… t.me/medicinaintern…

Test all adults for Lp(a)! doi.org/10.1016/j.jacl… @MarlysLPA @LipidJournal @nationallipid @foundationofnla @ACCinTouch @American_Heart @ASPCardio @DineshKalra @PamTaubMD @PamelaBMorris @rblument1 @EugeniaGianos @CBallantyneMD @hsbhatia @DrMichaelShapir @FamilyHeartFdn @Drlipid

👉 Inflammation in heart failure is not subtype-specific.
It’s phenotype-driven. And that quietly dismantles years of conceptual shortcuts. What the study actually shows From a global, real-world cohort (n = 11,809 HF patients): ~38% of patients have high inflammatory risk (hsCRP ≥2 mg/L) This is identical across HFpEF, HFmrEF, HFrEF Let that sink in: 👉 No meaningful difference across EF spectrum. The old narrative (that this paper challenges) We were taught: HFpEF → inflammation from comorbidities HFrEF → inflammation from myocardial damage Sounds elegant. Also… likely wrong (or at least incomplete). The new reality Inflammation clusters around a cardio–kidney–metabolic phenotype: - Obesity - CKD - Dyslipidemia - Diabetes - Worse NYHA class And this is consistent across all HF types Translation (clinically) EF is: 👉 a functional descriptor Inflammation is: 👉 a systemic biological state And the two are only loosely related The uncomfortable implication We may have been stratifying the wrong way. Instead of: 👉 HFpEF vs. HFrEF We should think: 👉 Inflammatory vs non-inflammatory HF phenotype Why this matters (a lot) 1. Trial design If inflammation is not subtype-specific: 👉 anti-inflammatory trials should not be EF-restricted Current approach risks: - underpowering - signal dilution - wrong conclusions 2. Patient selection hsCRP ≥2 mg/L: 👉 identifies ~4/10 HF patients globally That’s not a niche subgroup. That’s: 👉 a therapeutic population 3. Therapeutic targeting IL-6 axis: moderately correlated with hsCRP (r ~0.55–0.58 across all HF types) biologically consistent signal This is not noise. This is a coherent inflammatory pathway. My take This paper reinforces something we don’t say enough: 👉 Heart failure is not one disease.
 And EF is a poor organizing principle for biology. We keep slicing patients by: - EF - volumes - function But the real drivers are: - inflammation - metabolism - microvascular dysfunction If you connect this with imaging, this is where it gets interesting. Because: 👉 hsCRP is a crude systemic marker But imaging—especially advanced CT: plaque phenotype perivascular inflammation (FAI) tissue characterization (PCCT potential) …can localize the biology. Bottom line This is not “another inflammation paper”. It’s a quiet statement that: 👉 The HF classification system is lagging behind biology. And once you see it… you can’t unsee it.

Una vez se confirma con evidencia. En lesión renal aguda, la diálisis peritoneal, comparada a otras terapias extracorpóreas; tiene el mismo riesgo de morir y de recuperación renal Que no les vendan humo Metaanálisis de 10 ensayos clínicos Perit Dial Int 2026 10.1177/08968608261448781

çok sayıda amerikalı,Newyork'taki altında tüneller ve çocuk kalıntıları bulunan sinegog'a baskın yaptı ve şiddetli saldırılar gerçekleşti. bazı amerikan vatandaşları 2024'teki sinegog skandalını unutmamış...

📊 JAMA Clinical Guidelines Synopsis: #HelicobacterPylori infection is a leading cause of chronic #gastritis, #peptic #ulcers, and #gastric #cancer. The American College of Gastroenterology guideline for adults in North America recommends bismuth quadruple therapy for 14 days as first-line treatment in treatment-naive patients, due to superior eradication rates compared with proton pump inhibitor (PPI) triple therapy. ja.ma/4tq1d4x

At #HeartFailure26 congress: interesting mechanistic slide from the CADENCE trial discussion on obesity-related HFpEF and pulmonary hypertension. Key takeaway: activin type II receptor ligand trapping with sotatercept may improve both post-/pre-capillary pulmonary hypertension and structural pulmonary vascular disease by: ↓ pulmonary wedge pressure ↓ left atrial volume index ↓ pulmonary vascular resistance ↑ transpulmonary blood flow ↑ systolic blood pressure Presented by Milton Packer. Fascinating cardio-pulmonary-hemodynamic interplay in obesity-associated HFpEF. #CardioTwitter #HFpEF #PulmonaryHypertension #HeartFailure26

Daily home-based stellate ganglion phototherapy reduced ATP/ICD shock burden from 3.9 to 0.0 events/month (P<0.01) in 28 patients with refractory VT — no serious adverse events. A novel outpatient neuromodulation strategy ahajrnls.org/3PiETvA

SUBCUT HF II is a glimpse of where heart failure care may be heading: treating congestion at home instead of prolonging hospitalization.#HeartFailure26 In 172 patients across 20 UK hospitals, early discharge with wearable SC furosemide vs continued in-hospital IV diuretics led to: • +4 more days alive & out of hospital at 30 days • 5.5 fewer hospital days • p<0.001 A patient-centered shift in worsening HF management. #HeartFailure26 #CardioTwitter #HeartFailure #HFpEF #HFrEF @hfcollaboratory @SJGreene_md @gcfmd @MartaCoboMarcos @ShelleyZieroth @DrMarthaGulati @hvanspall

Age-related vascular changes contribute to disease. What drives vascular aging and how can these insights lead to new therapies? @AgingPitt ahajrnls.org/4d4CRbC

NEJM: New research reveals a massive concentration in medical malpractice: just 1% of all physicians account for 32% of all paid claims🩺⚖️ It seems risk isn't random—it's highly concentrated among a small group of practitioners. Full study: nejm.org/doi/pdf/10.105… @EricTopol

La adopción de la inteligencia artificial en las Administraciones públicas Oportunidades y retos para una gobernanza algorítmica 1drv.ms/b/c/a176902dca…

ALIMENTOS ULTRAPROCESADOS Y ENFERMEDAD CARDIOVASCULAR - Consenso @escardio La evidencia científica encontró asociación de UPF con riesgo de desarrollar: 🔴Obesidad 🔴Hipertensión arterial 🔴Diabetes tipo 2 🔴Insuficiencia renal 🔴Enf. hígado graso no alcohólico 🔴Insuficiencia renal 🔴Fibrilación auricular 🔴Enfermedad CV 🔴Muerte CV Vía @ESC_Journals academic.oup.com/eurheartj/adva…

2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines | JACC jacc.org/doi/10.1016/j.…

Check out our May issue! nature.com/neuro/volumes/…

🧠 L’IA sta davvero cambiando la cardiologia… o siamo ancora agli albori? Nicolosi analizza potenzialità e limiti attuali per un impatto reale nella pratica clinica quotidiana. giornaledicardiologia.it/archivio/4687/…

🫀⚡ CCTA is no longer “just a test.”
It is becoming the operating system of modern cardiology. This review makes something very clear: Coronary CT has crossed a threshold. It is no longer simply about detecting stenosis. It is now integrating: 👉 anatomy 👉 physiology 👉 plaque biology 👉 inflammation 👉 procedural planning 👉 AI-driven prediction —all inside one examination. For years, cardiac imaging was fragmented: - stress test for ischemia - angiography for anatomy - IVUS/OCT for plaque - separate risk scores for prognosis Now CCTA is starting to merge all of these layers together. The paradigm shift is obvious From: ❌ “Is there obstructive CAD?” To: 👉 “What is the biological trajectory of this patient?” The paper highlights how modern CCTA now provides: ✅ plaque characterization ✅ quantitative plaque burden ✅ CT-FFR ✅ PCAT inflammatory analysis ✅ radiomics ✅ AI-driven phenotyping And Photon Counting CT accelerates everything. Because PCCT is solving one of the oldest problems in coronary imaging: 👉 blooming 👉 limited spatial resolution 👉 poor stent evaluation 👉 calcium interference With PCCT: ⚡ spatial resolution approaches ~0.25 mm ⚡ calcium blooming is dramatically reduced ⚡ stent lumen visualization improves substantially But here’s the deeper implication We are moving away from: ❌ lumen-centric cardiology toward: 👉 multi-dimensional atherosclerosis phenotyping And AI becomes critical here. Not because it “replaces” physicians. But because humans cannot realistically integrate: ✅ plaque texture ✅ morphology ✅ inflammation ✅ radiomics ✅ flow dynamics ✅ longitudinal progression at scale. My take The future cardiac CT exam will not answer: 👉 “Is there a stenosis?” It will answer: 👉 “How dangerous is this artery biologically?” 👉 “How will this patient evolve?” 👉 “Which therapy changes the trajectory most?” Bottom line CCTA is evolving from: 👉 diagnostic imaging to: 👉 computational cardiovascular phenotyping ⚡ And once imaging becomes biology + AI + prediction… the entire architecture of cardiology changes. #CCTA #Cardiology #PhotonCounting #AI #PrecisionMedicine #Atherosclerosis #CardiacCT #PlaqueImaging #yesCCT