Miguel Puentes Chiachío

Diuretic resistance is not a therapeutic dead end → it’s a signal that we need a smarter strategy.” The perfect closing slide from Dr. Ana Belen Mendez Fernandez at #HeartFailure26 👏 5-step framework for smarter decongestion: 1️⃣ Recognize the problem Multifactorial, common, predictable — requires a structured approach 2️⃣ Objective assessment Weight, ultrasound, BNP, renal function, volume status, urine output 3️⃣ Optimize loop diuretics Adequate dose & frequency, IV route, check absorption 4️⃣ Sequential nephron blockade Target different nephron segments, overcome compensatory mechanisms 5️⃣ Treat the drivers Venous congestion, low cardiac output, neurohormonal activation And the line that should be on every HF ward wall: “Decongestion is not just symptomatic relief. It changes outcomes.” #CardioTwitter #HeartFailure #Cardiology #Decongestion #Diuretics

📄 2025 ESC/EACTS Valvular Guidelines: imaging perspective 🔗 DOI: doi.org/10.1093/ehjimp… 🫀 Core message The new guidelines mark a major shift: 👉 from a single decision (surgery vs transcatheter) 👉 to a lifetime management strategy ➡️ In this framework, imaging becomes central to Heart Team decision-making. 🔑 Key clinical updates Aortic stenosis: 👉 Age threshold for TAVI lowered to ~70 years 👉 Decisions now based on lifetime strategy (redo options, coronary access, anatomy) Primary mitral regurgitation: 👉 Surgery remains the gold standard 👉 Earlier intervention recommended in selected asymptomatic patients Atrial secondary MR: 👉 Recognised as a distinct entity 👉 New indications for surgery and transcatheter therapies Tricuspid regurgitation: 👉 Transcatheter therapies enter mainstream guidelines 👉 Strongly dependent on RV function and pulmonary hypertension 🧠 New role of imaging 👉 No longer just to “confirm severity” 👉 But to shape the entire clinical pathway Three key shifts: From single parameters → integrated phenotyping Right modality at the right time Standardisation and reproducibility 🖥️ Role of imaging modalities Echocardiography: first-line, now expected to be integrative (3D, stress) CT: crucial for anatomy, feasibility, and lifetime planning CMR: reference for volumes, regurgitation, and myocardial damage Multimodality imaging: essential for complex decision-making 🔄 Paradigm shift 👉 Imaging-driven pathway: DEFINE → SELECT → DELIVER → TRACK ➡️ Moving from thresholds → personalised, predictive care 🤖 Future: AI in imaging 👉 Not just automation, but: standardisation detection of discordance guideline-based decision support ⚠️ Must remain transparent, validated, and clinically accountable 🚨 Bottom line 👉 Imaging is now: a continuous, central, decision-making tool in valve disease 👉 Not just measuring valves ➡️ but guiding lifelong patient management strategies

Médicos y estudiantes, a la vez, pidiendo la dimisión de Mónica García. Decía que venía a mejorar el sistema sanitario y se lo ha cargado en unos meses. Tremendo. #MónicaGarcíaDimisión

¿Cómo estudias cardio? ¿Con el Topol o con el Braunwald? Yo con el Braunwald ! Pregunta esencial para los resis de cardio de mi época. Se ha ido uno de los padres de la cardiología moderna. Eugene Braunwald. Su visión pionera en investigación grupo #TIMI, su aportación en entender la fisiopatología de la IC, CI…. Nos deja un gran legado. Nuestro referente. DEP🕯️

Especial médicos🩺⚕️🏥👨🏻‍⚕️👩🏻‍⚕️. Os dejo esta carta en JAMA. Se la pondré a mis alumnos en la próxima clase: He elegido estas frases : 👇🏻⏰ «La medicina puede tener un significado extraordinario. Pero no puede sustituir el estar presente en tu propia vida. El mundo puede necesitarnos como médicos. Pero las personas que nos aman nos necesitan como nosotros mismos. Y ese es el rol que nadie más puede llenar.» «La residencia refuerza la lección de que las instituciones están diseñadas para perdurar más allá de los individuos. En cambio, las familias no.» «Creo en formar a la próxima generación. Creo en el significado de este trabajo. Lo que ha cambiado es mi disposición a absorber el desgaste sin cuestionarlo.» «Ya no estoy dispuesta a seguir posponiendo la vida. La medicina exige mucho. Y nosotros damos profundamente. Pero no puede tomarlo todo.» «El significado de mi trabajo es profundo. El significado de mi presencia en casa es irremplazable.»

#SPIRIT-HF #ACC26 🧑‍⚕️ HF with preserved or mildly reduced EF (HFpEF/HFmrEF)—a large, underserved group with limited therapies 🧠 Does Spironolactone reduce CV death and HF hospitalizations, building on signals from prior trials like TOPCAT 📊 Trial was underpowered (COVID impact, lower enrollment, high drug discontinuation) → unable to definitively test hypothesis ⚠️ No clear primary outcome benefit; side effects and drug withdrawal were common, potentially blunting efficacy 💡 Takeaway: Signal for benefit may still exist—but tolerability + adherence remain the real barriers in HFpEF therapy Great Discussion by @dranulala 👏👏

Designing Next-Generation Cardiometabolic Outcome Trials for Obesity Medicines Obesity increases the risk of cardiovascular, kidney, and metabolic (CKM) diseases. The optimal design of cardiovascular outcome trials (CVOTs) testing novel obesity medications is unclear. jacc.org/doi/10.1016/j.… @JACCJournals @ACCinTouch @CMichaelGibson @DrMarthaGulati @hvanspall @AndrewJSauer @Hragy @biljana_parapid

How does Lp(a) drive atherosclerosis? 🫀Delivers cholesterol to the arterial wall 🫀Carries oxidized phospholipids → vascular inflammation 🫀Interferes with plasminogen → impaired fibrinolysis 🫀Promotes an atherothrombotic environment Understanding these mechanisms strengthens the case for targeted Lp(a) therapies 📎 shorturl.at/Uudsc @drmarthagulati @AnnalisaFiltz @CardioMDPhD 🙏🏽 @DrDerekConnolly for inviting this review #Lpa #CardioTwitter #CVprev

❌ Un abogado del Estado desmonta con claridad muchas ideas. Y lo hace con razones simples. Muy recomendable 👇

Very high lipoprotein(a) levels are associated with increased 30-year risk of major #cardiovascular events, coronary heart disease, ischemic #stroke, and cardiovascular death among healthy women. ja.ma/4kcZvAm

Our new study in @ESC_Journals @ehj_ed : Aspirin Use, Lp(a), and CAVD Big thank you to the team @seamuswhelton @MichaelJBlaha @rblument1 @WendyPost9 @Lpa_Doc @hsbhatia @khurramn1 @BudoffMd @violavaccarino @OmarDzaye @ThanassoulisMD @n_marreromed LSperling VRamachandran MTsai

🧪🌿 Colchicine slows coronary plaque progression in stable CAD — first randomized imaging evidence A new randomized, double-blind, placebo-controlled trial in European Heart Journal – Cardiovascular Imaging tested whether low-dose colchicine — a classic anti-inflammatory drug — affects coronary plaque progression in patients with stable coronary artery disease (CAD). 📍 Study design: • 84 adults with angiographically confirmed CAD or a high coronary calcium score (>400) • Randomized to colchicine 0.5 mg/day vs placebo for 12 months • Standard care continued in both groups • Serial coronary CT angiography (CCTA) assessed plaque change 🧠 Why this matters Inflammation is a key driver of atherosclerosis progression and vulnerability. Prior clinical trials showed colchicine reduces cardiovascular events, but its direct effect on coronary plaque morphology and progression was unclear. 🫀 Key findings: • Colchicine significantly reduced progression of total plaque volume, particularly low-attenuation plaque — a marker of high-risk, lipid-rich, unstable plaque • Slower plaque progression was evident even when LDL levels were similar between groups • Treatment was generally well-tolerated at 0.5 mg daily 📊 Clinical implications: This trial provides mechanistic evidence that colchicine’s event-reducing benefits may be mediated through direct influence on plaque biology, not just systemic inflammation. Slowing plaque progression — especially of vulnerable components — aligns with reduced risk of future events. ⚠️ Nuances: • Modest sample size and single-timepoint imaging limits broad generalization • Plaque imaging biomarkers predict risk but are surrogate endpoints 📌 Bottom line: Low-dose colchicine, added to standard therapy, slows coronary atherosclerosis progression in stable CAD — supporting its emerging role in targeted residual risk reduction beyond LDL lowering.

Intravenous ferric carboxymaltose in patients with heart failure and iron deficiency: a systematic review and meta-analysis of randomized controlled trials with trial sequential analysis. #ESCHeartFailure @EJHFEiC @JanBiegus @Ppponikowski #HFA_ESC @hvanspall @ShelleyZieroth @FudimMarat @gcfmd @AlexMebazaa @MarcoMetra @GianluSava

SPARK score: comprehensive risk stratification in patients with moderate aortic stenosis 👉 #EAPCI26

A new state-of-the-art review that summarises adjunctive pharmacological strategies targeting lipids and inflammation to improve secondary prevention and long-term outcomes. Don't miss it! eurointervention.pcronline.com/article/adjunc… @johnwmcevoy @ToDoenst @DrFaisal_Sharif @Drroxmehran @BudoffMd @rkhamis @OnumaYoshinobu

Huelga de médicos (agotados y desesperados)

ESTRATIFICACIÓN DE RIESGO Y MANEJO DEL SCA NO ST #NSTEMI Buena revisión @EuroInterventio -Estratificación de riesgo -Tiempo a la estrategia invasiva -PCI vs CABG -Enf multivaso -MINOCA pubmed.ncbi.nlm.nih.gov/41342077/

"El tirano gobierna para su propio provecho. Y como nunca reconoce leyes por encima de su voluntad, busca perpetuar su poder mediante el miedo, el descrédito y la eliminación de los hombres respetables y eminentes". (Aristóteles. Política)

Clasificación CCS del Infarto Agudo de Miocardio (IAM). 🫀💥 🟥Durante décadas clasificamos el IAM como IAM-CEST 🆚️ IAM-SEST. Pero esa clasificación es electrocardiográfica y anatómica, no tisular. 🤔 🟥La Canadian Cardiovascular Society (CCS) propuso una nueva clasificación del IAM aterotrombótico agudo basada en la gravedad y progresión de la lesión miocárdica tras reperfusión. 📊 🟥No todos los infartos reperfundidos son iguales. El daño por isquemia-reperfusión evoluciona en etapas progresivas. Cada estadio añade un nuevo tipo de lesión. A mayor estadio mayor tamaño de infarto, mayor pérdida de miocardio salvable, mayor riesgo de IC y MACE. 📈☠️ 🟥Los 4 estadios CCS: 💚CCS Stage 1: infarto abortado. Solo edema miocárdico, sin necrosis reversible, excelente pronóstico (La “hora dorada”).🧐👌🏻 💛CCS Stage 2: necrosis miocárdica. Hay muerte de miocitos, sin lesión microvascular, tamaño de infarto limitado, pronóstico intermedio. 🫀⚠️ 🧡CCS Stage 3: necrosis + obstrucción microvascular, fenómeno no-reflow, disfunción microvascular persistente. Aumenta 2–4 veces el riesgo de eventos. Aquí el problema ya no es la arteria epicárdica, es el microvaso. 📈☠️ 💔CCS Stage 4: necrosis + OMV + hemorragia intramiocárdica. El estadio más grave. Asociado a expansión del infarto, remodelado adverso. Mayor riesgo de IC y muerte. Es la forma más letal de IAM reperfundido. 💀⚰️ doi.org/10.1016/j.jaca…

Los servicios mínimos de las huelgas médicas son un abuso, una vergüenza y un ataque frontal al derecho a ejercer la misma