Martin Matsumura

All the explanations I’ve heard today for the negative CLOSURE-AF result—some so strained they’re almost impressive. 1) The devices were “outdated” and therefore responsible for excess complications (the usual argument that things only go wrong elsewhere). 2) DAPT was used after LAAO, which is now said to be obsolete because of bleeding concerns compared with DOAC-based strategies (a claim that is often repeated, less often demonstrated). 3) Stroke rates were similar, so the signal is attributed mainly to bleeding and procedural issues—as if that were a minor point. 4) The composite endpoint is criticized for mixing different mechanisms, although if anything it should have favored non-inferiority. 5) The early phase of enrollment is invoked to argue that complications are not representative of current practice (again, complications seem to belong to others). 6) And then there are the usual remarks about loss to follow-up, crossovers, and lack of blinding. What seems to be missed in this accumulation of arguments is straightforward: the burden of proof lies with LAAO, not with the control arm. The issue is the strength of the evidence supporting LAAO, not medical therapy, which remains the reference standard.

Among patients with atrial fibrillation at high risk for stroke and bleeding, left atrial appendage closure was not noninferior to medical therapy in reducing the risk of stroke, embolism, major bleeding, or death at 3 years. Full CLOSURE-AF trial results: nejm.org/doi/full/10.10… Editorial: Left Atrial Appendage Closure — Another Overused Method in Cardiology? nejm.org/doi/full/10.10…

Students who took notes by hand scored ~28% higher on conceptual questions than laptop note-takers. Writing forces your brain to process and compress ideas instead of copying them.

Cardiac Screening for Conditions Associated With Sudden Cardiac Death: Yield, Interventions, and SCA/SCD Incidence in 104,369 Young Individuals jacc.org/doi/10.1016/j.… #athlete #SCD #prevention #ECG #Sportscardiology

Artificial intelligence–based quantification of breast arterial calcifications to predict cardiovascular morbidity and mortality Automatically quantified BAC is an independent predictor of MACE and mortality, adding prognostic value to the PREVENT score #Cardiology #MedTwitter #CardioTwitter #HeartHealth #Healthcare @ESC_Journals @escardio @DrMarthaGulati @hvanspall @CMichaelGibson @Hragy @biljana_parapid academic.oup.com/eurheartj/adva…

Peer review was supposed to be science’s quality filter, but somewhere along the way it started acting more like a bouncer who only lets in the regulars. It’s slow, it tends to favor established labs and familiar names, and it gets uncomfortable around anything too unconventional. Papers loaded with mountains of data tend to cruise through, while bold ideas that actually challenge the consensus get stuck in limbo or turned away at the door. The irony is that where a paper gets published almost never determines its real worth. What actually matters is what the scientific community does with it afterward, whether people cite it, argue with it, build on it, or use it to blow up a long-held assumption. That’s where the value lives, not in the journal’s logo. A major survey a few years back found that roughly 70% of researchers think the current system is fundamentally broken, and it’s not hard to see why. Publicly funded research hides behind paywalls, editors chase whatever topic is hot that month, and the whole incentive structure pushes toward safe bets over genuinely risky and potentially important work. Science has always been complicated and deeply human and full of ego and inertia, but the conversation is shifting.

Among pts undergoing percutaneous LAAO, shared decision-making (SDM) & decision aid reporting was high but varied by institution, & Medicare pts were not more likely to have reported SDM w/ decision aids, despite the CMS requirement. 🔗 bit.ly/3OV2bHl #LAAORegistry #NCDR

Genotype-positive #FamilialHypercholesterolemia in US adults was linked to higher atherosclerotic cardiovascular disease rates and lower achievement of guideline-recommended LDL-C targets. ja.ma/4sveLvd

Higher aldosterone-renin ratios in older adults were linked to increased risk of atrial fibrillation and ischemic stroke, supporting the aldosterone pathway as a target for cardiovascular disease prevention. ja.ma/46HoAxV

Reino Unido acaba de hacer el experimento de IA médica más grande de la historia. El resultado es un fracaso total. En ese país, hay 400.000 personas caminando con insuficiencia cardíaca sin saberlo y el 80% se va a enterar recién cuando llegue a una guardia. No porque no haya señales, sino porque el sistema de atención primaria no las detecta a tiempo. Entonces, le dieron a médicos de 205 clínicas un estetoscopio con Inteligencia Artificial que en 15 segundos analiza el corazón y te dice si hay insuficiencia cardíaca, arritmia o enfermedad valvular. Cuando se utilizaba, los resultados eran impresionantes: la detección se duplicaba. Pero, cuando miraron el resultado general, no había cambiado absolutamente nada. Misma cantidad de diagnósticos usando IA que sin usarla. El problema fue que el 70% de las clínicas lo había dejado de usar porque el estetoscopio le sumaba pasos a un médico que ya tiene 10 minutos por paciente, no se integraba con el sistema de historias clínicas y encima muchas alertas terminaban siendo de gente que no tenía nada. Eso es común en medicina (es lo que pasa, por ejemplo, con las mamografías), pero los médicos no estaban acostumbrados a esta nueva tecnología y cada falso positivo les fue sumando más y más desconfianza. No falló la IA: el error fue desarrollar tecnología de punta sin tener en cuenta que el sistema sigue siendo del siglo pasado.

Bradycardia & Pauses in Athletes ahajrnls.org/44CKDot

The problem isn't the availability of scientific research. It's the flood of people misinterpreting complex data with zero training and full confidence. Access to information is no longer the barrier. Understanding it is.

Two hs-troponin strategies—the ESC algorithm and High-STEACS pathway—perform well for diagnosing NSTEMI in emergency department patients with acute chest discomfort, based on prospective data from Europe. tctmd.com/news/some-mino…

90% of students “read” research papers and still can’t explain them….This is the method I use anytime I lead a Journal Club. I can tell in 30 seconds if you actually understood a research paper…. Most people don’t…. They “read” it… Then they can’t explain the question, the method, or the point. Here’s the reading method researchers are trained to use: The Three-Pass Method. ⸻ ★ PASS 1 (5–10 minutes) Get the map, not the details Read only: → Title → Abstract + intro → Section headings → Conclusion → References (quick glance) By the end, you should be able to say: ↳ What kind of paper is this ↳ What problem is it solving ↳ What are the main contributions ↳ Do the assumptions seem reasonable ↳ Is it worth your time If the answer is “no,” stop here. That’s not quitting. That’s focus. ⸻ ★ PASS 2 (up to 1 hour) Understand the argument Now read with a pen. Your job is to track: → What claim are they making → What evidence supports it → What figures/graphs prove it Study the visuals like your reputation depends on it: ↳ Are axes labeled ↳ Are error bars shown ↳ Do the results actually justify the conclusion At the end of pass 2, you should be able to explain the paper out loud to a friend. No notes. If you can’t, you don’t own it yet. ⸻ ★ PASS 3 (the “real researcher” pass) Rebuild the paper in your head This is the move that separates “I read it” from “I understand it.” Try to recreate the work mentally: → Why this method and not another → What assumptions are hiding in plain sight → What would break if one assumption fails → What would you change if you ran the study By the end, you should be able to reconstruct the whole paper from memory, including strengths and weak spots. ⸻ 💬 What trips you up the most when reading papers? ♻️ Repost if you know someone drowning in PDFs.

Most exercise advice focuses on how much you train. This paper shows the real question is what kind of cellular architecture you’re building. This systematic review and meta-regression synthesizes data from 425 human studies to quantify how different exercise modalities reshape mitochondrial content and skeletal-muscle capillarization, two core determinants of metabolic health and endurance capacity. The mechanistic takeaways: • Training intensity is the dominant driver of mitochondrial expansion. High-intensity and sprint-interval training produced ~2–4× greater increases in mitochondrial markers compared with traditional endurance training when normalized for time. • Volume still matters, but differently. Mitochondrial adaptations scale with training intensity × volume, whereas capillary growth depends more on intervention duration (≥8 weeks) than intensity alone. • Capillarization and hypertrophy are not the same adaptation. Capillary density and capillaries per fiber increased even when cross-sectional area did not, reinforcing that vascular remodeling is a distinct biological response. • Trainability is context-dependent. Untrained individuals showed larger relative gains, but well-trained individuals still adapted, especially under higher-intensity stimuli, contradicting the idea of a hard “adaptation ceiling.” • Age, sex, and disease status did not negate adaptation. Young vs. old, male vs. female, and healthy vs. cardiometabolic or pulmonary disease groups all demonstrated meaningful mitochondrial and vascular remodeling with appropriate training exposure. I'm sum, exercise is not merely a behavioral intervention, it is a dose-dependent biological signal that remodels mitochondrial density, oxidative capacity, and skeletal-muscle microvasculature. Intensity determines how much adaptation you get; duration determines how completely the tissue remodels.

@mavsmarie Relax it’s just TDS- Talarico Derangement Syndrome

It’s already starting on Facebook lmaooo

How to interpret the number needed to treat for clinicians 🔓doi.org/10.1093/ndt/gf… @EraRegistry

James Talarico’s message of religious faith and economic populism resonated with Hispanic voters in Texas. 🔗 on.wsj.com/3N28XdC

Higher aldosterone-renin ratios in older adults were linked to increased risk of atrial fibrillation and ischemic stroke, supporting the aldosterone pathway as a target for cardiovascular disease prevention. ja.ma/4seQLMK