Pedro Graziano Sanchez

What do you think ?

Heart failure w reduced ejection fractions

What do u expect in this 5 year child post Glenn?

What do you think about this LMCA ? Bi,tri,or quadri-furcates?

F. 60+ admitted to the emergency department with acute chest pain. Diagnostic cardiac catheterization demonstrated no significant CAD. PE was also ruled out. Then she was rushed to the cardiac OR. What happened? #echofirst @iamritu @CASivaram1 @DrRajeshG1 @Hragy @mmamas1973

High cortisol is the real reason you wake up at 3-4 AM. It also shaves 5 years off your life — tanks testosterone, locks belly fat, literally shrinks your brain. If I wanted to fix it without medication, here are 8 things I'd do every day: 1. No food 3 hours before bed.

Pulmonary vein perforation causing life-threatening pulmonary hemorrhage during pulsed field ablation for atrial fibrillation using a J-shaped radiofrequency transseptal puncture wire @yoshitake_3 heartrhythmcasereports.com/article/S2214-…

Think TTE can't diagnose sinus venosus defect in adults? This video walks you through how to visualize them. Test your 👀 tinyurl.com/3d3ku9fw #ACHDTTE #ACHDecho @wikimagen @ChamsiPash @valeriaduarteMD @NMerke @iamritu @ASE360 @DrRajeshG1 @GARCIAEDINSON95 #EchoFirst

Middle-aged male with isolated native pulmonary valve endocarditis and anterior cusp perforation #echofirst

🛠️ ECO SKILLS | Medición de la aorta Las guías ESC 2024 y recomendaciones TAVI/TAVR enfatizan la estandarización para lograr mediciones reproducibles y precisas. 📏 Medir bien = mejores decisiones clínicas. #SONECOM #ECOSKILLS #Aorta #Ecocardiografía

Aortopathy in #bicuspid_aortic_valve doi.org/10.3390/jcm150… #CHD

What's the value of CAC Scoring when Lp(a) is elevated? CAC scoring remains powerful, but risk is higher in those with higher Lp(a) levels in this MESA substudy jacc.org/doi/10.1016/j.… #JACC #cvLipids @DrNathanWong @khurramn1 @MichaelJBlaha @AlexRazavi @hsbhatia @MattRamsisMD

🫀 This paper is quietly dangerous. Not because it’s wrong—
but because it can be misunderstood. Let’s go straight to the core. What the study actually shows In 479 CCS patients undergoing CCTA: 👉 Lower LDL-C (<70 mg/dL) was associated with 👉 MORE severe CAD and higher plaque burden Even more interesting: 👉 These patients had - more diabetes / pre-diabetes - more metabolic syndrome - worse glucose metabolism markers And: 👉 Diabetes (OR ~6.1) and pre-diabetes remained strong independent predictors of CAD risk The uncomfortable observation 👉 The “best treated” patients (low LDL) had the worst arteries Before anyone panics: This is NOT saying LDL reduction is harmful. This is saying something much more subtle—and more important. What is really happening? 1. Reverse causality (the elephant in the room) Patients with: 👉 prior events 👉 higher baseline risk 👉 more aggressive treatment → end up with lower LDL So: 👉 Low LDL is a marker of treated high-risk patients Not the cause of disease. 2. Metabolic risk is the real signal The study shows very clearly: 👉 Glucose dysregulation dominates residual risk - Diabetes - Pre-diabetes - Insulin resistance - Metabolic syndrome → strongly associated with plaque burden and Leiden score This is the key shift For years, we simplified CAD risk to: 👉 LDL = bad → lower is better That’s still true. But incomplete. What this paper actually teaches 👉 You can have “perfect LDL” and still have high atherosclerotic risk Because: 👉 Atherosclerosis ≠ cholesterol alone 👉 It is a metabolic + inflammatory + vascular disease The imaging angle (the real gold here) CCTA shows: 👉 more non-calcified plaques in low LDL group 👉 higher plaque burden (SIS) 👉 higher Leiden risk scores This is exactly where imaging becomes decisive: 👉 Biology > numbers Clinical implication (the part guidelines are still catching up with) Treating LDL alone: ❌ does NOT eliminate risk Because: 👉 residual risk = metabolic + inflammatory + phenotypic My take This paper reinforces a concept that is still underused clinically: 👉 CAD is an atheroma disease, not a cholesterol disease The real mistake to avoid A superficial reading would lead to: ❌ “Low LDL is associated with more disease → LDL doesn’t matter” That would be wrong. The correct interpretation 👉 LDL lowering works 👉 BUT it does not address the whole disease Where this goes next This is exactly where: 👉 advanced CCTA (plaque quantification, phenotype) 👉 PCCT (microstructure, composition) 👉 AI-QCT will redefine risk stratification. Bottom line 👉 LDL reduction is necessary 👉 but absolutely not sufficient And if you only track LDL: 👉 you are managing a number 👉 not the disease

The author discovered the brain glymphatic system in 2012. She posits HRV as a way to assess brain clearance

The current physical activity guidelines are too low. I've been saying this for a while. And a new study confirms it. Meeting the standard 150 minutes/week was associated with only a modest ~8–9% lower cardiovascular risk. The biggest protection occurred at roughly 560–610 minutes/week, about 3–4× higher, where cardiovascular risk was 30% lower. We need to distinguish between the minimal activity volume required for basic protection, and the substantially higher volumes required for optimal resilience.

Dormir de más al día siguiente SÍ importa. 📍85,618 personas, 8 años de seguimiento: privarte de sueño sin recuperarte después aumenta mortalidad hasta 42%. Pero si duermes y repones el sueño la noche siguiente, el riesgo desaparece. La deuda de sueño crónica sin reponerlo sigue siendo dañina. By @Nature 🔗Descarga: t.me/DailyUrgencias… DOI: doi.org/10.1038/s41467…

His claim is correct. We have a fertility crisis. > 62% sperm count drop globally 1973 - 2018 > 23% drop in just 16 years > rate of decline accelerating > dropping 2.64% per year since 2000 I explain below how to improve yours. I've been working on improving my fertility markers for the past two years. They are elite for a early 20 something (I'm 48). Total motile count: 411 million Motility: 64% Morphology: 12% Concentration: 212 million Count: 642 million To put these numbers into perspective: the WHO considers a motile count above 42 million as normal, mine is 411 million, nearly 10x. And a normal concentration is 16 million (mL), mine is 212 million (mL). These personal-best fertility markers coincided with my first-in-human test result showing zero microplastics in my semen. Studies have shown 100% of men have microplastics in their semen. Microplastics hurt sperm. Human studies show the impact of various types of plastic, associated chemicals, and other toxins on male fertility: + 60% fewer normal shaped sperm (from PFAS) + 5x higher odds of low sperm count (from PTFE) + 10% lower sperm concentration (from PTFE) + 15% lower swimming ability (from PTFE) + 41% lower swimming ability (from PET) + 12% lower sperm swimming ability (from BPA) + 3x higher odds of low sperm count (from Phthalates) + 2x higher odds of poor swimming (from Phthalates) How to improve your fertility: > 7 to 9 hours of sleep, consistent bed and wake times > exercise: cardio fitness, strength, and muscle > reducing body fat and build lean mass > avoid alcohol, tobacco, and cannabis; each independently reduces sperm concentration, motility, and morphology, with cannabis also affecting sperm methylation. > cut junk food, added sugars, and excessive saturated fats > eat an anti-inflammatory, anti-oxidant diet (Mediterranean and green-Mediterranean): polyphenols, fiber, olive oil and other MUFAs, omega-3s (algal, fish, walnuts), plant protein, fresh veggies. > get full micronutrient coverage: zinc, selenium, folate, vitamins C, E, and D (blueprint solves this). > manage stress and cortisol load; chronic stress lowers testosterone and impairs spermatogenesis. Things I'm doing: 1. Sauna (dry). My toxin blood panel confirms sauna clears plastic related chemicals: BPA, phthalates, PFAS, flame retardants, pesticides. The plastic particles themselves are too big to sweat out directly. Heat may activate other clearance routes: bile flow through the liver, the cell's internal cleanup system, and the gut barrier. Humans have almost no enzymes that can break plastic apart, so the body has to physically push it out. 2. Reverse osmosis water filter. Drinking water is likely a major source of microplastic getting into your body. A reverse osmosis filter pushes water through a very tight membrane and strains the particles out. I filter everything I drink. 3. Trying to rid my environment of the big plastic items: cutting boards, cups, plates, food storage containers, non-stick pans, cling wrap, tea bags, water bottles, kitchen utensils, kettles, and synthetic clothing. Note, as hard as I try, I'm always finding new plastic things in my life. This can be all-consuming thing so try to just knock out the big ones. The studies: > meta-analysis with total 42,935 men; significant decline in both sperm concentration and total sperm count among men from Western countries, with total sperm count by about 59%, between 1973 and 2011. > A follow-up global meta-analysis, expanded the dataset to 223 studies and 57,168 men found the drop in sperm count was not only a Western phenomenon > total sperm count dropped by 62% globally between 1973 and 2018, including in men from South America and Asia. The rate of decline has also accelerated since 2000, reaching approximately 2.64% per year. > CDC data also showed US fertility rates peaking at the replacement level of 2.12 births per woman in 2007, then taking a sharp downward turn by 23% down to 1.62 in 2023.

📄 Hypertension-related LVH: not all phenotypes carry the same risk 🔗 DOI: doi.org/10.1093/ehjimp… 🫀 Hypertension is the most common cause of LV hypertrophy—but its cardiac expression is far from uniform. This large UK Biobank CMR study (n >24,000) provides a comprehensive look at LVH phenotypes and their prognostic impact. ✨ Four CMR-defined phenotypes: 👉 Normal LV 👉 LV remodelling 👉 Eccentric LVH 👉 Concentric LVH 📊 As shown in the graphical abstract (page 2): ➡️ each phenotype has distinct structural and functional signatures ✨ Key findings: 🔹 Eccentric LVH = worst phenotype ➡️ Most impaired LV function (EF + strain) ➡️ Largest chambers ➡️ Highest risk: MACE → HR 2.5 Heart failure → HR 9.0 🔹 Concentric LVH: ➡️ Highest wall thickness and native T1 (fibrosis) ➡️ ↑ Heart failure risk (HR 4.1) ➡️ No significant MACE association 🔹 LV remodelling: ➡️ Intermediate phenotype ➡️ Smaller chambers, milder changes 📊 Key pathophysiological insight: 👉 LVH is not a binary condition—but a spectrum of myocardial adaptation ➡️ From remodelling → concentric or eccentric hypertrophy ➡️ Driven by pressure load, volume load, and myocardial response 💡 Clinical take-home message: 👉 Not all LVH is equal ✔ Eccentric LVH → high-risk phenotype ✔ Concentric LVH → fibrotic, HF-prone phenotype 👉 CMR enables: precise phenotyping improved risk stratification potential tailored treatment strategies 🚨 Bottom line: In hypertension, LV geometry matters—because different phenotypes carry very different prognoses. #Cardiology #CMR #Hypertension #LVH #CardiacImaging #HeartFailure #RiskStratification #PrecisionMedicine #UKBiobank 🫀📊

Fruits & vegetables likely account for a majority of people's dietary microplastic and PFAS intake. What’s frustrating is that this isn’t something you can just rinse off. In many cases, the contamination appears to be taken up into the food itself. Organic may reduce some of that exposure, but even organic farms can be affected when they’re near contaminated land or water. Should you stop eating produce? No. We should be much more upset about how widespread these chemicals have become, especially when children are being exposed through foods we otherwise consider healthy. One practical thing I think is worth considering is beta-glucan. There’s some evidence it may help support the excretion of PFAS, and given how unavoidable these exposures are becoming, that may be a useful tool, especially for families who can’t realistically eliminate every source.

@bryan_johnson Well done sir. Plasticdetox.org is a great resource for plastic free living

The most powerful table in heart failure medicine. 🧵 Without treatment, 2-year mortality in HFrEF: 35% Add each pillar of GDMT and watch what happens: 💊 ARNI → 25.2% (↓28% RR) 💊 + Beta Blocker → 16.4% (↓35% RR) 💊 + Aldosterone Antagonist → 11.5% (↓30% RR) 💊 + SGLT2i → 9.5% (↓17% RR) Cumulative result: ✅ 72.9% relative risk reduction ✅ 25.5% absolute risk reduction ✅ NNT = 4 Treat 4 patients with all 4 therapies. Save 1 life. GDMT isn’t polypharmacy. It’s math. (Fonarow GC et al. Am Heart J 2011; Lancet 2008) #HeartFailure #HFrEF #GDMT #Cardiology #CardioTwitter #MedTwitter