Batman-Echo

@drbennisahmed @Hragy 3. Genetic susceptibility 4. Perpetuator mechanisms (inflamlation) triggered by inducers

🧬 Statins are not enough. Here’s what comes next: “Residual Lipid Risk in ASCVD” Nordestgaard BG et al. | European Heart Journal Even on maximal LDL lowering, many patients carry residual cardiovascular risk driven by two culprits: 1️⃣ Remnant Cholesterol •Triglyceride-rich lipoproteins penetrate the arterial wall •Drives atherosclerosis independently of LDL •Target: promote lipoprotein lipase activity → ↓ plasma TG → ↓ remnant cholesterol •Novel remnant-lowering drugs on the horizon 👀 2️⃣ Lp(a) •Genetically determined — diet & statins barely touch it •Promotes both atherosclerosis AND thrombosis •Target: reduce apo(a) production in hepatocytes or inhibit Lp(a) assembly •RNA-based therapies (siRNA/ASO) showing major promise 🎯 📋 The framework going forward: Initial lipid panel → max LDL lowering → reassess with apoB + remnant cholesterol + Lp(a) → treat residual hyperlipidaemia specifically The era of “LDL is all that matters” is over. Next-gen lipid management is here — and it’s targeted, mechanistic, and overdue. 💊 #Cardiology #Lipids #ASCVD #Lpa #RemnantCholesterol #EHJ #PreventiveCardiology #MedTwitter

@argulian Last thursday… small apical aneurysm too. ICD and DOAC for parox. AF.

Mid-ventricular HCM is one of the instances when Doppler can be misleading: despite high pressure gradient in the ventricle no high velocities are seen, which can be interpreted as non-obstructive physiology. Mid-systolic signal void is due to flow cessation explaining why gradients are not captured. The paradoxical low velocity flow then follows, which should prompt search for an apical akinetic chamber. onlinejase.com/article/S0894-…

@MKIttlesonMD My choice still depends on the “profile” of patients, but agree that CMIs will work (much) better on average compared to BB. Most of all, do not forget to discuss myectomy wirh your patients!

MAPLE-HCM randomized pts w/ sx and oHCM to beta-blocker vs aficamten. On aficamen: peak VO2 was +1.1 ml/kg/min vs −1.2 ml/kg/min on metop and better NYHA and KCCQ. Based on this, should we reach for aficamten or tried-and-true beta-blocker first for symptom relief in oHCM?

@saramoscatelli7 What is rhe gold standard to say something is better or worse?

🫀✨ Rethinking QTc: time to move beyond Bazett? A new study in the Journal of the American Heart Association evaluated QTc correction formulas in >3200 healthy Asian young adults (18–22 yrs) — and the results are striking. 📊 Key findings: 🔹 Bazett formula → ❌ strongest heart rate (HR) dependence & poorest consistency 🔹 Dmitrienko → 👍 best HR independence 🔹 Framingham & Rautaharju → 🤝 highest agreement 🔹 Framingham → ⭐ best overall performance across HR ranges ⚠️ Bazett tends to: ➡️ Overestimate QTc at high HR ➡️ Undercorrect at low HR ➡️ Potentially mislead clinical decisions ✅ Take-home message: 👉 The Framingham formula emerges as the most robust and clinically reliable method, especially in young populations. 📢 This study supports a shift toward precision-based QTc correction and challenges the routine use of Bazett in modern practice. 💡 Why it matters? Better QTc correction = better risk stratification, safer drug use, and improved arrhythmia assessment. #Cardiology #QTc #ECG #Arrhythmia #PrecisionMedicine #HeartRate #CardioTwitter #MedEd #YoungAdults #ClinicalResearch #Electrophysiology #CardioInsights 🫀📈

@dr_benoy_n_shah @Hragy @CASivaram1 @iamritu @kaulcsmc @djc795 @AnkurKalraMD @DocStrom @purviparwani @DrMarthaGulati @hvanspall Incredible and exceptional man. RIP!

RIP Eugene Braunwald (1929-2016) There'll never be another like Dr EB Shaped countless careers Mentored countless physicians Led countless landmark RCTs Discovered diseases (e.g.HCM) Pioneered treatments Authored the most famous ❤️ book Condolences to all family & friends

Great editorial on our recent research paper on a simple integrative Doppler index. 👉Under Pressure: Rethinking Pulmonary Hypertension Through Tricuspid Regurgitation Waveform Morphology - Journal of the American Society of Echocardiography onlinejase.com/article/S0894-…

In a paper from Guzzetti E et al in JASE 2020, LVOT to be measured < 2 mm of AV annulus correlated best with CMR-SV, but the paper didn’t provide details on where to put the PWD sample. Citing predecessors is a good way to get your work accepted but leaves a great Q open. Q is how much will it change scatter and clinical implications when putting PWD at vs. < 0.5 - 1 cm of AV valve?

🫀 Did you know where the recommendation to place the pulsed wave Doppler sample volume 0.5–1 cm from the aortic valve to measure LVOT VTI comes from? The answer is more interesting than it seems. It doesn’t come from a single study or an experiment designed for that purpose. It comes from a historical chain spanning nearly 40 years: 🔬 1982–1984 — The physical foundation Pasipoularides and Murgo demonstrated using invasive catheters and mathematical models that in aortic stenosis there is a real zone of flow acceleration in the LVOT, just proximal to the valve, without any second anatomic obstruction. Pure hemodynamics — no Doppler yet. 👉 Bird et al. Circulation 1982 → doi.org/10.1161/01.CIR… 👉 Pasipoularides et al. Am J Physiol 1984 → doi.org/10.1152/ajphea… 📐 1984 — The apical 5-chamber view Lewis, Kuo and Quinones were the first to validate cardiac output measurement using pulsed wave Doppler from the cardiac apex. They described placing the sample volume “immediately proximal to the aortic valve leaflets” — but without specifying any distance in centimeters. 👉 Lewis et al. Circulation 1984 → doi.org/10.1161/01.CIR… 📏 1985 — The first numerical distance Skjaerpe, Hegrenaes and Hatle (the Norwegian group) were the first to quantify this in Doppler: they empirically observed that flow acceleration began 0.5 to 1.5 cm proximal to the valve, and placed the sample volume just proximal to that zone. They directly cited Pasipoularides as supporting evidence. This was the first time a numerical distance appeared in the technique. 👉 Skjaerpe et al. Circulation 1985 → doi.org/10.1161/01.CIR… 📊 1986–1988 — Practical consolidation Otto et al. used ~1.0 cm. Oh, Tajik and the Mayo Clinic group explicitly established the range of 0.5 to 1.0 cm in 100 patients, justifying it as necessary to avoid the subvalvular acceleration zone. This is the figure we all recognize today. 👉 Otto et al. JACC 1986 → doi.org/10.1016/S0735-… 👉 Zoghbi et al. Circulation 1986 → doi.org/10.1161/01.CIR… 👉 Oh et al. JACC 1988 → doi.org/10.1016/0735-1… 📋 2002 — It becomes “official” Quinones, Otto, Zoghbi and colleagues codified it in the ASE guidelines as “~5 mm proximal to the aortic valve”… but without citing any specific study to support it. It had already become expert consensus. 👉 Quiñones et al. JASE 2002 → doi.org/10.1067/mje.20… ⚔️ 2017 — The debate reopens Baumgartner et al. (EACVI/ASE) maintained the 0.5–1 cm recommendation. However, Hahn and Pibarot responded with a critical letter pointing out that the original articles from the 1980s measured at the aortic annulus, not 0.5–1 cm below it, and that moving away from the annulus introduces errors due to the elliptical and irregular shape of the subannular LVOT. 👉 Baumgartner et al. Eur Heart J Cardiovasc Imaging 2017 → doi.org/10.1093/ehjci/… 👉 Hahn & Pibarot. JASE 2017 → doi.org/10.1016/j.echo… 💡 Bottom line: The 0.5–1 cm figure was never experimentally validated as the optimal distance. It emerged from empirical observations in the 1980s aimed at avoiding a flow acceleration zone that had been demonstrated with invasive catheters. It was adopted through accumulated clinical practice and later elevated to a formal recommendation by consensus. The debate over whether to measure at the annulus or 0.5–1 cm below it remains open to this day. One of those recommendations we all follow but few know where it actually came from 🙂 Dr Benigno Valderrábano Salas @MDBeni @JaeKOh2 @ottoecho @WilliamZoghbi @ASE360 @EACVIPresident @NephroP @iamritu @PPibarot @hahn_rt @MAecocardio @SISIACOficial @SONECOM_AC @VazyurVasquez @Cardiotweets83 @HEARTof_echo @echobasics

With deep sorrow, I received the news of Dr. Eugene Braunwald’s passing, one of the greatest figures in world cardiology. His scientific legacy, clinical vision, and immeasurable contribution to generations of cardiologists will continue to live on in our daily practice and in the history of medicine. My heartfelt condolences to his family, friends, students, and to the entire cardiology community. May he rest in peace.

@argulian Same for LBBB…😉

@echo_batman More common that people think!

An elderly hospitalized patient with irregular heart beat. The team is considering Afib. Mitral inflow PW Doppler is shown. What is the likely explanation?

@Irina67790690 @iamritu MR signal (reasoning: (1) very high velocity, (2) tiger tripes in the signal, (3) first part is dagger-shaped obstruction signal with peak around 3 m/s, followed by more straight MR scan signal)

What's going on here? I can't explain it.

@hvanspall @djc795 Ideally (but not feasible) the net result should be evaluated once all treated and non treated groups have died . Same holds true for eg. HF medication & hosp HF,

@djc795 gave us a spectacular presentation on #costeffectiveness analysis using #TAVR as an example🙏🏽 Pearls - cost-effectiveness is not the same as cost savings - for an intervention to be cost-effective, it must first be effective (& you can’t always get what you want 🎶🙂)

@saramoscatelli7 Isolated LVH on ECG or isolated left axis deviation is not considered abnormal.

⚽🫀 ECG screening in paediatric athletes: are we over-testing? I’m sharing this interesting study exploring the incidence and clinical significance of ECG abnormalities in healthy paediatric athletes, and what it means for screening strategies. 💡 Why this matters Sudden cardiac death in young athletes is rare—but devastating. The challenge remains: 👉 How do we identify at-risk individuals without over-screening? 🔬 Key findings from this real-world cohort: 📊 Abnormal ECGs are not uncommon ✔️ 18.5% of ECGs showed at least one abnormality ✔️ Most common findings: 👉 Left ventricular hypertrophy 👉 Axis deviations 🧠 But here’s the crucial point… ✔️ No clinically significant cardiac disease was identified after further evaluation ✔️ All athletes were safely cleared for sports participation 👉 Many “abnormalities” are actually physiological adaptations to training 🔄 ECG findings are dynamic ✔️ Abnormalities often: 👉 Appear and disappear over time 👉 Are not consistently reproducible ✔️ Only 4% had persistent abnormalities across years 👉 A single ECG may have limited predictive value 🌍 Important nuances ✔️ Higher prevalence of ECG abnormalities in African American and multi-racial athletes ✔️ Reflects known ethnicity-related physiological ECG patterns ⚠️ Clinical implications ✔️ High rate of false positives ✔️ Low yield for detecting true disease ✔️ Potential for: 👉 Unnecessary testing 👉 Anxiety 👉 Increased healthcare costs 🚀 So what should we do? 👉 Move toward targeted screening strategies 👉 Use ECG as a second-line tool, not universal screening 👉 Emphasise expert interpretation to distinguish physiology vs pathology 🫀 The take-home message Not every abnormal ECG is disease—especially in young athletes. 👉 Smarter screening, not more screening, is the key. 👏 A valuable contribution to the ongoing debate on cardiovascular screening in sports cardiology. #Cardiology #SportsCardiology #PediatricCardiology #ECG #Screening #AthleteHeart #SuddenCardiacDeath #Prevention #MedTwitter #CardioTwitter #Research doi.org/10.1017/S10479…

@StellEkaterina Very kind Ekaterina! Note that Vmax/Vmean in PAH has a differenr pathophysiological-hydraulic basis than in fTR. In PAH, it is most likely shaped by degree of afterload mismatch in these patients, evenrually leading to the “bistoury” in most mismatched ones we think.

@echo_batman Really nice work 👏 already using this in my talks, super helpful perspective on TR👍🏻✨

Tricuspid Regurgitation Peak-to-Mean Velocity Ratio: Linking Doppler Morphology to Right Heart Hemodynamics in Pulmonary Hypertension - Journal of the American Society of Echocardiography onlinejase.com/article/S0894-…

@SrihariNaiduMD @HcmPatient @hcmsociety @noshreza @tikuowens @MasriAhmadMD @purviparwani @DavidWienerMD @adityadoc1 @GiorgioMedranda @EllauziRama This was not an extended Morrow indeed. Personally, I would propose reintervention in ecperienced center but would first do trial with CMI to assess feasibility here and to assess impact on symptoms.

Of all we do in #HCM the procedures need to be done right the first time. Here’s a myectomy patient who flew in for a consult. Cut didn’t get to the SAM septal contact. Experience and isuprel challenge would have prevented or caught this. CMI v alc abl v repeat surgery?

Only partly agrree here. Guidelines are at least better than having nothing and on average, they do bring (some) order to the chaos for most physicians. However, I do share the concern with the author (“ But the more I read, the more I feel that guidelines are overly influenced by people with either financial or intellectual conflicts of interest), especially when it comes to devices; in facr, some of the paragraphs in recent ESC guidelines on valvular heart disease are exemplary in that case. Sio there is room for improvement and I think that it starts with the question on what basis are the authors of guidelines being selected?

Excellent Friday post from @adamcifu on @Sensible__Med Guidelines have indeed run amok

@EchoProsto @argulian @NephroP @IM_Crit_ @StellEkaterina @echo_stepbystep @iamritu @JGrapsa @denisamuraru @iceman_ex @purviparwani Severe primary MR due to Barlow given the timings of TR CWD signal. Great question!

@argulian @NephroP @echo_batman @IM_Crit_ @StellEkaterina @echo_stepbystep @iamritu @JGrapsa @denisamuraru @iceman_ex @purviparwani

A patient with dyspnea. CW Doppler interrogation across the tricuspid valve is shown. 1/2