Ariel Roguin

Head of Cardiology, Hillel Yaffe Medical Center. Professor of Cardiology, Technion Israel Institue of Technology.

[Eric Topol @EricTopol]

Getting it wrong for many decades.
Since the 1950's, pacemaker leads have been placed in the right ventricle. A new randomized trial challenging that dogma found marked superiority of outcomes for pacing from the left bundle branch. https://t.co/DzMUaStZjS

[Laliga News @laligaa_neews]

🔵⚪️ | Golpe fortísimo de Owono sobre Jesús de Miguel que hace que salten todas las alarmas. 🇪🇸👀

🙏🏼 Pronta recuperación a Jesús y que todo quede en un susto

🏟️ Tenerife - Andorra

[Eyal Braun @BraunEyal]

תובנות אחרי בחירות
לא מה שחשבתם :

בימים כאלו טוב להיות אוהד הפועל חיפה .
היכולת שלך לספוג מפלות ולהישאר אופטימי גבוהה לעין שיעור מאשר של אדם ממוצע.

[John Mandrola, MD @drjohnm]

Another sobering study in AF ablation. Melbourne group reports on 121 patients who have recurrent AF despite durable PVI. All have posterior wall isolation. [Because we can.]

The results are similar to the trials. Not good.

https://t.co/FtckPQI6zT

@peterkistler3

[Elad Asher @AsherElad]

ICI 2026 - Innovation in Cardiovascular Interventions. Tel Aviv, December 6 to 8.

Thirty-one years of a meeting that keeps coronary, structural heart, electrophysiology and AI on one program. Founded by Chaim Lotan and Rafael Beyar, who have organized it since.

[Dr Alo, DO, FACC @MohammedAlo]

🚨 Cardiology dogma says plaque only builds. It never breaks down.

Nine imaging trials from 2004 to 2023 prove that dogma wrong.

"But the data says otherwise."

And no, this is not just theory. This is IVUS, OCT, and NIRS imaging inside real coronary arteries.

I am a cardiologist. I have hundreds of patients on aggressive LDL-lowering therapy, and I track their numbers against this exact body of evidence.

🩺 Here is what the science actually says.

🔬 REVERSAL (2004): High-dose atorvastatin (LDL 79) halted plaque progression. Moderate pravastatin (LDL 110) let plaque grow +2.7%. Intensity at the artery wall matters.

✅ ESTABLISH (2004): Atorvastatin started immediately post-heart attack produced -13.1% plaque volume in 6 months. The fastest regression ever documented.

✅ ASTEROID (2006): Rosuvastatin drove LDL from 130.4 to 60.8 mg/dL. 63.6% of patients regressed. First frank proof reversal is real.

✅ SATURN (2011): 1,039 patients. Max-dose statins regressed plaque regardless of brand. Regression is a class effect of intensive LDL lowering.

✅ PRECISE-IVUS (2015): Adding ezetimibe to a statin nearly quintupled regression, 78% of patients regressed versus 58% on statin alone.

✅ GLAGOV (2016): Evolocumab drove LDL to 36.6 mg/dL. Regression correlated linearly down to LDL 20 mg/dL. No plateau. No floor.

✅ HUYGENS (2022): Evolocumab post-heart attack (LDL 28.1) nearly doubled fibrous cap thickening. ApoB below 65 mg/dL predicted nearly double the structural benefit.

✅ PACMAN-AMI (2022): Alirocumab (LDL 23.6) achieved triple regression, volume, lipid core, and cap thickness together. Event rate dropped to 8.3% versus 18.2% in non-regressors.

✅ YELLOW III (2023): Evolocumab cut dangerous thin-cap plaques from 48% to 13% in just 26 weeks. But 20% of patients did not respond despite LDL in the 30s and 40s.

That matters because LDL lowering is necessary but not always sufficient.

🫀 A patient who gets LDL below 50, gets ApoB below 65, and starts therapy immediately after a cardiac event can show measurable plaque regression within 6 months.

That is the difference between a plaque that ruptures and a plaque that heals.

❤️ Bottom line:

Plaque is not a one-way street. It is not permanent once it forms.

Over 4,000 patients across these trials prove regression is real, reproducible, and dose-dependent.

Stop targeting LDL of 100. Stop treating 70 as aspirational.

Measure ApoB. Target below 65 mg/dL.

Drive LDL below 60, then below 50, then below 40, with no floor yet identified for benefit or harm.

The question is no longer whether plaque can reverse. The question is why more clinicians are not treating it that way.

What is your LDL and ApoB right now?

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #ApoB #Statins #PCSK9Inhibitors #Lpa #PreventiveCardiology #LifestyleMedicine

[Gregg Fonarow MD @gcfmd]

🫀 DANCAVAS II: inviting men 60–64 to comprehensive CV screening including CAC testing

DID NOT cut ☠️ (9.3% vs 9.9%) or MACE ❌

⚠️ But it ⤴️ severe bleeding (6.0% vs 5.1%, HR 1.18), likely from aspirin 🩸

💊 Statin adherence? No better

Takeaway: screen ≠ improve outcomes

[د.مها @res_pian3]

الروابط الجديدة لموقع sci-hub لتحميل الابحاث العلمية المدفوعة مجاناً

👆👆
1- https://t.co/UQnyQf5TDZ
2- https://t.co/E0zrQnocEa
3- https://t.co/au71psQ8z8
4- https://t.co/plIeasHMOa
5- https://t.co/iYrUs0ww3m
6- https://t.co/YAy834EXBW

[Muthu Vaduganathan @mvaduganathan]

‘26 HF RCTs

HFpEF
GLP1: #MARITIME #HFPolaris #ELEVATE
sMRA: #SPIRRIT
nsMRA: #REDEFINE
ASi: #EASiHFPres
CMI: #AURORA #AMBER #EQUINOX

HFrEF
GLP1: #Enith
nsMRA: #FINALITY
ASi: #EASiHFRed
Myosin Act: #COMET
Colchicine: #COLHEF
IV Fe: #ICONIC

All LVEF
nsMRA: #BalanceD #CONFIRMATION

[Ariel Roguin @ArielRoguin]

@0DonaldTrumpJrQ 2208

[Sadhna @sadhna6389]

Netflix has 260 million subscribers. Netflix is betting that 250 million of them never open the settings menu.

One guy did. He worked Netflix customer support for 3 years. Handled 15,000 complaints. He told me something that should change the way you watch tonight:

"Every single complaint I got for 3 years was caused by the same 10 settings. Not bugs. Not content. Settings."

"'Why is my picture blurry?' Because Netflix set your streaming quality to Auto which doesn't mean best quality. It means lowest quality Netflix can get away with before you notice."

"'Why are my recommendations terrible?' Because 3 people are watching on your profile and the algorithm thinks you're one person who loves true crime, kids cartoons, and Korean dramas at the same time."

"'Why does every movie look like a soap opera?' Because a motion smoothing setting you've never seen is turned on making a $200 million film look like it was shot on a phone."

"'Why do I scroll for 45 minutes and give up?' Because autoplay previews are feeding the algorithm false data every single time you pause on a thumbnail. Netflix thinks you're interested. You were just reading the description. Now your homepage is full of content you'd never watch because you accidentally trained the algorithm to recommend it."

"'Why can't I find anything good?' Because your content maturity rating is set to a default that hides 40% of the library. Shows and movies that exist on your account right now that you're paying for right now are invisible to you because of one setting you've never checked."

"I spent 3 years answering the same 10 complaints. Every single time the fix was the same: 'Let me walk you through your settings.' Every single time the customer said the same thing: 'Why didn't Netflix tell me this?'"

"Because Netflix makes more money when you scroll. Not when you find something."

Here are 10 Netflix settings that are ruining your experience right now and exactly how to fix each one in under 5 minutes:

🧵

[Thomas Dayspring @Drlipid]

In view of all the Lp(a) interest, I thought it is a good timed to again explain and make less confusing Lp(a) and LDL metrics using my graphics. There is tremendous misuse of various particle metrics. Once again - LDL refers to a specific lipoprotein - THERE IS NO LAB TEST CALLLED LDL, Enlarge the graphic to study the subtleties. @nationallipid @foundationofnla @society_eas @ASPCardio @escardio @atherosociety @TheEndoSociety @FamilyHeartFdn @fhpatienteurope #cholesterol

[Davide Capodanno @DFCapodanno]

Novartis today announced that the phase III Lp(a)HORIZON trial of pelacarsen did not meet its primary endpoint of 4-point major adverse cardiovascular events in 8,323 patients with elevated Lp(a) and established CVD.

Three things were once said to be certain in life: death, taxes, and that lowering Lp(a) would improve health. What has always struck me is the confidence with which pelacarsen was described by some experts as a drug “on its way”. I remember a debate a year ago in which I pointed out that, if the clinical benefit of lowering Lp(a) were a certainty, there would be little reason to run an outcomes trial in the first place.

The fact that guidelines and consensus documents were already recommending Lp(a) measurement before cardiovascular outcomes trials had actually established clinical benefit seemed difficult to understand. It also contributed to the impression that the ongoing trial was essentially a formality and that it would inevitably be positive. Yet, as you may remember, Lp(a)HORIZON had to extend recruitment because fewer events than expected had occurred. Even then, that did not sound entirely reassuring.

I do not want to overinterpret one negative trial, particularly with phase III outcomes trials of olpasiran and lepodisiran still ongoing. But until those results are available, what do we make of the recommendation to measure Lp(a) at least once in everyone’s lifetime?

[Davide Capodanno @DFCapodanno]

The day after the announcement of the neutral results of HORIZON Lp(a), and while keeping in mind that nobody has yet seen the final results (although, in practical and regulatory terms, that may matter little), much of the discussion is focusing on Lp(a) as a prognostic risk-stratification marker.
The argument goes: “If you, as a patient, have high Lp(a), then you are a high-risk patient, and I will intensify the therapies I have available”—starting from the assumption that, without knowing your Lp(a), I would somehow not have done so based on other available biomarkers and clinical features.
But this raises at least two other questions.
First: what therapy has evidence specifically in patients with elevated Lp(a)? Are there trials of non-Lp(a)-lowering drugs conducted specifically in patients with elevated Lp(a) (all patients, not just a subgroup—no cheating)?
Second: if universal Lp(a) screening is indeed useful even though we have no evidence that lowering Lp(a) improves outcomes, are there at least studies showing that knowing the Lp(a) level improves outcomes? In other words, are there trials in which physicians—not patients—are randomized to know versus not know the Lp(a) value, and therefore to act accordingly (e.g., prescribing exercise or other therapies that physicians in the control group would presumably consider anyway)?

[Hany Ragy @Hragy]

This is what 40,000 cardiologists look like when using public transport to go to their event #ESCCongress at 8 am in Munchen….

[Prof Chris P Gale @cpgale3]

WOW!

Sham #AFib ablation RCT…. neutral

[Elad Asher @AsherElad]

The Fifth Universal Definition of Myocardial Infarction is out at ESC Congress 2026. Types 1-5 are gone. MI is now primary, secondary or procedure-related - classified by the pathophysiology behind it rather than by a number.

[Davide Capodanno @DFCapodanno]

The 10 trials I am most looking forward to at the ESC Hot Lines next week (in no particular order):

LIBREXIA-ACS, where milvexian could end up like apixaban in APPRAISE-2, perhaps with less bleeding. Rivaroxaban did not exactly have an easy story after ATLAS ACS 2 either, despite the positive results. Although we know the trial was stopped for futility, the data remain important in the rollercoaster of FXI inhibitor trials.

EPIDAURUS, because I will be the Discussant in Hot Line 3. It compares ticagrelor or prasugrel with clopidogrel in patients with atrial fibrillation and acute coronary syndrome. So I know everything about it, but I am not telling you.

SWITCH-SWEDEHEART, because if this trial is positive for prasugrel, this might finally be the moment when I call back all my patients on ticagrelor and switch them one by one. If not, we can say we have been joking all along and that ISAR-REACT 5 was just an episode.

PREMIUM, because after NEOMINDSET and STOPDAPT-3, a third negative trial for an aspirin-free strategy (meaning P2Y12 inhibitor monotherapy from the outset) would probably put this rather radical idea to rest, making it indefensible.

ISOLEDS, comparing OCT- versus IVUS-guided PCI in distal left main disease. After OPTIMAL and IVUS-CHIP, which we are still recovering from, we really need something that leaves angiography out of the comparison.

TAVI-PCI, because I don’t know about you, but after NOTION-3 and PRO-TAVI, I am still somewhat confused.

POPular-ACE, one of my favourites because it addresses a simple question with a potentially clear answer that we could implement in the cath lab the very next day: do we actually need protamine after TAVI or not?

AIR-STEMI, continuing the elemental saga of the Ferrara group (the same investigators behind FIRE) this time using angio-derived FFR to identify non-culprit lesions in STEMI. There is some confusion here too, given that FLOWER-MI was negative while FRAME-AMI was positive.

A-CLOSE, evaluating chronic clopidogrel monotherapy and continuing the story started by HOST-EXAM and SMART-CHOICE 3 against aspirin, while resembling OPT-BIRISK in its comparison with DAPT.

PRAGUE-26, which deserves a special mention because I really like the idea of tackling a complicated problem with an extremely simple and inexpensive approach. The results could surprise us and tell us that the solution has been sitting right there all along: alteplase directly instilled into the pulmonary arteries—a strategy we practically never use, and perhaps we are wrong not to.

[Ariel Roguin @ArielRoguin]

@miradreaamy 57

[Mamas A. Mamas @mmamas1973]

This is a really interesting paper- 1 in 300 citations are now fabricated with a 12- fold increase in past 2-3 years, probably reflecting use of AI. Via @ArielRoguin ( his sons paper)

Fabricated citations: an audit across 2·5 million biomedical papers - The Lancet https://t.co/u7ISubZGfm