1/ Good morning #MedTwitter, it’s time for another episode of #12LeadThursday! Remember to approach every EKG systematically. Grab your calipers, and let’s dive in!
What are potential causes of this pause?
5️⃣ PVI-SHAM-AF — one of the most provocative trials at ESC
🔹 What we knew
Catheter ablation reduces AF burden and improves symptoms and quality of life in many symptomatic patients.
But procedural trials have a major problem:
Patients know they underwent an intervention.
And invasive procedures can produce powerful placebo effects.
❓ The question
How much of the symptomatic improvement after AF ablation comes from actually eliminating AF — and how much comes from the procedure itself?
📊 PVI-SHAM-AF
262 symptomatic AF patients:
Catheter ablation
vs
sham procedure
At 6 months, AF-related quality of life improved substantially in BOTH groups — with no statistically significant difference between ablation and sham.
But:
Freedom from AF:
73% ablation
vs
52% sham.
📌 Take-home
Fascinating result.
Ablation clearly affects rhythm.
But improvement in rhythm and improvement in how patients feel are not necessarily identical outcomes.
Sham-controlled procedural trials force us to question assumptions that would otherwise be almost impossible to test.
#AFib #Ablation #ESC2026 #esccongress
4️⃣ SINGLE-AF — anticoagulation at intermediate stroke risk
🔹 What we knew
The benefit of anticoagulation is clear in AF patients at sufficiently high thromboembolic risk.
The dilemma is the intermediate-risk patient:
Is the absolute stroke risk high enough to justify lifelong anticoagulation and its bleeding risk?
Randomized evidence in this group has been limited.
❓ The question
Does anticoagulation improve outcomes in AF patients with only intermediate stroke risk?
📊 SINGLE-AF
1,803 patients with AF:
CHA₂DS₂-VASc 1 in men or 2 in women.
DOAC
vs
no anticoagulation.
At 24 months:
Primary composite: 0.5% vs 1.5%
HR 0.31
Ischaemic stroke: 0.1% vs 1.1%
Major bleeding: 0.3% vs 0.5%
📌 Take-home
Important randomized evidence supporting anticoagulation even in this lower-risk AF population.
But the absolute number of events was small.
This is potentially guideline-changing — while still requiring interpretation according to absolute stroke risk, bleeding risk and patient preference
#AtrialFibrillation #DOAC #ESC2026
3️⃣ AIR-STEMI — physiology beats the eyeball?
🔹 What we knew
In STEMI with multivessel coronary disease, complete revascularization improves outcomes compared with treating only the culprit lesion.
But an important question remains:
Which non-culprit lesions actually need PCI?
Angiographic stenosis severity does not always reflect physiological significance.
❓ The question
Could physiology derived directly from coronary angiography identify the lesions that actually matter — allowing more selective complete revascularization?
📊 AIR-STEMI
~1,800 patients with STEMI + multivessel CAD.
Functional coronary angiography-guided strategy
vs
conventional angiography.
Primary outcome:
4.6% vs 13.7%
Functional guidance substantially reduced major cardiovascular events.
Safety events including contrast-associated AKI/major bleeding were also lower:
4.6% vs 7.1%.
📌 Take-home
Complete revascularization doesn't necessarily mean stenting every lesion that looks severe.
Treat the lesions that matter physiologically.
This could move STEMI multivessel PCI closer to precision revascularization.
#STEMI #PCI #InterventionalCardiology #Cardiotwitter #ESCCongress
2️⃣ REACT — Atherosclerosis starts much earlier than we think
🔹 What we knew
Atherosclerosis develops silently for years — often decades — before MI or stroke.
Traditional risk scores estimate the probability of future events based on risk factors.
But risk factors and actual atherosclerotic burden are not the same thing.
❓ The question
If we actually look for atherosclerosis in apparently healthy people across adulthood, how common is it?
And how well do conventional risk scores identify those who already have disease?
📊 REACT
16,808 apparently healthy adults aged 18–70 underwent imaging for subclinical atherosclerosis.
Atherosclerosis was found in:
➡️ ~1 in 13 people aged 18–29
➡️ 57% overall
➡️ ~9 in 10 aged 60–70
Conventional SCORE2 identified only a minority of people with imaging-detected disease as high risk.
📌 Take-home
Perhaps the most important prevention message from ESC:
Risk factors estimate probability.
Imaging can show whether the disease is already there.
And atherosclerosis may begin much earlier than the age at which we traditionally start thinking seriously about prevention.
#Atherosclerosis #Prevention #ESC2026 #ESCCongress
1️⃣ STAREE — Statins after 70
🔹 What we knew
Statins clearly reduce cardiovascular events in younger and high-risk populations.
But primary prevention after age 70 remains an important evidence gap.
Older adults are underrepresented in statin trials, while competing risks, frailty, adverse effects and cognitive concerns make the risk-benefit calculation more complicated.
❓ The question
Should healthy adults ≥70 years without established CVD, diabetes or dementia receive statins to prevent cardiovascular events — and potentially prolong disability-free survival?
📊 STAREE
9,971 adults ≥70 years:
Atorvastatin 40 mg vs placebo
Median follow-up: 5.9 years
Major CV events: 6.0% vs 8.3%
HR 0.70
➡️ 30% relative reduction
But disability-free survival was not significantly improved.
📌 Take-home
Age alone should not make us dismiss statins for primary prevention.
The cardiovascular benefit in healthy older adults appears real.
But preventing cardiovascular events and extending disability-free survival are not necessarily the same thing.
#STAREE #Statins #Prevention #ESCCongress
🧵 ESC Congress 2026 🇩🇪 — the trials worth knowing
A huge ESC in Munich: 59 Hot Line trials.
Here are my picks of the studies most likely to influence how we think about cardiovascular prevention and treatment.
For each:
🔹 What we already knew
❓ What the trial asked
📊 What it found
📌 What it means
#ESCCongress #ESC2026
🎯 THE PRACTICAL TAKE-HOME
4th UDMI:
PCI → >5× troponin threshold
CABG → >10× troponin threshold
evidence of ischaemia/complication
→ Type 4a / Type 5 MI
5th UDMI:
Cardiac procedure
↓
Acute myocardial injury + suspected coronary complication
↓
Prove the complication and/or prove new ischaemic myocardial damage
↓
→ PROCEDURE-RELATED MI
The new philosophy:
Don’t diagnose procedural MI from the magnitude of troponin release alone.
After cardiac procedures, myocardial injury is common.
The diagnosis should identify a clinically meaningful coronary complication resulting in infarction.
#CardioX #MyocardialInfarction #PCI #CABG #ESCCongress
1/6 🚨 Procedure-related MI has changed substantially in the 5th Universal Definition of MI.
The old Type 4/5 classification is gone — and perhaps the biggest change is this:
❌ MI is no longer diagnosed by reaching an arbitrary troponin threshold after PCI or CABG.
Here’s the old vs new framework 👇
🔴 OLD — 4th UDMI
Type 4a MI (PCI-related)
Within 48 h of PCI:
cTn >5× the 99th percentile URL + evidence of new myocardial ischaemia, such as:
• new ischaemic ECG changes
• new pathological Q waves
• imaging evidence of new loss of viable myocardium/RWMA
• angiographic evidence of a procedural flow-limiting complication
Type 4b MI → Stent thrombosis
Type 4c MI → Restenosis
These could occur at any time after PCI.
Type 5 MI (CABG-related)
Within 48 h:
cTn >10× the 99th percentile URL + ≥1:
• new pathological Q waves
• angiographic evidence of new graft/native coronary occlusion
• imaging evidence of new loss of viable myocardium/RWMA
So what replaces this classification?
6/6 ⏱️ WHAT HAPPENS AFTER 30 DAYS?
Stent thrombosis, restenosis or graft failure >30 days after the procedure is no longer considered procedure-related MI.
👉 It is classified as PRIMARY MI.
Even within 30 days, an MI unrelated to the vessel/territory treated by the index procedure should be classified according to its actual mechanism — primary or secondary MI.
1/7 🚨 Secondary MI ≠ simply the new name for Type 2 MI.
The 5th Universal Definition of MI changes the framework.
And one important clarification:
Type 2 MI ALREADY required evidence of acute myocardial ischaemia.
So what actually changed? 🧵👇
🎯 The key change?
The 5th UDMI deliberately prioritizes SPECIFICITY for Secondary MI.
Not:
“Troponin ↑ + acute illness = MI.”
But:
Is there truly an infarction—or are we looking at acute myocardial injury?
That distinction matters.
2/7 OLD — Type 2 MI
Acute myocardial injury (troponin rise/fall) + O₂ supply–demand imbalance unrelated to acute atherothrombosis + Evidence of acute myocardial ischaemia
Type 2 MI
So requiring ischaemia is NOT new.
7/7 🟢 CONFIRMED Secondary MI
≥1 of:
• Obstructive CAD WITHOUT acute coronary pathology
(≥70% epicardial stenosis OR ≥50% if physiologically flow-limiting)
AND/OR
• New/presumed-new regional wall-motion abnormality or loss of viable myocardium consistent with ischaemia.