ECG_aficionado

[Waqas Haider, MD, MPH, FACC @WaqasHaiderMD]

Pericardial effusions have long been described in millimeters.

But when the clinical question is fluid burden, a single linear dimension may not be enough.

In our new JASE editorial with David Dudzinski, we discuss the practice-changing work by Kane et al. and the accompanying tutorial, which challenge us to rethink how we quantify pericardial effusions by echo.

The key shift:

From a single maximal width
to a more integrated assessment of volume, distribution, phenotype, and physiology.

Milliliters may bring us closer to the anatomic truth.

But tamponade remains a physiologic diagnosis.

Free access:
https://t.co/R2UgItJ6B3

#EchoFirst #CardioTwitter #PericardialDisease #JASE

[Ken Grauer, MD @ekgpress]

The ECG in the Figure is from a man in his 60s who is aware of his “irregular heart beat”. — Why is this rhythm irregular? — What is your differential diagnosis? — GO TO — https://t.co/CuTZVMvalV — :)

[ECG_aficionado @ecg_lover]

49/Male with seizures
@Ecgloverr @ecgandrhythmRoe @ecgrhythms @DrRazi4 @The_Nanashi_O @Jagdish26039718 @nihar_nayak2

[ECG_aficionado @ecg_lover]

60 Male palpitations
@Ecgloverr @ecgandrhythmRoe @ecgrhythms @The_Nanashi_O @DrRazi4 @EcgsOnly @PMcardioApp

[ECG_aficionado @ecg_lover]

@ecgandrhythmRoe @Ecgloverr @ECG_BUDDY_ARPI @EcgsOnly @ECG_BUDDY_ARPI @DrRazi4 @Ecgloverr

[ECG_aficionado @ecg_lover]

@ecgandrhythmRoe @Ecgloverr @ECG_BUDDY_ARPI @EcgsOnly @DrRazi4

[ECG_aficionado @ecg_lover]

15 year old
Routine ecg
@DrRazi4 @The_Nanashi_O @ecgchallenge @Ecgloverr @ECG_BUDDY_ARPI @Ecgloverr

[SREEVATSA NADIG DM FSCAI FESC @nadig_cardio]

I was Going through Af management - changes and nuances for a presentation
And some change that I read which are noteworthy #MedTwitter #CardioTwitter #NeuroTwitter #Epeeps

( updates from the new ESC / European Heart Rhythm Association guidelines)

1. CHA₂DS₂-VASc → CHA₂DS₂-VA
• Female sex ❌ no longer a risk factor
• It’s a risk modifier, not an independent predictor

2. Some AF cases = anticoagulate anyway (don’t calculate scores)
• HCM→ OAC irrespective of score
• Cardiac amyloidosis → OAC strongly favoured
• Significant valvular disease (esp. MS) → treat as high risk

“high-risk AF phenotypes”

3. DOACs
• No clear superiority of one DOAC over another
• Switching without reason = no benefit
• Dose correctly

4. Rhythm control is back favoured over rate ctrl except in PERMANET t AF
• Early rhythm control > rate control in:
– Paroxysmal AF
– Persistent AF

👉 Now Class I recommendation

5. Ablation early, preferred
• Early referral for catheter ablation
– Paroxysmal AF
– Persistent AF

👉 First-line strategy in selected patients (Class I)

6. AF + ACS (antithrombotics simplified) #cardiotwitter
• DOAC + DAPT → very short (≈1 week, up to 1 month)
• Then DOAC + single antiplatelet → up to 12 months
• Then DOAC alone lifelong

👉 Bleeding reduction is the priority

7. Transient / secondary AF
(e.g. sepsis, post-surgery, pericarditis)

• OAC ~ 4 weeks
• Reassess with monitoring (Holter/ELR)
• If no recurrence → stop OAC

8. No AF documented = no DOAC
• Even in cryptogenic stroke
• Need ECG evidence (Holter / ILR)

👉 No more “empirical anticoagulation”

9. Risk reassessment is dynamic
• Stroke risk ≠ static
• Re-evaluate periodically (age, DM, BP, etc.)

10. Lifestyle is now guideline-level therapy
• Weight loss
• Exercise
• Alcohol reduction
• Treat OSA

👉 Risk factor control = AF control

11. AF burden matters (but not fully there yet)
• Device-detected AF → still evolving
• Not all subclinical AF = anticoagulate

Bottom line

AF management is shifting from:
👉 “Rate control + late decisions”

to:
👉 “Early rhythm control + early ablation + precise anticoagulation”
Any other points?!

[Dr Sudhir Kumar MD DM @hyderabaddoctor]

Don’t wait for disease. Know your numbers.
Most heart attacks, strokes & diabetes are predictable years in advance, if you track the right markers.

For Indian adults, these cut-offs matter more than ever:

1. Blood Pressure (BP)
Target: <130/80 mmHg

Even “borderline” BP in Indians carries higher cardiovascular risk due to earlier vascular aging.

2. Fasting Blood Sugar (FBS) <100 mg/dL

Indians develop insulin resistance earlier, even at “normal” BMI.

3. HbA1c <5.7%

Prediabetes starts silently. By the time glucose rises, damage has already begun.

4. Insulin Resistance (HOMA-IR)
Ideal: <2

Insulin resistance (IR) is not routinely measured, but it is extremely useful in high-risk individuals. IR is a hidden driver of diabetes, fatty liver & PCOS.

5. Waist Circumference (Most important for Indians)

Men: <90 cm
Women: <80 cm

🔸“Thin outside, fat inside” (TOFI) phenotype is common.
🔸Waist circumference is better than BMI for risk prediction.

6. LDL Cholesterol
Target
<100 mg/dL (general)
<70 mg/dL (high-risk)

🔸Lower is better; there is no “safe high LDL.”

7. HDL Cholesterol>50 mg/dL

Low HDL is extremely common in Indians and amplifies risk.

8. Triglycerides (TG)<150 mg/dL
High TG is an insulin resistance marker, not just a lipid issue.

9. TG : HDL Ratio<2

🔸TG:HDL ratio is one of the simplest markers of metabolic health.
🔸A ratio of 2 or more is insulin resistance until proven otherwise.

10. hs-CRP (inflammation marker)<2 mg/L

Atherosclerosis is an inflammatory disease, not just high cholesterol.

11. ApoB (the underrated one)

Target: <80 mg/dL (general)
<65 mg/dL (high-risk)

ApoB is better than LDL at predicting risk, as it counts actual atherogenic particles.

12. Sleep Duration
Optimum: 7–9 hours/night

Less sleep is associated with ↑ insulin resistance, ↑ BP, ↑ appetite, ↑ CV risk.

▶️What makes this crucial for Indians?
🔸Higher risk at younger age
🔸More visceral fat at lower BMI
🔸Greater tendency for diabetes & heart disease
🔸Normal-looking person does not mean low risk

▶️If you are above these thresholds, do not panic. Start with exercise, healthy diet, optimum sleep, and consistency. Consult your physician for individual opinion.

Dr Sudhir Kumar @hyderabaddoctor

(Disclaimer: This is not a medical consultation. The information provided here is general in nature, and applies to healthy people, who are not on medications. In any case, consult your doctor for individual opinion)

[Ahmed Ammar @Dr_Ahmed_Ammar]

Back to Basic Electrophysiology

Nice educational case and discussion of different types and rare forms of AVNRT by Dr Christiane Jungen at #EHRA26

#EPeeps

[Ahmed Ammar @Dr_Ahmed_Ammar]

This ECG made me a better electrophysiologist

Fascinating talk by Dr Peter kistler at #EHRA26

[SREEVATSA NADIG DM FSCAI FESC @nadig_cardio]

For fellows bookmark this tweet for exams #cardiotwitter #MedTwitter
🧵
First of all What is a significant step-up?
👉remember 7-5-5-7 rule
•RA to mixed venous sats ≥7%
•RV to RA ≥5%
•PA to RV ≥5%
•. At any level >7%
{Mixed venous sats = (3* SVC + IVC)/4 )

Normally IVC sat is higher than SVC - please don’t say svc is higher (read up why )
1/n

[CardiovascularCorner @TrackYourHeart]

Pericardial Tamponade vs Constrictive Pericarditis ➡️Spot the Difference

Tamponade
⬇️
Accumulation of fluid in the pericardial space
⬇️
↑ intrapericardial pressure
⬇️
impairs diastolic filling throughout the cardiac cycle (early and late diastole).
Doppler shows blunted E and A waves due to restricted filling.

Constrictive Pericarditis
⬇️
Thickened, non-compliant pericardium
⬇️
rapid early diastolic filling that abruptly halts once volume limit is hit.
Doppler shows prominent E wave, reduced A wave, classic for constriction.

Recognizing the echocardiographic filling patterns is essential for diagnosis.

Ref: Catherine M. Otto, Textbook of Clinical Echocardiography

[Ritika Tuli @RitikaTuliMD]

#CardioNugget:

L wave = extra filling wave between E & A (mid-diastole)

Not normal → suggests ↑ LV filling pressures + abnormal relaxation

Seen in advanced diastolic dysfunction

E–L–A pattern = abnormal filling

#CardioNuggets #EchoBoards #Diastology

[Ritika Tuli @RitikaTuliMD]

#CardioNugget:

Diastology pearl 🫀

E wave = early filling (LA-driven) → correlates with PCWP
➡️ Best marker: E/e′ ↑ → ↑ filling pressures

A wave = atrial kick (LV resistance) → correlates with LVEDP
➡️ Marker: A-Ar → LV stiffness

#EchoBoards #CardioNuggets

[Milan Koštek @KostekMilan]

🟡 normalizing PVCs 🟡
* normalizing fusion *
🧵 with explanations 🧵

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🩻Contrast-induced AKI:
one of the biggest myths still shaping clinical decisions

For decades we were taught:

👉 “Contrast damages the kidneys”
👉 “Avoid CT with contrast in CKD”
👉 “Hydrate, protect, delay imaging if needed”

But what if… most of this is wrong?🤔

->The uncomfortable reality

Modern evidence shows:

👉 Low-osmolar contrast rarely causes true nephrotoxicity
👉 Even in CKD, AKI, and ICU patients
👉 The risk is often overestimated—or nonexistent

So where did the fear come from?

📍 1950s high-osmolar contrast (actually toxic)
📍 Poorly controlled observational studies
📍 “Creatinine rise = contrast injury” assumption

👉 Correlation became causation
👉 And the dogma stayed

⚠️What recent data tells us

✔ No difference in AKI rates with vs without contrast
✔ No benefit from bicarbonate, NAC, or aggressive hydration
✔ Even ICU and AKI patients show no worsening outcomes

->Translation to real life

👉 The patient was going to develop AKI anyway...Not because of contrast!!

->The real problem: “Renalism”

👉 Avoiding necessary imaging
👉 Delaying diagnosis
👉 Choosing inferior tests

And that leads to:

❌ Missed PE
❌ Delayed sepsis source control
❌ Worse outcomes

->Clinical mindset shift

Instead of asking:

👉 “Will contrast harm the kidneys?”

We should ask:

👉 “Will NOT doing the scan harm the patient?”

->Who still deserves caution?

✔ eGFR <30
✔ Severe hemodynamic instability
✔ Multiple nephrotoxins

Even then:

👉 Optimize volume
👉 Minimize dose
👉 Don’t delay critical imaging

🤓Bottom line

✔ Contrast nephrotoxicity exists… but is rare
✔ The fear is bigger than the risk
✔ The harm of NOT imaging is often greater

In critical care

👉 We don’t treat creatinine
👉 We treat patients

And sometimes…

👉 The most dangerous thing is NOT the contrast

👉 It’s hesitation.

📃Reference
Florens N, Demiselle J.
Kidney360 7: 445–449, 2026. doi: https://t.co/CWzi7WC9Wx

[ECG_aficionado @ecg_lover]

@Jagdish26039718 @ecgchallenge @ECG_BUDDY_ARPI @The_Nanashi_O @Ecgloverr @nihar_nayak2 Could this be fascicular VT?

[ECG_aficionado @ecg_lover]

22 Male dyspnea
@ecgchallenge @ECG_BUDDY_ARPI @The_Nanashi_O @Ecgloverr @nihar_nayak2 @Jagdish26039718

[ECG_aficionado @ecg_lover]

22 Male with dyspnea @The_Nanashi_O @ecgchallenge @Jagdish26039718 @nihar_nayak2 @Ecgloverr