Evan Hindoro

Cardiovascular Resident 🫀 at National Cardiovascular Center Harapan Kita, Indonesia

[Ritika Tuli @RitikaTuliMD]

CardioNugget™ 🫀

Why does diastolic MR occur in acute severe Aortic Regurgitation?

1️⃣ Acute severe AR → rapid filling of a noncompliant LV
2️⃣ LVEDP rises dramatically
3️⃣ LV diastolic pressure exceeds LA pressure → premature mitral valve closure
4️⃣ LV pressure continues to rise in late diastole → blood is forced back across the closed mitral valve = diastolic MR

Often accompanied by premature MV closure and a normal-sized LV in acute severe AR.

#CardioNugget™ #EchoBoards #EchoFirst #ASEcho #Cardiology #FOAMed #BoardPrep #AorticRegurgitation

[CardioNova @AppCardioNova]

Trombo ventricular izquierdo masivo
🔗DOI: 10.1016/j.case.2022.12.010

[Alexander Mladenow MD @alex1708ander]

Do’s ✅ and don’ts ❌ of PW Doppler Tracing Across the LVOT #echofirst @echo_batman @NMerke

[Ihtesham Ali @ihteshamali]

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Bookmark every single one. Your university will never tell you about most of these.

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[Sunil V. Rao @SVRaoMD]

Door-to-defecation time…

Defecation Patterns and Cardiovascular Outcomes in Acute Coronary Syndrome: The Influence of Stimulant Laxative Use
https://t.co/wypacDc2aH

[American Society of Echocardiography @ASE360]

We quantitatively assessed the degree of echogenicity in the proximal and mid segments of both coronary arteries to determine its additional diagnostic value in 109 patients with clinically suspected Kawasaki disease.

Read our @JournalASEcho article: https://t.co/fYoKY23ayt

[Dr G Rajesh (Gopalan Nair Rajesh). @DrRajeshG1]

patient with muscular dystrophy referred for echo.

[Edgardo Alania @Ed_Alania]

🔴Transthyretin Cardiac Amyloidosis Evaluation & Management: 2025 ACC Concise Clinical Guidance @JACCJournals #Cardiology #CardioEd #FOAMed #Amyloidosis #ATTR

[Diego Segura-Rodríguez @SeguraCardio]

📌Ventricular free-wall rupture, ventricular pseudoaneurysm & papillary muscle rupture complicating acute myocardial infarction

A clinical consensus statement of the @escardio & @EACTS

#PositionPaper #MechanicalComplications #MI

[Jorge Faerron @cardiopedhnn]

European Stroke Organization guideline on BP management in acute #ischemic_stroke & #intracerebral_hemorrage

https://t.co/owNdFiHkpV

[Dr. Filippo Cademartiri @FCademartiri]

🫀🔥 Not every myocarditis is myocarditis. And missing this… can kill your patient. Do not trust with your life CMR findings for final diagnosis.

We’ve all seen it:
👉 chest pain
👉 troponin ↑
👉 CMR positive

Diagnosis:
❌ “Acute myocarditis”
Case closed.

But this paper introduces a dangerous reality:
👉 Some of these patients don’t have myocarditis.

They have:
👉  Desmosomal “hot-phase” cardiomyopathy (HPC)
A genetic disease.
With:
⚠️ recurrent inflammation
⚠️ arrhythmias
⚠️ sudden death risk
The real problem?

HPC mimics myocarditis perfectly.
- Same symptoms.
- Same biomarkers.
- Same CMR criteria.

So what are we missing?

👉 RED FLAGS
🧬 Clinical
Family history of:
- cardiomyopathy
- myocarditis
- sudden death
- Recurrent troponin “bursts”

🧠 Imaging (this is where it gets interesting)
Ring-like LGE pattern
Right ventricular involvement
LGE that doesn’t regress over time
LV function that doesn’t normalize

⚡ Electrical
Low QRS voltages
High PVC burden (>1000/day)
Recurrent NSVT
VT/VF at young age

The key insight
Just 3 findings can identify most cases:
👉 ring-like LGE
👉 RV involvement
👉 family history
🎯 Diagnostic accuracy ≈ 93%

Let that sink in
We are:
👉 calling it myocarditis
👉 discharging the patient
👉 maybe giving NSAIDs

While the real disease is:
⚠️ arrhythmogenic cardiomyopathy in disguise
This is not semantics
This changes EVERYTHING:
👉 genetic testing
👉 family screening
👉 ICD consideration
👉 long-term management

My take
This paper is not about rare disease.
It’s about a diagnostic mindset error:
👉 We stop thinking too early.
The real shift
From:
❌ “Does this look like myocarditis?”
To:
👉 “What if this is NOT myocarditis?”
⚡ Because in cardiology:
The most dangerous diagnosis is the one that looks obvious.

And, when you lean into a tunneled vision because the standard semeiology of CMR looks like "myocarditis" you take a risk without contextualzing properly.

#Cardiology #CMR #Myocarditis #Cardiomyopathy #Arrhythmia #Imaging #PrecisionMedicine #CardiacMRI

[Jorge Faerron @cardiopedhnn]

Optimal lifelong roadmap post-#ACS : clinical consensus statement of the EAPC of the ESC.

https://t.co/k9DbGqtqLe

[CardiovascularCorner @TrackYourHeart]

Striking case of ventricular fibrillation during CPR, followed by successful return of spontaneous circulation

[Dr. Sou @SwissHeartDoc]

Honestly, AR, along with TR, is the most challenging valvular lesion to quantify. This will be so helpful!

[Jonny Wilkinson @Wilkinsonjonny]

🔝I presented on my TOP 10 LIFESAVING PAPERS in critical care at @CC_Symposium last week!

🎖️Which papers made it in? Why? What did they change for ICU care?

#FOAMed #POCUS #FOAMcc @veerappan91050

Lets take you on a little journey!

[Dr Rani Khatib FESC @DrRaniKhatib]

Resistant Hypertension
Hypertension on both sides of the Atlantic.
#ESCPrev26

[Sayed S Rahman @SayedSRahman1]

Approach to Patient with Cirrhosis and AKI :

Hepatorenal syndrome
⚠️ Occur 50% of hospitalized patients with cirrhosis
❗️PPt by overdiuress , GI Bleed,infection
✅️Vasoconstrictor + Albumin.
https://t.co/JDrDdOblcr

[Brian Locke, MD MSCI @doc_BLocke]

“Stewart Light” approach to acid-base and visualization

Classical ABG interp: use pH, PaCO₂, HCO₃⁻ [or SBE, base excess], and the Boston compensation rules to decide whether the respiratory response fits. It works well for single disturbance, but incomplete when several coexisting processes. For eg - if SBE = 0, there could be no metabolic disturbance, or two that are equal but opposite.

Stewart/Physiochemical approach = three indep vars: PCO2, strong ion difference (SID), and total weak acid concentration ([ATOT].. mainly alb and phos)

In “A pragmatic approach to complex acid base disturbances of critical illness: the ‘Stewart light’” the authors propose a hybrid approach:
- keep Boston rules for respiratory/compensation
- add pH-adjusted partition of metabolic SBE into chloride/SID effect (from Na - Cl), albumin effect, and unmeasured-ion reminder

Why? To tease out situations where multiple metabolic processes pull in opposite directions, for e.g. when a Strong Ion Difference and unmeasured-ion (or lactate) coexist.

Most useful for DKA, intoxication, sepsis, vomiting, NS administration, diuresis, or [my interest] chronic hypercapnia… Boston Rules can tell if you if the net secondary response(s) are as expected, but doesn’t tell what type of metabolic processes are present.

5 steps:
1. clinical context, pH, severity, and Boston rules (e.g. winters formula for met acidosis)
2. Quantify strong-ion effect SBE_SID = Na⁺ − Cl⁻ − 35; if pH is outside 7.30–7.50, adjust that reference 35 by 1.5 mmol/L for each 0.1 pH unit away from 7.40—upward in acidemia, downward in alkalemia. Negative values = strong-ion acidosis, positive values = stron-ion alkalosis
3. Quantify weak-acid effect from albumin SBE_Alb = 0.3 × (40 − albumin in g/L), so hypoalbuminemia is treated as an alkalinizing force.
4. Assign remainder: unmeasured ions: SBE_UI = SBE − SBE_SID − SBE_Alb; if lactate is available, subtract its contribution to see whether additional unmeasured anions remain

Then, 5.: synthesize all together.

(and clinically determine if a positive SBE_SID is due to chloride depletion primary process or expected renal repsonse to chronic hypercapnia).

They recommend visualizing it with a gamblegram and practicing… and this all seems to hard. So I vibe coded a visualization, available here:

Takes your blood gas and chemistries result -> gives “Stewart Light” interpretation and some visualizations/explanations.

[Oung Savly MD FACC FASE FESC FAAP FEACVI 🇰🇭 @OungSavly]

Right PVs draining into the IVC, is a classic clue to Scimitar syndrome.
@AEPCcongenital
@iamritu @jeffrey_vinocur @CASivaram1 @alex1708ander @alexsfelixecho @SIwa23288585 @swatigar @WithAScalpel @DavidWienerMD Digital walkthrough by @loomba_rohit
https://t.co/IWCqIR9DMC