ILLIASUL IBAD Profile picture
Oct 29, 2025 6 tweets 3 min read Read on X
🧵 Can we have cardiac dysfunction despite a normal ejection fraction?

Even with a normal LV ejection fraction (LVEF), early myocardial damage can exist — especially in conditions like systemic sclerosis, lupus, or diabetes.

Let’s explore how we can detect it early — before symptoms appear.

Lets explore about Speckle Tracking Echocardiography (STE) 👇

#Cardiology #Rheumatology #Echo #Rheumatology #Immunology
#Sullysrounds #MedX #Medtwitter #Mnemonics #Medicine #History
@DrAkhilX @IhabFathiSulima @Janetbirdope #MedTwitter #RheumTwitter @CelestinoGutirrImage
Tweet 2/6

The science behind it:

The LV myocardium has spiral architecture — fibers run longitudinally, circumferentially, and radially.
Each fiber layer contributes to a different “strain” during contraction.

When the myocardium weakens, strain changes before EF drops.

Image source-ecgwaveImage
Tweet 3/6

It tracks natural “speckles” in the myocardium on 2D echo frames — measuring how much each segment deforms during systole and diastole.

📊 Strain = (D₂ − D₁) / D₁
Values are negative (shortening from the original length).

Meet the hero: Global Longitudinal Strain (GLS)
GLS captures the average longitudinal shortening of the LV.

✅ Normal ≈ −18% to −22%

⚠️ Less negative values (e.g., −16%, −14%) suggest subtle systolic dysfunction — even when EF is 60%.Image
Tweet 4/6
So simply 👇

How do we calculate Global Longitudinal Strain (GLS)?

👉 GLS = % change in myocardial length between diastole & systole
📏 Formula: (Ldiastole − Lsystole) / Ldiastole × 100
🫀 Since the LV shortens, values are negative (normal ≈ −18% to −22%)

➡️ Less negative = early systolic dysfunction, even when EF looks “normal.”

#Echo #Cardiology #MedTwitterImage
Tweet 5/6

Why it matters in systemic sclerosis (SSc):

A large study (n=234, J Rheumatol 2019) followed patients with SSc using speckle tracking:

•LVEF remained stable
•But 19% had significant GLS decline (≥15%) over ~2.3 years
•These patients developed muscle weakness, lung fibrosis, and renal dysfunction

What this tells us:

🫀 LV dysfunction in SSc can progress silently.

GLS picks it up before EF falls — giving us a window for early intervention.Image
Tweet 6/6

Clinical takeaway:

•Use GLS for early detection of subclinical LV dysfunction
•Enables better risk stratification
•Allows timely treatment & closer follow-up

💡 Moral of the story:

Normal EF doesn’t always mean a normal heart

Sometimes, only a strain reveals the struggle.

#Echo #Cardiology #Rheumatology #SSc #Medtwitter

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with ILLIASUL IBAD

ILLIASUL IBAD Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @IlliasulK

Jan 28
🧵 Think about this carefully.

You get an implant for cosmetic reasons.
The surgery goes well.
Nothing seems wrong.

Months later, you are tired all the time.
Your joints ache.
Your eyes feel dry.
Tests don’t give clear answers.

This situation has a name doctors should know: ASIA 👇

@DrAkhilX @IhabFathiSulima @nileshnolkhaImage
1/9 Why this question matters

Modern medicine uses implants, fillers, meshes, and vaccines every day.
They help millions.

But doctors began noticing a pattern:

👉 some people developed delayed immune symptoms after exposure to immune-stimulating materials.
2/9 What ASIA actually is

ASIA means Autoimmune / Inflammatory Syndrome Induced by Adjuvants.

It is not a diagnosis like lupus.
It is a clinical framework to explain immune symptoms that appear after adjuvant exposure in susceptible individuals.
Read 10 tweets
Jan 8
CRP in Lupus -Why I Don’t Use It to Measure Disease Activity and when I will use it

For decades, we’ve been taught:

Inflammation → CRP ↑

That rule works — except in lupus.

Here’s why 👇

1/6- Lupus inflammation is real -CRP silence is not reassurance

Active SLE can have:

• Nephritis
• Cytopenias
• CNS disease
• High anti-dsDNA
• Low complement

…and a normal CRP.

This is not paradoxical.
It is biologically expected.

#MedTwitter
#Rheumatology
#Lupus
#SLE
#ClinicalPearls @DrAkhilX @IhabFathiSulima @CelestinoGutirr @Urchilla01 @schowardjdImage
2/6. Lupus is not an IL-6 disease

It is a Type I interferon disease.

That distinction matters.

In RA:
IL-6 → liver → CRP ↑

In SLE:
IFN-α dominates — and IFN actively suppresses CRP transcription in hepatocytes.How ?

• IL-6 → STAT3 → CRP ON
• IFN-α → STAT1 → blocks STAT3
• CRP gene transcription → OFF

Inflammation continues.
CRP stays low.Image
3/6.

Other reasons ?

Many lupus patients carry CRP-lowering polymorphisms.

So they begin with:

⬇️ baseline CRP

⬇️ acute-phase capacity

Add IFN-α -CRP becomes an unreliable reporter.

So CRP is low for four reasons in lupus

CRP is suppressed due to:

1.Type I IFN–mediated transcriptional inhibition

2.CRP-lowering genetic polymorphisms

3.Neutralization by anti-CRP antibodies

4.Local conversion to tissue mCRP (not reflected in serum)

This is why CRP fails as an activity marker.Image
Read 6 tweets
Jan 4
What is new in lupus (2025) ?

We now understand lupus as a disease of TLR7 dysregulation.
Three key genetic mechanisms illustrate this.

🧵👇

TLR7 gain-of-function

TLR7 recognizes ssRNA in endosomes.
Gain-of-function variants → constitutive TLR7 signalling → excess type I interferon → lupus.

UNC93B1 mutations

UNC93B1 controls trafficking of TLR7 from ER to endosomes.
Pathogenic variants → increased endosomal TLR7 availability → amplified interferon signalling → lupus.

The new addition: PLD4

PLD4 is an endosomal exonuclease that degrades self ssRNA/ssDNA.
Loss-of-function → nucleic acid accumulation → failure to terminate TLR7/TLR9 activation.

The clinical insight

This pathway is not limited to childhood lupus.
Adult-onset disease (>40 years) has been reported.
Monogenic lupus can present late.

The therapeutic implication

TLR7-driven interferon excess → JAK inhibition is rational.

📉 Baricitinib reduces interferon hyperactivation.

Take-home message:
Different genes. Same pathway.
TLR7 overactivation is central to lupus.It is time for genetics-guided lupus care.

#SLE #TLR7 #UNC93B1 #PLD4 #TypeIInterferon #MonogenicLupus #JAKinhibitors #Rheumatology @DrAkhilX @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1Image
1/3 Image
2/3 Image
Read 4 tweets
Dec 7, 2025
10 Erythemas in Medicine You Must Know, because every rash is a diagnosis in disguise.

A quick, high-yield thread for busy clinicians. 👇🧵

@IhabFathiSulima @hemo_shk @MoarSahitoPTI
@MRCEMPREP
@DrBassemKurdi
@mohammadalmogbi @Dr_Alhatlani @DrAkhilX @CelestinoGutirr @Urchilla01 Image
1/10

Erythema Nodosum

Tender nodular panniculitis on shins.

• TB, Streptococcus

• Sarcoidosis, IBD, Behçet’s

• Pregnancy

• Drugs – sulfa, penicillin, OCPs

Never ulcerates.

Image@dermatologyadvisor Image
2/10

Erythema Induratum (Bazin)

Lobular panniculitis linked to TB.

1- Posterior legs

2-ulcerating nodules

3-hypersensitivity reaction.

Image@americanjournalofdermatopathology Image
Read 12 tweets
Nov 26, 2025
🧵A must read

The rash that means “ischemia”
Painful, branching, non-blanching purple patches/plaques with central necrosis?

Think Retiform Purpura – a morphology that says:

“Blood vessels to the skin are compromised → ischemia → purpura → necrosis.”

Almost every case needs a systematic 6-step approach + biopsy.

A nice clinical trick 👇

A quick bedside hack: classify lesions as:

•Inflammatory → ≥2/3 erythema + ≤1/3 necrosis → vasculitis or infection

•Non-inflammatory → ≥2/3 necrosis + ≤1/3 erythema → occlusion/thrombotic

⚠️ But don’t be fooled

Cryoglobulinemia, sepsis, levamisole can hit both the vessel wall and lumen, causing overlap.

Read full 🧵👇
#RetiformPurpura #DermDetective #VascularRash #SkinCluesSaveLives
#RheumDerm #DICalert #HITteaching #ANCApearls
#MedEd #ClinicalPatterns #PatternToPunch #LupusMimics #IndiaMedEd @DrAkhilX @IhabFathiSulima @CelestinoGutirr @Urchilla01Image
🧵 2/7 – STEP 1: Morphology

✅ Define it first:

•Branching (reticular), non-blanching purpuric patch/plaque

•Persistent, often with frank or impending central necrosis/ulcer

🔍 Differentiate from other reticulate patterns:
•Livedo reticularis – complete rings, transient, temperature-related

•Livedo racemosa – broken, irregular fixed rings, rarely necrotic

@DrAkhilX @IhabFathiSulima @CelestinoGutirrImage
🧵 3/7 – STEP 2:

Status of the patient
Ask: “How sick is this patient?”

If acutely ill (fever, altered sensorium, organ failure, septic shock), think of:

•Sepsis ± DIC
•Purpura fulminans
•Heparin-induced thrombocytopenia
•Warfarin skin necrosis
•Catastrophic APS
•Calciphylaxis

Act fast:

•Send urgent labs (platelets, coagulation, etc.

•Do immediate skin biopsy (H&E ± DIF, tissue culture)

•Start broad-spectrum antibiotics/antifungals in septic or immunocompromised patients.Image
Read 7 tweets
Oct 8, 2025
🧵 Have you ever heard of MGTS?
Let me tell you a story about a clotting disorder that doesn’t play by the rules 👇

@DrAkhilX @IhabFathiSulima @Janetbirdope #MedTwitter #RheumTwitter
@drkeithsiau @CelestinoGutirr Image
Tweet 2/10

The patient who didn’t fit the pattern

A 55-year-old man came with repeated clots — in his legs, lungs, even the brain.
He was already on anticoagulants. Still, new thromboses appeared.

Platelets? Mostly normal.

No heparin. No recent vaccine.
Something didn’t add up.
Tweet 3/10

When common causes failed

He was tested for the usual suspects:

Antiphospholipid antibodies – negative
HIT assays – negative

Procoagulant and genetic markers of thrombosis -negative

Routine malignancy screening-negative

Yet the thrombosis kept recurring.
Read 10 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(