🧵 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) 👇
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-ecgwave
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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%.
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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 #MedTwitter
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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.
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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
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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 @nileshnolkha
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.
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.