Share this page!

Enter URL or ID to Unroll

You can paste full URL like: https://x.com/threadreaderapp/status/1644127596119195649
or just the ID like: 1644127596119195649

How to get URL link on X (Twitter) App

  1. On the Twitter thread, click on or icon on the bottom
  2. Click again on or Share Via icon
  3. Click on Copy Link to Tweet
  4. Paste it above and click "Unroll Thread"!
  5. More info at Twitter Help
Zdenek Vrozina Profile picture
@ZdenekVrozina
Apr 7 • 13 tweets • 2 min read • Read on X
Scrolly
The Karaviti study is finally in print, which makes this a good time to revisit it. It shows that subclinical myocardial injury in children after COVID-19 may not be something exceptional🧵
The key point is often missed. This was not mainly a comparison of children with Long Covid versus children without Long Covid. It compared
children after COVID-19
healthy controls without prior SARS-CoV-2 exposure
In that comparison, conventional echocardiographic measures did not differ significantly, but the post-COVID group showed worse left ventricular global longitudinal strain (LV GLS).
LV GLS can detect subtle myocardial dysfunction even when standard cardiac measures still look normal. In other words - the study points to silent, subclinical cardiac changes rather than obvious heart disease.
In children after COVID-19, there was a statistically significant group level shift toward worse myocardial function compared with healthy controls!
Put more simply - children after COVID-19 showed subtle subclinical changes in cardiac function.
The cohort included 137 children in the post-COVID group and 79 healthy controls, assessed 3 to 12 months after infection.
Long-COVID symptoms were reported in 23.6% of the post-COVID group, with fatigue the most common. But that figure should not be confused with the cardiac findings. The symptom rate is not the same thing as the proportion with altered GLS.
And that distinction is crucial.
What the paper shows is that the post-COVID group as a whole was shifted toward worse values.
That is why this study matters. It does support the view that COVID-19 can leave persistent, clinically silent myocardial footprints even in pediatric populations.
Sum:
Compared with healthy controls, children after COVID-19 showed a statistically significant shift toward worse LV GLS values, consistent with subtle subclinical myocardial dysfunction.
An this is exactly why follow-up matters. If standard measures look normal while more sensitive markers still detect change, the absence of overt disease should not be mistaken for the absence of impact.
Karaviti at al., Long term cardiovascular effects on COVID-19 infection in children. The need for monitoring. internationaljournalofcardiology.com/article/S0167-…

• • •

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

Keep Current with Zdenek Vrozina

Zdenek Vrozina 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 @ZdenekVrozina

Zdenek Vrozina Profile picture
Apr 12
COVID-19 is not just a story of inflammation. This review argues that it is also a story about what SARS2 does to mitochondria - and how that can turn infection into energy failure, cell injury, and worse oxygenation. This is an important mechanistic review🧵
Mitochondria are not framed here as passive bystanders damaged late in severe illness. In this model, they are active participants in disease - they shape ATP production, ROS, apoptosis, and oxygen sensing.
The review describes two main routes of damage -
very early changes in expression of mito-related genes (hours)
direct interactions between viral proteins and host mito proteins.
So not just the cell is stressed, but a more specific viral rewiring of core cell machinery.
Read 23 tweets
Zdenek Vrozina Profile picture
Apr 11
This interesting paper lays out a very specific idea for how severe COVID-19 may be driven not only by the virus itself, but by the way the immune system handles what the virus leaves behind🧵
The starting point is simple.
SARS2 can leave behind viral RNA and nucleocapsid protein (N). N naturally binds viral RNA, and during infection people also make antibodies against N.
The authors build the story from there.
Viral RNA + nucleocapsid (N) + anti-N IgG
= an immune complex carrying viral genetic material.
Read 18 tweets
Zdenek Vrozina Profile picture
Apr 10
Can Long COVID show up in a blood sample?
A new preprint @resiapretorius suggests it might. Researchers found much higher platelet-monocyte aggregates in people with Long COVID than in healthy controls - about 29% vs 4.6%🧵
That is a striking signal, and it hints that Long COVID may leave a measurable trace in blood.
In healthy controls, a monocyte was more likely to have just one platelet attached. In Long COVID, researchers more often saw multiple platelets attached to a single monocyte.
Why does that matter?
Because platelet-monocyte aggregates sit right at the intersection of clotting and inflammation. When they rise, it can point to ongoing thromboinflammatory activity - in simple words, blood clotting biology and immune signaling feeding into each other.
Read 7 tweets
Zdenek Vrozina Profile picture
Apr 9
Long COVID research badly needs studies that move beyond description and toward intervention. This is why this preprint is worth attention. It starts to sketch a possible treatment path.🧵
A new preprint is interesting because it points to something important
a potentially treatable biological mechanism.
Not a clinical breakthrough. More like a promising preclinical proof of concept.
This study is a strong mechanistic signal that at least some of the neurological problems after COVID may be driven by persistent neuroinflammation - and that shifting immune regulation can improve that state in mice.
Read 16 tweets
Zdenek Vrozina Profile picture
Apr 9
Do you have hypertension?
This study in Nature suggests that for people who already had hypertension before getting COVID, the infection was linked to a higher long-term risk of serious cardiovascular events.🧵
In people with hypertension, an infection can leave behind - or speed up - processes that raise the risk of cardiovascular disease over the months and years that follow.
The excess risk was more pronounced in people with poorer blood pressure control at baseline, and that signs of a stronger acute inflammatory response during infection predicted worse long-term outcomes.
Read 12 tweets
Zdenek Vrozina Profile picture
Apr 7
Another piece of the puzzle. Post-COVID changes are not just an isolated problem affecting a few unlucky individuals. They appear to have consequences at the population level🧵
A striking headline from Austria - 4 in 10 people report smell or taste problems.
That figure comes from a new cross-sectional survey of 2340 adults in Austria, Germany, and Switzerland looking at self-reported smell and taste disorders after the COVID era.
The key point is that this was not mainly about complete smell loss.
The most commonly reported problems were olfactory intolerance, phantosmia, and parosmia - in other words, abnormal, distorted, or intrusive smell experiences.
Read 12 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!

Send Email!

:(