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Zdenek Vrozina Profile picture
@ZdenekVrozina
Apr 7 • 13 tweets • 2 min read • Read on X
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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-…

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More from @ZdenekVrozina

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
Zdenek Vrozina Profile picture
Apr 6
This study suggests a possible mechanism for how SARS-CoV-2 could harm neurons in the inner ear.
Not mainly through inflammation, but potentially through a more direct effect on spiral ganglion neurons, involving disrupted mTOR signaling, abnormal stress granules, and eventually - apoptosis🧵
That matters because spiral ganglion neurons are not some minor supporting cells. They are the neurons - that carry sound information from the cochlea into the auditory pathway.
If they are damaged, the problem is not just in the ear. It affects the neural transmission of sound itself.
The authors try to map out an actual chain of events. In their model, infection - and especially spike related effects - seems to disturb the cell’s stress-response machinery.
Stress granules start accumulating abnormally, mTOR signaling drops, and the neuron is pushed closer to cell death.
Read 9 tweets
Zdenek Vrozina Profile picture
Apr 4
A new paper looks at shared molecular mechanisms between COVID-19 and Parkinson’s disease. It does not show that COVID causes Parkinson’s.
What it does ask is whether the two conditions share biologically meaningful pathways🧵
The authors identified 77 overlapping differentially expressed genes across COVID-19 and Parkinson’s datasets. The main signal points to inflammation-related pathways plus signs of dopaminergic neuron dysfunction!
Their main candidate is CHI3L1. In the single-cell analysis, CHI3L1 was especially elevated in astrocytes from severe COVID-19 brain tissue, which led the authors to propose an astrocyte - CHI3L1 - neuroinflammation axis as one possible explanation for why infection might worsen neurological outcomes.
Read 13 tweets
Zdenek Vrozina Profile picture
Apr 3
A new population based study from Stockholm sends a pretty troubling signal.
During follow-up, a cardiovascular event occurred in 20.6% of men and 18.2% of women with diagnosed long COVID.🧵
In the control group without long COVID, the numbers were much lower. 11.1% for men and 8.4% for women.
These were not mainly patients recovering from severe acute COVID or ICU stays. The study focused on non-hospitalized adults aged 18-65 with no prior cardiovascular disease!
Read 14 tweets
Zdenek Vrozina Profile picture
Apr 2
A new 2026 paper looks at a possible mechanism behind rare myocarditis after COVID-19 mRNA vaccination.
Not vaccines broadly damage the heart.
More like
some people may be biologically more vulnerable than others🧵
The paper’s central idea is mitochondrial vulnerability.
In simple English
your mitochondria can seem mostly fine under normal conditions, but still handle stress badly when the system gets pushed.
That matters because this study is trying to explain a rare adverse event, not argue that this is happening across the whole population.
That distinction is everything.
Read 25 tweets
Zdenek Vrozina Profile picture
Apr 2
This new important preprint study makes a strong mechanistic case that the SARS-CoV-2 E protein localizes to mitochondria and is linked to concrete mitochondrial dysfunction🧵
It pushes E beyond the idea of being just a structural protein involved in viral assembly. The paper suggests it may also directly disrupt host-cell function at the mitochondrial level.
The authors connect several findings into one coherent picture. Mitochondrial localization of E, reduced membrane potential, impaired respiration, increased ROS, and broad lipid/metabolic changes.
Read 13 tweets

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