Thread by @ZdenekVrozina

A new preprint (June 2025) shows that microclots formed during COVID-19 can obstruct capillaries and impair microcirculation.
And remarkably, an earlier peer-reviewed study reached the same conclusion - by a completely different method. 🧵

In the new study by Kell, Pretorius et al., SARS-CoV-2 is associated with abnormal blood clotting that produces fibrinaloid microclots - clots containing amyloid (!) fibrin that are resistant to fibrinolysis (breakdown). preprints.org/manuscript/202…

These microclots are made of amyloid-type fibrin - a misfolded version that resists not only natural fibrinolysis, but also standard clot-busting drugs.
In other words: your body can’t easily remove them. Neither can your meds.

Using laser Doppler and laser speckle imaging (LDI/LSI), the researchers found:
elevated blood pressure
reduced capillary blood flow
Consistent with capillary obstruction and rarefaction.
This suggests high blood pressure is an effect, not the cause!

Now compare this with a prior peer-reviewed study (Jalal et al., Scientific Reports, 2025):
Researchers trained an AI model (EfficientNet) to detect abnormalities in nailfold capillary images: dilated, hemorrhagic, and disorganized vessels nature.com/articles/s4159…

The AI model (CE-NFCNet) achieved perfect accuracy in distinguishing healthy vs abnormal capillaries- even in noisy images (eg low contrast, dark skin, glare).
Another line of evidence pointing to microvascular damage.

Two different technologies - one functional (blood flow), one structural (capillary morphology) - arrive at the same insight:
COVID-19 leaves a lasting mark on the microvasculature, even in mild or asymptomatic cases.

On the left: healthy nailfold capillaries.
On the right: capillaries one year after COVID.
The person on the right was never diagnosed with Long COVID!

Below:
A healthy individual
B asymptomatic COVID
C & D two patients with Long COVID
Different clinical stories, but a shared vascular footprint.

What we see in the skin (nailfold) is a window into systemic microcirculation.
If the capillaries are damaged here, it’s highly likely that similar damage exists in the lungs, brain, heart, kidneys - we just can’t visualize it as easily.

These changes are:
not rare
not limited to severe COVID
not always reversible
Capillary networks do not regenerate easily - if at all.

In future waves of SARS-CoV-2 - wearing a respirator isn’t extreme.
It’s one of the few ways to protect a system that doesn’t repair itself well - your microcirculation.

And while we're connecting dots - let’s go back to 2020.
Already then, a pediatric study showed that most children infected with SARS-CoV-2 had lab evidence of endothelial injury, even with mild or no symptoms.

In this Blood Advances study from CHOP (Children’s Hospital of Philadelphia),
86% of children met diagnostic criteria for microangiopathy (TMA) - based on elevated sC5b‑9,
a marker of complement-mediated capillary damage.
Even in regular COVID cases.

Worth noting: the 2020 CHOP study was done in hospitalized kids (COVID or MIS-C).
But importantly, many had no obvious symptoms of vascular injury - yet still showed strong lab signs (↑sC5b‑9).
Suggests subclinical damage may be broader than we think.

Later studies confirmed this:
increased circulating endothelial cells (CECs)
elevated MCP-1, VEGF-A, IL-8
= signs of ongoing endothelial activation and vascular inflammation - even in pediatric COVID.

All of this helps explain why:
breathlessness can linger
microvascular imaging looks abnormal
cognitive function dips
even when “routine tests” come back normal.
We're not just fighting a virus - but its systemic footprint.