Thread by @ZdenekVrozina

COVID-19 is not just an acute event - it is a long-term vascular insult.
This study shows that the risk of ischemic stroke remains elevated for at least four years after SARS-CoV-2 infection.🧵

The risk remains elevated including in people who
were not hospitalized,
had a mild or moderate course,
had no obvious neurological complications during the acute phase.

This strongly suggests that SARS-CoV-2 is consistent with lasting structural or functional vascular injury to the vascular system, rather than causing only a transient pro thrombotic episode.

One of the most striking and counterintuitive findings is that -
transient cerebral ischemia (TCI/TIA) is more than twice as common in non-hospitalized COVID-19 patients, while no significant increase is observed in hospitalized patients.

This is difficult to explain by disease severity alone, but it makes biological sense.
Hospitalized patients may have received earlier antithrombotic and anti-inflammatory treatment, and close monitoring.
Non-hospitalized patients received none of these, still experienced endothelial and microvascular injury.

In this context, TCI likely reflects persistent dysfunction of cerebral perfusion and vascular reactivity, rather than classic large vessel occlusion.

Ischemic stroke reflects structural failure (thrombosis, embolism, sustained hypoperfusion).
TCI/TIA reflects functional failure (microthrombi, endothelial instability, impaired autoregulation).

The pattern observed here - stroke risk increased in all COVID positive groups, while TCI increases mainly in mild cases - suggests
SARS-CoV-2 increases baseline cerebrovascular vulnerability across the population,
but in many individuals this manifests as recurrent, subclinical ischemic events rather than overt stroke.

Although mechanistic pathways were not directly measured, the findings are consistent with persistent endothelial dysfunction, chronic low-grade hypercoagulability, disruption of the neurovascular unit, impaired blood brain barrier regulation.

This aligns with evidence from (long) COVID research on microthrombi, BBB disruption, PET hypometabolism and EEG slowing, increased ischemic risk across multiple organs.

This is an uncomfortable result!Because it shows that cerebrovascular risk extends to mild and ambulatory infections, not limited to older or severely ill patients, cannot be easily dismissed, and it persists for years, not months.

Most importantly, it affects a population that was largely not targeted for long term cerebrovascular follow-up, and largely reassured that recovery was complete.

What this study does not claim?
It does not suggest that everyone who had COVID-19 will have a stroke.
It does not imply an extreme individual risk.
It does not define mechanisms at the individual patient level.

What it does show is clear?
SARS-CoV-2 infection is associated with a long-lasting increase in population-level cerebrovascular risk - even after mild disease.

Sum:
COVID-19 increases long-term risk of cerebral ischemia not only after severe illness but also after mild infection, likely through persistent endothelial and microvascular dysfunction that remains clinically silent until it manifests.

Changela et al., Risks of Stroke and Transient Cerebral Ischemia up to 4 Years Post-SARS-CoV-2 Infection in Large Diverse Urban Population in the Bronx. Diagnostics 2025. mdpi.com/2075-4418/15/2…

In public discourse, the limited follow up and the focus on clinically diagnosed events often create a false impression -
The risk is small - nothing is really happening.
In reality
we do not know how many vascular insults have already occurred
we do not know how many are yet to come
we do not know when or if the effect plateaus or reverses.

What we do know is this -
the risk curve has not returned to baseline even after four years.

That means -
no one has followed patients long enough to determine when or whether risk normalizes,
no one is counting the cumulative number of small vascular insults,
no one is systematically looking for subclinical ischemic events.

Transient ischemic attacks likely represent the visible tip of ongoing microvascular dysfunction - endothelial injury, impaired cerebral perfusion, and low-grade hypercoagulability that persist long after infection.

What we measure as stroke or TIA is likely only a fraction of a cumulative, silent vascular burden - one that may later manifest as cognitive decline, reduced brain resilience, or increased vulnerability to major stroke.

@szupraha @ZdravkoOnline @adamvojtech86 a @CzechCardiology, co pět let předstírá, že s tím nemá nic společného.