Zdenek Vrozina Profile picture
May 16 17 tweets 2 min read Read on X
Even in the Omicron era, SARS-CoV-2 was linked to a several-fold increase in serious thromboembolic and cardiovascular events - and that risk persisted for months after infection🧵
A new European preprint cohort study looked at ~780,000 people with COVID-19 and 7.6 million pre-pandemic controls across three health databases in the UK, the Netherlands and Spain.
The main finding is hard to ignore.
In the first 30 days after infection, the standardized incidence of venous thromboembolism was about 3.6-4.1 times higher than expected!
Even after 180 days, the risk had not returned to baseline. It remained roughly 1.9-2.4 times higher!
The strongest signal was pulmonary embolism - a potentially fatal condition caused by a blood clot blocking the circulation in the lungs.
But this was not only about venous clots.
The study also reported increased signals for arterial and cardiovascular outcomes, including ischemic stroke, acute myocardial infarction, heart failure, arterial thromboembolism, and major adverse cardiovascular events.
The risk was highest in the first month after infection, but part of the signal persisted for up to six months!
Higher risks were seen especially in immunocompromised people and in those without a prior recorded SARS-CoV-2 infection.
Vaccination and prior infection likely reduced the risk, but they did not erase it. The authors also caution that some vaccine-stratified estimates were imprecise because of small event numbers and wide confidence intervals.
As always. Observational design, possible confounding, differences between databases, changing testing policies.
But the overall message is clear.
Omicron COVID was not simply a short respiratory illness.
It was associated with a meaningful vascular and cardiovascular risk, even in a population with widespread vaccination and prior infection.
And it matters for public health.
People were repeatedly told that a milder variant meant the consequences were minor. But a milder acute illness does not automatically mean no post-infectious vascular risk.
The cardiovascular consequences of SARS-CoV-2 remain under-communicated - by public health agencies and, too often, by medical societies that should be leading on this.
@ZdravkoOnline @szupraha @adamvojtech86 @strakovka
Reducing infections and reinfections still makes sense.
Protecting still makes sense.
And communicating the real risks of SARS-CoV-2 honestly still matters.
Li at al., Venous and arterial thromboembolic events after COVID-19 during the Omicron period in three European countries. nature.com/articles/s4159…
Prevention, as presented by @czechcardiology, increasingly looks less like cardiovascular protection - and more like digging the grave in slow motion.

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More from @ZdenekVrozina

May 16
We are still trying to place Long COVID into a biologically coherent framework.
This study is interesting because immune activation, antiviral signaling, metabolism, mitochondria, cell survival do not appear as separate findings - but as parts of one connected system🧵
A possible axis is this
something keeps innate immunity on alert - immune cells produce inflammatory signals - their metabolism shifts - mitochondria come under stress - stressed mitochondria can further amplify immune activation.
That is a loop, not a list.
The study compared 50 people with Long COVID with 50 recovered controls around 10 months after SARS-CoV-2.
Both groups had been infected. The key difference was whether symptoms persisted.
Read 20 tweets
May 15
A new narrative review by Kell, Zhao & Pretorius looks at Long COVID through the lens of microcirculation. The idea that persistent fibrinaloid microclots may contribute to impaired blood flow in the smallest vessels.🧵
This is not a systematic review or meta-analysis. It is better read as a broad mechanistic argument. A way to connect existing findings on inflammation, endothelial dysfunction, coagulation, fibrinolysis and Long COVID symptoms.
The central idea is that, in some inflammatory states, blood may form abnormal microclots containing fibrin and other proteins in an amyloid-like form. Fibrinaloid microclots.
Read 19 tweets
May 14
A new warning study that deserves attention.
SARS-CoV-2 leaves a long-term endothelial and metabolic footprint in the blood months after infection - even in people without obvious Long COVID symptoms.
And that matters🧵
Researchers followed 262 adults in Germany and measured blood biomarkers about 37 weeks after infection - roughly 9 months later.
People who had previously had COVID showed higher markers of endothelial dysfunction and tissue stress, including soluble thrombomodulin and LDH, compared with never-infected controls.
Read 17 tweets
May 13
A new long COVID study found that standard autoimmune blood tests often looked normal. But when researchers tested patients blood directly against heart and blood vessel tissue, they found persistent immune reactivity - especially involving vascular tissue.🧵
The study found tissue-specific autoreactivity in many long COVID patients - especially against vascular tissue - while standard ANA screening often looked normal.
They found tissue-specific autoreactivity in 83% of long COVID patients vs 53% of pre-pandemic controls.
The clearest statistically significant difference was against vascular tissue.
34% in long COVID vs 8% in controls.
Read 7 tweets
May 12
SARS-CoV-2/spike RBD may act as a potential modifier of glioma progression in biologically susceptible cells. An interesting mechanistic study that raises a warning signal.🧵
Methods first.
This study combines single-cell RNA, bulk RNA-seq, spatial transcriptomics, survival analysis, pathway/enrichment analysis, and in vitro experiments on primary glioblastoma cells.
The authors looked at genes and proteins linked to SARS-CoV-2 cell entry
ACE2, BSG/CD147, NRP1, TMPRSS2, FURIN, FCGR1A, HSPG2.
These factors were mapped across healthy brain cells, COVID-19 brain samples, glioma cells, and glioma tissue.
Read 19 tweets
May 11
COVID-19 and the heart. A new narrative synthesis of 71 studies suggests that long-term cardiovascular effects are not limited to people who were hospitalised.
The risk is clearly highest after severe acute disease - but measurable abnormalities have also been reported after mild infections🧵
This is not a meta-analysis.
The authors did not calculate one pooled prevalence estimate because the studies were too uneven. Different LC definitions, different follow-up, tests, different populations, and often poor separation between hospitalised and non hospitalised groups.
Even with that messiness, the same warning signal keeps appearing.
COVID-19 can be followed by persistent cardiovascular problems - palpitations, chest pain, shortness of breath, fatigue, arrhythmias, dysautonomia, impaired heart function, and in higher-risk groups, major adverse cardiovascular events.
Read 16 tweets

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