Zdenek Vrozina Profile picture
Apr 9 12 tweets 2 min read Read on X
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.
The strongest signal was in patients who were hospitalized with COVID. Compared with COVID-negative patients with hypertension, their adjusted risks were
heart attack +40%
heart failure +59%
stroke +35%
all-cause mortality +151%
MACE +65%
Even in non-hospitalized patients, the risk increase was not zero. The study found
heart failure +17%
MACE +13%
In simple terms, COVID does not look like just a short-lived acute event here. It looks more like an amplifier of pre-existing vascular and cardiac risk.
And another important point. The effect was not the same for everyone. Among hospitalized patients, the risk of MACE was higher
with normal BP about 1.75×
with elevated BP about 2.26×
with stage 1 hypertension about 2.48×
with stage 2 hypertension about 1.69×
So the worse the baseline blood pressure profile, the more COVID seems to magnify existing cardiovascular vulnerability. The strongest signal appeared in people with elevated BP and stage 1 hypertension.
In hospi patients, several markers of more intense acute inflammatory stress also predicted worse long-term outcomes - higher CRP, creatinine, LDH, D-dimer, a higher neutrophil-to-lymphocyte ratio, and lower hemoglobin.
Clinically - a patient with hypertension is not automatically fine after COVID just because the acute infection has passed. Closer long-term follow-up and tighter control of cardiovascular risk factors make sense.
A retrospective observational study. But as a warning signal for long-term cardiovascular monitoring, it is a strong one. Probably nothing new, but a good reminder.
Hadidchi at al., COVID-19 and cardiovascular outcomes in patients with pre-existing hypertension. nature.com/articles/s4137…

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More from @ZdenekVrozina

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
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
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
Apr 7
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).
Read 13 tweets
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
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

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