Great rundown at https://siderea.dreamwidth.org/1617381.html

Summary: plenty of evidence that COVID-19 is causing blood clots in younger people, which leads to noticeable increases in strokes and cardiac arrests, which may not be counted in the official statistics as of now.

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Oh joy, just when I thought I'd absorbed the bad news about viral load, there's something new to worry about.

The stroke patients were on average '15 years younger than' stroke patients without the virus - so younger, as elsewhere in article it says median age for strokes is 74, so around 60. There's mention of ages 33-49 suffering from these Covid-19 strokes. It also fits with a few one-off weird news stories about sudden deterioration in younger people that I've read over the last month or two and mostly ignored as flukes. No good statistics, except its clear this can't be a rare occurrence.

“We are used to thinking of 60 as a young patient when it comes to large vessel occlusions,” Raz said of the deadliest strokes. “We have never seen so many in their 50s, 40s and late 30s.”

This sounds like the same deal as Covid-19 pneumonia - it hits people younger than the normal age for the condition, tailing off at a younger age, but still predominately affects the old to middle-age. These stroke patients still have Covid symptoms, fever and cough, they would still probably be tested if hospitalised and still test positive. Obviously they'd be undercounted because of missing tests, but not by way more than the other ways Covid-19 presents. Apparently being healthy matters less for the stroke than for the pneumonia route to death, but age still matters.


In the UK, total excess deaths are about twice the official figures for deaths with Covid-19 - so that's our upper limit on how much worse things might be. With a massive fraction of those unrecorded excess deaths being deaths in care homes, and much of the rest being due to inadequate testing to catch 'normal' Covid-19, there is some leftover that might be Covid-19 cases so weird nobody realises they're Covid-19 in the first place.

That still doesn't leave room for mysterious stroke deaths we don't diagnose as Covid-19 to be making the disease much worse than we already think it is from hospital deaths and excess deaths in care homes. So, not an entirely new nightmare - just the same nightmare we're already dealing with.


What's the strategy here? Not a doctor - just wild speculation - I'm not even going to do this myself without real medical advice - would aspirin possibly make a difference as it helps for 'normal' blood clots? That and make sure you still call emergency services if you have stroke symptoms, no matter what. Hospitals in the UK are starting to empty out as we pass the peak - in the rest of Europe things have improved further, so you will get the care you need.


Possibly also relevant - the UK released a detailed breakdown of ICU patients with Covid-19 - there's a very strong skew between male and female (the skew is stronger for older age groups, barely there for younger age group, suggesting gender is a proxy for pre-existing conditions) and the usual, very strong age skew (image here).

I've done some digging through the UK's ONS statistics for the last month - for ages 15-44 the average deaths from 2016-2019 was 288 for this past week. This week it's 353, and the total deaths linked to Covid-19 were 101, so you'd 'expect' the non-covid average to be 252.


In other words - no significant (in size compared to the 101 covid deaths) wave of missing deaths from Covid-19 in younger people - at least in the past week in the UK. I've eyeballed the data for the weeks before then, and the pattern is the same there - no giant shadow of excess deaths in younger people (and barely any excess deaths due to covid before 3 weeks ago) so most of that doubling in deaths compared to official figures is coming from older people (presumably care home residents). Not sure how this fits with the spike in stroke cases.

EDIT: turns out writing 'Covid-19' on a death certificate and being included in the official statistics aren't the same since you need a positive test result. So the above tells us there aren't many extremely weird Covid-19 deaths where a coroner can't make an educated guess that that's what it is.

The article seems more of a "this is a thing that's happening" article than a "this is a major cause of death" thing.

Still, it looks like it'll be important to follow recoveries for an increase in circulation issues going forward.

Not a doctor - just wild speculation - I'm not even going to do this myself without real medical advice - would aspirin possibly make a difference as it helps for 'normal' blood clots?

I forget, what's the current epistemic status of "don't use NSAIDs if you might have COVID-19"? I think they were recommended against for a while, then said to be fine. And I haven't seen them mentioned on LW recently.

All else being equal you don't want to use antipyretics because fever is beneficial (to a point). Aspirin might reduce your chance of stroke but increase the strength of the infection.

increase the strength of the infection.

I'd be interested in a link for this.

https://www.nejm.org/doi/full/10.1056/NEJMc2009787?query=RP is one of the primary sources.

I like the theory that this coronavirus is a blood disease that just mostly seems to hit the lungs because it causes respiratory symptoms.

Diabetes and metabolic syndrome and heart disease seem like the most significant risk factors for serious covid19 cases. I haven't noticed the weight of patients being noted in any of the primary sources on this, but I strongly suspect that most are obese or at least overweight.

Looks like the data is largely NY. Any indication that this is more widely supported in the data?

NY is the place in America we have the most data, and are most likely to notice less common effects.


It fits with all the autopsy and clinical data that coagulation issues are a major cause of morbidity in severe cases, and the fact that children with non-severe cases are having an anomalously high rate of skin lesions in fingers and toes characteristic of circulation problems.

What I was really wondering about was does the particular strain of the virus matter here. My understanding is there are several different strains and what is primarily in the USA is not what was primarily in China or Europe.

Now that might just be poor news reporting on the facts as I'm not seem anything about -A, -B, -C versions.

For the most part, all those labels are just labels for where on the tree of all sequences it falls. There is almost no evidence of widespread functional mutants. They're useful for tracking the spread of the virus around the globe.

There is one mutation in the S protein at the root of the European strains that you could *imagine* having an effect on the function of the fusion protein but there is no particularly strong evidence that it's doing much - a little equivocal difference in the measured PCR cycles required for detection from samples, but that could have to do with the fact that they happened at different times when people were getting tested at different disease stages or on different equipment. It is more common more recently relative to the other lineages in Europe and America, but that could very easily just be because it is the only lineage in Italy and once Italy exploded its shrapnel founded a lot of new transmission chains all over Europe and America. It could very easily just be a bottleneck effect having to do with breaking into a new area.

Much more interesting are a few small lineages that have actually lost whole accessory proteins involved in suppressing the innate immune response, but that's a total of like 7 patients found to have them.