
SARSCoV2 findings in iPSC- heart cells and autopsy indicate it's a heart virus - Brajeshwar
https://twitter.com/EricTopol/status/1299027542272172032
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rolph
preprint is available here. its a better view of the particulars

[https://www.biorxiv.org/content/10.1101/2020.08.25.265561v1](https://www.biorxiv.org/content/10.1101/2020.08.25.265561v1)

bioRxiv preprint doi:
[https://doi.org/10.1101/2020.08.25.265561](https://doi.org/10.1101/2020.08.25.265561)
. this version posted August 25, 2020. The copyright holder for this preprint
(which was not certified by peer review) is the author/funder. It is made
available under a CC-BY-ND 4.0 International license .

also:: Competing Interest Statement

>> B.R.C. is a founder of Tenaya Therapeutics
([https://www.tenayatherapeutics.com/](https://www.tenayatherapeutics.com/)),
a company focused on finding treatments for heart failure, including genetic
cardiomyopathies. B.R.C. and T.C.M. hold equity in Tenaya. <<

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mrfusion
Wow so more than 25% of NYC got their hearts damaged? Someone should let them
know.

* [https://newyork.cbslocal.com/2020/04/27/coronavirus-antibodi...](https://newyork.cbslocal.com/2020/04/27/coronavirus-antibodies-present-in-nearly-25-of-all-nyc-residents/)

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thu2111
I find myself sceptical about this. And not only because so many claims about
COVID-19 have turned out to be false.

We start with the opening claim, " _COVID-19 causes cardiac dysfunction in up
to 50% of patients_ ". I wonder how they are defining patient and cardiac
dysfunction in this sentence, as it is well known that virtually all people
who get COVID have an extremely mild infection, and often no symptoms at all.
If we look at e.g. the UK report of hospital admissions [1] then we can see
that cardiac admissions plunged during the lockdown period and then returned
to normal. If COVID was really damaging hearts at such a high rate, that would
presumably have been noticed before now in more people being admitted to
hospital with heart problems. Instead there was a huge drop.

But perhaps by dysfunction they mean a mild sort of damage that would take a
fairly long time to detect. Where did they get this 50% figure from?

The abstract doesn't use citations but the introduction does cite three
studies. It says:

 _" Notably, multiple independent reports have found that COVID-19 patients
frequently present with significant myocardial damage6–8, even without prior
cardiovascular disease9 (CVD), indicating that viral infection may be directly
responsible for the cardiac damage"_

Obviously we would expect CVD to be co-present with COVID-19 in many patients
because COVID-19 only kills the very old and frail, but they also cite one
study as evidence it also shows up in patients who didn't previously have any
heart damage. That study is a statistical meta-analysis [2]. This study
contains the following curious statement:

"SARS-CoV-2 may invade cells by binding to ACE2, causing direct damage to
cardiomyocytes. However, the autopsy results of COVID-19 cases failed to
detect SARS CoV-2 virus components in myocardial tissue by electron microscope
observation, immunohistochemical staining or PCR"

... which seems to contradict the headline. However this new study works by
bathing heart cells derived directly from stem cells with virus in a lab, so
it's not really a close equivalent of the real body. Their claims about
autopsy specimens also showing SARS-CoV-2 invasion of the heart must be taken
with a dose of salt, as:

"The alarming clinical consequences of COVID-19 on the heart have been
puzzling since the vast majority of pathological studies of autopsy patients
have not shown any specific signature of COVID-19 in cardiomyocytes ... We
obtained autopsy specimens from three COVID-19 positive patients, one of whom
was diagnosed with viral myocarditis"

So their claim that it's a "heart virus" requires discarding the majority of
the evidence from prior studies that it doesn't show up in the heart, and
extrapolating from a whole three patients. In fact the meta-analysis they cite
in support of their primary alarming claim speculates the the heart damage
isn't caused by the virus at all, but rather by general increased stress on it
due to breathing difficulties stemming from the respiratory infection, which
would make more sense.

The meta-analysis meanwhile is heavily biased towards people who died, and is
thus not at all representative of the real population. They admit this:

"The overall mortality rate was 23.5% in our meta-analysis, which is much
higher than the value of 2.3% of 44,672 confirmed cases reported in the study
of the Chinese Centers for Disease Control and Prevention. A possible reason
is that these involved studies included a high proportion of critically ill
patients."

So it's really not obvious how these findings generalise to the actual
population, where doctors are not reporting huge waves of previously healthy
patients turning up with otherwise inexplicable heart damage.

[1]
[https://assets.publishing.service.gov.uk/government/uploads/...](https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/886455/EDSSSBulletin2020wk20.pdf)

[2]
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189258/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189258/)

