Thread by @anish_koka

The coverage of this wildly speculative paper linking sars-cov2 is much worse than the actual paper is.

To give you a flavor.

The study is based on 8 autopsies of patients with a diagnosis of COVID.

Let’s take Patient 1.

🧵

59 year old black man with a history of CAD.

He was admitted to the hospital 3 times before dying.

Hospitalizations 1 was with a clot in his lungs. His only treatment was heparin and xarelto. This means he didn’t present with a COVID pneumonia.

Hospitalization 2 was listed for heart failure. His ejection fraction was 40-45%. He spent 5 days in the hospital. He was still COVID positive.

Hospitalization 3 was with an acute heart attack. A circumflex artery occlusion associated with rupture of a component of the mitral valve — the papillary muscle. He was now COVID negative. He died of the heart attack and resultant heart failure, I assume.

The authors of this study took coronary artery tissue and looked for evidence of sars-cov2

They show representative samples of tissue in their main figure. They do not , even in their supplement, show all tissue sampled and stained.

The presence of sars-cov2 rna In patients who were infected by itself doesn’t mean much, but researchers probed tissue for the antisense strand of the S gene (S antisense), which is only produced during viral replication.

They go on to write “In the coronary arterial wall, vRNA encoding the S protein and the antisense strand of the S gene were detected to different degrees in all the sections from all patients, indicating the presence of vRNA and replicative activity of the virus.”

So patient 1 died 140 days AFTER testing negative for sars-cov2.

The authors are making a pretty incredible claim — sars cov2 actively replicates in the coronary tree long after an acute infection resolves, and lead to rupture of coronary plaque and death in this patient 140 days after testing -ve for xovid in the respiratory tree!

With this data in hand , med page interviews some academics who propose this as a potential novel mechanism for COVID heart damage given the fact the initial concern that sars-cov2 directly infects heart muscle turned out NOT to be true.

Puntnam , the researchers opining was author of a paper in 2020 that suggested up to 70% of recovered COVID pts may have heart damaged as seen on cardiac mri.

This was a really bad paper that I went into here :
medscape.com/viewarticle/93…

A stunning claim of viral replication long after an initial xovid infection means either something completely novel has been found.. or that the method used to find active viral replication is bogus.

There is a near 100% likelihood this finding is bogus bc

1. there has been no tsunami of cardiac patients noted by clinical cardiologist beyond what one would expect from the stresses put on the heart with any severe viral illness.
2. There are no negative controls provided in the study. I mean I would have used the patient who died 140 days after a negative covid test of a heart attack as a negative control, but pretty sure these authors view anyone with a prior covid test who dies as a potential covid victim.

The problem here is that this poor gentleman who never appeared to have a bad COVID pneumonia — the hallmark of sars-cov2, and likely had a significant coronary stenosis that was causing ischemia that probably lead to his 2nd heart failure admission (Note to trainees, HFpEF is a diagnosis of exclusion) — is the type of patients cardiologists have been seeing for a long time prior to the pandemic.

We never went to this much work in the past to rule out a respiratory infection in the 6 months prior to a heart attack before..

I mean, maybe all coronary disease is deemed some
Day to be infectious , but it won’t be because of research like this.

I’m embarrassed there’s a lab in the US doing this type of research, and embarrassed for journalists who keep going to the same really bad sources over and over again to amplify this shoddy work.