OT: Keyontae Johnson UF | Page 4 | The Boneyard

OT: Keyontae Johnson UF

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ctchamps

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Screaming is probably the right word, because there is virtually zero evidence of any meaningful long term effects in young people.
There have been at least 2 studies suggesting potential long term effects from myocarditis in young people. Both were retracted/corrected.

The problem here is very obvious. There is a massive bias among researchers to be the first to publish any novel results concerning SARS-CoV-2 and the impact of Covid-19. That bias led the PennState researchers to publish unscientific, unsupported conclusions that they retracted. Same thing with the German study. Bizarrely, to me, it seems that there are many people who want young people to be affected more than thy are - misery loves company, I guess.

A study published earlier this month in Cardiovascular Pathology examined actual autopsies performed on Covid-19 fatalities. The conclusion? The rate of myocarditis in Covid-19 fatalities, as determined from an actual examination of the heart, and not a scan or troponin assay, is very small, and is, "not the dominant mechanism of cardiac injury."

I've noted this elsewhere - one of the big challenges with SARS-CoV-2 is all the emotion and bizarre cultural polarization it has caused, none of which is based on science.

This young man has suffered an incredible tragedy. We owe it to him, and to decency, to not use him as an unwilling pawn.
Last sentence totally agree with.

You are incorrect about the German study. Data errors in their original paper reported in JAMA on July 27th were found. The German authors of that study agreed with those data errors and corrected the original JAMA paper which satisfied the concern.

On August 25th a second JAMA paper from the German authors was published indicating they made corrections to the data. They wrote this:

We are pleased to confirm that reanalysis of the data has not led to a change in the main conclusions of the study. As we originally reported, compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volume, and elevated values of T1 and T2. However, the corrected findings no longer show higher left ventricular mass in these patients.

You are dismissing a valid scientific paper and it's potential findings. JAMA Cardiology editor Robert Bonow, MD, and deputy editor Clyde Yancy, MD (both Northwestern University Feinberg School of Medicine, Chicago, IL), also weighed in, issuing a brief letter accompanying the correction. They proceeded with a repeated statistical review—and requested reanalysis and revision by the original investigators—following questions raised after the study’s publication, they write. “A rigorous review has confirmed that the findings as originally reported remain valid.”
 

ctchamps

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A study published earlier this month in Cardiovascular Pathology examined actual autopsies performed on Covid-19 fatalities. The conclusion? The rate of myocarditis in Covid-19 fatalities, as determined from an actual examination of the heart, and not a scan or troponin assay, is very small, and is, "not the dominant mechanism of cardiac injury."
Now this part of the post has some merit.

By definition myocarditis indicates the presence of inflammatory infiltrate with adjacent myocyte injury. They conclude that the autopsy data indicates a low incidence of myocarditis present in autopsies of patients who died from Covid-19. The article reviews autopsy reports and they state histological reports are vastly different and perhaps too subjective. But even at low numbers they believe myocarditis from Covid -19 is important.

From that article: Even a low myocarditis rate of ∼1.4% among fatal cases would still predict hundreds of thousands of worldwide cases of myocarditis in severe COVID-19 due to the enormous numbers of infected individuals. Low rates of myocarditis do not indicate that SARS-CoV-2 individuals are not having cardiovascular problems, but rather those complications are likely due to other stressors such as endothelial cell activation, cytokine storms, or electrolyte imbalances.

They write there appears to be a disconnect between MRI clinical findings and incidences of histological myocarditis. The low incidence of COVID-19 myocarditis across this large series stands in sharp contrast to the reports of COVID-19 survivors having a myocarditis rate of 60% as determined by cardiac MRI. It will be incumbent on our colleagues in radiology to better interpret the meaning of cardiac MRI changes and other study data in light of this low incidence of histopathologic myocarditis.

So how do you rectify MRI observations such as the German study and this review of autopsies. A clue might be this:

In this issue of JAMA Cardiology, Lindner and colleagues4 report on 39 autopsy cases of patients with COVID-19 in whom pneumonia was the clinical cause of death in 35 of 39 (89.7%). While histopathologic evaluation did not meet criteria seen in acute myocarditis, there was evidence of virus present in the heart in 24 of 39 patients (61.5%) with a viral load more than 1000 copies per microgram of RNA in 16 of 24 patients (66.7%). Evidence of active viral replication was also noted. In situ hybridization suggested that the most likely localization of the viral infection was in interstitial cells or macrophages infiltrating the myocardial tissue rather than localization in the myocytes themselves. Further using a panel of 6 proinflammatory genes, the investigators demonstrated increased activity among hearts with evidence of viral infection compared with hearts with no SARS-CoV-2 viral infection detected.4 These new findings provide intriguing evidence that COVID-19 is associated with at least some component of myocardial injury, perhaps as the result of direct viral infection of the heart.
 
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Low rates of myocarditis do not indicate that SARS-CoV-2 individuals are not having cardiovascular problems, but rather those complications are likely due to other stressors such as endothelial cell activation, cytokine storms, or electrolyte imbalances.

This sentence alone can explain a lot of things. If it's determined his collapse was related to his earlier case of covid, it doesn't have to relate to myocarditis. If your blood vessels have been impacted by covid, that in itself can lead to blood pressure deregulation, which frequently causes cardiovascular problems, and indeed leads people to collapse especially under stress situations. This is why cardiologists and sometimes neurologists are the main doctors who treat post-viral infection syndromes.
 

ctchamps

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This sentence alone can explain a lot of things. If it's determined his collapse was related to his earlier case of covid, it doesn't have to relate to myocarditis. If your blood vessels have been impacted by covid, that in itself can lead to blood pressure deregulation, which frequently causes cardiovascular problems, and indeed leads people to collapse especially under stress situations. This is why cardiologists and sometimes neurologists are the main doctors who treat post-viral infection syndromes.
This certainly is a possible explanation. Another is that viral loads are reaching the heart in sufficient numbers and damaging or interfering with enough myocardial cells to get radiological results that mimic myocarditis.

My concern with this virus is that it might have more capability to reach vital organs than influenza or respiratory viruses. Unfortunately we won't know this until after the fact.

The following study supports your hypothesis. The thing to consider in this BBC article is that the new scanning system they employ may be revealing vascular problems in the lungs as opposed to damage to the lung tissue itself or fluid in the lungs both of which are detectable with normal MRIs.

Covid-19: Lung damage 'identified' in study
 

BParkDog

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The following study supports your hypothesis.
Study relates to Covid-19 pneumonia, as far as I can tell (can't find peer-reviewed publication). It appears to involve people who were hospitalized with pneumonia related to Covid-19 disease, then released.
If that's the case, then this is likely inapplicable to young, healthy, asymptomatic or mildly symptomatic athletes who did not have pneumonia.
 
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Who is using him as a pawn? Seems like you're sensationalizing this not being covid related more so than those speculating a possible link. Do you have scientific evidence there aren't lasting effects?

Would you tell his doctor not to consider possible effects, so you can use him as a pawn to grind your axe?

Gathers died from the 2nd time he collapsed 3 weeks after the first collapse. Its a shame we don't take medical conditions more seriously. But he had to play, he was a superstar.

Will you clear this kid to play in 3 weeks because you only have one case of a player dying after collapsing a second time? Florida's fans might get depressed if they don't have a winning season.

I had no idea Scott Atlas was a UConn alum.

Does your Dr. Atlas comment mean you revere Dr. Fauci's leadership?
 
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Oh...so, with health care, there are no financial contracts or implications? (I did not know that, even after having been in the biz for more than 25 years...thanks!) :rolleyes:
The way things are going you won’t be able to get auto insurance with a pre-existing health issue.
 
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Remote learning, hybrid models, smaller class sizes - a lot transmitted in schools. Early season numbers for vaccinations against the flu were double what they were last year at the same time.

'New data from the health IT firm IQVIA finds that 23.5 million people got the flu shot from Aug. 7 through Oct. 2, compared with 12.6 million during the same timeframe in 2019.'
 
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Johnson had help from the start....as he went down, the Florida trainers rushed out...they then waved FSU's trainers over...the paramedics came in from the NW corner of the stadium.....an FSU fan who is a cardiologist came out of the stands and assisted...Johnson was put on a gurney and taken to Tallahassee Memorial...the FSU fan/cardiologist rode with him....no update yet this morning.
 

Dream Jobbed 2.0

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Not talked about is how hard he hit his head...he fell forward unconcious right onto his face...no hands breaking the fall...face hit first....
That’s something that count my eye too. Almost guaranteed concussion
 
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A lot of us woke up and had flu shots...I know my wife and I did this year.
 
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There was a Johns Hopkins study that came out recently that concluded that the overall death rate for elderly people in the United States since the pandemic began have been fairly similar to prior years, with an overall increase of just over 11,000 from 2018 peaks. Why? Because the deaths attributed to Covid-19 have been offset by fewer deaths from all other causes. Dr. Genevieve Briand concluded that it's likely that many deaths have been misreported as Covid-19. In other words, she concluded that it is statistically impossible that all deaths from heart disease, aneurism, and so on went down almost exactly as much as Covid-19 caused deaths. This study was pulled, not because her numbers were bad - they were taken directly from the CDC. Her analysis was irrefutable, because it was just number crunching. The study was pulled because, bizarrely, some people were concerned it would be used for improper purposes.

BTW - pneumonia kills about 45k a year in the U.S., including, tragically, many children. Covid-19 has, by official numbers, killed almost a third of a million, and fewer than 200 children - so not comparable, officially.

According to a NY Times article yesterday, in 2020 USA there are at least 356,000 more deaths than usual from all causes. In addition to the COVID 19 deaths, there have been higher than normal numbers of deaths reported from diabetes, Alzheimer's, high blood pressure, and pneumonia.

 
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According to a NY Times article yesterday, in 2020 USA there are at least 356,000 more deaths than usual from all causes. In addition to the COVID 19 deaths, there have been higher than normal numbers of deaths reported from diabetes, Alzheimer's, high blood pressure, and pneumonia.

May be hard to quantify the reasons, but I would guess the stress and social isolation of the pandemic and being isolated from extended family (for those who have done so and followed protocols strictly), and the reluctance of many to seek medical care especially in an institutional setting, may have some bearing on it.

No studies, nothing peer-reviewed, just my guess.

FWIW.
 

BParkDog

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According to [CDC Data] yesterday, in 2020 USA there are at least 356,000 more deaths than usual from all causes.
You are absolutely correct. Better to ignore the NYT, however, which is fairly radical now, and go right to the source the NYT writer cites, which is the CDC - here's the link . . . Excess Deaths Associated with COVID-19 (cdc.gov) . I recommend scrolling down to the blue histogram, which shows the data. The Hopkins author pointed out that the peak weekly death rate in '18, about 67,664, was only exceeded by 12,000/week at the peak of Covid-19 mortality in March, and was only exceeded for 4 weeks during that peak period. In other words, total deaths in U.S., per week, since Covid began, were less than those experienced week-ending Jan 13, 2018 for all but 4 weeks. Her point was that non-Covid-19 deaths have been swapped with Covid-19 deaths. Others have extended her point to - unscientifically - attempt to minimize what this is, by making the point, "well if fewer people died in pandemic week ending Dec. 14, 2020 than did pre-pandemic early January 2018, then how bad can this pandemic really be?" Terrible logic, of course.

This is a severe pandemic, no doubt. How severe? That's a question for history, I suppose.
 
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The social distancing, masking, and probably just as important the work/school from home stuff we are doing which is only moderately effective against COVID is incredible against regular influenza. We should very much consider encouraging as a society more mask usage during the winter months each year, especially for susceptible individuals or anyone with flu symptoms like they do in Asia.
 
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"You are absolutely correct. Better to ignore the NYT, however, which is fairly radical now, and go right to the source the NYT writer cites, which is the CDC - here's the link . . . Excess Deaths Associated with COVID-19 (cdc.gov) . I recommend scrolling down to the blue histogram, which shows the data. The Hopkins author pointed out that the peak weekly death rate in '18, about 67,664, was only exceeded by 12,000/week at the peak of Covid-19 mortality in March, and was only exceeded for 4 weeks during that peak period. In other words, total deaths in U.S., per week, since Covid began, were less than those experienced week-ending Jan 13, 2018 for all but 4 weeks. Her point was that non-Covid-19 deaths have been swapped with Covid-19 deaths. Others have extended her point to - unscientifically - attempt to minimize what this is, by making the point, "well if fewer people died in pandemic week ending Dec. 14, 2020 than did pre-pandemic early January 2018, then how bad can this pandemic really be?" Terrible logic, of course.

This is a severe pandemic, no doubt. How severe? That's a question for history, I suppose.
Data generation and collection is one of the most underreported shortcomnigs of this pandemic, especially considering this data is what drives life and death decisions made by governments.

"Death caused by Covid 19" is an incomplete statistic. It neglects the level of impact Covid had on the person's death. Was Covid the primary contributing factor? Was Covid the straw the broke the camel's back? Was Covid even a factor at all?

Similar logic applies to "cases." While it's important to know how many people test positive to gauge the prevalence of the virus, that doesn't tell us much about its impact. What is the rate of cases that lead to symptoms? What is the rate of cases that lead to hospitalization? What is the rate of cases that lead to deaths? How is this distributed across segments of the population by age, gender, socioeconomic status, etc.

This level of data would lead to much more informed decisions on public health measures and increase public trust that leaders aren't just winging it.
 
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The social distancing, masking, and probably just as important the work/school from home stuff we are doing which is only moderately effective against COVID is incredible against regular influenza. We should very much consider encouraging as a society more mask usage during the winter months each year, especially for susceptible individuals or anyone with flu symptoms like they do in Asia.
You won't get public buy-in on universal mask wearing in the winter for regular flu. Masks are a key and necessary tool to prevent Covid, absent immunity and other therapies.

But there are inconveniences and drawbacks to universal masking in a "just to be safe" scenario - especially for a virus like influenza that does not overwhelm hospitals, there are extensive therapies for, and is not as transmittable as Covid.
 
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