3/4 of Covid Recovered Patients have Heart Problems

"The patients and ourselves were both surprised by the intensity and prevalence of these findings, and that they were still very pronounced even though the original illness had been by then already a few weeks away," study co-author Dr. Valentina Puntmann, a consultant physician, cardiologist and clinical pharmacologist at University Hospital Frankfurt in Germany, told UPI.
reads like a lingering marker -like myocarditis.
It's a risk factor until/if it clears
 
Isn't amazing, that there are feeble minded Trumpoids on this thread who believe Trump, when Trump said that 99% of covid-19 cases are benign, and are trying to trivialize the effects of covid-19 after more than 150K deaths, and are not smart enough to understand that they could be next.
I suggest you seal yourself in a tin can for the duration
 
The more seriously ill Covid patients have some type of underlying conditions which their immune systems had difficulty fighting off the virus.
 
And yet 3/4 of all recovered covet patients have cardiac damage

Not according to the medical publication. That's according to the People magazine headline. You castigate me for overlooking the link in the article yet you don't bother to read the link :doh:
 
The more seriously ill Covid patients have some type of underlying conditions which their immune systems had difficulty fighting off the virus.

Yet even the patients who are not hospitalized end up with heart muscle damage. Are you going to blame them for not taking garlic and vitamins too? :rolleyes:
 
Yet even the patients who are not hospitalized end up with heart muscle damage. Are you going to blame them for not taking garlic and vitamins too? :rolleyes:
D3 helps the immune system, which helps the overall condition of the human body, which then helps to enable the body to fight off and/or recover quicker from viruses.
$12 for a year's supply of D3? Yeah, it's worth it.
 
D3 helps the immune system, which helps the overall condition of the human body, which then helps to enable the body to fight off and/or recover quicker from viruses.
$12 for a year's supply of D3? Yeah, it's worth it.

I take it too, but I do not consider a substitute for avoiding crowded places, not wearing a mask in public, not washing my hands frequently, and condemning those who don't take it.

Care to address the several credible sources I posted that concur on heart damage even in patients w/o comorbidities or severe cases of the virus? I thought not.

Here's an interesting article on possible reasons why some ppl have less severe cases then others. Notice that it has little to nothing to do with vitamins. lol Silliness aside, it's fascinating and intriguing and may hold the key to science helping us beat this thing by using the tools our bodies already have on hand.

https://www.cnn.com/2020/08/02/heal...cross-reactivity-immunity-wellness/index.html
 
Yet even the patients who are not hospitalized end up with heart muscle damage. Are you going to blame them for not taking garlic and vitamins too? :rolleyes:
damage is more of a marker -temporary. I'm not a cardiologist but from what I gleaned from the link if you are healthy the heart will repair itself.

If not -then it is a cardiac event. just hiow serious is beyond my abilities to say
 
I take it too, but I do not consider a substitute for avoiding crowded places, not wearing a mask in public, not washing my hands frequently, and condemning those who don't take it.

Care to address the several credible sources I posted that concur on heart damage even in patients w/o comorbidities or severe cases of the virus? I thought not.

Here's an interesting article on possible reasons why some ppl have less severe cases then others. Notice that it has little to nothing to do with vitamins. lol Silliness aside, it's fascinating and intriguing and may hold the key to science helping us beat this thing by using the tools our bodies already have on hand.

https://www.cnn.com/2020/08/02/heal...cross-reactivity-immunity-wellness/index.html

D3 is a hormone. You still don't get the connection? After all these months? The idea is to simply HELP your otherwise healthy body fight off other milder
disorders like colds, sinus infections, etc. so your body THEN has a better CHANCE of weathering (or not getting in the 1st place) a more severe disease.

And, what about WBC and RBC counts? Most (maybe not you or I) people have no idea how their WBC's, RBC's and platelets are doing.
Right after a Covid patient dies, I hear their kid or cousin or whoever say, "No, they didn't have any pre-existing condition". They don't really know that.
Most patients don't have advanced blood-work to see what shape their defense system looks like.


**************


May 20, 2020 03:42 PM
Low white blood cell counts linked to severe COVID-19 cases
Modern Healthcare

Host factors rather than viral genetic differences appear to influence disease outcomes among COVID-19 patients, according to a new study from China.

Researchers in Shanghai examined clinical, molecular, and immunological data from more than 300 people with confirmed COVID-19. While infection with SARS-CoV-2 can lead to severe respiratory disease and death, it also can result in more mild pneumonia in some patients.

As they reported Wednesday in Nature, researchers led by Hongzhou Lu at Fudan University uncovered two different SARS-CoV-2 strains within their patient cohort, but found these genetic viral variations did not significantly affect patient outcomes. Instead, having low levels of lymphocytes appeared to predict disease severity.

"The determinants of disease severity seemed to stem mostly from host factors such as age, lymphocytopenia, and its associated cytokine storm, whereas viral genetic variation did not significantly affect the outcomes," Lu and his colleagues wrote in their paper.

The researchers analyzed data collected from 326 individuals. Of these, five were asymptomatic and had no fever, respiratory symptoms, or radiological evidence of disease, though they had confirmed SARS-CoV-2 infections. Most of the cohort, though, 293 individuals, had mild disease, defined as having a fever and radiological evidence of pneumonia. Twelve patients had severe disease with shortness of breath and ground-glass opacity in their lungs, and 16 patients had critical disease, developed acute respiratory distress syndrome, and needed a ventilator or extracorporeal membrane oxygenation. As of the beginning of April, almost all of these patients had been discharged, but six had died.

Viral sequencing data was available for 112 samples. When the researchers compared their viral genome data from patients in Shanghai to the initially reported SARS-CoV-2 virus from Wuhan, they identified 66 synonymous and 103 non-synonymous variants in nine protein-coding regions.

Using the viral genomes from 94 cases and 221 other SARS-CoV-2 sequences in the German public-private database known as GISAID, the researchers conducted a phylogenetic analysis of their samples. They separated into two major clades and indicated the earliest zoonotic spillover event may have occurred in late November, which the researchers noted was in line with others' findings.

However, viruses from both clades led to similar disease among patients. The researchers uncovered no statistical differences in disease severity, lymphocyte count, CD3 T cell count, C-reactive protein, D-dimer, or viral shedding duration.

Instead, host factors appeared to affect disease severity. In particular, leukocytopenia was more common among severe and critically ill patients, which the researchers said confirmed prior reports. CD3+ T cells were most severely affected and were suppressed in severe and critical patients. They also noted that CD4+ and CD8+ cell counts were reduced in these patients.

Additionally, patients with critical and severe COVID-19 had high levels of the cytokines IL-6 and IL-8 upon admission and treatment. These levels correlated with decreased lymphocyte count and suggested a link between inflammatory cytokines and COVID-19 severity.

"y closely monitoring the molecular and immunological data in 326 cases of COVID-19 patients, we suggest that adverse outcome is associated with depletion of CD3+ T lymphocytes that is tightly linked to bursts of cytokines such as IL-6 and IL-8," Lu and his colleagues wrote.

Age, the presence of pre-existing conditions, and gender also influenced disease severity, they noted.

https://www.modernhealthcare.com/clinical/low-white-blood-cell-counts-linked-severe-covid-19-cases
 
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Higher levels of destructive white blood cells associated with more severe COVID-19

Researchers believe the NETs may be relevant to numerous aspects of novel coronavirus as thrombosis and inflammation are hallmarks of the severe infection.
FeaturedNeuroscience
·April 25, 2020

Summary: Patients with severe COVID-19 infections have higher blood levels of neutrophil extracellular traps (NETs), which produce NETosis, an inflammatory type of neutrophil cell death. Researchers believe the NETs may be relevant to numerous aspects of novel coronavirus as thrombosis and inflammation are hallmarks of the severe infection.

Source: University of Michigan

New research finds a connection between destructive white blood cells and a more severe disease course in patients with COVID-19.

“We found that patients with COVID-19 infection have higher blood levels of neutrophil extracellular traps, also called NETs, which are a product of an inflammatory type of neutrophil cell death called NETosis,” says first author Yu (Ray) Zuo, M.D., a Michigan Medicine rheumatologist.

Zuo worked on the study with Yogen Kanthi, M.D., a cardiologist and vascular medicine specialist at the Michigan Medicine Frankel Cardiovascular Center, and Jason Knight, M.D., Ph.D., a rheumatologist at Michigan Medicine, who study inflammation and neutrophils. The researchers analyzed blood samples from 50 patients with COVID-19 for this publication.

Zuo and colleagues say, in light of the COVID-19 pandemic, there is an urgent need to better understand what causes the inflammatory storm and blood clots triggered by SARS-CoV-2 infection—a storm that leads to respiratory failure and a requirement for mechanical ventilation in many patients. They believe NETs may be relevant to many aspects of COVID-19 research, given that thrombosis and inflammation are hallmarks of severe infection.

This is the first publication to come out of the Frankel CVC’s CV Impact Research Ignitor Grant program, which was created to address COVID-19 from both basic science and clinical perspectives.

About this neuroscience research article

Source:
University of Michigan
Media Contacts:
Haley Otman – University of Michigan
Image Source:
The image is credited to Stephanie King.

Original Research: Closed access
“Neutrophil extracellular traps in COVID-19”. by Yu Zuo et al.
JCI Insight doi:10.1172/jci.insight.138999

https://neurosciencenews.com/nets-blood-covid-19-16241/
 
in summary, most of the people who caught the coronavirus in their nursing homes but survived, had heart problems as well as a variety of other pre-existing life threatening illnesses......
 
D3 helps the immune system, which helps the overall condition of the human body, which then helps to enable the body to fight off and/or recover quicker from viruses.
$12 for a year's supply of D3? Yeah, it's worth it.

beware.....people who take D3 and hydrochloroquine are at high risk of being conservatives......
 
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