Interesting. Would love to know what is going on with this one.
Uh-oh Another development: Strokes in th... - Cure Parkinson's
Uh-oh Another development: Strokes in the young???
Same thing. Zinc deficiency -> Blood clots -> stroke
A reason to take aspirin for pain with COVID-19, also vitamin E. These are known to thin the blood.
Marion,
NYC where significantly more acute, large vessel strokes in young (<50 years) adults infected with COVID-19. (n=5) The five cases had either no (so what, asymptomatic is the norm), or mild, COVID-19 symptoms. The destruction was in the larger vessels, not the smaller ones.
Not much information to go on to draw any conclusions. Perhaps this toxic virus for some reason attacks young adults with reasonably decent immune systems in a cytokinetic storm (CRS) fashion where we find uncontrolled release of proinflammatory cytokines regardless of their age or underlying illness.
I do have to agree with rescueme regarding a possible zinc deficiency. Unfortunately, I doubt whether zinc (or anything else) by itself will alter the negative impact of CRS (if that is what is happening) in some individuals.
Yup. A big "uh-oh"
Sharon
Here is a quote from from a Dr Ruschitzka, chairman of the heart centre and cardiology department at the university hospital in Switzerland from the South China Morning Post newspaper;
scmp.com/news/china/science...
'Ruschitzka suggested strengthening vascular health may be key to treating Covid-19 patients.
“All patients who are at risk and the elderly should be treated very well for the underlying cardiovascular conditions. The better they are treated, the more likely they are to survive the Covid-19 infection,” he said.
“We know that angiotensin-converting enzyme inhibitors [heart medications used to treat high blood pressure] and anti-inflammatory drugs [make the endothelium stronger],” he said.'
I believe the Lancet article referred to is the following, authored in part by the Dr.
thelancet.com/journals/lanc...
The article ends as follows;
'COVID-19-endotheliitis could explain the systemic impaired microcirculatory function in different vascular beds and their clinical sequelae in patients with COVID-19. This hypothesis provides a rationale for therapies to stabilise the endothelium while tackling viral replication, particularly with anti-inflammatory anti-cytokine drugs, ACE inhibitors, and statins.7, 8, 9, 10, 11 This strategy could be particularly relevant for vulnerable patients with pre-existing endothelial dysfunction, which is associated with male sex, smoking, hypertension, diabetes, obesity, and established cardiovascular disease, all of which are associated with adverse outcomes in COVID-19.'
This is of course directed to the clinician or research doctor not advice for lay person.
Uh, oh.
I've been thinking about this and I am going to sleep on it. If I make it to retirement I am may take up smoking again as a hobby.
It really seems to be so. Here is an article by the authoritative Italian hospital cardiologist.
sanitainformazione.it/salut...
“Not pneumonia, but a thrombosis that caused so many coronavirus deaths. The latest discovery bears the signature of Professor Maurizio Viecca, head of Cardiology at the Sacco Hospital in Milan, who, after having tackled the virus and studied the evolution of the disease in its most acute phase, has developed a therapy based on antiaggregants and anti-inflammatory drugs already renamed "Viecca protocol", which is now in the main international scientific publications.
"More than a month ago - he told Sanità Informazione - I observed that these patients went from the CPAP helmet phase to the intubation phase within an hour and a half, and this is impossible only with pneumonia because there is no virus in the world that can give a pneumonia that suddenly no longer responds to the helmet or even to intubation. There had to be some other mechanism. So I started looking at the medical records of these patients and found that in some cases there was a blood test called D-dimer that was particularly high. When you find this altered blood test in the individual, it means there's a thrombosis going on. Then I spoke to the anatomopathologist of the Sacco, Dr. Nebuloni, who told me that she had done thirty autopsies and in all of them she had found the embolism of the small pulmonary capillaries".
Gio:
"...in all of them she had found the embolism of the small pulmonary capillaries". The NYC study found just the opposite if I'm not mistaken.
Therefore, we need to ask ourselves 2 critical questions: 1) "Is the virus found in NYC a variant of the virus found in northern Italy? 2) Is the "thrombosis" the same?
Answers: 1) probably yes. 2) probably no.
Sharon
Italy is the only place that I have heard the C strain was the active strain. Europe and the east coast have the B strain and the west coast has the A strain, supposedly the mildest of the three strains.
Art
Who did you talk to? or what study?
It was a video of some research that I had put in my post for covid-19, let me see if I can grab it and paste it here.
She has a link to the research paper, but it is only available on youtube itself.
I read the paper...I turned her off after a couple of minutes.
Without going into the weeds, it simply states that in their analysis the individuals infected in NYC had infections from different areas of the world (a brilliant deduction given the transient nature of parts of the NYC population).
Another inadequate sampling study where n= 88 with only 68 having hospital info.
"A limitation of our analysis is the relatively small number of isolates from cases identified in the first week of March 2020 which means that our model relies on inferences based on sequences deposited in the GISAID database. Since sequencing efforts vary by country, the fraction of sequences available by region/country is not necessarily representative of the number of cases reported for each of these regions."
IOW, scientific conjecture in a rush to publish something.
sharon
I have read the recent (4/14/2020) preprint study about possible mutations prepared by Chinese microbiologists.
The virus according to them (and other Chinese studies re: SARS-cov-2) enters cells via ACE2. Using data from 750 miles away from Wuhan (how interesting!) they found as many as 1-5 (which is it?) mutations.
They believe that their studies show that the observed
mutations can have a direct impact on the viral load, which means different gradients will result in different levels of end state mortality.
My hangup with this study and similar ones claiming strains or mutations is that the numbers are tiny, here n= 11. Nice lab work, but crummy statistical validity.
Too early to tell.
Sharon
Gio:
In English, his "Viecca protocol" for coronary thrombosis specific to covid-19;
The protocol provides for the administration of an antiplatelet agent "which is a hundred times more powerful than the aspirin that is given to heart patients , the antiplatelet agent (a cocktail of clopidogrel (Plavix), ticagrelor (Brilinta), prasugrel (Effient) ? - sharon)by definition". But as the drug ends, "we supplement it with aspirin and other drugs in order to maintain this fluidity of the blood and prevent the platelets from joining together giving life to the so-called white thrombus, which is what closes the capillaries". (a thrombus here is a blood clot - sharon).
Does this approach mean ARDS is not the issue?
Sharon
Non lo so
insanitas.it/coronavirus-e-...
I quote
“How is Coronavirus countered in light of new discoveries?
"What we have been talking about are now standard protocols applied everywhere, the difference with which Doctor Viecca operates lies in the introduction of double dose of heparin (which is an anticoagulant) also to an antiplatelet agent. They both thin the blood, but with two different actions. So, within a month, he went from nothing to heparin, then to a single administration, then to a double and now to the addition of the antiplatelet agent. We have understood, especially in the North where the epidemic is still widespread, that the mortality rate in resuscitation has been decreasing a lot since we focused not on the lungs or the virus - for which unfortunately we still have no cure - but on thrombosis and microembolies . Therefore, it is not the cure against Covid-19, but the double administration of heparin, with the addition of antiplatelet agents, is perhaps the only economic strategy we have, in the sense that it is the therapy with the most important cost / benefit ratio. In addition to the basic therapy that chloroquine, cortisone, antivirals are doing, we are directing our attention to the venous walls and lung micro-embolisms induced by excessive inflammation. The difference lies only in the dosages and timing. However, I remember that, despite the encouraging data on mortality and the decrease in complications, everything is still to be validated, to be analyzed properly ».
The copied links don't go through HU? I'll try again.