What is the Real Cause of ‘COVID-19’ Deaths?
Written by Dr. Harry Ambrose
All the facts seem to point out that the death of the patients by the Sars Cov-2 virus (COVID-19) is not an interstitial pneumonia that has been talked about so much in the media. There is a real cause which we explain in detail and chronologically in this chapter, and about which not much is said in the official journalistic media.
I’ve loosely transcribed the audio from Spanish to English. In short, SARS COVID2 patients are not dying from interstitial pneumonia (which is why ventilators aren’t working and often cause more harm than good) but rather from DIC (disseminated intravascular coagulation) – a medical term for blood clotting causing a lack of oxygen.
HERE’S THE LOOSE TRANSCRIPT:
Autopsies revealed a number of micro-thrombi, generalized venous, this means that in the capillaries, blood clotting occurred with obstruction blood flow, this caused the inability of oxygen to reach the alveoli, and for more mechanical respirator than the patient had, he was going to die anyway, because he had occluded blood vessels that carry oxygenated blood to the lungs, they also found micro throbs, in the heart, brain, and kidneys. Which means the patients did not die of interstitial pneumonia as told initially, they died from a blood condition called disseminated intravascular coagulation (DIC) also found in the x-rays of the lungs that interstitial pneumonia can be easily confused with images caused by micro thombus.
These discoveries of Italian pathologists in more than 50 autopsies performed in Bergamo and Milan Italy, center of the largest number of cases in that country, was corroborated by another more recent study in the U.S. by the doctor specializing in pathology, Sharon Fox and collaborators, in April in New Orleans, but only in 4 patients.
So in total 74 autopsies and other Chinese studies by Dr. Ning Tang etal., between Feb and March that confirm these facts. Increased D-dimers in the blood and coagulopathy indicators are related with worse prognosis of hospitalized patients.
SARS, COVID2 WAS INVENTED IN A BRITISH LAB (PIRBRIGHT INSTITUTE) FROM A U.S. PATENT (BICKERTON ET AL.) WHICH HAS 4 GENETIC INSERTS:
- most likely Dengue or Zika, which most likely were carried out in the biosafety lab in Wuhan China, and then escaped or were released.
Of these diseases Malaria, Dengue, Zika, and HIV can cause Thrombocytopenia, which means decreased platelets and formation of micro clots or thrombus, which produces purpuric lesions on the skin, which results in red dots on the limbs, that have been reported in some patients asymptomatic but infected with COVID-19 – mainly in young people, and the worst cases are capable of inducing coagulation, Disseminated Intravascular, which is a systemic event triggered by damage in the blood vessels, caused by inflammation. This has two consequences:
- Severe, localized micro thrombus formation OR
- Generalized or localized bleeding
The video states that while some scholars will say “severe infections can trigger DIC,” which is true, but among those infectious processes are HIV, Malaria, ZIKA, and Dengue, which is irrefutable.
IT SHOULDN’T BE SURPRISING THAT THE GENETIC CODES INSERTED INTO THE NEW SARS INVENTION, COVID2 ARE THOSE OF THESE PATHOLOGIES.
THE FIRST ACTION WHEN THE PATIENT STOPS BEING ASYMPTOMATIC AND BEFORE HOSPITALIZATION SHOULD BE BLOOD STUDIES TO ANALYZE COAGULATION BECAUSE DIC MUST BE AVOIDED AT ALL COSTS.
- Prothrombin time or PT, which measures the external path of the cascade of coagulation
- Partial thromboplastin time, of PTT, which measures intrinsic and common pathway, the amount of D-dimers,
- Level of fibrinogen, platelet count and hematocrit will show quickly what is happening.
This clotted blood is mainly in the lungs, heart, brain and kidney. It is feasible that many died of hemorrhagic vascular brain ischemia, others with kidney failure, and others with heart disease such as myocardial infarction or failure of cardiac dilation of the heart.
Pathologist Sharon Fox found dilation of the right ventricle that means the heart was dilated, by the effort of pumping blood to the lungs that were occluded by micro thrombus, covered by platelet accumulation, and exudates inflammatory, characteristic of coagulopathy or DIC.
Another study just published by Wuhan General Hospital by Zhang et al., in more than 300 hospitalized patients from Jan 1999 to March 2020, the scale levels, D-dimers like prognostic factor of higher or lower mortality, and the conclusion was that patients with increased elevation of this blood factor had a greater risk of dying.
All of this evidence points to the fact patients are dying of micro thrombus (DIC) in the lungs, mainly, without ruling out heart, brain, and kidneys, NOT by interstitial pneumonia as reported and continues being reported today.
These studies raises a very suspicious question:
WHO TOLD THESE RESEARCHERS IN WUHAN, CHINA TO STUDY D-DIMERS SPECIFICALLY JUST 12 DAYS AFTER THE PANDEMIC WAS DECLARED? THIS IS SUSPICIOUS AND INDICATES THEY ALREADY KNEW IT WAS A DISEASE THAT CAUSES DIC AND HAD PROBABLY DONE AUTOPSIES PRIOR TO DECEMBER AND THEY KNEW WHICH BLOOD ELEMENT WAS INDICATED.
THIS PROVES THAT THIS PLAGUE CAME LONG BEFORE THEY GAVE THE ALERT, ALLOWING IT TO SPREAD WIDELY.
And, they already knew about the micro thrombus and coagulopathies as the vital element in the the cause of mortality.
IT TOOK 3 MONTHS AND THOUSANDS OF PEOPLE DYING UNTIL THE STUDIES PRESENTED IN THIS VIDEO HAPPENED. A HARSH REALITY OF WHAT WENT ON.
Dr. Harry Abrose, et al.
THIS ALSO EXPLAINS WHY HYDROXYCHLORQUINE (HCQ), AN ANTIMALARIAL (ALONG WITH ZINC)IS WORKING, AS WELL AS AZITHROMYCIN AS IT STOPS THE GROWTH OF BACTERIA LIKE TB.
- alkalizes the blood, reducing the virus’ ability to replicate
- causes 02 to dissociate from hemoglobin, similarly as carbon monoxide replaces the 02 molecule
- reduces cytokine storm
“Hydroxychloroquine prevents the virus from binding to the hemoglobin which causes the oxygen to plummet and desaturate, and it prevents the iron from getting released from the hemoglobin molecule and causing damage in the lungs,” said Melbourne Family Dr. Stephanie Haridopolos. https://www.fox35orlando.com/news/hydroxychloroquine-what-is-it-and-why-the-debate-in-the-fight-against-covid-19
Evidently, HCQ also improves the following:
- anticoagulant in Lupus patients. See: https://www.ahajournals.org/doi/full/10.1161/01.cir.96.12.4380,
- improves muscle and joint pain
- skin rashes
- pericarditis (inflammation of the lining of the heart)
- pleuritis (inflammation of the lining of the lung)
- fatigue and fever
- may prevent activation of plasmacytoid dendritic cells, a component of the immune system that is responsible for making interferon https://www.hopkinslupus.org/lupus-treatment/lupus-medications/antimalarial-drugs/
MOST OF THESE ISSUES ARE INVOLVED WITH COVID2, SHOWING WHY HCQ WOULD BE A GOOD CHOICE.
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