COVID-19 Can PREDISPOSE Individuals to Thrombotic Disease

COVID-19 and Thrombotic Disease interaction

Coronavirus disease-2019 (COVID-19) is a viral illness caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2).

COVID-19 is associated with high mortality due to respiratory failure with thrombosis playing an important pathophysiological role. 20-40% of patients with COVID-19 have a likelihood of developing blood clots (thrombosis in both venous and arterial circulations) because of excessive inflammation, platelet activation, endothelial dysfunction, and stasis.
Individuals who already have risk factors, such as: Thrombotic Disease, Cancer, Heart Disease, Diabetes are at increased risk of thrombotic events with devastating Clinical Outcome: Venous Thromboembolism, Myocardial Infarction, Disseminated Intravascular Coagulation.
Even COVID-19 patients WITHOUT a history of cardiovascular disease are at risk for incident cardiovascular complications.

Importance of Abnormal D-Dimer, HsC-Reactive Protein, and Fibrinogen levels

Published data shows that the majority of patients with progressive COVID-19 infection have Abnormal D-Dimer, HsC-Reactive Protein, and Fibrinogen levels, which indicate a hypercoagulable state due to cytokine storm syndrome:
Occasionally (due to genetic factors or strong viral infections like COVID-19) our immune system can become overzealous and start attacking and killing everything in sight, even healthy cells in the body. When that happens it is referred to as a cytokine storm and it kills around 50% of severe COVID-19 patients.

D-Dimer – Protein fragment that’s made when a blood clot dissolves in your body.

HsC-Reactive Protein – High-sensitivity C-reactive protein is a substance produced by the liver in response to inflammation.

Fibrinogen – Produced by the liver protein, specifically a Clotting Factor (Factor I), that is essential for proper blood clot formation.

Endothelial damage and subsequent clotting is common in critical COVID-19 patients. Clots in the small vessels of not only the lungs, but also in the heart, the liver, and the kidneys are noticed in these patients. It is believed that COVID-19 can activate the coagulation cascade through various mechanisms, leading to severe hypercoagulability. Early anticoagulation may block clotting formation and reduce microthrombus, thereby reducing the risk of major organ damages.

At this time, there are no specific vaccines or treatments for COVID-19. However, there are many ongoing clinical trials evaluating potential treatments. More than 200 clinical trials have been organized mainly for the study of anti-viral drugs.

Ayass Bioscience, LLC research and development has, over the years, published many articles on the coagulation cascade and antiphiospholipids. With years of experience in treating patients with autoimmune diseases and coagulopathy, Dr. Ayass has stated that all people with positive COVID-19 can be saved if we pay attention to their vascular components, including Factors II, VII, VIII, IX, X, XI, and XII, plasminogen inhibitor, fibrinogen, HsC-Reactive Protein and D-Dimer. By monitoring these components, we can direct the therapy toward recirculating the lungs. He believes that physicians should follow anticoagulation management protocols not only for treatment of patients, but also as a preventative measure.


There is a strong association between blood thinners and reduced probability of death from COVID-19 Infection. Therapeutic and prophylactic doses of anticoagulants reduced mortality by roughly 50% compared to patients without it.

Also, patients on both therapeutic or prophylactic blood thinners have 30% fewer intubations than those who did not receive anticoagulation therapy.

All regimens of anticoagulants – drugs that prevent blood clotting – are far superior to no anticoagulants in COVID-19 patients.

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