In all 12 Coronavirus Autopsy cases, the cause of death was found within the lungs or the pulmonary vascular system. Those who did not die of large pulmonary emboli died of extensive inflammation, meaning pneumonia with ARDS. In these Coronavirus Autopsy cases, the lungs were wet and heavy, much like a sponge that is saturated with water.

The lung surfaces often had a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish-blue Hypercapillarized areas. This indicates areas of intense inflammation, with endothelial dysfunction that can be seen at the microscopic level. When they look at the lungs’ slices under the microscope, they found diffuse alveolar damage in 8 Coronavirus Autopsy cases. Specifically, they saw hyaline membrane formation, tiny clots in the capillaries, capillaries engorged with red blood cells, and other inflammatory findings. All these findings represent ARDS. They also found lymphocytes, a type of white blood cell, infiltrated these areas of infiltration. This fits the picture of viral pathogenesis.

* VALUABLE Covid Updates from Dr. Hansen

They also looked at the pharynx of these COVID patients, meaning in their throat. The lining of the throat, or mucosa, was hyperemic, meaning very red and irritated. At the microscopic level, they saw lymphocytes invading there, which is consistent with a viral infection. In one Coronavirus case, a COVID patient had lymphocytes invade his heart muscle, findings that are consistent with what we call viral myocarditis. More than half of the COVID patients in this study had large blood clots. One-third of the COVID patients had pulmonary embolism as the direct cause of death. All the others died of intense inflammation in their lungs related to pneumonia with ARDS (Acute Respiratory Distress Syndrome). Recently, studies show that about 1/3rd of COVID patients with severe COVID have blood clots. In another study of 191 COVID patients, half of those who died had clots, compared with 7% of survivors. And levels of D-dimer that were greater than 1000 µg/L were associated with a fatal outcome. So it’s pretty clear now that the Coronavirus has caused many clots to form in moderate to severe COVID disease.

How is this happening?
It’s likely a combination of reasons that have to do with downregulation of the ACE2 receptor in the lung alveoli, with a subsequent shift towards having more angiotensin II in the lungs, and less angiotensin 1-7 and 1-9 in the lungs, and when this happens, this leads to more cytokine storm with more inflammation, more constriction of pulmonary arteries, and more clots that develop. That, in turn, leads to more endothelial dysfunction in the capillaries that surround the alveoli. Also, there is evidence that the virus attaches to the ACE2 receptors of those endothelial cells that line those capillaries, which further propagates inflammation and clotting. And in the cytokine storm that develops there, RANTES, a chemokine, binds to the CCR5 receptor of CD4 and CD8 lymphocytes, and that causes those lymphocytes to infiltrate those areas of inflammation, and in doing so, further contributes towards the inflammatory reaction. This is why we are seeing low levels of CD4 and CD8 lymphocytes in severe COVID. Endothelial damage can also lead to the development of antiphospholipid antibodies, and these antibodies are bad because they trigger blood clots formation. That’s why COVID patients who have clots with antiphospholipid antibody syndrome need to be on blood thinners.

11 out of the 12 COVID patients in this study had underlying heart disease and were obese. These are known risk factors for cardiovascular disease and known risk factors for endothelial dysfunction and are known risk factors for COVID. So the big takeaways from the findings in this study are that most people who die of COVID are primarily a lung problem. Either related to inflammation with ARDS and/or blood clots.

Antiphospholipid syndrome might be a commonality among patients with thrombosis in COVID patients.

Doctor Mike Hansen, MD

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