More evidence emerges on why COVID-19 is so much worse than the flu

Researchers who examined the lungs of patients killed by COVID-19 found evidence that it attacks the lining of blood vessels there, a critical difference from the lungs of people who died of the flu, according to a report published Thursday in the New England Journal of Medicine.

Critical parts of the lungs of patients infected by the novel coronavirus also suffered many microscopic blood clots and appeared to respond to the attack by growing tiny new blood vessels, the researchers reported.

The observations in a small number of autopsied lungs buttress reports from physicians treating COVID-19 patients. Doctors have described widespread damage to blood vessels and the presence of blood clots that would not be expected in a respiratory disease.

“What’s different about COVID-19 is the lungs don’t get stiff or injured or destroyed before there’s hypoxia,” the medical term for oxygen deprivation, said Steven Mentzer, a professor of surgery at Harvard Medical School and part of the team that wrote the report. “For whatever reason, there is a vascular phase” in addition to damage more commonly associated with viral diseases such as the flu, he said.

The research team compared seven lungs of patients who died of COVID-19, the disease caused by the coronavirus, with lung tissue from seven patients who died of pneumonia caused by the flu. They also examined 10 lungs donated for transplant but not used. The lungs, acquired in Europe, were matched by age and gender.

They did not look at blood vessels in organs such as the kidneys and heart, where other researchers have described finding attacks from the virus and unexpected blood clots.

In larger blood vessels of the lungs, the number of blood clots was similar among COVID-19 and flu patients, the researchers wrote. But in COVID-19 patients, they found nine times as many micro-clots in the tiny capillaries of the small air sacs that allow oxygen to pass into the blood stream and carbon dioxide to move out. The virus may have damaged the walls of those capillaries and blocked the movement of those gases, the researchers wrote.

They also found inflamed and damaged cells in the lining of blood vessels in the COVID-19 patients.

Most surprising was evidence that the lungs of people attacked by the SARS-CoV-2 virus grew new blood vessels.

“The lungs from patients with COVID-19 had significant new vessel growth,” a discovery the researchers described as “unexpected.” In an interview, Mentzer speculated that may have been an attempt by the lungs to pass more oxygen to hypoxic tissue.

“That may be one of the things that gets people better,” he said.

The researchers looked for genetic and other differences that might help predict who is most susceptible to severe illness from the virus but did not find any in their tiny sample. So far in the pandemic, COVID-19 has hit certain groups, including older people, African Americans and people with underlying diseases such as diabetes, the hardest.

“Patients who do fairly well have a purely respiratory disease, and the patients who have trouble have a vascular component as well,” Mentzer said. But efforts to determine or explain who will fall into each group have not panned out, he said.