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  • Writer's pictureVirus-Guard Disinfectant Srl

Cardiovascular effects of COVID-19

A number of studies have shown that there is an association between age, cardiovascular (CV) disease, and COVID-19. In a summary of a report from the Chinese Center for Disease Control and Prevention among 72 314 cases records of COVID-19 [confirmed cases: 44 672 (62%)], a total of 10.5%, 7.3%, 6.3%, 6.0%, and 5.6% had a history of CV disease, diabetes, chronic respiratory disease, hypertension or cancer, respectively. The overall case-fatality rate (CFR) was 2.3%, but in the age-group 70 - 79 and >80 years the CFR increased to 8.0% and 14.8%, respectively. Similarly, in a meta-analysis that included 1527 subjects with COVID-19 the prevalence of hypertension, as well as the cardiac and cerebrovascular disease was 17.1% and 16.4%, respectively. Therefore, preexisting CV disease may be a risk factor for COVID-19. Moreover, small studies in China have shown that patients with established CV disease may be more prone to severe or fatal infection from SARS-CoV-2, although a study from Italy suggests similar mortality but increased risk for death in people with comorbidities.

A second wave

Several days after the innate immune response begins, the body begins the second wave of attacks against the viral invader. This adaptive immune system response is more targeted than the first, methodically destroying cells infected by this specific virus.

But in older bodies, the adaptive response not only takes longer to get into gear, it arrives to find a scene of inflammatory pandemonium, said Amber Mueller, a postdoctoral researcher at Harvard Medical School who co-authored published in May about Covid-19 and aging. Think of firefighters coming to put out a house fire, she said.

“You have a whole neighborhood of pedestrians or bystanders that are just hanging around, screaming their heads off, causing chaos,” she said. “To the point that it makes it harder for the firefighters to find the fire — to find the infection — and then put it out effectively.”

These delays mean that the pathogen has already made many copies of itself by the time the adaptive immune system gets to work and gains a foothold that might not have been available in a younger person. Additionally, older people have fewer fresh T cells, important players in the adaptive response that are trained to hunt down cells infected with a specific pathogen. When everything is working correctly, successful T cells make copies of themselves so that at the height of the infection, the body is swarming with them. Afterward, a few remain to prime us against return attacks from the same virus.

The supply of T cells that hasn’t already been assigned a pathogen dwindles over the decades. Those that remain may not be as good at copying themselves as the cells in younger people. And they may have trouble making the transition to patrolling the body against future attacks, said Dr. Shabnam Salimi, a professor of epidemiology and public health at the University of Maryland School of Medicine who wrote about the interaction between aging and Covid-19.

“All these together make the immune system less functional during aging,” Dr. Salimi said.

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