COVID-19 Infects Coronary Arteries, Increases Plaque Inflammation


Small study shows infected macrophages and foam cells cause cytokines to be released and may help explain why patients have cardiovascular complications long after getting the infection.

What You Should Know

The study reveals that SARS-CoV-2, the virus responsible for COVID-19, can directly infect the arteries of the heart, even in individuals with pre-existing plaque build-up.

The research highlights that SARS-CoV-2 can infect and replicate in arterial cells, including macrophages (white blood cells) and foam cells, which are involved in cholesterol removal. Infected foam cells appear to be particularly susceptible to the virus and struggle to clear it efficiently.

The study underscores the multifaceted nature of SARS-CoV-2 infection and its ability to trigger inflammation in various cells and tissues throughout the body.

SARS-CoV-2 can directly infect the arteries of the heart and cause plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke, according to a small study.

The findings were published in Nature Cardiovascular Research.

“Since the early days of the pandemic, we have known that people who had COVID-19 have an increased risk for cardiovascular disease or stroke up to one year after infection,” Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH, said in a statement. “We believe we have uncovered one of the reasons why.”

SARS-CoV-2 infects and replicates in the arteries no matter the levels of plaque, the investigators wrote.

Prior to the study, less was understood about coronary arteries and the effects of the virus on patients. Medical science previously knew that after SARS-CoV-2 reaches the cells, the body’s immune system releases macrophages (white blood cells) to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialized type of cell called foam cells.

The study’s investigators surmised that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, MD, PhD, associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID-19 and confirmed the virus was in those tissues. Then they took arterial and plaque cells, including macrophages and foam cells, from healthy patients and infected them with SARS-CoV-2 and examined them ex vivo. They found that the virus had also infected those cells and tissues.

They also found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus, the investigators reported. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID-19.

“This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID,” Olive said.

Limitations for the study include a small group of older individuals with COVID-19 who had pre-existing atherosclerosis and other medical conditions and comorbidities, the investigators wrote.

They also point out the study looked at cases that occurred during the early phases of the COVID-19 pandemic, so it was limited to the SARS-CoV-2 strains that circulated in New York City between May 2020 and May 2021.

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