Damage to pacemaker cells may explain arrhythmia

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SARS-CoV-2 can infect pacemaker cells, causing rhythm problems. the_burtons/Getty Images
  • Specialized cells in the heart that regulate its rhythm can be selectively infected with SARS-CoV-2, the virus that causes COVID-19, according to a new study.
  • Infection of these cells, called pacemaker cells and including the sinoatrial node (sinus node), can lead to an irregular heartbeat, causing it to race (tachycardia) or slow down (bradycardia).
  • The study’s findings offer a possible explanation as to why some COVID-19 patients report disturbed heart rhythms.

A new study explore the link between SARS-CoV-2 infection and irregularities in heart rate and rhythm (arrhythmia) sheds light on how the virus disrupts the body’s cardiovascular system.

The research, reported in the journal Traffic Researchexplores recent findings that cardiac abnormalities are a common symptom of COVID-19 and may be a consequence of SARS-CoV-2 affecting specialized pacemaker cells.

The research was led by a team from Weill Cornell Medicine in New York, which included Shuibing Chen, Ph.D.associate professor of surgery, chemical biology and biochemistry; Robert Schwartz, MD, Ph.D., assistant professor of medicine; and Todd Evans, Ph.D.professor and vice-president of research, in addition to Benjamin tenOever, Ph.D.faculty member of New York University’s Grossman School of Medicine and NYU Langone Health.

It has been reported that almost 17% of hospitalized patients with COVID-19 experienced heart irregularities.

Electrocardiogram (ECG) studies of COVID-19 patients described tachycardia as one of the most frequently observed abnormalities. In addition, studies have observed that 56% of COVID-19 patients hospitalized with fever also have bradycardia.

Mounting evidence suggests that SARS-CoV-2 can infect specialized heart cells called pacemaker cells. Once pacemaker cells are infected with SARS-CoV-2, the process of self-destruction of ferroptosis ⁠— iron-dependent cell death that begins in the sinus node.

the sinus node is the main pacemaker and damage to its structure causes bradycardia or too slow heart rate. The node monitors heart rate and rhythm as part of the conduction system.

However, few reports have documented whether the sinus node can become infected with SARS-CoV-2 in people with COVID-19.

The Weill Cornell Medicine team used a type of pluripotent stem cell (hPSC) called human embryonic stem cells (hESC) to derive human sinus node-like pacemaker cells.

Researchers have also observed Syrian golden hamsters (Mesocricetus auratus) because they are susceptible to SARS-CoV-2 infection.

Following nasal exposure to SARS-CoV-2, the researchers noted that their pacemaker cells were infected.

Restoration of normal rhythm (sinus)

Among the cell types they studied, the researchers found that the heart’s pacemaker cells were particularly vulnerable to ferroptosis induced by SARS-CoV-2 infection.

They further investigated whether the toxic effects of ferroptosis could be reversed using chelating agents, chemical compounds that bind tightly to metal ions. The researchers wanted to see if these agents could remove iron from the bloodstream and stop ferroptosis.

A chemical screening revealed that the drugs deferoxamine and imatinib could inhibit SARS-CoV-2-induced ferroptosis on pacemaker cells.

Medical News Today spoke with Dr. Chen about his findings. She said:

“[A]Although arrhythmia has been reported in many patients with COVID-19, the cause of COVID-associated arrhythmia is unknown. Here, we found that pacemaker cells of the sinoatrial node are highly susceptible to SARS-CoV-2 infection.

“We compared many tissue organoids, including lung organoids, intestinal organoids, pancreatic endocrine organoids, liver organoids, etc., for their responses to SARS-CoV-2 infection,” he said. she declared. DTM.

Dr. Chen confirmed that of all the cells and organoids they studied, they only detected ferroptosis in pacemaker cells infected with SARS-CoV-2.

“This underscores the importance of applying disease-relevant cells/organoids to study viral infection,” she pointed out.

According to study author Dr. Evans, the results reveal the potential for new therapies.

“[A]Although physicians can currently use an artificial electronic pacemaker to replace the function of a damaged sinoatrial node, here it is possible to use sinoatrial cells such as those we have developed as an alternative pacemaker therapy. cell-based,” he said.

A limitation of the research is that it was a preclinical study involving animals and stem cell-derived pacemaker cells. Further research would be needed to confirm these findings in humans.

DTM also spoke with Zunaid Zaman, MD, Ph.D., cardiologist at Keck Medicine of USC. He said he had recently observed the cardiovascular effects of SARS-CoV-2 in his patients.

“The study shows that COVID-19 can directly infect key cells responsible for maintaining a normal heart rhythm. I’m not surprised as I’m starting to see many patients, especially younger ones, who have abnormal fast or slow heart rhythms after COVID infection.
– Zunaid Zaman, MD, Ph.D.

The research also raised questions for Dr. Zaman, which he believes could be addressed in further research.

“[D]Is COVID exacerbating a pre-existing condition that they would later develop, or is it a direct effect? The results of this study prove the latter and suggest two FDA-approved drugs that block this effect. This should motivate further preclinical and clinical studies to confirm these findings in humans,” he said.

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