How coronavirus infections can damage the heart – healing practice

How the SARS-Cov-2 coronavirus attacks the heart

Numerous studies have already shown that severe courses of COVID-19 are associated with organ damage. Heart complications are also among the possible consequences of a coronavirus infection. A German research team has now been able to follow the virus’s journey through the heart and show how the pathogen attacks the heart.

Researchers from the Ruhr University in Bochum led by Dr. Nazha Hamdani in a recent study discovered how the SARS-CoV-2 coronavirus infects human heart muscle cells and that this infection of the heart is mainly promoted by the inflammation and oxidative stress. The results were recently presented in the International Journal of Cardiology.

Heart damage in coronavirus infections

Especially in people with underlying diseases such as obesity, diabetes and high blood pressure, cardiac complications occur in severe courses of COVID-19. But so far it is not known exactly how the corona virus damages the heart.

Using state-of-the-art technology, the Bochum University Hospital task force has now analyzed heart tissue structures from patients who had contracted COVID-19, some of whom died from the infection. .

SARS-Cov-2 can directly attack heart muscle cells

One of the team’s key early findings is that the virus is actually able to directly infect heart muscle cells. SARS-Cov-2 has been detected directly in the heart muscle cells of those affected.

“Our observations show that the virus puts pressure on the heart muscle, which attacks and weakens the force of contraction, that is to say the pumping function of the heart,” explains Hamdani, head of the research.

How does the corona virus reach the heart?

A key question arising from this is how the virus reaches the heart and enters the organ. Researchers have discovered a possible mechanism associated with dysfunction of heart muscle cells in people with severe SARS-Cov-2 infections.

This leads to the activation of certain enzymes that break down proteins. The process is known in technical terms as proteolytic activity.

Taken together, the results indicate that SARS-Cov-2 enters cells via spike protein activation by enzymes responsible for protein degradation, and entry into cells is dependent on these enzymes. a break.

Heart cells are stimulated to commit suicide by SARS-Cov-2

Special proteins responsible for cell suicide (apoptosis) are involved in the process. “The results imply that apoptosis contributes to the deterioration in cardiac contractility observed in Sars-Cov-2 patients,” says Dr. Hamdani.

As the research team was able to show in a later stage of the study, the processes described above were considerably aggravated when they took place in an environment characterized by oxidative stress and inflammatory reactions.

This appears to be why heart damage during coronavirus infection occurs particularly frequently in people with underlying conditions.

So-called neutrophils are responsible for the deterioration. They are primary cell types that play an essential role during inflammatory reactions and migrate rapidly from the bloodstream to damaged tissues.

SARS-Cov-2 can spread through the heart in several ways

In addition, the team was able to prove that SAR-Cov-2 also uses the protein neuropilin-1 (NRP-1) as an entry gate into cells. Therefore, according to Hamdani, the corona virus has several mechanisms to spread in the heart.

“Sars-Cov-2 is able to spread in the infected heart in a receptor-dependent and receptor-independent manner”, summarizes Dr. Hamdani. (vb)

Author and source information

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This text corresponds to the specifications of the specialized medical literature, medical guidelines and current studies and has been verified by health professionals.

Author:

Graduate editor (FH) Volker Blasek

Sources:

Ruhr-Universität Bochum: How the corona virus attacks the heart (published: June 29, 2022), news.rub.deMelina Tangos, Heidi Budde, Nazha Hamdani et al. : Sars-Cov-2 infects human cardiomyocytes promoted by inflammation and oxidative stress; in: International Journal of Cardiology (2022), internationaljournalofcardiology.com

Important note:
This article contains general advice only and should not be used for self-diagnosis or treatment. It cannot substitute a visit to the doctor.

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