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Two potential drugs — how Corona attacks the heart — today

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In lab­o­ra­to­ry tests, a team from the Ger­man Cen­ter for Car­dio­vas­cu­lar Research shows that the virus­es can also pen­e­trate cells and mul­ti­ply there. Because they can clear­ly see the mech­a­nisms, the researchers also con­clude that there are two pos­si­ble treat­ment meth­ods. prob­lems are repeat­ed­ly found in patients suf­fer­ing from Covid-19. As ear­ly as July, researchers at the Uni­ver­si­ty Med­ical Cen­ter Ham­burg-Eppen­dorf (UKE) found out that the coro­n­avirus can infect cells and mul­ti­ply in them. A work­ing group from the Ger­man Cen­ter for Car­dio­vas­cu­lar Research has now shown the infec­tion takes place on car­diac mus­cle cells. Their results have been pub­lished in the jour­nal Car­dio­vas­cu­lar Research. To this end, mus­cle cells were first gen­er­at­ed from stem cells that have not yet been assigned to a spe­cif­ic tis­sue type. These were then treat­ed with iso­lat­ed virus mate­r­i­al from the first Ger­man patient who had returned to Ger­many from Wuhan, Chi­na, in March. The cells took up the virus, the virus RNA mul­ti­plied and the virus-typ­i­cal spike pro­tein was also formed.

In order to repro­duce the heart more close­ly, the researchers built small clumps of cells from heart mus­cle cells, blood ves­sel cells and con­nec­tive tis­sue cells. They also detect­ed the spike pro­tein in this. Sars-CoV2 could also mul­ti­ply in real human heart tis­sue. Over­all, how­ev­er, the exper­i­ments sug­gest­ed that heart cells are slight­ly less sus­cep­ti­ble to the virus than oth­er cell types. The rate of cell death trig­gered by the infec­tion was there­fore low­er and it also took a lit­tle longer for the heart cells to die. The experts also observed the “heart­beat” of the twitch­ing heart cells in the test tube. “The cells get real­ly stressed when they are exposed to the virus. The so-called ‘beat­ing rate’ only increas­es sharply and falls after three days because the cells die,” says Ste­fanie Dim­mel­er, who coor­di­nat­ed the exper­i­ments Com­mu­ni­ca­tion from Goethe Uni­ver­si­ty Frank­furt cit­ed.

Anoth­er gate­way

Appar­ent­ly the virus fol­lows a slight­ly dif­fer­ent mech­a­nism in heart cells than in lung cells, for exam­ple. Heart mus­cle cells do not have the mem­brane pro­tein TMPRSS2, which the coro­n­avirus needs in lung cells in addi­tion to the ACE2 recep­tor in order to pen­e­trate the cells. In heart mus­cle cells it uses anoth­er pro­tein, cathep­sin.

Experts: Sick peo­ple avoid clin­ics Fear of coro­na could be fatal

This already results in treat­ment options. Because active sub­stances that inhib­it this pro­tein, so-called cathep­sin inhibitors, suc­cess­ful­ly stopped the virus from mul­ti­ply­ing in the heart mus­cle cells in the lab­o­ra­to­ry tests. The drug Remde­sivir, which is already used for coro­na ther­a­py, was also appar­ent­ly able to pre­vent the pathogen from mul­ti­ply­ing. It is still unclear whether this can also be used in acute ther­a­py. “The heart mus­cle cells are nor­mal­ly well pro­tect­ed because the virus first has to pen­e­trate the vas­cu­lar bar­ri­er. In order to exam­ine the virus infes­ta­tion of the heart in the human body in the acute phase, we would have to take reg­u­lar biop­sies from the heart of sick peo­ple, which is almost impos­si­ble,” says Dim­mel­er . How­ev­er, one could try to treat coro­na patients with prob­lem­at­ic heart reac­tions with cathep­sin inhibitors.

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