COVID-19 and Patients with Heart Failure

Angiotenzin konvertirajući enzim 2 (ACE2) je protein koji služi kao ulazno mjesto SARS-CoV-2 u stanice ljudskog organizma. Strukturno je sličan angiotenzin konvertirajućem enzimu, ali u usporedbi s njim ima antagonističku ulogu u renin-angiotenzin-aldosteronskom sustavu, te drugačiju ciljnu molekulu. ACE2 protein prisutan je u raznim tkivima u ljudi, uključujući epitel pluća i miokard. Trenutna saznanja upućuju da su srčane manifestacije COVID-19 prvenstveno povezane sa zahvaćenošću krvnih žila u SARS-CoV-2 infekciji. Zatajivanje srca opisivano je u bolesnika s COVID-19 od samog početka pandemije, s učestalosti od oko 25 %. Iako trenutno nema dovoljno podataka vezano za tip zatajivanja srca u COVID-19 bolesnika, trenutno dostupni podaci upućuju na češću pojavnost zatajivanja srca sa smanjenom ejekcijskom frakcijom. Zbog uloge ACE2 proteina u renin-angiotenzin-aldosteronskom sustavu, nameće se pitanje učinka lijekova koji inhibiraju navedeni sustav (inhibitori angiotenzin konvertirajućeg enzima i blokatori receptora za angiotenzin II) u pogledu susceptibilnosti bolesnika liječenih navedenim lijekovima na obolijevanje od SARS-CoV-2, kao i pitanje izazivanja težega kliničkog tijeka bolesti. S druge strane, valja uzeti u obzir opasnosti ukidanja lijekova iz ove skupine u bolesnika sa zatajivanjem srca. Prema dosadašnjim spoznajama, uporaba ovih lijekova ne povećava sklonost zarazi SARS-CoV-2 niti je povezana sa značajnim porastom rizika razvoja teškoga ili smrtonosnoga kliničkog tijeka COVID-19 te se nastavak liječenja ovim skupinama lijekova preporučuje od strane vodećih kardioloških društava.Angiotensin-converting enzyme 2 (ACE2) is a protein which serves as the entry point for SARS-CoV-2 into human cells. Although structurally similar to angiotensin-converting enzyme, it serves an antagonistic purpose in the renin-angiotensin-aldosterone system (RAAS), and has a different target molecule. The ACE2 protein is present in various human tissues, including the lung epithelium and myocardium. It is currently thought that cardiac manifestations of COVID-19 are primarily linked to vascular involvement in SARS-CoV-2 infection. Heart failure has been described in COVID-19 patients since the start of the pandemic, with a frequency of around 25%. Although at present there is insufficient data regarding the type of heart failure in COVID-19 patients, current available data suggests a more common occurrence of heart failure with reduced ejection fraction. Due to the role of the ACE2 protein in the RAAS, questions have arisen regarding the effect of medications that inhibit the aforementioned system (angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers), on the susceptibility of patients treated with the said drugs to SARS-CoV-2 infection, as well as on the development of a more severe clinical course of the disease. Conversely, it is important to consider the dangers of discontinuing medications from this group of drugs in patients with heart failure. According to current insights, the use of these drugs does not increase susceptibility to SARS-CoV-2 infection, nor are they associated with an increased risk of developing a more severe or fatal clinical course of COVID-19; thus, continuation of therapy is recommended by leading cardiac societies