Abstract
The coronavirus disease-2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) that first appeared in Wuhan, China. COVID-19 was found to have significant connection with the cardiovascular system by causing complications such as myocarditis and arrhythmias. Furthermore, medications for COVID-19 have been shown to induce cardiovascular side effects. The emergence of COVID-19 spreading also raised questions on the need for modification of life support algorithms to protect vulnerable healthcare workers.
Highlights
Coronavirus disease-2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARSCoV2) that first appeared in Wuhan, China.[1,2]
SARS-CoV2 rapidly spread to almost every country in the world and COVID-19 was declared a pandemic by the World Health Organization on 11 March 2020.2 In Indonesia, COVID-19 has affected 11.192 confirmed patients with 1.871 patients recovered and 845 patients deceased (4 May 2020).[3]
ACE inhibition, as the holy grail of heart failure therapy; debatable regarding its use in COVID-19 infection, it was recommended and proven beneficial in COVID-19 patients with hypertension or heart failure
Summary
Coronavirus disease-2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARSCoV2) that first appeared in Wuhan, China.[1,2] SARS-CoV2 rapidly spread to almost every country in the world and COVID-19 was declared a pandemic by the World Health Organization on 11 March 2020.2 In Indonesia, COVID-19 has affected 11.192 confirmed patients with 1.871 patients recovered and 845 patients deceased (4 May 2020).[3]. From the QRS-T morphology, we may determine the possibility of myocarditis, acute coronary syndrome, and the baseline of QT interval.[13] Frequent monitoring of QT interval should be done especially if COVID-19 drugs are started (Figure 1); mainly azithromycin (risk of Torsades de pointes 4.7-6.7%) and chloroquine (or hydroxychloroquine) which may increase the risk of QT prolongation and the risk of Torsades de Pointes (TdP).[14] This was caused by activation blockage of potassium channel IKr (hERG/KV11.1) and both treatments metabolized by CYP3A4 which delay its clearance in the plasma.[15,16]. Hydroxychloroquine act on the entry and post-entry stages of COVID-19 infection, likely via effects on endosomal pH and the resulting under-glycosylation of ACE-2 receptors that are required for viral entry.[29] Both of chloroquine and hydroxychloroquine are known to prolong QT interval They can provoke pro-arrhythmia via mechanisms beyond the block of IKr implicated in usual cases of torsade de pointes.[30,31] Azithromycin, a frequently used macrolide antibiotic, lacks strong pharmacodynamic evidence of IKr inhibition.
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