ABC | Volume 114, Nº5, May 2020

Review Article Askin et al. COVID-19 and cardiovascular diseases Arq Bras Cardiol. 2020; 114(5):817-822 inhibition of lysosomal enzymes in myocytes. 48 Furthermore, due to the effects of chloroquine on CYP2D6 inhibition, beta-blockers (such as metoprolol, carvedilol, propranolol, or labetalol) metabolized via CYP2D6 may cause increased drug concentration that requires careful monitoring of heart rate and blood pressure changes. Finally, both agents are associated with the risk of conditional torsade de pointes in patients with electrolyte abnormalities or in combination with agents that prolong QT. Short-term exposure to these agents as expected in the treatment of COVID-19 poses a lower risk for these dose-dependent side effects. 49 COVID-19 cases complicated by severe acute respiratory distress syndrome (ARDS) are currently treated by methylprednisolone. 50 This steroid cause fluid retention, electrolyte irregularity, and hypertension, and it also interacts with warfarin through an unknown mechanism. Clinicians advise observing these drug interactions. Finally, severe COVID-19 may create difficulties in the application of routine cardiovascular medications; for this reason, patients at a risk of ischemic heart disease or heart failure may worsen. 47 Other recently published studies Recent studies provide promising information for treatment and follow-up of COVID-19. Diaz et al. 51 showed that ACEi and ARB therapy increased the number of ACE2 receptors in experimental animals. ACE2 receptors serve as binding sites for SARS-CoV-2 virions in the lungs. This increase can produce serious disease outcomes. COVID-19 can suppress cardiac functions and cause myocardial damage. History of CAD and increased levels of cTnI are two major independent markers that affect clinical evolution of patients with COVID-19. 52 In HT and DM, ACE2 enhancing drugs pose a risk for serious COVID-19 infection, so ACEi and ARB therapy require close monitoring. As calcium channel blockers (CCBs) have not been shown to affect ACE2 expression or activity, they may be an alternative therapy in COVID-19 patients. 53 Age, presence of underlying diseases, secondary infection, and high inflammatory indicators in the blood are determinants ofmortality inCOVID-19. COVID-19 mortality develops due to virus-activated “cytokine storm syndrome” or fulminant myocarditis. 54 Previous cardiovascular metabolic historymay further increase the severity of COVID-19 and greatly affect the prognosis of COVID-19. On the other hand, a marked increase inmyocardial damage is observed in patients with COVID-19. 55 Recent studies have focused on the beneficial effect of chloroquine, an antimalarial drug, which is effective on the treatment of patients with SARS-CoV-2. Due to previous experiments with chloroquine in the field of antiviral research, the scientific community is more concerned with the treatment of chloroquine 56 Among cases of COVID-19, patients with comorbidities haveworse clinical results than thosewithout comorbidities. More comorbidity is associated with worse clinical outcomes. 57 Recognizing acute myocarditis as a complication associated with COVID-19 is important for close follow-up of patients affected by COVID-19 and increased knowledge of public health officials about this type of complication. Clinical surveillance and laboratory tests, including troponin levels, are essential for proper identification of COVID-19 and reduction of transmission. More studies areneeded todetermine the effectiveness of corticosteroids in suppressing the myocardial inflammatory response. It cannot be denied that antiviral drugs or chloroquine can contribute to the recovery of patients with COVID-19. 58 Myocardial injury has fatal consequences for COVID-19. Patients with a history of CAD without myocardial damage have relatively better prognosis. Myocardial damage triggers cardiac dysfunction and arrhythmias. Inflammation is one of the possible causes of myocardial injury. Closer follow-up and multiple treatment regimens should be considered for patients with a high risk of myocardial injury. 59 Cardiac damage has been common among patients hospitalized with COVID-19, and it is closely related to the risk of in-hospital mortality. More research is needed to clarify the mechanism of cardiac injury, and complications should be carefully monitored in COVID-19 management. 60 Chen et al. 61 observed that the elderly, male patients, and/or patients with high ACE2 expression-related diseases had worse prognosiswhen exposed toCOVID-19.Withpreclinical evidence, renin-angiotension system blockade was thought to alleviate COVID-19. Multicentre studies are needed to test the hypothesis beforemaking recommendations on potentially essential drugs. 62 Conclusion SARS-CoV-2 causing COVID-19 is a global pandemic problem. KVH is more common in COVID-19 patients. Morbidity and mortality rate is high in these patients. Whether CVD is an independent risk or whether it is mediated by other factors (e.g. age) has not been clarified yet. Myocardial damage occurred in more than a quarter of critical cases. Clinical ACEi and ARB medications do not present problems according to the current evidence. Research is currently promising in terms of treatment. Author contributions Conception and design of the research: L.A., O.T., H.S.A. ; Acquisition of data: L.A., O.T., H.S.A. ; Analysis and interpretation of the data: L.A., O.T., H.S.A. ; Writing of the manuscript: L.A., O.T., H.S.A. ; Critical revision of the manuscript for intellectual content: L.A., O.T., H.S.A. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding There were no external funding sources for this study. Study Association This article is not related to any study association Ethics approval and consent to participate This article does not contain any studies with human participants or animals performed by any of the authors. 820