COVID-19, MYOCARDIAL INFARCTION AND HEART FAILURE. FEATURES OF THE CLINICAL COURSE AND MANAGEMENT

Since its discovery, the SARS-CoV-2 virus has spread extremely quickly around the world, causing a global pandemic. One of the most common complications of COVID-19 is pneumonia, but SARS-CoV-2 also affects the brain, kidneys, and liver. The course of chronic heart failure, as well as myocardial damage in COVID-19, are extremely pressing issues. ACE-2, transmembrane serine proteases TMPRSS2, and furin all play an important role in the virus entry into the host cell. In patients with heart failure, the level of ACE-2 is elevated, therefore, on the one hand, this can promote SARS-CoV-2 entry into the host cell, and on the other hand, ACE-2 may have a protective effect, since it converts angiotensin II into angiotensin (1-7), which functions as an antagonist of the renin-angiotensin-aldosterone system. The benefit/harm ratio of ACE and ARB is poorly understood. There are active debates concerning whether an increase in plasma ACE-2 levels mediated by ACE inhibitors and angiotensin II receptor blockers (ARBs) exacerbates the clinical course of COVID-19. However, this hypothesis is still unconfirmed and according to the recommendations of the British and Irish Hypertension Society, these drugs should not be abolished if they are taken for the treatment of hypertension and heart failure. Currently, there are ACE-2 inhibitors (camostat, nafamostat) that could theoretically be effective for the treatment of COVID-19, but there is not yet sufficient evidence for their use in real clinical practice. Mortality in COVID-19 is three times higher in patients with chronic heart failure. There are several mechanisms of myocardial damage by the SARS-CoV-2 virus: direct damage to cardio myocytes; hyper activation of lymphocytes, leading to myocarditis; excessive production of cytokines (cytokine storm); impaired blood supply to the myocardium due to microvascular endothelial cell injury and thrombi formation. An increase in pro-inflammatory interleukins (especially IL-6) is an important marker of cytokine storm and it has a significant prognostic role. Cardiac biomarkers (mainly troponin) are used to confirm the myocardial injury. But troponin levels may be elevated in acute heart failure, pulmonary embolism, myocarditis, hypertension, arrhythmias, cardiac surgery, stress-induced cardiomyopathy, and in some non-cardiological states (acute kidney injury, sepsis, anemia, hypoxia, rhabdomyolysis). NT-proBNP is used to determine the presence of heart failure. Damage to the myocardium can manifest itself as a disorder of the rhythm and conduction, and the occurrence of acute heart failure and myocardial infarction. To diagnose these conditions, electrocardiography, echocardiography, MRI of the heart with contrast enhancement and coronary angiography are used. For all hospitalized patients, low molecular weight heparins are recommended for the period of hospitalization. For patients at high risk of venous thromboembolism and low risk of bleeding, NOAC or enoxaparin may be considered for up to 45 days from discharge.