Authors

• Duška Glavaš — Croatian Cardiac Society, Croatia — ORCID: 0000-0003-2649-0936

DOI

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## Acute heart failure Acute heart failure is one of the possible complications in the clinical course of COVID infection, especially in more severe cases. The underlining condition can be acute myocardial ischemia, infarction, inflammation/myocarditis, stress-induced cardiomyopathy, tachyarrhythmia, acute respiratory distress syndrome (ARDS), acute kidney injury, and hypervolemia. COVID-induced pneumonia leads to deterioration of the patient’s condition due to hypoxemia, dehydration, and hypoperfusion. The patient’s clinical presentation, comorbidities, imaging methods, and elevated natriuretic peptides (NP) can indicate HF. Application of a bedside transthoracic echocardiogram (TTE) is important for the diagnosis (care should be taken not to transmit the infection to the staff and device). Data on acute HF with COVID infection are lacking. In one report, 23% of all hospitalized patients developed HF, and HF was a significantly prevalent diagnosis in mortal outcomes in comparison with those who survived the infection (52% vs. 12%, P< 0.0001) ( 5 ). There are several mechanisms that cause the development of acute HF in COVID infection, such as: Acute myocardial injury (changes in troponin levels, ECG, TTE) manifests in 8% of patients ( 3 ). The causes can be ischemia, infarction, or myocarditis. In severe infections, damage to the myocardium was reported in 22.2-31.0% of patients ( 6 ). A meta-analysis of 4 studies (n=341) reported that troponin was already significantly elevated on hospital admission in patients with severe infection, that it remained higher in those who survived the infection, and that troponin levels increased as the disease became more severe ( 5 ). HF was more common in patients with acute myocardial damage (14.6% vs. 1.5%), with elevation of NT-proBNP levels ( 7 ). Comorbid diseases can contribute to the development of HF (such as acute respiratory distress syndrome, hypoxemia, acute kidney injury, hypovolemia, stress-induced cardiomyopathy, systemic inflammatory activation – a “cytokine storm”, or severe infection with multi-organ dysfunction). Arrhythmia can lead to deterioration of heart function. It has been reported in 16.7% of all hospitalized COVID patients and in 44.4% of those who required intensive care ( 6 ). The limited data we have indicate that SARS-CoV-2 infection can lead to fulminant myocarditis. This diagnosis can be suspected in case of acute onset of chest pain, ECG changes, arrhythmia, and hemodynamic instability. Dilatation of the left ventricle (LV) can usually be observed, along with global hypocontractility, significantly elevated troponin and NP values, but with no significant changes in the coronary arteries. Myocarditis should also be suspected in patients with COVID-19 and HF. Imaging using MSCT coronarography is desirable when we want to exclude CAD comorbidity. Magnetic resonance imaging (MR) can be used as an additional diagnostic tool. Endomyocardial biopsy is not recommended in patients with COVID. The exact mechanism of this myocarditis is still unclear ( 8 ). ## Chronic heart failure Risk of COVID-19 infection can be high in patients with HF, as well as those at an advanced age and with comorbidities. A number of tests are used in diagnosis: body temperature measurement (with non-contact devices), ECG (arrhythmia, myocardial ischemia, myocarditis), chest X-ray (cardiomegaly, COVID-induced pneumonia), and laboratory tests (elevated erythrocyte sedimentation rate, fibrinogen, CRP, and lymphocytopenia) can facilitate establishment of the diagnosis. Due to low chest X-ray sensitivity, chest MSCT scan is used to discover pneumonia. TTE is very important to show LV dysfunction and spot myocarditis. During all of the above, it is important to prevent virus transmission. Patients with chronic HF should adhere to protective measures (masks, medical gloves, hand hygiene, social distancing, disinfectants, self-isolation), and hospital checkups should be avoided during the stable phase. Telemedicine (internet, phone) should be used as much as possible. This helps reduce virus transmission while monitoring stable patients. Support from psychologists and home delivery of medication is recommended. SARS-CoV-2 uses ACE2 receptors to enter the cell, and some data indicate that angiotensin receptor blockers (ARB) and angiotensin-converting-enzyme inhibitors (ACE inhibitors) can increase the number of ACE2 receptors, which might hypothetically increase susceptibility to infection ( 9 ). A study on 12 patients with COVID-19 infection and ARDS showed that plasma angiotensin II was significantly increased with viral infection and damage to the lungs ( 10 ). Therefore, treatment with the ARB group of medications can have a beneficial effect on suppressing angiotensin II-mediated lung damage. Data available so far indicates that treatment in chronic patients with HF according to guideline recommendations (ACE inhibitors, ARB, beta-blockers, sacubitril/valsartan, aldosterone receptor antagonists) should be continued regardless of COVID infection ( 2 , 11 ). Termination of chronic therapy can lead to HF deterioration ( 12 ). Further research on the role of ACE inhibitors and ARB in this disease is expected. Patients with a left ventricular assist device (LVAD) and with heart transplants are especially susceptible to infections, and strict adherence to preventive measures against virus transmission is necessary. There have been few publications on transplant patients with COVID-19 infection; some studies with SARS and MERS infection are available ( 13 - 16 ).