Authors

• Duška Glavaš — Radna skupina za zatajivanje srca, Hrvatsko kardiološko društvo, Hrvatska — ORCID: 0000-0003-2649-0936

DOI

Full Text

Heart failure represents one of the most significant diseases due to its high morbidity and mortality, despite the availability of various treatment methods that are being continuously improved. It is more common in older populations, and with the aging of the population it has become a growing global issue. On the other hand, many diseases, especially heart diseases, can manifest as heart failure (HF). Although those of us who work in the field might feel that the issues surrounding HF are well-known, we can still be surprised by (new) data. Over the last few months, we have witnessed the rise of the COVID-19 (COVID) virus pandemic, that has changed all of our lives and affected many people, in many cases with a lethal outcome. COVID infection primarily affects the respiratory system, but once it has spread it can influence the whole organism via different mechanisms, and HF can also be one of its manifestations, especially in the terminal phase. It should be noted that as many as 80% of patients can have mild or no symptoms while still transmitting the disease. The COVID pandemic has made us face new challenges and taught us or warned us of current problems or of issues that will arise in the near future with regard to both new and previously known infections and diseases. The working groups of the European Society of Cardiology and Heart Failure Association are continuously developing and implementing numerous activities in addition to providing guidelines and organizing congresses, trainings, and meetings, with the ultimate goal of improving the prognosis of patients with heart failure, and the Croatian Cardiac Society is part of this process. Notably, this participation includes the Heart Failure III Registry, the ATLAS project (with epidemiological data from individual countries), the Heart Failure Awareness Week (this year from May 4 to May 10), and an initiative for general practitioner patient care for patients with HF with the help of specialized medical nurses, and telemedicine support (which was especially useful during the pandemic). In the rest of this article, we will provide a review of the treatment of acute and chronic HF during the COVID-19 pandemic. Guidelines of the European Society of Cardiology for the diagnosis and treatment of cardiovascular diseases during the COVID-19 pandemic in relation to heart failure Patients with comorbidities are infected by COVID more often with a higher disease severity and mortality, especially if the comorbidity involves cardiovascular (CV), respiratory, renal, or malignant diseases, diabetes, and arterial hypertension (1). One study (n=8910) followed patients with COVID based on comorbidities. The mortality was 5.8%, and the risk was especially pronounced in the older age group (>65, 10%: 5.8%), in coronary artery disease (CAD, 10.2%: 5.2%), heart failure (15.3%: 5.6%), chronic obstructive pulmonary disease (COPD, 14,2%: 5,6%), arrhythmia (11.5%: 5.6%), and smoking (9.4%: 5.6%). CV diseases significantly increased mortality (2). In a meta-analysis of 6 studies, hypertension and CV diseases were present in 17.1% of those hospitalized for COVID, with up to 3 times higher risk of higher disease severity (3). COVID affecting the heart usually manifests as cardiac damage and heart failure, arrhythmia, and cardiac arrest. Different signs of infection can be prevalent in patients with COVID (high fever, muscle and joint pain, sore throat, headache, fatigue, skin changes, smell and taste disorders, and disorders of the digestive and urinary systems), and breathing problems accompanied by chest pain are common, which can resemble myocardial infarction. All known clinical methods must be used to establish a diagnosis. If performed, coronarography is usually normal. In a study on patients with COVID from China (1/2020; 552 hospitals, n=1099, average incubation – 4 dana, febrility 43%, lymphocytopenia 83.2%, typical changes observed on lung CT 56%), the severe form of the disease was observed in 6.1% of patients (5% were admitted to intensive care, 2.3% were placed on a respirator, and 1.4% died) (4). A fifth of the infected had signs of myocardial damage, in which case the mortality rate was several times higher. In the deceased, the heart was affected in about 40% of cases, 12% did not have prior CV diseases, whereas 25-50% of patients with pneumonia had comorbidities. Patients with COVID-19 infection can develop a new CV disease or present with progression of an existing disease (CAD, cardiomyopathies, various form of HF). Heart failure can be the consequence of acute viral myocarditis and a “cytokine storm”, but also the result of exacerbation of chronic HF. The high cardiometabolic burden during infection causes overwork of the heart, while cytokines can exacerbate shock and circulation changes, including the coronary vessels and microthrombosis. Respiratory infections accompanied by hypoxia lead to a higher incidence of mortal outcomes. Approximately one third of patients with the severe form of the infection can develop HF. ## 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: 1. 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). 2. 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). 3. 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).

Literature

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