Coronavirus Disease 2019 (COVID-19) and its implications for cardiovascular care: expert document from the German Cardiac Society and the World Heart Federation

Abstract

Coronavirus diseases 2019 (COVID-19) has become a worldwide pandemic affecting people at high risk and particularly at advanced age, cardiovascular and pulmonary disease. As cardiovascular patients are at high risk but also have dyspnea and fatigue as leading symptoms, prevention, diagnostics and treatment in these patients are important to provide adequate care for those with or without COVID-19 but most importantly when comorbid cardiovascular conditions are present. Severe COVID-19 with acute respiratory distress (ARDS) is challenging as patients with elevated myocardial markers such as troponin are at enhanced high risk for fatal outcomes. As angiotensin-converting enzyme 2 (ACE2) is regarded as the viral receptor for cell entry and as the Coronavirus is downregulating this enzyme, which provides cardiovascular and pulmonary protection, there is ongoing discussions on whether treatment with cardiovascular drugs, which upregulate the viral receptor ACE2 should be modified. As most of the COVID-19 patients have cardiovascular comorbidities like hypertension, diabetes, coronary artery disease and heart failure, which imposes a high risk on these patients, cardiovascular therapy should not be modified or even withdrawn. As cardiac injury is a common feature of COVID-19 associated ARDS and is linked with poor outcomes, swift diagnostic management and specialist care of cardiovascular patients in the area of COVID-19 is of particular importance and deserves special attention.

Keywords: CORONA; COVID-19; Cardiovascular risk; Heart failure; Hypertension; Myocardial injury.

Fig. 1

Summary of consequences of SARS-Cov2 infection on the cardiovascular system summarizing primary targets (left) and secondary comorbidities (right)

Fig. 2

Distribution of comorbidities in different intensities of COVID-19 infections

Fig. 3

Hypothetical scheme for the interaction of the CORONA virus and angiotensin converting enzyme-2 (ACE2). The CORONA virus binding with its spike protein to ACE2, which is processed by the proteinase ADAM17 leading to the internalization of the CORONA virus and ACE2 into the cell where the viral genome is released. The internalization as well as the shedding of ACE2 from the cell surface and its release into the circulation reduces membrane-bound ACE2. Furthermore, ACE2 is reduced by pathological conditions like pulmonary fibrosis, asthma, COPD, pulmonary hypertension, smoking and old age [17]. On the contrary, membrane-bound ACE2-concentrations are higher following treatment with ACE-inhibitors, AT1-blockers and potentially ibuprofen, and ACE2 is more abundantly expressed in childhood and at young age. As ACE2 forms more Ang 1–7 from angiotension-II to stimulate the MAS-receptor mediating anti-proliferative, anti-inflammatory action, hypothetically enhanced ACE2-expression might cause more infection by acting as a receptor for viral cell entry and protect from pulmonary complications. In conditions where is downregulation of ACE2, less infection might occur, but severity of COVID-19-related ARDS can be more severe. This hypothesis fits with the higher likelihood of pulmonary complications in certain disease conditions and in aging. Notably, these data are derived from experimental and observational data, but not from controlled clinical studies and need to be scrutinized in clinical conditions

Fig. 4

Manifestations of myocardial injury and potential pathomechanisms of release of cardiac troponin during COVID-19 infection