COVID-19: from epidemiology to treatment

Abstract

The COVID-19 pandemic has greatly impacted the daily clinical practice of cardiologists and cardiovascular surgeons. Preparedness of health workers and health services is crucial to tackle the enormous challenge posed by SARS-CoV-2 in wards, operating theatres, intensive care units, and interventionist laboratories. This Clinical Review provides an overview of COVID-19 and focuses on relevant aspects on prevention and management for specialists within the cardiovascular field.

Keywords: COVID-19; Coronavirus; Prevention; Prognosis; Risk factors; Treatment.

Figure 1

Life cycle of SARS-CoV-2 and potential medical countermeasures. The positive-sense RNA genome of SARS-CoV2 is encapsulated in a viral envelope studded with four viral structural proteins: spike (S), envelope (E), membrane (M), and nucleocapsid (N). SARS-CoV-2 gains entry into the host cell via binding of the S protein to the cellular receptor angiotensin-converting enzyme 2 (ACE2). Spike glycoprotein rearrangement that primes fusion of viral and host membranes is driven by host proteases (TMPRSS2, cathepsins, HAT, furin, etc.), after which the genome is deposited into the cytoplasm and translation of ORF1a/b ensues. The polyproteins generated from ORF1a/b are cleaved by viral proteases liberating 16 non-structural proteins that guide virus replication. The replication complex is formed on double membrane vesicles, creating both genome-length RNA as well as subgenomic RNAs that encode structure genes S, E, M, and N as well as accessory ORFs that probably play roles in modulating the host response. New virus particles are assembled on membranes derived from the ER–Golgi complex and then transported out of the cell via the secretory pathway. Medical countermeasures are shown in italics adjacent to the viral function they are thought to attack. Convalescent sera and neutralizing monoclonal antibodies should inhibit virus binding to ACE2 and entry. Chloroquine is thought to interrupt entry and/or egress. Protease inhibitors such as lopinavir/ritonavir are thought to prevent polyprotein proteolysis. Nucleoside analogues such as remdesivir and ribavirin are thought to prevent viral RNA synthesis. *Interferons induce the expression of antiviral and immunomodulatory genes that could affect multiple aspects of the virus replication cycle HCQ/CQ, hydroxychloroquine/chloroquine.

Figure 2

Clinical stages of COVID-19 (adapted with permission from Siddiqu and Mehra¹²⁵). During the first days from disease onset, patients typically present a first phase with symptoms resembling an upper respiratory tract viral infection, mostly characterized by fever and coughing. Over days 8–12 there is a transition to an inflammatory phase during which pulmonary symptoms such as shortness of breath might appear. In those patients progressing to the hyperinflammatory phase with relevant lung involvement, the risk of ARDS is notable. In addition, during this late phase, patients are at higher risk of suffering thrombotic and embolic events due to a procoagulant state. ARDS, acute respiratory distress syndrome; CRP, C-reactive protein; IL-1, interleukin 1; IL-6, interleukin 6; LDH, lactate dehydrogenase; NT-pro-BNP, natriuretic pro-brain natriuretic peptide; SIRS, systemic inflammatory response syndrome.

Figure 3

Proposed scheme of prevention measures in different settings involving cardiovascular patients during the COVID-19 pandemic. ECMO, extracorporeal membrane oxygenation; PPE, personal protective equipment.

Figure 4

Proposed organization of an ICU during the COVID-19 pandemic (see text for explanation). FFP3, filtering facepiece protection 3; PPE, personal protective equipment.