CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
Anticoagulation Strategies in Non-Critically Ill Patients Hospitalized with COVID-19: A Randomized Clinical Trial (FREEDOM COVID)
The FREEDOM COVID Anticoagulation Strategy Randomized Trial was an international, multicenter, randomized, open label, three-arm active-controlled trial comparing prophylactic-dose enoxaparin, therapeutic-dose enoxaparin, or therapeutic-dose apixaban for patients hospitalized with COVID-19. Read More
This chapter reviews the current understanding of cardiovascular manifestations of COVID-19. Although primarily a respiratory virus, SARS-CoV-2 can produce an inflammatory reaction manifested by cytokine storm, endothelial activation, and hypercoaguability that can broadly affect the cardiovascular system (see Fuster and Hurst's Central Illustration). Initial binding of the virus's spike protein to the angiotensin-converting enzyme 2 (ACE-2) receptor on vascular endothelium sets off a chain of events resulting in loss of ACE-2 receptor density, down-regulation of ACE-2 activity, and accumulation of angiotensin II leading to a vasoactive state that is profibrotic, hypertrophic, and vasoconstrictive. Evidence of myocardial injury (eg, elevated troponin) is common in hospitalized patients. It is usually minor in degree but is associated with more severe illness and higher mortality. Venous thromboembolism, arterial thrombosis, and microvascular thrombi occur more commonly in severe COVID-19 and may result in multiorgan failure. Epidemiological and mechanistic associations of cardiometabolic-based chronic disease with COVID-19 substantiate a COVID-related cardiometabolic syndrome (CIRCS) spanning the pre-, acute, and postinfection stages propelled by four key metabolic drivers: abnormal adiposity, dysglycemia, dyslipidemia, and hypertension. Treatment with anticoagulants, antiviral agents, and corticosteroids have some demonstrated efficacy, with additional clinical trial evidence forthcoming.
eFig 84-01 Chapter 84: Cardiovascular Manifestations of COVID-19
In December 2019, a cluster of pneumonia cases from an unknown etiology emerged in Wuhan, China.1 Originating from a wet market, the source of these infections was later identified as SARS-CoV-2 and the clinical syndrome it produced became labeled as COVID-19. What started as a local cluster spread rapidly from Asia to Europe and the United States. The World Health Organization declared a global pandemic on March 11, 2020, and 9 months later there were more than 70 million reported cases and 1.5 million deaths worldwide. Although initial attention was focused on its pulmonary involvement, it soon became apparent that COVID-19 was a multisystem inflammatory and thrombotic disorder that both directly and indirectly affected the cardiovascular system.2,3 This chapter will focus on the cardiovascular manifestations of COVID-19 by discussing its epidemiology, pathophysiology, clinical manifestations, and reported outcomes. The full extent and impact of postacute sequelae of COVID-19 (PASC) are not yet known, but are expected to have lasting implications for cardiovascular health.
Global Cases and Transmission
As of November 2021, more than 250 million cases of COVID-19 infection and 5.1 million deaths related to COVID-19 were reported worldwide, across all continents (Figs. ...