Introduction

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus first identified in an outbreak of pneumonia in Wuhan, Hubei Province, China in December 2019. Despite mitigation of the initial epidemic, the viral syndrome now named coronavirus disease (COVID)-19 has since spread rapidly throughout the world, representing a pandemic with profound implications for human morbidity and mortality. In turn, the capacity of diverse healthcare and economic systems to cope with rising infections and associated intensive care requirements is strained.

The most extensive clinical experience of this virus to date comes from the more than 80 000 positive cases identified in Hubei Province.1–4 These early clinical reports clearly indicated that although most clinical manifestations of COVID-19 requiring hospitalisation are respiratory, there is a substantial minority of patients who undergo progressive and severe cardiovascular compromise.1 2 4 Subjects at highest risk of death appear to be more elderly patients with pre-existing cardiovascular disease and/or classical risk factors that accompany advanced cardiovascular illness.3 The goal of this viewpoint article is to examine whether the nature of SARS-CoV2 infection and the homeostatic status of high-risk cardiovascular patients can be linked in a mechanistic framework that provides insights into corrective therapy over and above current and emergent antiviral approaches to COVID-19.

There are a number of reasons why COVID-19 may be associated with cardiovascular complications that include inter alia-specific aspects of SARS-CoV-2 structure and receptor targeting, and target cell location and its relationship with cardiovascular disease homeostasis. In addition, there are potential risk amplifiers including hitherto unanticipated interactions between viral targets within the host and established homeostatic pathways that may already be perturbed in patients with advanced cardiovascular disease.

In this viewpoint, we underscored specific alterations in renin angiotensin system-ACE 2 (RAS-ACE2) homeostasis that may contribute to more adverse COVID-19 outcomes in …