Twindemic of Coronavirus Disease (COVID-19) and Cardiometabolic Diseases

Metabolic diseases, like hypertension, excess weight, obesity, type 2 diabetes, and vascular diseases, have rapidly increased to epidemic proportions worldwide. Metabolic risks (such as oxidative stress, chronic inflammation, insulin resistance, altered glucose and lipid metabolism, changes in hemodynamics, endothelial dysfunction, and subclinical atherosclerosis) contribute significantly to the progress of vascular disease and drive it eventually to acute vascular events like heart attacks and stroke. Although this situation has been noticed and discussed extensively by the global public health experts, and professional societies, the unprecedented SARS-CoV-2 pandemic has demonstrated for the first time the interdependency or syndemic nature of metabolic diseases and a pathogenic virus that takes advantage of the compromised metabolic function in these diseases. The most common clinical symptoms reported are fever, cough, fatigue, shortness of breath, dyspnea, chest pain, sore throat, and sputum production. The main mode of transmission is through respiratory particles containing viral virions. Both asymptomatic and symptomatic patients seem to be infectious. The spike (S) protein of SARS-CoV-2 seems to have a 10- to 20-fold higher affinity to the human ACE2 receptor than that of SARS-CoV. Since these receptors are highly expressed on a variety of cells, including vascular endothelial cells and adipose tissue, individuals with compromised function of these tissues are more vulnerable to greater infection, replication, and severity with COVID-19. In most cases, the severity of the coronavirus disease is associated with pre-existing comorbidities, which include metabolic diseases such as hypertension, obesity, diabetes, and vascular diseases. Those with such diseases, or with elevated risk factors for such diseases, will have a compromised endothelium, favoring endothelial dysfunction. The infection of the endothelium by SARS-CoV-2 and resulting endothelialitis seems to add to this problem by further damaging the endothelium, causing dysfunction, disruption of vascular integrity, and endothelial cell death. These events lead to the exposure of the thrombogenic basement membrane and result in the activation of the thrombotic and clotting cascade. Because of these observations, critical care clinicians recommend aggressive anti-thrombotic and thrombolytic therapies in the management of acute COVID-19 cases. In the absence of a cure for coronavirus disease, se