Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV2), emerging in Wuhan, China and developing into a pandemic with rapidly emerging cardiovascular manifestations. In the United States, there are approximately 1.7 million reported cases with over 100,000 deaths as of 30 May 2020 [1]. Severe SARS-CoV-2 infection is more commonly observed in patients with specific comorbidities, including cardiovascular disease, diabetes and obesity, yet the mechanism of this relationship is unclear. SARS-CoV2 binds to the angiotensin-converting enzyme 2 (ACE2) receptor, which is abundantly expressed in human tissues including lung epithelium, myocardium, and vascular endothelium [2]. The virus has been shown to directly infect engineered human blood vessel organoids in vitro [3]. A rapidly accumulating body of evidence suggests that COVID-19 causes vascular derangements as a consequence of endothelial cell infection by the virus, contributing to observed cardiovascular and pulmonary complications. Advanced age, hypertension, diabetes, smoking and coronary artery disease are risk factors for severe COVID-19, conditions which are all associated with vascular endothelial dysfunction. Recent reports have also shown a robust and independent association between obesity and the severity of COVID-19 infection, even in the absence of other co-morbidities [4, 5]. Obesity is a chronic inflammatory state associated with dysregulated endocrine and paracrine actions of adipocyte-derived factor, which in turn disrupt vascular homeostasis and cause endothelial dysfunction. While the mechanisms through which obesity exacerbates COVID-19 infection are not fully understood, endothelial dysfunction may be the common link [6, 7]. A prothrombotic state is evident in COVID-19 patients, with elevated D-dimer levels, arterial and deep venous thrombosis, pulmonary embolism, strokes, and intracardiac and microvascular thrombi. It is postulated that endothelial dysfunction and endotheliitis (inflammation of the blood vessel wall) result in thrombus formation. A new pulmonary complication called microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome (MicroCLOTS) has been described in severe COVID-19 and likely represents an atypical form of acute respiratory distress syndrome (ARDS)[8]. MicroCLOTS is a progressive, diffuse endothelial thromboinflammatory syndrome which is characterized by the development of microvascular pulmonary thrombosis. On a background of endothelial dysfunction, endotheliitis (endothelialitis) likely plays a central role in the development of COVID-19 related thromboembolic phenomenon and pulmonary injury [8]. Since the vascular endothelium is a dynamic endocrine, paracrine, and autocrine organ with a vital role in regulating vascular tone and homoeostasis [9], its dysfunction leads to detrimental shifts in