Mechanistically, COVID-19 is found to be linked to Angiotensin-Converting Enzyme 2, a membrane-bound aminopeptidase highly expressed in lung, intestinal, and heart tissue. Beyond being implicated in hypertension and diabetes, ACE-2 further functions as a receptor for coronaviruses [58•]. COVID-19 translocates into lung parenchyma via damaging epithelial cells, resulting in respiratory symptoms, with symptom severity worsening in patients with cardiovascular disease. ACE2 secretion is noted to be elevated in CVD patients due to increased reliance on angiotensin-receptor blockers for management of hypertension. At the receptor level, the receptor-binding domain of SARS-CoV spike protein specifically recognizes ACE2, which contributes to both cross-species and human-to-human transmission [59, 60]. Documented variability is demonstrated between various strains of SARS-CoV in terms of binding affinity and viral attachment, which is preserved across both humans and animal models of disease transmission [61]. The preserved domains across MERS/SARS may contribute to the heightened inflammatory response and cytokine milieu that leads to severe pneumonia [62].