Table 2.

Cardiovascular severity in diabetes and non-diabetes coronavirus disease 2019 patients

Pathophysiology of CVD	Non-diabetes	Diabetes	Reason
Hypoxia	↑	↑ ↑	In COVID-19 patients compared with non-DM cases, DM reduced pulmonary function by reduced levels of FVC and FEV1 this condition further deteriorated in COVID-19 causing hypoxia[126-128,134] ongoing ischemia results in hypoxia causing CVD
Cytokine storm	↑	↑ ↑	In COVID-19 patients compared with non-DM cases, DM increases the severity of the cytokine storm is due to exaggerated inflammatory response[138-141]. Thus, it increases the endothelial dysfunction causing a decrease in plaque stability, and an increase in plaque rupture results in CVD
RAAS Dysregulation	↑	↑ ↑	DM patients using ACE inhibitors and ARBs have increased ACE2 expression is beneficial to vascular health by reducing profibrotic and proinflammatory function. But increased ACE2 levels increase the entry of SARS-CoV-2 infection, which potentially results in loss of ACE2 in blood vessels in diabetes patients causing vascular complications like CVD (see Obukhov et al[154])

ACE: Angiotensin-converting enzyme; CVD: Cardiovascular disease; COVID-19: Coronavirus disease 2019; DM: Diabetes mellitus; FEV1: Forced expiratory volume in 1 sec; FVC: Forced vital capacity; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.