The current COVID-19 pandemic, caused by the SARS-CoV-2 virus (Severe Acute Respiratory Syndrome-Coronavirus-2), represents the largest medical challenge in decades. It has exposed unexpected cardiovascular vulnerabilities at all stages of the disease (pre-infection, acute phase and subsequent chronic phase). The major cardiometabolic drivers identified to have epidemiological and mechanistic associations with COVID-19 are abnormal adiposity, dysglycemia, dyslipidemia, and hypertension. Hypertension is of particular interest, because components of the renin-angiotensin system (RAS), which are critically involved in the pathophysiology of hypertension, are also implicated in COVID-19. Specifically ACE2, a multifunctional protein of the RAS, which is part of the protective axis of the RAS, is also the receptor through which SARS-CoV-2 enters host cells causing viral infection. Cardiovascular and cardiometabolic co-morbidities not only predispose to COVID-19, but are complications of SARS-CoV-2 infection. In addition, increasing evidence indicates that acute kidney injury is common in COVID-19, that it occurs early and in temporal association with respiratory failure and is associated with poor prognosis, especially in the presence of cardiovascular risk factors. Here we discuss cardiovascular and kidney disease in the context of COVID-19 and provide recent advances on putative pathophysiological mechanisms linking cardiovascular disease and COVID-19, focusing on the RAS and ACE2 as well as the immune system and inflammation. We provide up-to-date information on the relationship between hypertension, diabetes, and COVID-19 and emphasize the major cardiovascular diseases associated with COVID-19. We also briefly discuss emerging cardiovascular complications associated with long COVID-19, notably postural tachycardia syndrome (POTS).