In March 2020 the World Health Organization (WHO) declared the Coronavirus disease 2019 (COVID-2019) outbreak a global pandemic. Almost two years later, there have been more than 600 million cases and more than 6.5 million deaths worldwide [1]. Despite the exact mechanisms underlying severe COVID-19 remaining unknown, it has been suggested that during the response to SARS-CoV-2 the immune dysregulation and the high levels of pro-inflammatory cytokines might represent pivotal causes of tissue damage. In this context, statins, which are usually used to treat dyslipidemia, gained attention due to their potential role in COVID-19 prognosis [2]. Several studies highlighted their anti-inflammatory, immunomodulatory, antithrombotic, and antiviral properties that may translate into improved short- and long-term outcomes in COVID-19 patients. Apparently, vascular lesions in COVID-19 are more significant than the cytotoxicity of the virus in cardiomyocytes. Of course, cardiovascular implications of COVID-19 are most dangerous for those who, on the basis of preexisting atherosclerosis, already have chronic lesions of the coronary/cerebral arteries and marginally reduced perfusion reserves of the myocardium and other vital organs.

COVID-19 ,dyslipidemia, inflammation, cytokines.

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Synergy Between NK Cells and Monocytes in Potentiating Cardiovascular Disease Risk in Severe COVID-19.