COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Abstract

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) was first identified in December 2019 as a novel respiratory pathogen and is the causative agent of Corona Virus disease 2019 (COVID-19). Early on during this pandemic, it became apparent that SARS-CoV-2 was not only restricted to infecting the respiratory tract, but the virus was also found in other tissues, including the vasculature. Individuals with underlying pre-existing co-morbidities like diabetes and hypertension have been more prone to develop severe illness and fatal outcomes during COVID-19. In addition, critical clinical observations made in COVID-19 patients include hypercoagulation, cardiomyopathy, heart arrythmia, and endothelial dysfunction, which are indicative for an involvement of the vasculature in COVID-19 pathology. Hence, this review summarizes the impact of SARS-CoV-2 infection on the vasculature and details how the virus promotes (chronic) vascular inflammation. We provide a general overview of SARS-CoV-2, its entry determinant Angiotensin-Converting Enzyme II (ACE2) and the detection of the SARS-CoV-2 in extrapulmonary tissue. Further, we describe the relation between COVID-19 and cardiovascular diseases (CVD) and their impact on the heart and vasculature. Clinical findings on endothelial changes during COVID-19 are reviewed in detail and recent evidence from in vitro studies on the susceptibility of endothelial cells to SARS-CoV-2 infection is discussed. We conclude with current notions on the contribution of cardiovascular events to long term consequences of COVID-19, also known as “Long-COVID-syndrome”. Altogether, our review provides a detailed overview of the current perspectives of COVID-19 and its influence on the vasculature.

SARS-CoV-2 Spike- and Nucleoprotein-Specific Antibodies Induced After Vaccination or Infection Promote Classical Complement Activation

“…In addition, in humans challenged with influenza virus increased levels of C3a and C5a were detected in the upper respiratory tract ( 47 ), intriguingly most often during the recovery phase rather than the acute infection phase, presumably concomitant with when antibody responses are established. Other effects of complement activation may include the destruction of host cells due to the formation of the membrane attack complex (MAC) and the activation of the coagulation cascade and effects on the vasculature ( 38 , 46 , 48 , 49 ).…”

Combining L-Arginine with vitamin C improves long-COVID symptoms: The LINCOLN Survey

“…Therefore, we inferred that associating Vitamin C with other nutraceuticals playing similar actions, like L-Arginine, could be useful. On these grounds, considering that both L-Arginine and Vitamin C are known to improve endothelial function and reduce vascular permeability during infectious disorders 75 , 83 , 84 , 85 , 86 , and based on the emerging role of vascular permeability in Long-COVID 87 , 88 , we designed a study to assess the effects of a combination of L-Arginine and Vitamin C in Long-COVID.…”

Impact of breakthrough COVID-19 cases during the omicron wave on vascular health and cardiac autonomic function in young adults

“…The COVID-19 pandemic has affected nearly 80 million Americans to date, many of whom are young adults without preexisting conditions ( 1 ). Although initially thought to be a respiratory disease, it is increasingly recognized that COVID-19 induces vascular dysfunction in persons who become infected ( 2 ). Indeed, we and others have previously shown that COVID-19 resulted in reduced endothelial function indicated by decreased flow-mediated dilation (FMD) ( 3 – 5 ), impaired microvascular reactivity (i.e., blunted reactive hyperemia) ( 3 , 4 ), and increased arterial stiffness ( 3 , 6 ).…”