https://orcid.org/0000-0001-9303-7790
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ABSTRACT
Introduction
both symptomatic and asymptomatic SARS-CoV-2 infections – coined Coronavirus disease 2019 (COVID-19) – have been linked to a higher risk of cardiovascular events after recovery.
Areas covered
our review aims to summarize the latest evidence on the increased thrombotic and cardiovascular risk in recovered COVID-19 patients and to examine the pathophysiological mechanisms underlying the interplay among endothelial dysfunction, inflammatory response and coagulation in long-COVID. We performed a systematic search of studies on hypercoagulability, endothelial dysfunction and inflammation after SARS-CoV-2 infection.
Expert Opinion
endothelial dysfunction is a major pathophysiological mechanism responsible for most clinical manifestations in COVID-19. The pathological activation of endothelial cells by a virus infection results in a pro-adhesive and chemokine-secreting phenotype, which in turn promotes the recruitment of circulating leukocytes. Cardiovascular events after COVID-19 appear to be related to persistent immune dysregulation. Patients with long-lasting symptoms display higher amounts of proinflammatory molecules such as tumor necrosis factor-α, interferon γ and interleukins 2 and 6. Immune dysregulation can trigger the activation of the coagulation pathway. The formation of extensive microclots in vivo, both during acute COVID-19 and in long-COVID-19, appears to be a relevant mechanism responsible for persistent symptoms and cardiovascular events.
Article highlights
Patients after the acute phase of COVID-19 present a higher incidence of cardiovascular events and higher mortality than patients who did not undergo the infection.
Patients who recovered from COVID-19, and in particular those reporting persistent symptoms and chronic fatigue syndrome, are characterized by persistent endothelial dysfunction.
There is evidence for the spreading of SARS-CoV-2 into different organs and persistence for weeks to months after initial infection.
A compromised ability to switch from the innate to the adaptive immune response can be detected in subjects affected by persistent symptoms after COVID-19 infection.
Post-COVID patients may be characterized by a procoagulant state with high levels of D-dimer and coagulation molecules. Moreover, there is evidence for an exaggerated platelet activation pattern.
Most guidelines do not advocate for universal use of post-discharge thromboprophylaxis, rather suggesting a stratification of the thrombotic and bleeding risk of each individual patient.
List of abbreviations
| CV | = | Cardiovascular |
| COVID-192019 | = | Coronavirus Disease |
| US | = | United States |
| HR | = | Hazard ratio |
| CI | = | Confidence interval |
| VTE | = | Venous thromboembolism |
| OR | = | Odds ratio |
| ICU | = | Intensive care unit |
| IL | = | Interleukin |
| ACE | = | Angiotensin-converting enzyme |
| Ang | = | Angiotensin |
| ROS | = | Reactive oxygen species |
| NO | = | Nitric oxide |
| VWF | = | von Willebrand factor |
| PAI-1 | = | Plasminogen activator inhibitor-1 |
| MVs | = | Microvesicles |
| NETs | = | Neutrophil extracellular traps |
| miRs | = | Micro ribonucleic acids |
| TNF | = | Tumor necrosis factor |
| IFN | = | Interferon |
| AT | = | Antithrombin |
| C1inh | = | C1-esterase-inhibitor |
| α1AT | = | Alpha-1-antitrypsin |
| Ag | = | Antigen |
| IQR | = | Interquartile range |
| NF-κB | = | Nuclear factor kappa B |
| ADAMTS-13 | = | A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 |
| PF4 | = | Platelet factor 4 |
| TF | = | Tissue factor |
| VCAM-1 | = | Vascular cell adhesion molecule-1 |
| PS | = | Phosphatidylserine |
| PMVs | = | Platelet-derived MVs |
| EMVs | = | Endothelium-derived MVs |
| PDGF-β | = | Platelet-derived growth factor subunit β |
| Protease-activated receptor type 1 | = | (PAR-1) |
| SOFA | = | Sequential organ failure assessment score |
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.