Abstract / Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was initially regarded as a pathogen of the respiratory epithelium, yet clinical, histopathological and functional observations have shown that the vascular endothelium is one of the most consistently affected tissues during and after COVID-19. Background. Post-COVID-19 condition is characterised by fatigue, dyspnoea, exercise intolerance, cognitive complaints and multisystem symptoms that often cannot be explained by a single organ lesion. Materials and Methods. A structured narrative review of peer-reviewed publications and documents of international health organisations was performed, focusing on endothelial activation, coagulation abnormalities, capillary perfusion, tissue hypoxia and their downstream structural consequences in the lungs, heart, kidneys, skeletal muscle and nervous system. Results. The analysed evidence indicates that endothelial injury links several otherwise separate processes: increased vascular permeability, leukocyte adhesion, platelet activation, procoagulant activity, reduced nitric oxide–dependent vasodilation and impaired capillary oxygen delivery. Chronic microvascular hypoperfusion may sustain oxidative stress, mitochondrial dysfunction and profibrotic signalling, thereby converting a transient inflammatory injury into persistent tissue remodeling. The vascular contribution is best documented in the lungs after severe disease, but plausible microcirculatory correlates have also been described in myocardium, kidneys, skeletal muscle and the neurovascular unit. The strength of evidence differs between organs, and concepts such as persistent “microclots” still require validation. Conclusion. Endothelial dysfunction can be considered a cross-organ pathogenetic axis of post-COVID-19 condition rather than a local vascular complication. Assessment of vascular function, coagulation status and tissue perfusion may help to stratify patients and to design targeted rehabilitation and follow-up strategies.