The results of this study suggest that the celiac axis compression syndrome exists and that the actual ischemia can be detected by gastric exercise tonometry and treated safely, with success.

Gastric exercise tonometry proved crucial in the evaluation of possible intestinal ischaemia. Comparing patients with single- and multiple-vessel stenoses, there were significant differences in clinical presentation and mortality rates.

The endoscopic retroperitoneal approach for the release of the CA in CACS, with additional endovascular treatment of persistent stenosis, is feasible and effective. Short-term results were comparable with the open procedure.

ER appears to be preferential in the treatment of elderly patients and in patients with comorbidity, severe cachexia, or hostile abdomen. Long-term results after OR are excellent. OR can still be proposed as the preferred option for relatively young and fit patients.

This study shows that stenosis in either the CA or SMA increases flow velocities in the other unaffected mesenteric artery. This increase was correlated with the presence of collaterals. Collaterals and stenoses in one of the mesenteric arteries may lead to mimicking or overgrading of stenosis in the other mesenteric artery.

Introduction Endothelial damage and thrombosis caused by COVID-19 may imperil cardiovascular health. More than a year since the WHO declared COVID-19 pandemic, information on its effects beyond the acute phase is lacking. We investigate endothelial dysfunction, coagulation and inflammation, 3 months post-COVID-19. Materials and methods A cohort study was conducted including 203 patients with prior COVID-19. Macrovascular dysfunction was assessed by measuring the carotid artery diameter in response to hand immersion in ice-water. A historic cohort of 312 subjects served as controls. Propensity score matching corrected for baseline differences. Plasma concentrations of endothelin-1 were measured in patients post-COVID-19, during the acute phase, and in matched controls. Coagulation enzyme:inhibitor complexes and inflammatory cytokines were studied. Results and conclusions The prevalence of macrovascular dysfunction did not differ between the COVID-19 (18.6%) and the historic cohort (22.5%, RD −4%, 95%CI: −15–7, p = 0.49). Endothelin-1 levels were significantly higher in acute COVID-19 (1.67 ± 0.64 pg/mL) as compared to controls (1.24 ± 0.37, p < 0.001), and further elevated 3 months post-COVID-19 (2.74 ± 1.81, p < 0.001). Thrombin:antithrombin(AT) was high in 48.3%. Markers of contact activation were increased in 16–30%. FVIIa:AT (35%) and Von Willebrand Factor:antigen (80.8%) were elevated. Inflammatory cytokine levels were high in a majority: interleukin(IL)-18 (73.9%), IL-6 (47.7%), and IL-1ra (48.9%). At 3 months after acute COVID-19 there was no indication of macrovascular dysfunction; there was evidence, however, of sustained endothelial cell involvement, coagulation activity and inflammation. Our data highlight the importance of further studies on SARS-CoV-2 related vascular inflammation and thrombosis, as well as longer follow-up in recovered patients.

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