Background Microvascular dysfunction, serum cytokines and chemokines may play important roles in pathophysiology of coronavirus disease 2019 (COVID-19), especially in severe cases. Methods Patients with COVID-19 underwent non-invasive evaluation of systemic endothelium-dependent microvascular reactivity - using laser Doppler perfusion monitoring in the skin of the forearm - coupled to local thermal hyperemia. Maximal microvascular vasodilatation (44° C thermal plateau phase) was used as endpoint. A multiplex biometric immunoassay was used to assess a panel of 48 serum cytokines and chemokines. Severe COVID-19 (S-COVID) was defined according to WHO criteria, while all other cases of COVID-19 were considered mild to moderate (M-COVID). A group of healthy individuals who tested negative for SARS-CoV-2 served as a control group and was also evaluated with LDPM. Results Thirty-two patients with COVID-19 (25% S-COVID) and 14 controls were included. Basal microvascular flow was similar between M-COVID and controls (P=0.69) but was higher in S-COVID than in controls (P=0.005) and M-COVID patients (P=0.01). The peak microvascular vasodilator response was markedly decreased in both patient groups (M-COVID, P=0.001; S-COVID, P<0.0001) compared to the healthy group. The percent increases in microvascular flow were markedly reduced in both patient groups (M-COVID, P<0.0001; S-COVID, P<0.0001) compared to controls. Patients with S-COVID had markedly higher concentrations of dissimilar proinflammatory cytokines and chemokines, compared to patients with M-COVID. Conclusions In patients with COVID-19, especially with S-COVID, endothelium-dependent microvascular vasodilator responses are reduced, while serum cytokines and chemokines involved in the regulation of vascular function and inflammation are increased.

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ObjectiveEndothelial progenitor cells (EPCs) are produced in the bone marrow and mobilized to the peripheral blood playing a key role in endothelial repair. The objective of this study was to evaluate circulating EPC before and after percutaneous coronary intervention (PCI) with stent implantation and their associations with coronary restenosis and adverse cardiovascular events. Venous blood was obtained before and the day after PCI. Quantification of total white blood count and identification of EPCs (CD45−CD34+CD31+CD133/2+CD309+) through immunophenotyping by flow cytometry was performed. The primary outcome was either restenosis detected by new coronary angiography or angina with myocardial ischemia at the territory of the stented coronary artery. Secondary outcomes were angina without demonstrable myocardial ischemia, acute coronary syndrome or all-cause death.Results37 patients were followed for 1 year. The median EPC count before PCI was 320 cells/mcl and after PCI 286 cells/mcl. A decrease of EPC count was found in 65% of the patients, while 35% displayed an increase. Primary outcomes occurred in 10.8% and the secondary in 37.8% of the patients. Despite a higher level of EPC before (402 cell/mcl) and after PCI (383 cell/mcl) in patients with the secondary outcomes, there was no significant association between EPC and cardiovascular events.Electronic supplementary materialThe online version of this article (10.1186/s13104-018-3401-y) contains supplementary material, which is available to authorized users.

This study compared macro‐ and microvascular endothelial function and redox status in active vs inactive HIV‐infected patients (HIVP) under antiretroviral therapy. Using a cross‐sectional design, macro‐ and microvascular reactivity, systemic microvascular density, and oxidative stress were compared between 19 HIVP (53.1 ± 6.1 year) enrolled in a multimodal training program (aerobic, strength and flexibility exercises) for at least 12 months (60‐minutes sessions performed 3 times/wk with moderate intensity) vs 25 sedentary HIVP (51.2 ± 6.3 year). Forearm blood flow during reactive hyperemia (521.7 ± 241.9 vs 361.4% ± 125.0%; P = 0.04) and systemic microvascular density (120.8 ± 21.1 vs 105.6 ± 25.0 capillaries/mm2; P = 0.03) was greater in active than inactive patients. No significant difference between groups was detected for endothelium‐dependent and independent skin microvascular vasodilation (P > 0.05). As for redox status, carbonyl groups (P = 0.22), lipid peroxidation (P = 0.86), catalase activity (P = 0.99), and nitric oxide levels (P = 0.72) were similar across groups. However, superoxide dismutase activity was greater in active vs inactive HIVP (0.118 ± 0.013 vs 0.111 ± 0.007 U/mL; P = 0.05). Immune function reflected by total T CD4 and T CD8 counts (cell/mm3) did not differ between active and inactive groups (P > 0.82). In conclusion, physically active HIVP exhibited similar immune function, but greater macrovascular reactivity, systemic microvascular density, and superoxide dismutase activity than inactive patients of similar age.