Background: Rising data suggest that COVID-19 affects vascular endothelium while the underlying mechanisms promoting COVID-19-associated endothelial dysfunction and inflammatory vasculopathy are largely unknown. The aim was to evaluate the contribution of COVID-19 to persisting vascular injury and to identify parameters linked to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy.Methods: In a cross-sectional design, flow-mediated dilation (FMD), nitroglycerine-related dilation (NMD), pulse-wave velocity (PWV), augmentation index, intima-media thickness (IMT), compounds of the arginine and kynurenine metabolism, homocysteine, von Willebrand factor (vWF), endothelial microparticles (EMP), antiendothelial cell antibodies, inflammatory, and immunological parameters, as well as nailfold capillary morphology were measured in post-COVID-19 patients, patients with atherosclerotic cardiovascular diseases (ASCVD) and healthy controls without prior or recent SARS-CoV-2 infection.Results: Post-COVID-19 patients had higher values of PWV, augmentation index, IMT, asymmetric and symmetric dimethylarginine, vWF, homocysteine, CD31+/CD42b– EMP, C-reactive protein, erythrocyte sedimentation rate, interleukin-6, and β-2-glycoprotein antibodies as well as lower levels of homoarginine and tryptophan compared to healthy controls (all with p < 0.05). A higher total number of pathologically altered inflammatory conditions and higher rates of capillary ramifications, loss, caliber variability, elongations and bushy capillaries with an overall higher microangiopathy evolution score were also observed in post-COVID-19 patients (all with p < 0.05). Most parameters of endothelial dysfunction and inflammation were comparably altered in post-COVID-19 patients and patients with ASCVD, including FMD and NMD.Conclusion: COVID-19 may affect arterial stiffness, capillary morphology, EMP and selected parameters of arginine, kynurenine and homocysteine metabolism as well as of inflammation contributing to COVID-19-associated endothelial dysfunction and inflammatory vasculopathy.

Aims We assessed the outcome of hospitalized coronavirus disease 2019 (COVID‐19) patients with heart failure (HF) compared with patients with other cardiovascular disease and/or risk factors (arterial hypertension, diabetes, or dyslipidaemia). We further wanted to determine the incidence of HF events and its consequences in these patient populations. Methods and results International retrospective Postgraduate Course in Heart Failure registry for patients hospitalized with COVID‐19 and CArdioVascular disease and/or risk factors (arterial hypertension, diabetes, or dyslipidaemia) was performed in 28 centres from 15 countries (PCHF‐COVICAV). The primary endpoint was in‐hospital mortality. Of 1974 patients hospitalized with COVID‐19, 1282 had cardiovascular disease and/or risk factors (median age: 72 [interquartile range: 62–81] years, 58% male), with HF being present in 256 [20%] patients. Overall in‐hospital mortality was 25% ( n = 323/1282 deaths). In‐hospital mortality was higher in patients with a history of HF (36%, n = 92) compared with non‐HF patients (23%, n = 231, odds ratio [OR] 1.93 [95% confidence interval: 1.44–2.59], P < 0.001). After adjusting, HF remained associated with in‐hospital mortality (OR 1.45 [95% confidence interval: 1.01–2.06], P = 0.041). Importantly, 186 of 1282 [15%] patients had an acute HF event during hospitalization (76 [40%] with de novo HF), which was associated with higher in‐hospital mortality (89 [48%] vs. 220 [23%]) than in patients without HF event (OR 3.10 [2.24–4.29], P < 0.001). Conclusions Hospitalized COVID‐19 patients with HF are at increased risk for in‐hospital death. In‐hospital worsening of HF or acute HF de novo are common and associated with a further increase in in‐hospital mortality.

A 51-year-old woman attended our emergency department with a 3-day history of dyspnoea, fatigue, and cough; 11 days earlier she had the ChAdOx1 nCoV-19 vaccination. On examination she was afebrile, her peripheral oxygen saturation was 98% (fraction of inspired O 2 21%), blood pressure was 150/90 mm Hg, heart rate was 98 beats per min, and body-mass index was 31 kg/m².Laboratory investigations showed a severe thrombocytopenia of 37 × 10⁹ platelets per L; 3 days earlier it had been 178 × 10⁹ per L (normal 140-440). Serum concentrations of D-dimer (>34 mg/dL; normal <0•5) and C-reactive protein were increased (42 mg/L; normal <0•5); prothrombin time, partial thromboplastin time, fibrinogen, creatinine, electrolytes, aspartate aminotransferase, alanine aminotransferase, and high-sensitivity troponin T were within normal range. SARS-CoV-2 RT-PCR on a nasopharyngeal swab was negative.CT pulmonary angiography showed a central pulmonary embolism without right ventricular dysfunction (figure). Magnetic resonance venography showed venous thrombus formation in the left internal iliac vein-including the common iliac vein-with extension into the inferior vena cava (figure; appendix).

: Background: The white blood cell count to mean platelet volume ratio (WMR) is increasingly gaining importance as a promising prognostic marker in atherosclerotic disease, but data on lower extremity artery disease (LEAD) are not yet available. The principle aim of this study was to assess the association of the WMR with the occurrence of CLTI (chronic limb-threatening ischemia) as the most advanced stage of disease. Methods: This study was performed as a retrospective analysis on 2121 patients with a diagnosis of LEAD. Patients were admitted to the hospital for the reason of LEAD and received conservative or endovascular treatment. Blood sampling, in order to obtain the required values for this analysis, was implemented at admission. Statistical analysis was conducted by univariate regression in a first step and, in case of significance, by multivariate regression additionally. Results: Multivariate regression revealed an increased WMR (p < 0.001, OR (95%CI) 2.258 (1.460–3.492)), but also advanced age (p < 0.001, OR (95%CI) 1.050 (1.040–1.061)), increased CRP (p < 0.001, OR (95%CI) 1.010 (1.007–1.014)), and diabetes (p < 0.001, OR (95%CI) 2.386 (1.933–2.946)) as independent predictors for CLTI. Conclusions: The WMR presents an easily obtainable and cost-effective parameter to identify LEAD patients at high risk for CLTI.

Background and aims:Observational studies support an association between periodontitis and cardiovascular diseases. The study objective was to assess vascular inflammation after periodontal treatment in patients with peripheral arterial disease. Methods: Ninety patients with peripheral arterial disease (PAD) and severe periodontitis were enrolled in a randomized, controlled trial. Thirty patients underwent non-surgical periodontal therapy and received additional systemic antibiotics (PT1 group), while 30 patients received the same therapy without antibiotics (PT2 group). The remaining thirty patients did not receive periodontal therapy (CG, control group). The primary outcome of this treatment was a reduction in vascular inflammation three months after periodontal treatment as determined by 18 F-FDG PET/CT values. Secondary outcomes were changes in the inflamed periodontal surface area (PISA) and other periodontal parameters, changes in vascular biomarkers, and adverse cardiovascular events. Results: After three months of treatment, a significant improvement in periodontal health was observed in the treatment groups. However, no difference in the primary outcome in the aorta was observed in the three study groups (median target to background ratio follow-up/baseline, PT1 1.00; 95% CI 0.97-1.10, PT2 1.00; 95% CI 0.98-1.1, CG 1.1; 95% CI 0.99-1.1, p = 0.75). No significant differences were detected in most diseased segments and active segments. In addition, no differences were observed in 18 F-FDG uptake in the carotid, iliac, femoral, and popliteal arteries. No differences with regard to relative changes in vascular biomarkers were noted, and no serious cardiovascular adverse events occurred. Conclusions: Periodontal treatment was effective and safe but did not reduce vascular inflammation in patients with PAD.