Impaired flow-mediated dilation in hospitalized patients with community-acquired pneumonia

Background Community-acquired pneumonia (CAP) is complicated by cardiovascular events as myocardial infarction and stroke but the underlying mechanism is still unclear. We hypothesized that endothelial dysfunction may be implicated and that endotoxemia may have a role. Methods Fifty patients with CAP and 50 controls were enrolled. At admission and at discharge, flow-mediated dilation (FMD), serum levels of endotoxins and oxidative stress, as assessed by serum levels of nitrite/nitrate (NOx) and isoprostanes, were studied. Results At admission, a significant difference between patients with CAP and controls was observed for FMD (2.1 ± 0.3 vs 4.0 ± 0.3%, p < 0.001), serum endotoxins (157.8 ± 7.6 vs 33.1 ± 4.8 pg/ml), serum isoprostanes (341 ± 14 vs 286 ± 10 pM, p = 0.009) and NOx (24.3 ± 1.1 vs 29.7 ± 2.2 μM). Simple linear correlation analysis showed that serum endotoxins significantly correlated with Pneumonia Severity Index score (Rs = 0.386, p = 0.006). Compared to baseline, at discharge CAP patients showed a significant increase of FMD and NOx (from 2.1 ± 0.3 to 4.6 ± 0.4%, p < 0.001 and from 24.3 ± 1.1 to 31.1 ± 1.5 μM, p < 0.001, respectively) and a significant decrease of serum endotoxins and isoprostanes (from 157.8 ± 7.6 to 55.5 ± 2.3 pg/ml, p < 0.001, and from 341 ± 14 to 312 ± 14 pM, p < 0.001, respectively). Conversely, no changes for FMD, NOx, serum endotoxins and isoprostanes were observed in controls between baseline and discharge. Changes of FMD significantly correlated with changes of serum endotoxins (Rs = − 0.315; p = 0.001). Conclusions The study provides the first evidence that CAP is characterized by impaired FMD with a mechanism potentially involving endotoxin production and oxidative stress.