Kinetics of Circulating Extracellular Vesicles Over the 24-Hour Dosing Interval After Low-Dose Aspirin Administration in Patients at Cardiovascular Risk.

Extracellular vesicles (EVs) are small vesicles deriving from all cell types during cell activation, involved in transcellular communication, and regarded as predictors of vascular damage and of cardiovascular events. We tested the hypothesis that, in patients on chronic low-dose aspirin treatment for cardiovascular prevention, aspirin may affect the release of EVs within the 24-hour interval. We enrolled 84 patients, mostly at high or very high cardiovascular risk, on chronic low-dose aspirin treatment. The numbers of circulating EVs (cEVs) and annexinV+ cEVs (total, platelet-derived, endothelial-derived, and leucocyte-derived) were assessed immediately before, and after 10 and 24 hours of a witnessed aspirin administration. Platelet cyclooxygenase 1 (COX-1) recovery was characterized by measuring serum thromboxane B2 (sTXB2 ) at the same timepoints. Nine healthy participants were also enrolled. In patients, daily aspirin administration acutely inhibited after 10 hours following aspirin administrations the release of cEVs (total and leukocyte-derived) and annexinV+ cEVs (total, platelet-derived, endothelial-derived, and leukocyte-derived), with a rapid recovery at 24 hours. The inhibition after 10 hours suggests a COX-1-dependent mechanism. Interestingly, the slope of platelet-derived and of annexinV+ platelet-derived cEVs were both directly related to sTXB2 slope and COX-1 messenger RNA, raising the hypothesis that vice versa, cEVs may affect the rate of COX-1 recovery and the subsequent duration of aspirin effect. In healthy participants, no circadian difference was observed, except for leukocyte-derived cEVs. Our findings suggest a previously unappreciated effect of aspirin on the kinetics of a subset of cEVs possibly contributing to the cardioprotective effects of this drug.

A case of Legionella pneumophila evaluated with CT and ultrasound.

A 36-year-old man was admitted to the emergency department of "SS Annunziata" hospital in Chieti complaining of a sharp chest pain arisen some hours before admission. On examination, the patient looked sweaty; his vital signs showed tachycardia and augmented breath rate; sinus tachycardia and normal ventricular repolarization were observed on ECG, and no abnormalities were observed in the echoscan of the hearth. According to the clinical and electrocardiographic findings, and to previous episode of DVT in anamnesis, a thorax CT scan was performed in order to rule out pulmonary embolism. It showed an "area of parenchymal consolidation involving almost all the left lower lobe with patent bronchial structures"; given the patient's CURB 65 score, he was then admitted to the pneumology ward where empiric treatment with levofloxacin (750 mg PO once daily) was initiated. Thoracic ultrasound was performed using a multifrequency convex transducer, and the posterior left area was examined through intercostal approach, placing the patient in a sitting position. A subpleural patchy hypoechoic lesion with irregular boundaries was detected; the maximum diameter was 11 cm, and the multiple hyperechoic spots inside it (elsewhere defined as "air bronchogram") showed no Doppler signal. Given the positive result of the Legionella urinary antigen test, antibiotic treatment was switched to Levofloxacin 1000 mg PO once daily and Claritromicin 500 mg PO twice daily. After 3 days, his clinical conditions improved dramatically. Ultrasound performed after 5 days from the diagnosis showed decreased dimensions of the lesion previously identified (maximum diameter 8.25 cm) and a marked reduction of the hyperechoic spots in it. The patient was discharged in good clinical conditions, and both thorax CT scan obtained after 1 and 4 months from the diagnosis showed radiological resolution of the parenchymal consolidation. The key to ultrasound visualization of pneumonia is its contact with the pleural surface (86-98% in cases of CAP) and the relative loss of aeration of the portion involved by the infection and a concomitant increase in the fluid content. A paradigmatic US image for parenchymal inflammatory infiltrate has not been established yet; anyway, some typical findings, when combined with the clinical features, can confirm the diagnostic hypothesis.