Organizational Learning in Healthcare Contexts after COVID-19: A Study of 10 Intensive Care Units in Central and Northern Italy through Framework Analysis.

The rapid spread of the SARS-CoV-2 virus has forced healthcare organizations to change their organization, introducing new ways of working, relating, communicating, and managing to cope with the growing number of hospitalized patients. Starting from the analysis of the narratives of healthcare workers who served in the intensive care units of 10 hospitals in Central and Northern Italy, this contribution intends to highlight elements present during the pandemic period within the investigated structures, which are considered factors that can influence the birth of organizational learning. Specifically, the data collected through interviews and focus groups were analyzed using the framework analysis method of Ritchie and Spencer. The conducted study made it possible to identify and highlight factors related to aspects of communication, relationships, context, and organization that positively influenced the management of the health emergency, favoring the improvement of the structure. It is believed that the identification of these factors by healthcare organizations can represent a valuable opportunity to rethink themselves, thus becoming a source of learning.

Partial inhibition of platelet thromboxane A2 synthesis by aspirin is associated with myonecrosis in patients with ST-segment elevation myocardial infarction.

Heterogeneity in response to aspirin (ASA) treatment, or "aspirin resistance," could be of importance in patients with ST-segment elevation myocardial infarction (STEMI). Decreased effects of ASA in platelets could be due to partial inhibition of cyclo-oxygenase-1 (COX-1) or to COX-1-independent mechanisms. We evaluated the effect of ASA treatment in patients with STEMI for (1) platelet thromboxane A(2) (TXA(2)) synthesis, (2) platelet recruitment elicited by TXA(2)-dependent and -independent mechanisms, and (3) a possible association of these aspects of platelet reactivity with serum markers of myonecrosis. We studied 62 ASA-treated patients within 48 hours of onset of the acute event and 69 ASA-free and 10 ASA-treated controls. TXA(2) synthesis and platelet recruitment (fluid-phase proaggregate activity of cell-free releasate) were assessed after collagen stimulation (1 micro g/ml) of whole blood. Partial inhibition of TXA(2) by ASA was found in 21 patients (34%). This was associated with significant increases in troponin T, creatine kinase-MB mass, creatine kinase, and recruiting activity versus 41 patients with blocked TXA(2) production. This was independent of fibrinolysis, and platelet COX-2 expression was not augmented. TXA(2) blockade was achieved after subsequent daily treatments or platelet incubation with ASA in vitro, suggesting lower sensitivity of COX-1 to ASA. In addition, 28 patients (45%) had an abnormally increased recruiting activity despite TXA(2) blockade, which was also associated with increased myonecrosis. In conclusion, ASA resistance, elicited by TXA(2)-dependent and TXA(2)-independent mechanisms, was prevalent in patients with STEMI. This study describes, for the first time, the association of partial platelet TXA(2) inhibition with myonecrosis.