Incidence and predictive factors of acute diseases in patients with syncope: the ESCAPE study

According to the 2018 ESC guidelines, emergency physicians shall primarily aim to identify syncopal episodes associated with an underlying acute principal disease. Therefore, in this study, we aimed to assess the incidence of syncope associated with acute principal diseases (APDs) and to identify predictive factors reflecting the presence of these underlying conditions. We retrospectively evaluated all patients presenting with syncope during a 6-month period to the local emergency department, collecting incidence of syncopal cases associated with APDs, personal information, clinical features, and laboratory abnormalities, which were compared between syncopal patients with or without APDs. A syncope-associated APD could be diagnosed in 346/1279 patients (27.1%). In the majority of cases, the cause was a non-cardiovascular acute condition (67%), mostly non-life-threatening such as infectious diseases (34.4%) and acute diseases with pain, fluid loss or hypotension (23.7%). Severe acute cardiovascular conditions were less frequent (4.2%). Cardiogenic syncope, no previous history of syncopal episodes, not full agreement with typical clinical features of syncope, alterations of vital parameters, and laboratory abnormalities were also found to be independently associated with syncope-associated APDs. Syncope may be frequently associated with APDs of varying severity, though mostly non-clinically threatening, thus confirming that this condition shall be considered a symptom and not a disease. Emergency physicians should hence be first engaged in troubleshooting an underlying pathology when facing patients with syncope, for timely identifying patients at higher risk of short-term adverse events and reducing inappropriate admissions and diagnostic investigations, especially in the presence of hypotensive syncope elicited by non-severe concurrent conditions

Cell Senescence in Cardiac Repair and Failure

Although the lack of a robust cardiomyocyte proliferative response has been considered to be a crucial determinant of cardiac pathology and Heart Failure in adult mammalians, the emerging picture is that myocardial regeneration is a complex phenotype involving many actors, including acute cellular senescence and inflammation. However, three major and interconnected events occur in response to tissue injury: loss of protein homeostasis, accumulation of dysfunctional mitochondria and chronic inflammation. These events blunt the reparative response of the heart, are associated with the accumulation of chronically senescent cells and progressively lead to cardiac dysfunction. Therefore, it is crucial to understand which are the pivotal players of this process, in order to devise strategies aimed at reducing the occurrence of chronic cell senescence in the heart in vivo