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Intravenous thrombolysis (IVT) is the treatment of choice for most patients with acute ischemic stroke. According to the recently updated guidelines, IVT should be administered in absence of absolute exclusion criteria. We aimed to assess the proportion of ischemic strokes potentially eligible and actually treated with IVT, and to explore the reasons for not administering IVT. We prospectively collected and analyzed data from 1184 consecutive ischemic stroke patients admitted to the 22 Stroke Units (SUs) of the Veneto region from September 18th to December 10th 2017. Patients were treated with IVT according to the current Italian guidelines. For untreated patients, the reasons for not administering IVT were reported by each center in a predefined model including absolute and/or relative exclusion criteria and other possible reasons. Out of 841 (71%) patients who presented within 4.5 h of stroke onset, 704 (59%) had no other absolute exclusion criteria and were therefore potentially eligible for IVT according to the current guidelines. However, only 323 (27%) patients were eventually treated with IVT. Among 861 (73%) untreated patients, 480 had at least one absolute exclusion criterion, 283 only relative exclusion criteria, 56 only other reasons, and 42 a combination of relative exclusion criteria and other reasons. Our study showed that only 46% (323/704) of the potentially eligible patients were actually treated with IVT in the SUs of the Veneto region. All healthcare professionals involved in the acute stroke pathway should make an effort to bridge this gap between eligibility and reality.

Syncoilin may have a role in linking the desmin-associated intermediate filament network of the muscle fiber with the dystrophin-associated protein complex (DAPC). We have evaluated syncoilin in a range of neuromuscular disorders including Duchenne and Becker muscular dystrophy, central core disease, congenital muscular dystrophies, and neurogenic disorders. Our results show that syncoilin immunolabeling is not only altered in muscle fibers with alterations in the DAPC but also in response to a variety of genetic defects, including those associated with proteins of the extracellular matrix and the intracellular Ca2+-release channel (ryanodine receptor). The pattern of syncoilin immunolabeling in these diseases appeared to reflect a rearrangement of the intermediate filament-associated cytoskeleton that characterizes both muscle fiber development and conditions in which the cytoskeletal organization of the muscle fiber is significantly affected. These observations raise the possibility that mutations in the gene encoding for syncoilin may underlie some forms of muscle disease.