Objective: The chances of surviving an out-of-hospital cardiac arrest depend on early and high-quality cardiopulmonary resuscitation (CPR). Our aim is to verify whether the use of feedback devices during laypersons’ CPR training improves chest compression quality. Methods: Laypersons totalling 450 participating in Basic Life Support and Automated External Defibrillation (BLS/AED) courses were randomly divided into three groups: group No Feedback (NF) attended a course without any feedback, group Short Feedback (SF) a course with 1-minute training with real-time visual feedback, and group Long Feedback (LF) a course with 10-minute training with real-time visual feedback. At the end of each course, we recorded 1 minute of compression-only CPR. The primary end point was the difference in the percentage of compressions performed with correct depth. Results: There was a significant improvement in the percentage of compressions with correct depth in the groups receiving feedback compared to the other (NF v. LF, p=0.022; NF v. SF, p=0.005). This improvement was also present in the percentage of compressions with a complete chest recoil (71.7% in NF, 86.6% in SF, and 88.8% in LF; p<0.001), compressions with the correct hand position (93.2% in NF, 98.2% in SF, and 99.3% in LF; p<0.001), and in the Total CPR Score (79.4% in NF, 90.2% in SF, and 92.5% in LF; p<0.001). There were no significant differences for all of the parameters between group SF and group LF. Conclusions: Real-time visual feedback improves laypersons’ CPR quality, and we suggest its use in every BLS/AED course for laypersons because it can help achieve the goals emphasized by the International Liaison Committee on Resuscitation recommendations.

It is well established that direct oral anticoagulants (DOACs) are the cornerstone of anticoagulant strategy in atrial fibrillation (AF) and venous thromboembolism (VTE) and should be preferred over vitamin K antagonists (VKAs) since they are superior or non-inferior to VKAs in reducing thromboembolic risk and are associated with a lower risk of intracranial hemorrhage (IH). In addition, many factors, such as fewer pharmacokinetic interactions and less need for monitoring, contribute to the favor of this therapeutic strategy. Although DOACs represent a more suitable option, several issues should be considered in clinical practice, including drug–drug interactions (DDIs), switching to other antithrombotic therapies, preprocedural and postprocedural periods, and the use in patients with chronic renal and liver failure and in those with cancer. Furthermore, adherence to DOACs appears to remain suboptimal. This narrative review aims to provide a practical guide for DOAC prescription and address challenging scenarios.

TRIM5α is a natural resistance factor that binds retroviral capsid proteins and restricts virus replication. The B30.2/SPRY domain of TRIM5α is polymorphic in rhesus macaques, and some alleles are associated with reduced simian immunodeficiency virus (SIV) SIV _mac251 and SIV _smE543 replication in vivo . We determined the distribution of TRIM5α alleles by PCR and sequence analysis of the B30.2/SPRY domain in a cohort of 82 macaques. Thirty-nine of these macaques were mock vaccinated, 43 were vaccinated with either DNA-SIV/ALVAC-SIV/gp120, ALVAC-SIV/gp120, or gp120 alone, and all were exposed intrarectally to SIV _mac251 at one of three doses. We assessed whether the TRIM5α genotype of the macaques affected the replication of challenge virus by studying the number of SIV variants transmitted, the number of exposures required, the SIV _mac251 viral level in plasma and tissue, and the CD4 ⁺ T-cell counts. Our results demonstrated that TRIM5α alleles, previously identified as restrictive for SIV _mac251 replication in vivo following intravenous exposure, did not affect SIV _mac251 replication following mucosal exposure, regardless of prior vaccination, challenge dose, or the presence of the protective major histocompatibility complex alleles (MamuA01 ⁺ , MamuB08 ⁺ , or MamuB017 ⁺ ). The TRIM5α genotype had no apparent effect on the number of transmitted variants or the number of challenge exposures necessary to infect the animals. DNA sequencing of the SIV _mac251 Gag gene of the two stocks used in our study revealed SIV _mac239 -like sequences that are predicted to be resistant to TRIM5α restriction. Thus, the TRIM5α genotype does not confound results of mucosal infection of rhesus macaques with SIV _mac251 .

Background: Acute kidney injury (AKI) has been associated with increased mortality in ST ‐segment elevation myocardial infarction. We compared the mortality predictive accuracy of the 3 AKI definitions used most widely for patients with ST ‐segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Methods and Results: We included 3771 patients with ST ‐segment elevation myocardial infarction treated with primary percutaneous coronary intervention at 2 Italian hospitals. AKI incidence was evaluated according to creatinine increases of ≥25% ( AKI ‐25), ≥0.3 mg/dL ( AKI ‐0.3), and ≥0.5 mg/dL ( AKI ‐0.5). The primary end point was in‐hospital mortality. Overall, 557 (15%), 522 (14%), and 270 (7%) patients developed AKI ‐25, AKI ‐0.3, and AKI ‐0.5, respectively ( P <0.01). All AKI definitions independently predicted in‐hospital mortality (adjusted odds ratio 4.9 [95% CI 3.1–7.8], 5.4 [95% CI 3.3–8.6], and 8.3 [95% CI 5.1–13.3], respectively; P <0.01 for all). At receiver operating characteristic analysis, the addition of each AKI definition to combined clinical predictors of mortality (age, sex, left ventricular ejection fraction, admission creatinine, creatine kinase‐ MB peak) found at stepwise analysis significantly improved mortality prognostication (area under the curve increased from 0.89 for clinical predictor combination alone to 0.92 for AKI ‐25, 0.92 for AKI ‐0.3, and 0.93 for AKI ‐0.5; P <0.01 for all). At reclassification analysis, AKI ‐0.5 added to clinical predictors, provided the highest score in mortality (net reclassification improvement +10% versus AKI ‐0.3 [ P =0.01] and +8% versus AKI ‐25 [ P =0.05]). Conclusions: Each AKI definition significantly improved the mortality prediction beyond major clinical variables. AKI ‐0.5 showed a mortality discrimination advantage, suggesting it should be the preferred definition in studies addressing ST ‐segment elevation myocardial infarction and focusing on short‐term mortality.