The Disparity Between Public Utilization and Surgeon Awareness of the STS Patient Education Website.

BACKGROUND: Many online resources currently provide healthcare information to the public. In 2015, the Society of Thoracic Surgeons (STS) created a multimedia web portal (ctsurgerypatients.org) to educate the public regarding cardiothoracic surgery and provide an informative tool to which cardiothoracic surgeons could refer patients. METHODS: A patient education task force was created, and disease-specific content was created for 25 pathological conditions. After launching the website online, a marketing campaign was initiated to make STS members aware of its availability. Website visits were monitored, and an online survey for public users was created. An email survey was sent to STS members to evaluate awareness and content. Surveys were analyzed for effectiveness and utilization by both public users and STS member surgeons. RESULTS: From 2016 to 2018, the website had more than 1 million visits, with visits increasing yearly. Surveyed user ratings of the website were positive regarding quality and utility of the information provided. STS member response was poor (379 responses of 6347 emails), and 78.3% of responders were unaware of the website. Surgeon responders were positive about the content, though many still refrain from referring patients. CONCLUSIONS: Online education for cardiothoracic surgery is seeing increased public use, with high ratings for content and utility. Despite aggressive marketing to STS members, most remain unaware of this website's existence. Those who are aware approve of its content, but adoption of referring patients to it has been slow. Improved strategies are necessary to make surgeons aware of this STS-provided service and increase patient referrals to it.

Carbon monoxide donors or heme oxygenase-1 (HO-1) overexpression blocks interleukin-18-mediated NF-kappaB-PTEN-dependent human cardiac endothelial cell death.

The objective of this study was to determine whether heme oxygenase-1 (HO-1) or heme metabolites exert cytoprotective effects on interleukin-18-mediated endothelial cell (EC) death. Treatment with interleukin (IL)-18 increased NF-kappaB activation and PTEN induction, suppressed Akt activation, and stimulated EC death. While ectopic expression of p65 enhanced PTEN transcription, adenoviral transduction of dnIkappaB-alpha, dnp65, or dnIKKbeta was inhibitory. Furthermore, IL-18 suppressed HO-1 mRNA expression via enhanced mRNA degradation. Overexpression of HO-1, treatment with HO-1 inducer hemin, or the CO donor cobalt (III) protoporphyrin IX all reversed IL-18-mediated NF-kappaB activation, PTEN induction, Akt suppression, and EC death. Furthermore, hemin induced HO-1 expression, and HO-1 knockdown, HO-1 inhibition, or CO scavengers all reversed the prosurvival effects of hemin. In addition, the CO donors CORM-1 and CORM-3 and the heme metabolites biliverdin and bilirubin attenuated IL-18-induced EC death via a similar signaling pathway. IL-18 induced p38alpha MAPK activation, and suppressed p38beta isoform expression. While p38alpha knockdown attenuated, p38beta knockdown potentiated IL-18-mediated EC death. Hemin and HO-1 reversed IL-18-mediated p38alpha induction and restored p38beta levels. These results demonstrate that IL-18 suppresses HO-1 expression and induces EC death. HO-1 overexpression, HO-1 induction, or treatment with heme metabolites all reverse IL-18-mediated p38alpha MAPK and NF-kappaB activation, PTEN induction, Akt suppression, and EC death. Thus, HO-1 inducers and CO donors may have the therapeutic potential to effectively block IL-18 signaling and reduce IL-18-dependent vascular injury and inflammation.