Aloha. Welcome, everyone. It's a nice full house. I'm Brittany Duchesne. I'm one of the moderators. We're just going to give a few instructions for our speakers. Thank you so much for being here. Remember to talk about your disclosures. Each presentation is eight minutes. We'll give a one-minute warning prior to wrapping up. And then we have a two-minute question period after every talk. It would be very helpful to use the microphone in the room. I would not make a great Vanna White. And I think if everyone's ready, we can get started. I encourage everyone, including the speakers, to stay after for the whole presentation. The first speaker in our session is Dr. Sherif El-Tawansi. Do COPD patients have a higher risk for atrial fibrillation re-admission? A nationwide study. Welcome. Good morning, everyone. And my name is Dr. Sherif El-Tawansi. My study title is about COPD and AFib. They are two of the most common diseases with higher morbidity and mortality re-admission and cost in the U.S. and all over the world. So my title is, Do COPD Patients Have a Higher Risk for Atrial Fibrillation Re-Admission? Analysis from Nationwide Re-Admission Database. Thanks again for participating in this session. My name is Dr. Sherif El-Tawansi, MD. I have a Master's in Public Health and a Fellowship of FACP, Assistant Professor of Internal Medicine at Hackensack University School of Medicine, Academic Hospitalist at Jersey Shore University Medical Center in Neptune, New Jersey. I have no financial interest to disclose in this session. So the lesson objectives here, patients with chronic obstructive pulmonary disease are known to have an increased risk for atrial fibrillation, which may in turn increase the risk of hospitalization. COPD might lead to unfavorable outcome for AFib patients through the increased burden of inflammatory markers, hypoxia, use of beta agonist, and ventricular dysfunction with increased atrial afterload in COPD patients. We aim to investigate the outcome associated with patients with AFib with co-existing COPD compared to those without COPD. So our study population is the AFib patient and we are studying COPD versus non-COPD. So it's a visual cycle between COPD and atrial fibrillation. COPD patients carry an increased risk of developing AFib and not only developing, it can provoke its progress, carry a higher recurrence risk of AFib after catheter ablation according to Kochhauser 2016. COPD works negatively alongside the AFib, increasing morbidity, mortality, and healthcare costs. And this was a graph, an illustrative one from Goudis 2017. He posted that graph to show how the COPD would provoke the initiation and recurrence of AFib through hypoxia, hypercapnia, pulmonary hypertension, ventricular injury, inflammatory and exudative stress, and respiratory drugs like beta to agonist. So we conducted a retrospective court study of patients admitted with AFib between 2016 and 2020 using the Healthcare Cost and Utilization Project nationwide readmission database with variables were identified using the ICD, the International Classification of Diseases. Admissions were included if patients at least 18 years old with primary diagnosis of AFib stratified by presence or absence of COPD. So this kind of nationwide database is the readmission. So we are looking only for readmission, not for the admission only, but if someone is admitted with AFib and then readmitted later, like if there is a readmission for AFib with RVR, with flare-up, this is our study population. It's like a nationwide database. It doesn't need IRB approval. It's online to be used. And the primary outcome was 30-day readmission while secondary outcome with other criteria including length of stay, mortality, and others. We used the status 17 for statistical analysis. We used multivariate, linear, Cox, and logistic regression analysis with B value less than 0.05 was considered statistically significant. So we found 1,064,982 patients admitted with AFib between 2016 and 2020 were identified meeting the inclusion criteria all over the country. 18% of them had COPD. 52% were female, a slight increase in female. And the mean age for COPD was 73.2. And for the non-COPD group, 70.8. So the COPD was a little older and with a statistically significant B value here. We used multivariate logistic regression models adjusting for clinical variables showing higher odds for readmission for patients with COPD compared with the non-COPD with odds ratio as we see 1.35 and the P value is less than 0.001, statistically significant. There is a higher length of stay mortality in the COPD group also compared to the non-COPD group as we will see in the table 1 and 2. So all the P values were significant for the COPD group. And after managing the confounding factor, we still found that the COPD has an independent risk impact on the AFib patients. So there is a higher risk of readmission. There was one table that showed the length of stay was lower compared to patients without COPD. But it was not statistically significant. So the length of stay was not like very significant. What was more significant was the readmission risk and the mortality. There was also a group that shows no significant difference in patient mortality between two groups. So the most significant one was the readmission more than other factors. COPD adds a burden to patients with AFib and better control may help limit frequent readmission in these patients. Our clinical implications show that in patients with AFib, the concurrent presence of COPD increases increases the risk of readmission. Better management of both may lead to better outcome and decreased readmission. So these are the tables that we see here. The P values were statistically significant in all of the age, length of stay, total cost, and the elixir comorbidity more towards the COPD group. More significant was in the readmission risk itself. Okay. So we use that elixir comorbidity in our, like I just want to identify, it's more of the comorbidity index. And this is another table showing a statistically significant P value for mortality and length of stay and total cost. There were other tables I couldn't include, but there were other conflicting results. But the most important was the readmission itself. The readmission risk was higher in the COPD patients. Thank you and don't forget to evaluate this session on that. Good morning and welcome to this session. My name is Eva Yabuakwadie. I'm a second year internal medicine resident at Mester Health Baltimore. I have no financial disclosures or no conflict of interest to disclose. My interest is in the research and clinical practice of pulmonology and critical care medicine and also in health equity research. Our topic for research today was the association between alcohol use and development of chronic obstructive pulmonary disease. We used data from the NIH funded All of Us research data set. Now the purpose of the research was to find out if there was a relationship between alcohol use and development of COPD and to find out if that relationship was dependent on the amount of alcohol use. Why did we take this topic or why did we select this topic? So as we all know, COPD has been found to be the third leading cause of mortality globally. We found out that in high income countries about 70% of COPD cases have tobacco smoking implicated as a cause. Now, instead of about 80% of people who are alcohol dependent smoke tobacco. There are existing studies that have been done to look at the relationship between COPD exacerbation and alcohol use, but we found very limited studies on COPD development and alcohol use. So that's the study. Now, I already mentioned we used data from NIH funded All of Us data set, which is a publicly available data. For our variable, so COPD was basically gotten from ICD classification of COPD in the data set that's J44. For alcohol use we defined it as ever users versus never users where never use was taken anything less than a taste or a sip of alcohol. We used audit C to classify alcohol users into normal alcohol use versus hazardous drinking. Where in audit C having a total point of less than three women and less than four in men was defined as normal alcohol use. Whilst having a total score of greater than four or more than four in men and three or more than three women was defined as hazardous drinking or alcohol dependent. For cigarette smoking we classified this as never users, former users and current users. Where never assistants have never used cigarette, former people who quit in the last five years and current is those who are currently smoking. So we excluded everybody who had COPD at the time of the initial survey. So in other words we excluded all those who had COPD at baseline and our statistical analysis was mainly done in our using cost regression analysis. So this is just a summary of baseline characteristics of our participant. So we had a total of about a little over 200,000 participants with less than 10% being never users for alcohol. Our average age was 51.1 for never users versus 55.4 for ever users. Our study was predominantly female and predominantly white. Now among the smoking status we noticed that about 78.2% of our alcohol users never smoked tobacco or cigarette. We also found that about 57.2% of our alcohol ever users never smoked cigarette. With regards to current smoking, 9.7% of our never users were current cigarette smokers and 19% of our alcohol ever users smoked cigarette. With regards to COPD we noticed that 2.1% of our steady population of alcohol ever users had the diagnosis of COPD during the time of the survey. In other words they developed COPD at some point during the survey. Whilst 1.9% of our alcohol never users developed COPD at some point in the survey. Alright, so using the cost analysis we noticed that alcohol users associated with the hazard ratio of 0.87, that's about 13% reduction in development of COPD. Our results were almost statistically significant. I just put this here just to reiterate that we know that cigarette smoking is associated with development of alcohol, development of COPD and that was also seen in the study. We adjusted for race, education, income and smoking status. Now further classifying alcohol use into hazardous drinking versus normal alcohol use, we noticed that interestingly hazardous drinking was associated with about 10% reduction in the development of COPD in the steady population. This was also adjusted for race, education, income and smoking status. I put this first plot here just to illustrate our unadjusted versus adjusted indicators or hazard ratios in our three groups. Unadjusted alcohol ever use was associated with development of COPD but after adjusting for the socioeconomic factors and for tobacco we noticed that alcohol use may be protected. Now what's the conclusion of the study? So previous literature has actually shown that alcohol use has a J-shaped correlation with COPD exacerbation where moderate alcohol use has been protective and hazardous or the extreme ends have been harmful. Our initial analysis is consistent with that existing data. Alcohol use or alcohol consumption is protective in some inflammatory states and COPD may be one of those states. Now moving forward we are doing further analysis to see if this association is found between all the types of alcohol like beer, wine, different categories of alcohol. We have a couple of acknowledgements so we want to acknowledge the contribution of all participants of who volunteered their data and all of us research data set and for my internal medicine residency programs. Thank you. Thank you and good morning. I bring you greetings from the University of Tennessee Graduate School of Medicine in Knoxville, Tennessee and I want to tell you the conflicts of interest. The study was funded by Mylan and Theravans but they provided nebulizers and medications for the study but they had no role in the conduct of the study data analysis or and I have received honoraria from Teva and up-to-date and research support from Mylan, Theravans and Byatris. So the goal committee recognizes and recommends that in stable patients with COPD we use long-acting bronchodilators because they have several advantages over the use of short-acting agents. They also recommend that we use a combination of long-acting beta agonist or a LABA with a long-acting muscarinic antagonist or a LAMA because the combination therapy provides greater bronchodilation than each component alone. However for acute exacerbations of COPD which affects about a million patients annually admitted in the United States we still use short-acting inhaled beta agonists and although the goal committee says although there is no high-quality evidence from RCTs to support their use they go on to note that there are no clinical studies of inhaled long-acting agents in this setting. So we planned a prospective randomized parallel group study to assess the feasibility, safety and efficacy of a LABA-LAMA combination among patients hospitalized for exacerbations of COPD and compared that with the standard of care therapy with albuterol and aprotropium and our goal was to see if the peaks and troughs as shown in the figure, the peaks and troughs associated with the use of short-acting bronchodilators could be smoothed over by the use of longer-acting bronchodilators that would provide more sustained bronchodilation, increase the trough FEV1 and also reduce hyperinflation. So we've for this study we enrolled 60 patients, 30 patients in each group. We followed the tenets of good clinical practice and patients were equal to the age or more than 40 years in age regardless of sex or race and we enrolled patients within 36 hours of their admission to the UT Medical Center in Knoxville with a primary diagnosis of exacerbation of COPD or acute respiratory failure with a secondary diagnosis of ECOPD and all these patients tested negative for COVID-19. We excluded patients who were intubated or mechanically ventilated or who were rapidly decompensating. We excluded patients with unstable cardiovascular disease, decompensated congestive heart failure, low bar pneumonia, other pulmonary diseases, lung cancer on treatment and a variety of other comorbidities. So we did a one is to one randomization to either nebulized albuterol 2.5 milligram in combination with aprotropium 0.5 milligram Q6 hours or nebulized formodrol 20 microgram Q12 hours and revifenesin 175 microgram Q24 hours. So the pharmacist assigned the treatment according to a predetermined true random number generator schedule with stratification for age groups and we did not blind the clinical investigators to the assigned treatment. So the primary outcome measure was the modified Borg-Disney scale which is a numerical scale going from one which is very slight, Disney up to 10 which is maximal and we had a number of predetermined secondary outcomes which I will talk more about in the result section. So we analyzed data using the standard statistical techniques using SPSS version 29 and statistical significance at two-sided alpha value of 0.05. So coming to the results we see that the groups did not differ in their demographics and comorbidities as shown in that third column. The patient's average age was about 63 years. They were mostly majority were males and they were mostly current smokers. They had high level of comorbidities and the mean length of stay in the hospital was a little over four days. So the modified Borg-Disney scores did not differ between the two groups on days one and day three. As we see on the left of the figure we found that patients in the long-acting group had higher Disney scores at baseline and there was a significant decrease in the score by day three. On the other hand we did see a decline in patients in the short-acting group but this was not statistically significant and the significance of this observation I think needs to be evaluated in future studies. There was no difference in the supplemental oxygen requirement and we studied the total doses of study drugs administered. You can see that on day one and day three we required significantly lower doses in the long-acting group that was 1.4 doses per patient versus 1.83 doses per patient on day one and 3.21 doses versus 5.13 doses on day three. The difference on day seven was not significant. Overall the total doses were reduced by about 30% in the long-acting group. However patients in the long-acting group required more rescue visits for therapy that is 29 versus 8 and those were mainly because of the two patients who required five and six additional doses on day one and day three. There were no differences in the other outcomes the need for supplemental oxygen, biochemical or hematological parameters, chest x-ray, electrocardiographic changes, antibiotic use, other respiratory medicines as prescribed by the treating physicians and there were no serious adverse events. So the limitations of the study is that it delay in enrollment to allow COVID-19 testing. As you know there are limitations to doing PFTs in these patients. We did not blind our investigators. There were no previous studies to allow calculation of sample size to adequately power our study and we did not study the cost effectiveness of the Lama-Lava combination. So in summary we find that fewer doses of a combination of nebulized formotrol and revifenesin achieve comparable efficacy and safety with the standard albuterol and polypertropin combination and we conclude by saying that long-acting bronchodilators provide more convenient dosing with similar efficacy and safety than short-acting bronchodilators in non-ventilated hospitalized patients with ECOPD. I would like to acknowledge some of my fellow investigators and the sponsors of this study. Thank you very much, and I hope you get to enjoy the surf and stand in beautiful Hawaii. Thank you very much. Good morning, I'm Libby Rosenthal. I'm a pulmonary critical care fellow at Dell Austin Medical Center in Texas. I have no disclosures. So today I wanna talk to you about how we might be able to change spirometry in patients with advanced COPD using respiratory muscle training. So we're gonna explore the concept of COPD as a neuromuscular disease. We'll talk about some physiology for why that is probably the case, and then we'll talk about a potential high-value intervention. This was a study that was a collaboration between the University of Texas, Ascension-Seton Medical Center, and Texas State. First, some background. We know from prior data that respiratory muscle training can improve quality of life, symptoms, PI max and PE max in patients with COPD, but there's limited data showing actual changes in FEV1, FVC, and there's also limited data stratifying by severity of disease. COPD patients have at least a component of neuromuscular disease. They have atrophy of the diaphragm, they're at a mechanical disadvantage, and these ideas have not been targeted as potential therapies for these patients. The diaphragm in a patient of a COPD is very different than the diaphragm in a patient that doesn't have COPD. When you look, there's a 30% reduction in myosin heavy chain content. There's a 30 to 40% reduction in muscle cross-sectional area, and for even a single muscle fiber, there's reduced contractile force. The diaphragm is also at a distinct mechanical disadvantage. Because of air trapping, the shape of the diaphragm changes from a nice dome shape on the right to a flattened shape on the left, and this has major implications for the work of breathing and respiratory muscle fatigue in patients with COPD. So through the law of Laplace, we know that the tension generated by the diaphragm is a function of the radius, and so a patient who's unable to generate the negative intrathoracic pressure required to get a deep breath in is gonna have a problem producing an FEV1, and you can't even see the radius on that slide. It's totally off the page. So this leads to a reduced ability to generate flow and pressure, increased work of breathing, and overall diaphragmatic fatigue in these patients. So our methods were, we had a cohort of patients, we collected some data on them, we put them through eight weeks of respiratory muscle training, and then we collected data on them afterwards. The data we collected was biometric data, height, weight, we collected simple spirometry, no lung volumes, PI max, PE max, and then we had them do three surveys of quality of life and symptoms. The protocol we used was an eight-week protocol. We used Teach Back to make sure they were able to do the actual, use the device. Three sets, 10 breaths, twice a day. It was a spring-loaded device, and we had them increase the resistance of the device if it felt easy. This is not the device we used, but this is like the device we used. It is important to note that this device is a pressure resistor, not a flow resistor device, so the patient has to generate a certain amount of inspiratory or expiratory pressure to actually move the needle here, as opposed to a flow device, where you have to generate a certain amount of flow. What we found, we had 27 patients enrolled, which is a pretty small study, and kind of consistent with the rest of the literature in this realm. Most of the studies that we were able to find on respiratory muscle training in COPD patients were very low numbers as well. Nobody dropped out, and all 27 patients completed the study requirements. We were split about 50-50, male-female. The baseline FEV1 of our patients, nobody had a good FEV1, so this is before the new COPD classification, so we're still in the one, two, three, based on baseline FEV1. Seven patients were under 30% predicted, 12 patients were 30-50% predicted, and eight patients were in the 50-80% predicted, so this corresponds to gold stage one, two, three, and four. We found significant improvement in maximum inspiratory pressure, maximum expiratory pressure, and the surveys on quality of life and symptoms. Interestingly, though this did not reach statistical significance, five out of the seven patients in the previously gold stage four disease showed an improvement in their FEV1 by 14 to 29% from their baseline. This corresponded to about an average of 94 cc's of improvement, which is right below that kind of MCID for changes in spirometry to affect patient satisfaction. So the discussion on this is really, you know, it's a non-significant finding, but could it be still a signal that we wanna continue to pursue? We think there's a physiologic basis that this probably is signal and not just noise based on the fact that improving your respiratory strength increases your inspiratory volume, which is gonna increase elastic recoil and give you a better FEV1, better FEC, and it may even affect your expiratory reserve volume and decrease residual volume and therefore augment the horrible diaphragmatic mechanics that these patients are facing. So the next thing we wanna do is undergo a larger study with more patients in these COPD 3-4 groups. We wanna look at full lung volumes with residual volume to see if we're affecting that. And then we'd like to, you know, extend the study treatment period from eight weeks to 12 weeks. And we'd also like to stratify based on whether they are chronic bronchitis phenotype or emphysema. Knowing that this might be mediated through elastic recoil, we're very interested to know if maybe the chronic bronchitis folks do a little bit better, understanding that they may have more baseline elastic recoil than someone with, say, an emphysematous sub-phenotype. I'm very interested in this because I think it might represent an opportunity for high-value care if these patients maybe can't make it to pulmonary rehab. Potentially, they could get some benefit. Potentially, this device might be able to get approved by insurance. Currently, it's not. So we hope that this could represent a high-value care for patients with a really high burden of disease. I want to thank my mentors, Dr. Shapiro, my entire faculty, and Sharon is here from Texas State who collaborated with us. So this was a team effort. Thank you. Okay, next we have Dr. Mayers, short-acting beta-agonist antibiotics, oral corticosteroid, and risk of mortality in cardiopulmonary events in patients with COPD. Great. Thank you very much. I'm happy to be able to present this data on behalf of my colleagues who are at University of Alberta in Canada, AstraZeneca Canada, and MedliOrg. So this study was funded by AstraZeneca Canada, and several of the team members do have some potential conflicts of interest. The rationale for this really is there's limited real-world evidence looking at what rescue medication in COPD may impact mortality as well as cardiopulmonary outcomes. We want to identify the associations between SAB, a short-acting beta-agonist, courses of antibiotics, courses of oral corticosteroids, OCS, and look at risk of mortality and cardiopulmonary outcomes among a cohort of patients with COPD who reside in Alberta, Canada. The data source is an administrative, a set of administrative health databases. The population we looked at were adults greater than 35 years of age with COPD residing in Alberta, and the timeframe was from 2011 to 2020. We looked at one-year history of SABA canister use, antibiotic dispensations, and OCS burst days, and the outcomes, as mentioned, were mortality, so all-cause mortality as well as COPD-specific mortality, and we also looked at major adverse cardiac events, including cardiovascular death, both overall as well as specifically post-COPD exacerbation. This is really how the study was designed, that there was a case ascertainment window between April 1, 2011 to March 31, 2019 with a one-year look-back period. The cohort size was roughly 190,000 adults with COPD, and we had an incident rate between about 11,000 to 12,000 patients per year. The mean follow-up or median follow-up was around five years, roughly equally distributed male to female, and the age of COPD patients in just about every study, not unusually near 70 years of age. These are results, so all-cause mortality, and you can see that, sorry, that's very sensitive. You can see comparing zero dispensations of SABA to two to five dispensations to greater than six, there's a dose-response curve in terms of all-cause mortality. Similarly, when you look at antibiotic dispensations, there seems to be a dose-response curve between zero, one to two, greater than six, so increasing all-cause mortality with increasing dispensations of both SABA and antibiotics, and OCS birthday follow a similar pattern. If you look at just COPD-related mortality, the same patterns persist. With increasing SABA dispensations, there's a greater COPD-related mortality. As antibiotic dispensations increase, greater COPD mortality, and again, OCS birthday, same thing. For major adverse cardiac events, the events aren't quite as clearly related, but CV deaths are. So again, as the dispensation of SABA increases up to six plus, you see an increasing CV mortality. If you look just at post-exacerbation data, then you see a relationship between canister dispensations and the major adverse cardiac events, both that as well as CV deaths. So there's a known relationship between COPD exacerbations and cardiac events, and there's this interrelationship, increasing SABA dispensations in the preceding year, increased CV death, increased major adverse cardiac events. So this study gives us a look using real-world data at what our patients are actually taking, both for relief, the SABAs, as well as for any intercurrent deterioration. The higher the SABA, the higher the antibiotic dispensations, more OCS births, greater mortality. Higher dispensation of SABA was also associated with a greater risk of post-exacerbation cardiac events. This study suggests that we can use these patterns of drug dispensations to find high-risk patients and try and intervene before these bad events occur. So I'd like to thank everyone for listening and happy to take any questions. Aloha, everyone. So this study was a retrospective data analysis study comparing the impact of biologics versus standard therapy in patients with moderate and severe persistent asthma post-hospital admission. I am Sushant Gupta. I'm one of the residents in Department of Internal Medicine at Carl Foundation Hospital in Champaign, Illinois, and I don't have anything to disclose. Briefly talking about the basis of this study. So we understand that the therapeutic approach to asthma has undergone a paradigm change after the introduction of biologics. They have reduced healthcare utilization, incidence of asthma exacerbation, and improved the overall quality of life. But the robust real-world data that looks at the impact of biologics post-hospital admission after an asthma exacerbation is still missing. So our purpose of our study, the primary objective was to determine the impact of biologics on hospitalization outcomes. Post-asthma exacerbation. And a secondary objective was to see if there are any racial or gender disparities in our population. So this was a retrospective data analysis where we used Slicer Dicer, which is a self-service cohort exploration tool that's embedded in Epic. This study lasted for over five years, from February 15, 2018 to February 15, 2023, and the site was a Midwest tertiary care teaching hospital. Our population, we included patients with moderate and severe persistent asthma. Amongst this population, we divided the population into two groups, those on biologics and those not on biologics. And we looked at the incidence of asthma exacerbation, including the incidence of severe exacerbation needing hospital admission, intensive care unit admission, invasive ventilation, overall length of stay post-exacerbation. The secondary outcome here was the demographic distribution in biologic popular prescription to see if there are any racial or gender disparities. Statistical analysis, we divided our population into clusters which were expressed in absolute values to see for the strength of association, we did do chi-square test. Let's go and talk about the results. So if you, these were our population, so in biologics, we had 316 patients, and not on biologics, we had 9,645 patients. Amongst the age group, most population was between 27 to 82 in both the groups. Males were 30% in the biologic group, which was similar in non-biologic group as well. In terms of ethnicity, Caucasian were predominant population in both the groups. Since this was the time when COVID had also struck, so we wanted to see if COVID infection would affect our outcomes, and we found that the incidence of breakthrough COVID cases in both the groups were very similar. We'd also looked at the vaccination, if we felt that that could impact our outcomes, and those were also pretty similar in both the groups. Smoking, we had higher proportion of patients in non-biologic groups who were actively still smoking. So as we talked about, we had total of 9,960 patients with higher population in 54 to 82 year growth in females, Caucasians, and non-smokers. So this was when we looked at the gender and racial disparities. There was slightly higher proportion of male patients in the non-biologic group, which was sort of touching the statistical significance mark, but the confidence interval was very, very, almost touching each other, so I'd be, but in terms of the race, there was no racial disparities in both biologics and non-biologic groups. So these were our outcomes. So hospital admissions, we had 0.9% of patients who needed hospital admissions for asthma exacerbation as compared to 6.5, which was very statistically significant. Also, the incidence of ICU admissions was also significantly lower in patients on biologics. In terms of ICU length of stay, we only had, sorry, mechanical ventilation. We did not have any patient in the biologic group over the past five years who needed any intubation or mechanical ventilation for asthma exacerbation. Interestingly, for ICU length of stay, we only had one patient who got admitted to the ICU and was discharged in a day, so we didn't really calculate significance in both the groups for ICU length of stay, and for hospital length of stay, we, again, had only three patients who were admitted, so we didn't really compare the significance amongst the length of stays in both the groups. So now, briefly going over the discussion, in terms of the biologics, we did not, we used all the five biologics, including tezepulimab, to compare, to see in a biologic group. Let's, and looking at the other published data, so briefly summarizing our own, so this was a retrospective comparative data analysis on patients with moderate and severe persistent asthma, and we found that biologics had significantly lesser proportion of patients needing hospital and ICU admission, no incidence of mechanical ventilation, and no racial disparities. Now, this is as compared to the other published data, one published by Trevor et al. in Annals of Allergy, Asthma and Immunology. We found that, very similar to ours, they had significantly lower proportion of patients who needed an ED visit, lower proportion of patients with asthma needing hospitalization, ICU admission, and they did have some patients who needed mechanical ventilation, unlike our study. They did find, in their study, that there was some racial disparities with Caucasian being more likely to get a prescription for biologics for asthma, which was unlike our, where we did not find any racial disparities. This was another study from Britain. This was a retrospective two-year data analysis from the southwest of Britain, and again, they had very similar results to us. They had significantly lower proportion of patients who needed fewer ED admissions, and also the relative risk for fewer hospital discharges after biologic initiation, which suggests that they had fewer hospital admissions as well. They, however, did not comment on racial disparities. This was another study that was, again, very similar to us, real-life omalizumab data, and they had found that, from 2009 to 2019, after two years, the hospitalization rate with use of biologics had reduced by 75%, which kind of is on the same line as what our study also entails. But our study has certain limitations, as one would expect. It's a retrospective data analysis design. There are confounders. We, Concomitant Administration of Systemic Steroids, we don't have an idea on that. We don't know about the compliance with inhalers, so that's another confounder. Also, we had a limited representation of races other than Caucasians, so it's really difficult to extrapolate this data to other races as well, and we did not conduct a safety analysis. But then again, there are future road ahead. One is to see, they are with multiple biologic options, to see the eligibility of biologics in clinical practice, and to see if one switches to other biologics, does it affect the overall outcomes? Investigation into the clinical trajectory. We do need more real-world data in terms of switching or discontinuation of biologics. Implications, conclusions, yes, biologics does improve post-hospital outcomes of hospital admissions post-asthma exacerbation. We did not have any racial disparities, which suggests that possibly to keep a lower threshold in initiating early biologic therapy in patients with asthma, moderate to persistent asthma, can possibly reduce morbidity and mortality in this population group. Thank you.

COPD

Chronic Obstructive Pulmonary Disease

atrial fibrillation re-admission

alcohol use

respiratory muscle training

biologics

short-acting beta agonists

cardiopulmonary events

COPD

Chronic Obstructive Pulmonary Disease