 vaccinations has evolved over the years. We have successfully made HIV part of the primary care visit, but many patients are still hesitant to undergo testing due to the stigma associated with the disease. Similarly, fears persist about the COVID-19 vaccine – primarily because some patients unfortunately still don’t trust our science-based institutions. 

Yet for most people, solid trust in their primary care doctor has not wavered. For that reason, clinicians have a great opportunity to increase COVID-19 vaccinations and testing for HIV. It begins with a candid conversation; but starting that dialogue can be difficult. From our experience, here are a few key approaches that can help open the door.

Being open and honest with patients must always be our top priority. Many patients doubt the safety of the COVID vaccines when seeing friends and family members fall sick after vaccination. As clinicians, we have to remind patients that vaccines were never meant to prevent infections 100% of the time. Instead, their greatest use is preventing 

 infections, hospitalizations, even deaths. But in the messaging to patients, we may have oversold the capability of vaccines. 

Similarly, the stigma and misinformation surrounding HIV has led many to question why vaccines have been quickly developed for emergent infections such as COVID-19 and Monkeypox, yet we still don’t have a vaccine for HIV. This has spurred even more distrust and fueled skepticism about the origins of HIV.

When we as clinicians provide explanation, we help debunk these dangerous myths and misunderstandings. Honesty builds trust, and every subsequent conversation becomes a little easier.

Your patients see you as a highly reliable source of information. They will look to you for direction and trust your guidance. But if they have questions, they’ll be able to quickly tell if you aren’t sure of the answers. We always have to do our best to stay up to date on new research, guidelines, and recommendations. But obviously, we won’t always have all of the answers.

One way to build trust is to actually look up the information with your patient right there in the exam room. So when starting a conversation about HIV testing, you can actually show the patient the latest recommendations of the U.S. Preventive Services Task Force for testing based on patient demographics. You can show them which specific guidelines are recommended for them. And when you want to discuss COVID vaccines, show them the CDC.gov website, walk them through the recommendations, and guide them toward the answers.

When it comes to HIV and COVID-19 discussions, it’s crucial that patients don’t feel targeted. Questions should never feel accusatory or taboo, and the best way to avoid this is to make testing and screening questions part of your routine in every primary care visit. Patients will then come to expect this discussion, and even if they aren’t willing to undergo testing or screening, it won’t cause any ill feelings between you and the patient.

The CDC recommends that we keep our feet on the gas pedal, continually having conversations with patients about the dangers of COVID-19. This should also be the approach with HIV testing. We hope that we can reach a point when COVID vaccines and HIV testing become routine topics just like screenings for breast cancer, diabetes, and other diseases. 

There are efforts to help inform clinicians about navigating conversations with patients on these topics. For instance, the "Two in One: HIV + COVID Screening and Testing Model" from George Washington University has launched a training series for all clinicians to routinize HIV screening and COVID-19 vaccine screening for all of their patients. The next free webinar in the training series will take place in May. More information can be found on the 

We must help our patients by sharpening our skills in using the simple but powerful tools of patience, transparency, and honesty based on evidence.

Annette Gadegbeku, MD, is Associate Dean of Community Health at Drexel University College of Medicine and an Associate Professor in the Department of Family, Community & Preventive Medicine and Chief of the Division of Community Health. She is on the advisory board for George Washington University’s 

Two in One HIV +COVID Screening and Testing Model.

Leon McCrea, MD, MPH, is the Senior Associate Dean of Diversity, Equity & Inclusion at Drexel University College of Medicine and an Associate Professor in the Department of Family, Community & Preventive Medicine. He is on the advisory board for George Washington University’s 

Clinicians and experts interested in replying to this piece or submitting an article to HCPLive can 

The Power of the Primary Care Visit to Combat COVID-19 and HIV

Annette Gadegbeku, MD

To watch the video series component of this episode, click here. 

5:11 Classifying the Severity of Plaque Psoriasis

8:30 Laboratory Tests for Systemic Therapy

13:22 Monitoring Systemic Therapy in Plaque Psoriasis

16:50 New Oral Systemic Therapies for Plaque Psoriasis

28:03 Long-term Safety Data of Deucravacitinib

34:52 Selecting the Right Treatment for the Right Patient


A panel of dermatologists have a comprehensive discussion on exciting developments in the treatment of plaque psoriasis, focusing on treatment approaches, patient monitoring strategies, and recent clinical trial data.

Beyond the Surface: Monitoring your Patients with Moderate to Severe Plaque Psoriasis

Bruce Strober, MD, PhD, FAAD

Daniel Tashnek, JD

 Let’s shift to the other stuff coming in the future. There are other mechanisms being investigated in therapeutics in atopic dermatitis. I’ll start with topicals.

There’s a new topical JAK inhibitor that has been studied in ages 12 and older. It’s probably as strong or a little stronger than triamcinolone 0.1% as a steroid, but it’s a nonsteroid. There’s no atrophy. It may have more potency than our other nonsteroidals without a lot of irritancy, burning, or stinging at all. We’re really excited about that.

Tapinarof is a drug in a totally different class of medicines. It’s an aryl hydrocarbon receptor modulator. This is being developed both for psoriasis and atopic dermatitis. 

Another PDE4 inhibitor is under study as well. Another topical JAK inhibitor, delgocitinib, is being studied in both chronic hand eczema and atopic dermatitis. They’re not ready to be written yet, but these are other medicines that will give us different topical options.

Peter, do you want to talk about biologics?

Absolutely. We have some new biologic agents that are in development. In particular, we have 2 new IL-13 inhibitors that are in late-stage development, so that’s going to be exciting. It seems they’ll be similar to dupilumab but a different molecule. It may be for patients who have had an adverse event with dupilumab or if it didn’t work fully. This may be another option. This is going to be nice. It seems like they’re going to have a similar safety profile and lack of lab monitoring. That’s exciting.

We have an IL-31 inhibitor that’s also in development. That’s interesting because some people call IL-31 the master itch cytokine. That would be neat because that could answer our question we asked at the beginning. Is this the itch that rashes? If so, how much? Of course, nothing is quite that pure. IL-31 is doing other things too, but the early data seem very promising, so that’s exciting to me as well.

 There are some oral JAK inhibitors coming down the pike as well. They are well along the way. Baricitinib and upadacitinib have been approved for other indications and are being studied in phase 3 trials for atopic dermatitis. There’s also a new molecule, abrocitinib. These will be different. They’ll be oral. There are some more issues with monitoring blood work, but that will give another potential approach to some of our patients. Two of the 3 JAKs have been studied in ages 12 and older, and the other is being studied in adults but going younger. There’s lots of new stuff happening. 

This has been an incredible discussion and very practical, reflecting on all the changes that are happening in the field. Let’s get final thoughts from each of our participants. Jeffrey? 

I’ll go back to education. Educate the pediatrician and make sure the pediatrician educates the family and takes the time. This is not an easy process. This is not an easy disease state. If we do a good job outlining to the families what they need to do, we can see much better outcomes. That goes without saying for everything that primary care doctors do. This forum is going to be great for people to take a look and hear what’s coming on and where we should be.

We all have to work together in a therapeutic alliance. We need to get the patients on board. We need all of the specialists and primary care practitioners to work together because we’re all together for the same concept. We want the patient and their family to be better. When we bring all our forces together, it’s so much more powerful. There’s great synergy.

These are exciting times in the world of atopic dermatitis. The world is going to be a better place with all these new therapies on the way and with the advent of Dupixent 4 years ago. It’s a good time to have atopic dermatitis. We can do many more things to help.

Thank you. Great contributions from everyone today. Thank you for watching this HCPLive® Peer Exchange. If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming Peer Exchanges and other great content right in your in-box. Thank you.

Lawrence F. Eichenfield, MD; Jeffrey M. Bienstock, MD, FAAP; Peter A. Lio, MD; and Elizabeth A. Swanson, MD, review additional mechanisms being investigated in the pipeline for the treatment of atopic dermatitis. 

Emerging Agents for the Treatment of Atopic Dermatitis 

Elizabeth A. Swanson, St. Luke’s Children’s Hospital 

Drs. Sperling and Gianos introduce the HCPLive Special Report on Lipoprotein Apheresis

HCPLive Lipoprotein Apheresis Special Report Part 1

On October 07, 2024, the American Heart Association (AHA) 

 outlining the role and supporting data for using lipoprotein apheresis in clinical practice.

At 18 pages in length, citing 104 references, and featuring a multitude of charts and colorized graphics, the scientific statement’s specific aim is to provide an overview of the history of lipoprotein apheresis, mechanisms of action, cardiovascular and renal outcomes data, indications, and options for treatment. Composed on behalf of several AHA councils, including the Council on Arteriosclerosis, Thrombosis, and Vascular Biology; Council on Cardiovascular and Stroke Nursing, and Council on Clinical Cardiology, the document was created by a volunteer writing committee chaired by Laurence Sperling, MD, Katz Professor in Preventive Cardiology and founder of the Emory Center for Heart Disease Prevention.

, Sperling is joined by committee vice-chair Eugenia Gianos, MD, director of Cardiovascular Prevention at Northwell Health, for a deep dive into the AHA’s scientific statement, their personal experiences with lipoprotein apheresis, and future considerations in the evolving landscape of lipodology.

In the introduction video featured above, Sperling explains the importance of raising awareness of this underutilized treatment for patients with severe hypercholesterolemia, including familial hypercholesterolemia (FH) and elevated lipoprotein(a) [Lp(a)]. Gianos highlights key points from the statement, focusing on the specific patient populations that benefit most from this therapy, such as those with homozygous and heterozygous familial hypercholesterolemia, as well as those with elevated Lp(a) levels. Both experts emphasize the importance of the central illustration in the statement, which concisely presents the treatment’s benefits, including reductions in LDL, Lp(a), and inflammation markers.

Clinical Application of Lipoprotein Apheresis

Laurence Sperling has no disclosures to report. Relevant disclosures for Gianos include Amgen, AstraZeneca,Eli Lilly and Company, kaenka, Novartis, and Med-IQ.

Gianos E, Duell PB, Toth PP, et al. Lipoprotein Apheresis: Utility, Outcomes, and Implementation in Clinical Practice: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. Published online October 7, 2024. doi:10.1161/ATV.0000000000000177

Iapoce C. AHA scientific statement promotes expanded use of lipoprotein apheresis. HCP Live. October 11, 2024. Accessed October 17, 2024. https://www.hcplive.com/view/aha-scientific-statement-promotes-expanded-use-of-lipoprotein-apheresis.

The American Heart Association released a comprehensive scientific statement on October 7, 2024, detailing the role of lipoprotein apheresis in clinical practice. This document, created by a volunteer committee led by Dr. Laurence Sperling, aims to provide an overview of the treatment's history, mechanisms, and outcomes. It highlights the therapy's benefits for patients with severe hypercholesterolemia, including familial hypercholesterolemia and elevated lipoprotein(a) levels. The statement emphasizes the importance of raising awareness about this underutilized treatment and includes a central illustration summarizing its benefits.

Laurence Sperling, MD, and Eugenia Gianos, MD, discuss the historical context and underutilization of lipoprotein apheresis in part 1 of a 3-part video series.

Exploring the Role, History of Lipoprotein Apheresis, with Laurence Sperling, MD, and Eugenia Gianos, MD

Eugenia Gianos, MD

A shift in the management of BCG-unresponsive non–muscle invasive bladder cancer (NMIBC) has been the inevitable culmination of over a decade’s worth of work.

Traditional approaches to the management of NMIBC were limited to intravesical immunotherapy or chemotherapy––relying primarily on BCG, with the only other approved alternative being valrubicin. With the BCG shortage taking hold in 2012, urologists found themselves grappling with an even more constrained set of options. Considering this reality, pharmaceutical companies, investigators, and the FDA itself recognized the need for new therapeutics in this space, thus beginning the arm’s race for novel innovations.

In recent years, the fruits of this effort have become apparent, with 3 new approvals in the NMIBC realm and many more agents in phase 3 development.

However, even after the BCG shortage resolves, the need for agents in the BCG-unresponsive setting will remain.

“In the future, we are going to probably have other BCG strains, but this concept of BCG failure or BCG refractory disease is not going to go away,” said Siamak Daneshmand, MD, a professor of urology and director of clinical research at the University of Southern California, in an interview with 

®. “Not everybody responds to BCG. There's a global need for patients who don't respond to BCG, and then there's a small percentage of patients who don't tolerate BCG very well. We're so used to it because we've been using it for so long, but there are some patients who have a really difficult time with BCG.”

As 2024 comes to a close, the excitement for these new agents could not be more apparent. The BCG-unresponsive NMIBC space has gone from a dearth of options to a wave of new treatments, and now urologists are faced with an encouraging challenge: choosing the best one.

The wave of new treatment options began in January 2020 with the approval of intravenous pembrolizumab (Keytruda), an anti-PD-1 therapy for patients with high-risk, BCG-unresponsive NMIBC with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Although this approval offered a new bladder-sparing option for patients, long-term outcomes showcased its downsides. Pembrolizumab was the first approved agent in the space with a 3-month complete response (CR) rate of 41%, but only 18.8% of the initial treatment cohort (n = 96) remained disease-free at 12 months.

Daneshmand noted, “Pembrolizumab has been around for several years now for [NMIBC], but the efficacy is not very high, especially when you start to look at 3 years. That safety-profile-to-benefit ratio is just not quite there.”

It wasn’t long before a new option rivaled the efficacy seen with pembrolizumab. In December 2022, the FDA approved nadofaragene firadenovec-vncg (Adstiladrin), an oncolytic adenovirus for patients with high-risk BCG-unresponsive NMIBC with CIS with or without papillary disease.

The approval was supported by data showing a 3-month CR rate of 53.4%.

 At 2 years following its initial approval, the therapeutic continues to demonstrate tolerability and safety in these patients, with promising cystectomy-free survival outcomes.

 The dosing schedule is also convenient for patients, as nadofaragene is dosed every 3 months as opposed to once per week like many of the other treatments that are available.

However, this drug comes with its own set of challenges, primarily in its storing and handling. Nadofaragene arrives frozen and needs to be thawed before use, making it challenging for hospitals to manage in a busy environment.

Vikram Narayan, MD, an assistant professor of urology at Emory University in Atlanta, Georgia, explained, “The company has provided some additional guidance on how to make that piece easier, but I think in a lot of urology practices, being able to do that in an efficient way in a busy clinical practice remains a challenge.”

This year saw the approval of a third new agent––the interleukin-15 (IL-15) superagonist nogapendekin alfa inbakicept (N-803; Anktiva). Anktiva is indicated for use in combination with BCG for the treatment of patients with BCG-unresponsive NMIBC with CIS with or without papillary tumors. The approval was based on data showing a CR rate of 55% at 3 months and 71% at any time point.

 However, real-world outcomes with this agent remain to be seen.

Although all 3 novel therapies have served as catalysts in bringing renewed hope to the BCG-unresponsive NMIBC space, there is optimism for further advancements in the near future.

Narayan noted, “I think it's fair to say that we haven't been as excited about the durability of a lot of these agents. So, we want to see better durability.”

Fortunately, it appears the wait for this progress will not be nearly as long as the decades leading up to these new options. Several agents already having demonstrated encouraging results in phase 2/3 studies, including TAR-200, cretostimogene grenadenorepvec, and TARA-002. Impressively, these agents boast CR rates at any time point of 83.5%,

Moving away from the BCG-unresponsive setting, there is even more potential with TAR-210, UGN-102, and combination regimens with BCG.

These agents are ushering in a new era of intravesical treatments, which appear to have comparable efficacy to systemic agents with less toxicity.

 Such treatments are anticipated to provide an additive impact to the profound progress that has already been seen in the BCG-unresponsive setting.

Thus, with a dizzying amount of activity in the management of NMIBC, urologists are now faced with new questions. The current treatment options were approved based on single-arm trials, so there are limited data on comparative efficacy. In the absence of head-to-head data, patient selection and treatment sequencing remain a challenge. As Sarah P. Psutka, MD, MSc, explains, these factors are a “black box,” and more data are needed to be able to make more informed decisions.

“Real-world data hopefully will help us to start to be able to use a data-driven approach to intelligently guide patients towards the therapies that they are most likely to respond to, but we're obviously not there yet. In the absence of comparative trials, it's just really challenging to know,” said Psutka, an associate professor of urology at the University of Washington in Seattle.

Patients will also face some considerations of their own.

“My understanding of the data is that most of these agents are about the same in terms of their efficacy. So, I think what it's going to boil down to, for the most part with patients, is going to be tolerability,” said Mark D. Tyson, II, MD, MPH, a urologic oncologist at Mayo Clinic in Phoenix, Arizona. “I also think there's going to be some other drivers of utilization. I'm sure the payers going to have something to say about this when the costs––for all of these agents––come out into full view. For the most part, I think patients are going to look at convenience, administration methods, tolerability, those sorts of things.”

Despite all of these unknowns, one thing remains clear: the future for NMIBC is bright.

Undoubtedly, this shift––deciding which agent to choose from–– is a welcome challenge in consideration of the previous era where bladder-sparing options were limited. This year has been a marked reflection of the past decade’s worth of progress in this space, and 2025 is poised to provide even more practice-changing advancements.

Balar AV, Kamat AM, Kulkarni GS, et al. Pembrolizumab monotherapy for the treatment of high-risk non-muscle-invasive bladder cancer unresponsive to BCG (KEYNOTE-057): an open-label, single-arm, multicentre, phase 2 study. 

. 2021;22(7):919-930. doi:10.1016/S1470-2045(21)00147-9

Boorjian SA, Alemozaffar M, Konety BR, et al. Intravesical nadofaragene firadenovec gene therapy for BCG-unresponsive non-muscle-invasive bladder cancer: a single-arm, open-label, repeat-dose clinical trial. 

. 2021;22(1):107-117. doi:10.1016/S1470-2045(20)30540-4.

Narayan VM, Boorjian SA, Alemozaffar M, et al. Efficacy of Intravesical Nadofaragene Firadenovec for Patients With Bacillus Calmette-Guérin–Unresponsive Nonmuscle-Invasive Bladder Cancer: 5-Year Follow-Up From a Phase 3 Trial. 

. 2024;212(1):74-86. doi:10.1097/JU.0000000000004020

Chamie K, Chang SS, Kramolowsky E, et al. IL-15 Superagonist NAI in BCG-Unresponsive Non–Muscle-Invasive Bladder Cancer. 

. 2023;2(1):EVIDoa2200167. doi:10.1056/EVIDoa2200167

Daneshmand S, Zainfeld D, Pieczonka C, et al. Safety and tolerability of TAR-200 monotherapy in patients with bacillus Calmette–Guérin (BCG)-unresponsive high-risk non–muscle-invasive bladder cancer (HR NMIBC) in SunRISe-1. Presented at: Society of Urologic Oncology 25th Annual Meeting. December 4-6, 2024. Dallas, Texas. Abstract 135. Accessed December 5, 2024. https://suo-abstracts.secure-platform.com/a/gallery/rounds/21/details/3800

Tyson M, Uchio E, Nam J-K, et al. Topline results from BOND-003: a phase-3 study of intravesical cretostimogene grenadenorepvec for the treatment of high-risk BCG-unresponsive NMIBC with CIS. Presented at: Society of Urologic Oncology 25th Annual Meeting. December 4-6, 2024. Dallas, Texas. Late-breaking abstract.

Mazzarella B, Jayram G, Shore S, et al. ADVANCED-2: phase 2 open-label study to evaluate safety and anti-tumor activity of intravesical instillation of TARA-002 in adults with high-grade non-muscle invasive bladder cancer. Presented at: Society of Urologic Oncology 25th Annual Meeting. December 4-6, 2024. Dallas, Texas. Abstract 119. Accessed December 5, 2024. https://suo-abstracts.secure-platform.com/a/gallery/rounds/21/details/3637

Guerrero-Ramos F, Boormans JL, Daneshmand A, et al. Novel Delivery Systems and Pharmacotherapeutic Approaches for the Treatment of Non-muscle-invasive Bladder Cancer. 

. 2024;7(6):1267-1279. doi:10.1016/j.euo.2024.05.012

The management of BCG-unresponsive non-muscle invasive bladder cancer (NMIBC) has evolved significantly due to a decade-long effort to develop new treatments. Traditional options were limited, but recent years have seen the approval of three new therapies: pembrolizumab, nadofaragene firadenovec, and nogapendekin alfa inbakicept. These advancements offer new hope, though challenges remain in terms of treatment durability, patient selection, and real-world efficacy. Future developments are promising, with several agents in advanced trials, potentially transforming the therapeutic landscape for NMIBC.

The BCG-unresponsive non-muscle invasive bladder cancer space has gone from a dearth of options to a wave of new treatments.

A New Era for NMIBC: How a Decade of Progress is Reshaping Treatment

Hannah Clarke

Thoughts on the Current State of PBC Management

Video content above is prompted by the following:

Please share your concluding thoughts about management of PBC.

Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by the progressive destruction of small and medium-sized bile ducts within the liver. This destruction is primarily mediated by autoreactive T lymphocytes targeting the epithelial cells of the bile ducts. The ensuing cholestasis leads to the accumulation of toxic bile acids, causing hepatocellular damage and inflammation. Over time, this chronic inflammatory process results in fibrosis and eventually cirrhosis. The pathophysiology of PBC is influenced by genetic predispositions and environmental factors, contributing to its complex etiology and progression.

The panel of experts offers expert insights and concluding thoughts on the management of primary biliary cholangitis (PBC), emphasizing the importance of personalized treatment strategies, monitoring, and the evolving role of new therapies in improving patient outcomes.

John Vierling, MD, FACP, FAASLD, AGAF

Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA

A panel of expert cardiologists share their clinical pearls for managing patients with hyperlipidemia.

Clinical Pearls on Lipid Management

Keith C. Ferdinand, MD, FACC, FAHA, FNLA:

 I’m going to give each of you about a minute or so to give what we call a take-home message: a clinical pearl for the physicians, nurse practitioners, physician assistants, [and] pharmacists who may be listening, something that will motivate them to do better. We’ve heard from the Family Heart Foundation that we’re not recognizing these patients early enough and that those patients at high risk are not getting high-intensity statin. We heard from Dr Michos that there is a whole world of alternatives. Christie, you suggested [that] we combine these agents [to] reach lower [lipid] levels vs pushing [the dose of] a drug to toxicity level. Dr Kohli, you’ve been very persistent that education, culturally appropriate [and] literacy-appropriate education, is one of the linchpins to success.

 We’ve talked about education, but it starts with [this]: “You can prevent heart attacks and strokes.” Patients need to know their numbers; that’s an education process. We help them get there. We’re their guides to get there. One thing that is a frustration, a practical point in terms of when you use some of the nonstatin therapies, [is] the approval process. It turns out—we have fellows coming [in] every year—if you say this patient has a family history of very high cholesterol [level] and premature heart disease, [you’re] denied. You [have] to say heterozygous familial hypercholesterolemia [FH]. There’s an 

International Classification of Diseases, Tenth Revision

] code for that. Put those words in there. If you say [the patient] “has heart disease or ASCVD [atherosclerotic cardiovascular disease] with MI [myocardial infarction]”…put the right information. Have a lipid measurement within a month, [provide] the LDL [low-density lipoprotein] cholesterol [level], [and state], “It was unacceptably high; therefore, [I’m] using this agent.” Some pragmatic steps will reduce the frustration for both [patient and provider], because if the patient doesn’t get it and you don’t get it, it’s frustrating. But you can do it. It’s easier.

 Dr McGowan, thank you for your great work with the Family Heart Foundation. Can you give us some clinical pearls to help our clinicians out there do better?

 When you screen patients, and hopefully you’ll screen all your patients, [but] when you screen patients with a lipid profile, if it’s an adult person and you see an LDL [level] greater than 190 mg/dL, you want to think familial hypercholesterolemia. With that in mind, you want to have a conversation with the patient [that] this is unlikely to be chance. This is your genetics, and, therefore, your children need to be screened, your siblings need to be screened, and it’s important. People who hear that it might [affect] their children are more likely to take action. So take action. The other big thing, [because] I’m coming from the Family Heart Foundation, [is] don’t forget to measure lipoprotein(a) [Lp(a)] [level]. Don’t think it’s unactionable. I’m going to tell you one quick story about a patient of ours who’s an advocate for Lp(a). This young woman was 44 years old [with a] completely normal lipid profile. [She] did have a history of cardiac disease [and] attributed her father’s early cardiac disease to his type A behavior. She waited 18 hours with chest pain before going in and finding that she was having a cardiovascular event: a myocardial infarction. What she said to us was, “If I had known I had such a high Lp(a) [level], I would have gone in earlier.” That was important information to me. So even if you feel like there aren’t agents currently [available], as everybody else has said, you can reduce other risk factors. Measure that Lp(a) [level] and then take action. And educate your patients about it.

 There’s so much burnout in medicine. It is so hard, what we do on a day-to-day basis. But the thing that keeps me most engaged is knowing that I made an impact on somebody’s life. If you could take 2 or 3 minutes at the end of every visit, no matter what it’s for (eg, knee pain, urinary tract infection, back pain), to look at those lipid [levels and] focus on prevention, [then] you are going to have a tremendous impact on [a] number of lives out there that you won’t even realize. That will give you the highest degree of engagement: knowing their numbers, not just knowing your numbers, but knowing your patients’ numbers and phenotyping at every visit so [that] you’re delivering a personalized care plan. You’re not lumping every secondary prevention to less than 70 mg/dL or less than 55 mg/dL. You’re using your risk modifiers to reclassify that risk in an iterative fashion at every visit for your primary and secondary prevention. So if Mrs Jones had a stroke since the last time you saw her, her risk just changed. You bump her down to the next level, δ LDL of 50%, and get [her level] below those thresholds. If you can work it into your busy practice, just spend 2 minutes at the end of each visit looking at those lipid [levels] and making a little plan. It’ll be tremendous how many lives you’ve changed and how many trajectories of atherosclerosis you’ve modified.

 That’s a wonderful message. Dr Michos, you have the last take-home [message].

 I want to circle back to something that Dr Kohli said at the beginning about cholesterol years. This is something that might resonate with patients and other clinicians when they’re familiar with pack-years of smoking. It’s not only the magnitude of elevation; it’s the duration [that] one’s [had] that value. There’s been some modeling thinking that the theoretical onset of clinical ASCVD may be around 5000 mg/dL-years. Individuals who have had high cholesterol [level] since birth—our patients with FH—if left untreated, they’ll cross that threshold of clinical ASCVD very young in life. Whereas individuals who have favorable genetics, healthy lifestyle, or early treatment may never cross that threshold for clinical ASCVD. [And] don’t forget about those with mild to moderate hyperlipidemia. The LDL [level] is [in the] 130s mg/dL [or] 160s mg/dL. A lot of these patients are ignored. But [if] left untreated for a sufficient number of years, those individuals will have earlier onset ASCVD than their counterparts who have had lifelong low LDL [levels]. The message is [that] we want to get LDL [levels] lower for longer and get there faster.

 Wonderful message. Thanks to you all for this rich and informative discussion. And thank you for watching this 

. If you enjoyed this content, please subscribe to our e-newsletters to receive upcoming 

 [videos] and other great content right in your inbox.

Mary McGowan, MD, FNLA

 Karl, there’s a drug that was mentioned by Nate called daridorexant. It’s a new drug. Can you tell us a little bit about this and what’s new and different about it?

 As Nate mentioned, it’s a dual orexin receptor antagonist [DORA], and it seems to have a shorter half-life than the other DORAs. And it may, for that reason, have different clinical effects. But one of the interesting things about the clinical development of this medication is that it’s also been looked at for daytime functioning disturbances with insomniacs. It has been shown to have some improvement in some areas of daytime functioning, which I think is very interesting, since we’ve been speaking about daytime functioning as being a critical area for insomniacs. I think we need more studies like this. It would be very helpful in the future if we could also develop more objective ways of quantifying daytime dysfunction with insomniacs and see if these medications could be helpful. This medication was also studied in, I believe, a 3-month trial where there was a rapid discontinuation. Of course, that’s a clinical issue with many of our patients who discontinue sleep medications, stop taking them. In this particular case, there was no rebound insomnia, which was very interesting to find out.

 Yes, this is interesting. You mentioned having effects on daytime functioning. When you survey patients, you find that daytime functioning is the biggest complaint, and I think you mentioned that at the beginning of the program. The fact that this medication has shown some benefit, not only at night, but also during the daytime, I think is a good direction. Hopefully, we will have other medications for insomnia that will address this as well and look at various daytime consequences of insomnia, not just look at how it’s improving the nighttime.

 Another medication, Michael, I want to mention in the pipeline is something called IMB-115; it does not have an official name yet. It is a medication being developed for not only insomnia, but also for insomnia associated with alcohol cessation. It actually acts at the receptors that are important for both pain as well as for mood and other issues and those susceptive receptors. And interestingly, it may have some effects on drug addiction as well. Thus, it has been developed as a way of possibly treating alcohol cessation insomnia as well as insomnia, period.

 Yes, I think this is particularly interesting because it’s a whole new different mechanism of action for a hypnotic [medication]. As you said, it’s affecting these pain receptors, it’s a pain receptor agonist. This medication is under investigation at the present time. What’s yet to be seen is whether it will eventually get FDA approved, of course. But it’s nice to think that there are new receptor types that could be affected by medications to help people sleep and not just the traditional ones.

Expert panelists share their excitement for novel agents that may impact the insomnia treatment landscape.

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