Podcasts about cardiomems

In this episode of AbbottTalks, Kartik Sundareswaran, PhD, divisional VP, global clinical and regulatory affairs, Abbott Heart Failure, discusses Abbott's pioneering work in heart failure care, focusing on technologies that improve outcomes and empower earlier interventions. Sundareswaran's path to MedTech began with a shift from computer engineering to biomedical research, where his early work studying blood flow patterns in children with congenital heart disease sparked a passion for solving cardiovascular challenges. This passion led him to roles at Thoratec, St. Jude Medical, and ultimately Abbott, where he has spent years advancing heart failure care. The conversation highlights Abbott's CardioMEMS™ Heart Failure System, a device enabling remote pulmonary artery pressure monitoring to reduce hospitalizations, and the HeartMate 3 LVAD, which provides life-extending support for patients with advanced heart failure. Sundareswaran also discusses the new TEAM-HF clinical trial, which combines CardioMEMS and HeartMate 3 to identify patients earlier and deliver timely, effective interventions. This conversation comes to you courtesy of our episode sponsor, Tecan Group Ltd. To learn more about how Tecan works with medical device companies, visit: https://partnering.tecan.com/ Thank you for listening to the AbbottTalks Podcast. Tune in and subscribe to DeviceTalks on all major podcast channels to never miss an episode.

Abbott celebrated the 10 year anniversary of the FDA approval of CardioMEMS. On this podcast Chris Bell talks to Rebecca (Beki) Angerstein about the legacy of CardioMEMS. Beki is currently the Manager in Medical Affairs at Abbott. Her clinical background includes managing CV patients at the bedside and in a large cardiology practice for many years. She continues to practice clinically working prn in the hospital. Her passion is heart failure which led her to Abbott where she worked with clinicians on HF research trials.

Joining us for episode #107 was Mr. Jason Kroh, the Chief Technology Officer at Strados Labs.Jason comes to the show with over 25 years of experience in Med-Tech. At the front end of his career he held positions in both Product & Electrical Engineering and began to work his way into Executive leadership roles overseeing R&D, Engineering & eventually becoming a CTO. He's worked for companies like Vero Biotech, CardioMEMS, & Cybersonics to name a few.Jason has simultaneously been a Panel Reviewer for the National Science Foundation reviewing both Phase I and II SBIR & STTR grant applications. Jason holds his Bachelors of Science in Biomedical Engineering & his Masters of Science in Electrical Engineering. Since 2018 Jason has been the CTO at Strados Labs. For those unfamiliar with the organization, Strados is home to the world's only FDA-cleared device called the RESP Biosensor which is clinically validated to capture lung sounds including coughing, wheezing, rhonci & other adventitious breathing sounds over time without requiring episodic patient intervention. This leads to a stronger understanding of treatment response & earlier insight into exacerbations to prevent uncessary hospitalizations…especially for people suffering from chronic respiratory diseases such as COPD & Ashtma.Some highlights of what we discussed:-How Jason got into Med-Tech-The roles & responsibilities that were pivotal for propelling his career to the Executive level-Making the transition from contributor to leader-How Jason manages the stress of Executive responsibilities & balances with other aspects of life-The difference between average & top performance, especially in Engineering-The future of Cybersecurity in the Medical Device industry...and so much more!

This episode's Community Champion Sponsor is Ossur. To learn more about their ‘Responsible for Tomorrow' Sustainability Campaign, and how you can get involved: CLICK HERE---Episode Overview: Is it possible to revolutionize kidney disease treatment and redefine conventional care? Our next guest, John Erbey, is doing just that as the founder and CEO of Roivios. With over 25 years of pioneering experience in the medical field, John brings a unique blend of analytical rigor, physiological insight, and deep understanding of customer needs, which has driven ground-breaking advancements across the medical device and pharmaceutical sectors. Inspired by personal experiences with kidney disease in his family, John is on a mission to transform patient lives. Join us as we explore how Roivios is reshaping kidney health management, potentially saving billions in healthcare costs, and paving the way for a future where kidney function can be sustained and enhanced. Let's go!Episode Highlights:Embracing discomfort for true innovation in healthcareAddressing kidney disease's $250 billion annual cost in the USTargeting renal impairment during cardiac surgeryDeveloping JuxtaFlow technology with future wearable applicationsEnvisioning implantable devices to prevent kidney disease progressionAbout our Guest: John Erbey, a visionary with over 25 years of experience in the medical field, is the founder and CEO of Roivios. His dynamic leadership and pioneering approaches have led to substantial advancements in therapeutic development and medical devices.At Roivios, John has revolutionized the treatment of kidney disease by introducing an innovative approach that redefines conventional wisdom about kidney filtration. This led to the creation of the groundbreaking JuxtaFlow® Renal Assist Device (RAD), marking a significant evolution in kidney health management.John's leadership extends across the medical device and pharmaceutical sectors, where he has led the launch of CardioMEMS and defined the EU pricing strategy for Ezetrol (Zetia). As a strategist, his mission is to enhance patient lives by providing superior tools to healthcare providers. His unique blend of analytical rigor, physiological insight, and deep understanding of customer needs has enabled him to leverage scientific innovations, creating value for brands like CardioMEMS™, Zetia™, Vytorin™, and Avandia™.Since founding Roivios in 2015, John's personal journey has been a driving force behind his commitment to transformative healthcare solutions. Having witnessed the profound effects of kidney failure within his own family and through poignant stories shared by potential investors, John's resolve to make a positive impact on patients facing similar challenges has only strengthened over time.John holds a Ph.D. in epidemiology from the University of Pittsburgh's Graduate School of Public Health, where his groundbreaking research in this field has earned him induction into Delta Omega, the prestigious National Honor Society for Public Health.Links Supporting This Episode:Roivios Website: CLICK HEREJohn Erbey LinkedIn page: CLICK HERERoivios LinkedIn page: CLICK HERE Mike Biselli LinkedIn page:

The Filtrate:Joel TopfNayan AroraSophia AmbrusoWith Special Guest:Boback Ziaeian @boback Assistant Professor of Medicine David Geffen School of Medicine at UCLA. His Google Schoolar page is better than yours. And returning for her fourth time (why do we keep inviting her back?)Sadiya Khan @heartDocSadiya Assistant Professor of Medicine (Cardiology) and Preventative Medicine at Northwestern Feinberg School of Medicine. LinkEditor:Priya YenebereShow Notes:Diuretic Therapy review by. Craig Brater NEJMThe manuscript in JAMA | NephJCMetoprolol vs Carvedilol: Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial (Lancet)EMPULSE: The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial (Nature Medicine)Effect of Aliskiren on Postdischarge Mortality and Heart Failure Readmissions Among Patients Hospitalized for Heart Failure The ASTRONAUT Randomized TrialEffects of Oral Tolvaptan in Patients Hospitalized for Worsening Heart Failure The EVEREST Outcome TrialSophia ended up placing fifth in NephMadness 2023. (Link)Joel finished 697thAfter winning in the opening round, Northwestern lost to UCLA, in the second round of the March Madness tournament, 68-63.Torsemide to furosemide equivalents CardioMems positive trial: Sustained efficacy of pulmonary artery pressure to guide adjustment of chronic heart failure therapy: complete follow-up results from the CHAMPION randomised trial (The Lancet)CardioMems negative trial: Haemodynamic-guided management of heart failure (GUIDE-HF): a randomised controlled trial (The Lancet)Estimation of the Absolute Risk of Cardiovascular Disease and Other Events: Issues With the Use of Multiple Fine-Gray Subdistribution Hazard Models (Circulation)Torasemide in chronic heart failure: results of the TORIC study (PubMed)Tubular SecretionsNayan: Louise Penny A World of Curiosities: A Novel (Amazon)Sadiya: Ted Lasso season threeSophia:The Last of Us on HBO and SNL skit Mario Cart as Prestige DramaBoback: Duolingo for Japanese

Interviewees: Associate Professor Jasper Brugts, Erasmus University Medical Centre of Rotterdam, The Netherlands; Professor John Cleland and Doctor Ross Campbell, University of Glasgow, United Kingdom of Great Britain & Northern Ireland; Doctor Jeroen Dauw AZ Saint-Lucas, Ghent, Belgium and Interviewers: Doctor Antonio Cannata, King's College London, United Kingdom of Great Britain & Northern Ireland; Doctor Jozine Ter Maaten, University Medical Centre Groningen, The Netherlands; Doctor Sotiria Liori, Attikon University Hospital, Athens, Greece; Doctor Francesca Musella, Royal Brompton Hospital, London, United Kingdom of Great Britain & Northern Ireland. This podcast discusses the results of four late breaking clinical trials presented at the Heart Failure congress 2023 in Prague, Czech. First, dr. Brugts shares the results of the MONITOR-HF trial, an open-label, randomized trial showing that haemodynamic monitoring using a cardioMEMS device, significantly improved quality of life and reduced heart failure hospitalizations in patients with moderate-to-severe heart failure. This trial was simultaneously published in the Lancet (Remote haemodynamic monitoring of pulmonary artery pressures in patients with chronic heart failure (MONITOR-HF): a randomised clinical trial - The Lancet). Second, dr. Cleland walks us through a population study from the greater Glasgow area that found that use of loop diuretics in patients without a diagnosis of heart failure was associated with poor outcomes. He consequently discusses possible explanations and clinical consequences. Third, dr. Campbell shares the results of the DAPA-RESIST trial, that found that in patients with diuretic resistance, dapagliflozin was not superior to metolazone at relieving congestion (Dapagliflozin versus metolazone in heart failure resistant to loop diuretics | European Heart Journal | Oxford Academic (oup.com)). Fourth, dr. Dauw discusses the results of the ENACT-HF trial where a strategy of natriuresis guided therapy as recommended by the HF guidelines, in an open label, sequential roll-out (first 10 patients standard of care, followed by 10-30 patients in the natriuresis arm), was shown to improve natriuresis and reduced length of hospital stay. No effect on change in congestion score or in-hospital mortality was observed. The podcast is concluded with a brief discussion of some HFA Young highlights at the congress. 

In Episode 49 of The Healthcare Leadership Experience Jim Cagliostro is joined by Todd Nicklas, Senior Clinical Trial Manager and Head of Clinical Operations at Trevena to discuss the benefits and challenges of clinical research trials.    Episode Introduction Clinical trials can transform healthcare and the patient experience, yet they are not without their challenges. In this episode, Jim Cagliostro, VIE's Clinical Operations Performance Improvement Expert, interviewed Todd Nicklas to discuss his experience with clinical research, including the positive impact for hospitals that participate in clinical trials, overcoming patient hesitancy, and the high cost of achieving FDA approval.    Show Topics   Why clinical trials matter to healthcare From bench research to real life scenarios Clinical research can reduce patient readmissions Trialing heart donors with Hepatitis C Overcoming patient hesitancy  The $2.6 billion cost of successful clinical trials The impact of COVID-19     01:55 Why clinical trials matter to healthcare Todd said clinical research can attract patients to hospitals by giving them access to brand new treatments.     ‘'Physicians and patients have access to cutting edge new technologies and that's brand new technologies and medicines that maybe are a few years down the road in development, or maybe that just got approved and that hospital has it ready to go in their formulary and ready to be used. They're maybe ahead of the game versus other hospitals around their area. And that might get people excited to come to their institution. I worked in clinical research on the hospital side for about 10 years, and some patients would come to our hospital for the very reason of trying out a research medication or trying to work with a physician that's doing a trial with us with a medication. Got them excited to come to that institution versus maybe their own hospital that they're at.''     03:56 From bench research to real-life scenarios  Todd shared an early example of artificial hearts, trialed in a cow.   ‘'Another great thing, I would say, is a fair amount of hospitals have translational bench research and they want to translate that into real life scenarios and putting it in patients and giving it to patients. So you see something that maybe was developed 30, 40 years ago. You and I worked at Penn State Hershey Medical Center for a few years, and I love the story in the, I believe it was the 1970s. They were working on the first total artificial hearts. And this device was pretty primitive at the time. It's developed a good bit as of today, but they put it in a cow and they have a neat story that it was a pneumatic system. It was an air compressed system and they plugged it in, it was back in the 70s, they had the plugs in and I guess some electrical problem happened, and the cow dropped like it was dead because the power went out and somebody thought to blow on the pneumatic tubing that was in the back of the machine to have the blood pump for that cow and, to bring it back to life until they get the electrical power back on. And the cow lived for weeks and months after that. But it gets people excited, "Oh, Hershey Med's doing this? And look at this neat story." And then the years to come, the cow survived, they put it in patients a few years after that, but it's doing great and people can get that now at home. They can actually go home with a total official heart and a driver. ‘'     05:24 Clinical research can reduce patient readmissions  Todd said new medications can improve patient outcomes, leading to fewer readmissions, rehospitalizations and ER visits.    ‘'….Physicians that are so used to certain procedures, certain medications, certain devices, they might have good outcomes and they might do fine. But what if there's a new medication that gives them 50% better outcomes or 50% less hospital burden where people are coming into the hospital, 70% less, or pick a number. Why wouldn't that be something that's a top priority or a top consideration in your mind? I worked with the CardioMEMS device, which was a really neat device that was bought by a larger company. But at the time, it was the small company that was running it. And it's a device implanted into your pulmonary artery to measure heart pressures, and to tell you when your heart pressures are not doing well, and even if you're not symptomatically feeling that change… And the biggest reason why it got FDA approved was the fact that it was reducing re-hospitalizations, readmissions, and even people coming back for ER visits, even for heart failure. So why wouldn't that get hospitals excited saying, "Hey, we can reduce our heart failure admissions by X percent." That's less burden on the hospitals, less burden on the doctor, nursing staff, supplies, beds.''     12:45 Trialing heart donors with hepatitis C Todd shared his experience working in heart failure and transplant, when patients were out of options.    ‘'I worked in heart failure and transplant where people are at the end of their rope and last ditch options with heart failure.... Hospitals did a study where they would have patients be able to get hepatitis C hearts from donors that had hepatitis C. But the goal was that if they did receive that heart, that they could get a treatment that would immediately t rid of the hepatitis C. And it would open the doors to more options when you're waiting on a heart transplant for years, and you never know if you're going to make it to get a heart or not. I remember talking to the second patient that got it at Upenn, and he was ecstatic about how he got... I think he got a heart within two weeks of signing up with the study and it would've been months and months. So yeah, it was a leap of faith. It was a little bit of nerves with him, but he read the consent form. He talked with his physicians, he understood the safety behind it, and what he could know and not know at the present. And he made his own decision.''     13:39 Overcoming patient hesitancy  Todd highlighted the importance of transparency around risks and benefits for patients.    ‘'Clinical research is very focused still today on the patient first and safety first. You can quit a trial at any time and you can work with the physicians to do so. And I'll talk about this a little further down the road, but I think a big hesitancy is the fact that research in the past, maybe 30, 40, 50 years ago, there were times where people wouldn't tell people that they were doing... Physicians or clinicians wouldn't tell people that they were doing a trial on someone, or wouldn't be as transparent about the risks and the benefits, or maybe say, "Oh yeah, this is the next best thing, but not really tell both sides of the equation of saying, "Well yeah, but we don't know X, Y, Z about it. But nowadays, I've given patients consent forms that are 20 to 26 pages long, just to say every single thing about the study and how your data is going to be shared and confidentiality and safety, benefits, visits, little bit of everything. So I think it's really developed even the last 10 or 15, 20 years, but I think that's a big hesitancy in the past is, if you think about the Tuskegee studies in the 1930s and forties come up pretty often here. I know that was about 80 years ago, but that's a big one where people were not told at all about multiple things.''     19:56 The $2.6 billion cost of successful clinical trials Todd outlined the complexities and huge costs of achieving FDA approval.    ‘'That's a tough thing to know because one, it wastes cost and money to put all that forth, that effort, if you're not really learning a lot from it, and it's not slam dunk at the end of the day, but we don't know what we don't know sometimes. And it is speculation. There's so much money that has to go into these trials. I looked up a 2018 study, they said that 12% of drugs in clinical development stages get approved 12%. And it costs about $2.6 billion on average to get a drug from the very first stages of it being studied, maybe in animals or even before that to getting it FDA approved. So people don't understand that it takes so many different iterations of trials and money and understanding all the, how does it affect your kidneys? How does it affect your heart? How does it affect your brain? How is it broken down? How effective is it? All these studies have to be done for the FDA to make a good decision. And sometimes knowing how to asset in a protocol could make or break protocol, the development of that some people might just toss it aside and say, "Well, we can't develop that anymore because we don't have the money for it and we missed the target on this." So that's a tough one, I would say upfront.''     23:11 The impact of COVID-19 Todd said that the pandemic showed how participation in research studies can have a positive impact.    ‘'I think people across the board are still hesitant to research in the sense that they think they're their Guinea pig. I came across it a lot where people would say, "Are you just trying this out on me because I'm a Guinea pig and I'm just saying yes to it?" And the misconception I think is because, until there's a big cure for cancer or a big cure for something major where people are saying, "Wow," from a societal perspective, like we really now appreciate research and understand I think COVID vaccine a little bit, but it also has some political components to it where people were like, "Look at the impact of the COVID vaccine. But then some people kind of are worried about different sides of how that data has landed. But I think when there's big things that really hit the clinical medical world where people are like, "Wow, this is great that we have research that people are willing to do." Then you get the sense of people jumping all in. We actually had that in 2020, 2021 where people are, were really banging down the doors to say, "I want to do research," because they saw how much COVID was affecting the world, and how maybe their participation in a research study could help our understanding of it.''     Show Links Connect with Jim Cagliostro on LinkedIn Connect with Todd on LinkedIn Check out VIE Healthcare Consulting     You'll Also Hear:   The benefits of clinical trials for your hospital – from attracting new patients, to building partnerships with pharma companies and device manufacturers as ‘'first adapters.'' ‘'…People will say, "Well, do I want to go to a hospital that has 10 years of experience with it, or they just started last month?" You're going to have a hospital that's really well respected in that landscape.''   Taking a leap of faith: The true story of Dr Forssmann and the first (self-administered) catheterization, ‘'He actually performed the first catheterization on himself. What he did was he actually took a fully catheter and put it into a vein in his arm... Because he believed that this was a doable procedure. This was 100 years ago, 1929.''   Overcoming cultural issues: why participation on a clinical trial can't be based on patient-doctor relationships alone. ‘'There's been times where I've had to fight and advocate for my patients to say, "Hey, I don't think this patient knows enough about what they're saying yes to."   The red tape around clinical research and why it's always ‘'safety first'' for patients.    Why it's important to understand that most patients don't meet the criteria to successfully enrol on clinical trials. ‘'I think it's like 70% of the people tend to not meet the criteria. And then another 30% to 50% tend to decline the study. So when you already take those numbers down, let's say you have 1,000 people that would meet the criteria.''   What To Do Next:   Subscribe to The Cost Advantage for Healthcare Leaders and receive a special report on 15 Effective Cost Savings Strategies. Learn more about the simple 3 step process to work with us. If you are interested in learning more, the quickest way to get your questions answered is to speak with one of our margin improvement experts. Schedule a call with our team here.

An update to CardioMEMs post, ARBs and cancer, troponins, empagliflozin, and low-value care are the topics discussed by John Mandrola, MD, in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I – Invasive Monitoring for HF - FDA Expands Eligibility for CardioMEMS Heart Failure System https://www.medscape.com/viewarticle/969004 - Haemodynamic-guided management of heart failure (GUIDE-HF): a randomised controlled trial https://doi.org/10.1016/S0140-6736(21)01754-2 II – ARBs and Cancer - ARBs and Cancer Risk: New Meta-Analysis Raises Questions Again https://www.medscape.com/viewarticle/969510 - Risk of cancer with angiotensin-receptor blockers increases with increasing cumulative exposure: Meta-regression analysis of randomized trials https://doi.org/10.1371/journal.pone.0263461 - Marciniak Meta-analysis in FDA Medical Review 206316Orig1Orig2s000 https://rb.gy/myhlvy III – Troponins and Cardiac Surgery - What Troponin Level Indicates Injury After Cardiac Surgery? https://www.medscape.com/viewarticle/969617?src= - High-Sensitivity Troponin I after Cardiac Surgery and 30-Day Mortality https://www.nejm.org/doi/full/10.1056/NEJMoa2000803 - Five-Year Outcomes after PCI or CABG for Left Main Coronary Disease https://www.nejm.org/doi/full/10.1056/nejmoa1909406 IV – Empagliflozin in HFpEF - FDA Okays Empagliflozin for HF Regardless of Ejection Fraction https://www.medscape.com/viewarticle/969118 - Empagliflozin in Heart Failure with a Preserved Ejection Fraction https://www.nejm.org/doi/full/10.1056/NEJMoa2107038 - Angiotensin-Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction https://www.nejm.org/doi/full/10.1056/NEJMoa1908655 V – Low-Value Care - AHA Targets 'Low-Value' Heart Care in New Scientific Statement https://www.medscape.com/viewarticle/969107 - Strategies to Reduce Low-Value Cardiovascular Care: A Scientific Statement From the American Heart Association https://www.ahajournals.org/doi/abs/10.1161/HCQ.0000000000000105 You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

FDA approval of CardioMEMS, statins, VT storm, and fish oil and AF are the topics covered by John Mandrola, MD, in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I - Invasive Monitoring for HF - FDA Expands Eligibility for CardioMEMS Heart Failure System https://www.medscape.com/viewarticle/969004 - Haemodynamic-guided management of heart failure (GUIDE-HF): a randomised controlled trial https://doi.org/10.1016/S0140-6736(21)01754-2 - Wireless pulmonary artery haemodynamic monitoring in chronic heart failure: a randomised controlled trial https://doi.org/10.1016/S0140-6736(11)60101-3 II - Statin Use in Primary Prevention - USPSTF Tweaks Primary Prevention Statin Recommendations in New Draft Guidance https://www.medscape.com/viewarticle/968963 - Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: Preventive Medication https://www.uspreventiveservicestaskforce.org/uspstf/document/draft-evidence-review/statin-use-primary-prevention-cardiovascular-disease-adults - The Case Against Coronary Artery Calcium Scoring for Cardiovascular Disease Risk Assessment https://www.aafp.org/afp/2019/1215/p734.html III - VT-Storm - Transcutaneous Magnetic Stimulation Promising Against VT Storm https://www.medscape.com/viewarticle/968955 - Effect of Transcutaneous Magnetic Stimulation in Patients With Ventricular Tachycardia Storm https://jamanetwork.com/journals/jamacardiology/fullarticle/2788915 IV - Fish Oil and AF risk - Fish Oil Supplements May Increase the Risk for Atrial Fibrillation: What Does This Mean? https://www.medscape.com/viewarticle/967159 You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

In this edition of Device Week, Medtech Insight's Reed Miller chats with UK-based reporter Barnaby Pickering about Abbott's recent supplementary premarket submission to its CardioMEMS platform, recent safety data for Dexcom's G7 continuous glucose monitor, and where KPMG expects life sciences investment to be focused in 2022. Medtech Insight articles addressing topics discussed in this episode: -Abbott Hopes To Prevent Heart Failure Hospitalizations With New CardioMEMS HF Labeling - https://medtech.pharmaintelligence.informa.com/MT145103/Abbott-Hopes-To-Prevent-Heart-Failure-Hospitalizations-With-New-CardioMEMS-HF-Labeling -KPMG Speaks On What 2022 Medtech Investment May Look Like -Dexcom Shows Off More G7 Data - https://medtech.pharmaintelligence.informa.com/MT145078/KPMG-Speaks-On-What-2022-Medtech-Investment-May-Look-Like

In this episode, we'll dive deep into the Heart Failure business at Abbott. First we'll connect with Philip Adamson, MD, chief medical officer of the group. Dr. Adamson uses an explanation of CardioMEMS to give a vivid portrait of how patients live with heart failure. Technology, he says, makes turns those patients into their own health care workers. This podcast is sponsored by KNF. Then, we'll talk with Kevin Bourque, vice president of research and development, and Robert Kormos, division VP, global affairs of heart failure, about the advances of Heartmate 3. Both also detail how Abbott is working to help children suffering from the condition. Dr. Kormos also shares the most gratifying part of his job. The entire editorial staff joins the podcast to share their personal top stories of 2021. News includes mentions from Vicarious Surgical, ResMed, Philips, Pfizer, BioNTech, Abbott, Dexcom and Insulet. Happy New Year!!! We'll see you in 2022. LIKE! FOLLOW! SUBSCRIBE!

Topics: "Pink Tax" in the ER for chest discomfort; Chagas Disease & cardiomyopathy; PAPP & CardioMEMS; Pets & CV risk

Dr Carolyn Lam: Welcome to Circulation on the Run! Your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Greg Hundley, Associate Editor, Director of the Pauley Heart Center, VCU Health in Richmond, Virginia. Dr Carolyn Lam: Greg, we got double features today. Now, the first one's all about fruit and vegetables. Now, before you switch off, this is a very important one, okay? So, listen on. And the second is on the EMBRACE heart failure trial. Now, this was a late breaker, very important, more data on empagliflozin, that SGLT2 inhibitor. So really, really fun discussions coming right up. But first, can I dig into one of the papers that I'm really dying to tell you about? Dr. Greg Hundley: Absolutely. Dr Carolyn Lam: Okay. This is all about the diagnostic performance of high-sensitivity cardiac troponin T strategies, that super hot topic. We know that European data support the use of low high sensitivity troponin measurements or a 0/1 hour algorithm for myocardial infarction or to exclude MACE among emergency department patients with possible acute coronary syndrome. However, there's really very modest U.S. data to validate these strategies. This study today from Dr. Allen and colleagues from University of Florida, really evaluated the diagnostic performance of an initial high sensitivity cardiac troponin T measure below the limit of quantification. And that is six nanograms per liter, a 0/1 hour algorithm, and their combination with heart scores for excluding MACE in a multi-site U.S. cohort. And this is the largest prospective multi-site U.S. study of high sensitivity troponin T strategies to date. Dr. Greg Hundley: Wow, Carolyn you've really piqued my interest. So what did they find? Dr Carolyn Lam: Okay. And initial high sensitivity, cardiac troponin T below that level of quantification of six nanograms per liter was associated with a negative predictive value of 98.3% for 30-day MACE. Okay. That was that value itself. Now the 0/1 hour algorithm rolled out 57.8% of patients with a negative predictive value of 97.2% for 30-day MACE. The addition of a low-risk heart score to that initial high sensitivity troponin T level below that six nanogram per liter and the 0/1 hour algorithm improved the negative predictive value for 30-day MACE to 99% and 98.4% respectively. Dr. Greg Hundley: Wow. Carolyn, it looks like a really comprehensive analysis of the high sensitivity troponin. So tell us what are the clinical implications of this study? Dr Carolyn Lam: So these data seem to imply that when used without a risk score and initial high sensitivity troponin T below six nanograms per liter, or a 0/1 one hour algorithm, may not have sufficient sensitivity or negative predictive value to exclude 30-day MACE in the U.S emergency department patients. But the addition of that low-risk heart score to those measures improves the negative predictive value, but rolls out fewer patients. And so in totality, these results suggest that in the U.S. Emergency departments, adding a risk score to either of these strategies really increases their safety. Dr. Greg Hundley: Boy, great new information in our journal. Well, Carolyn, I'm going to switch to the world of basic science and start to evaluate in this next paper, the regulation of cellular signatures in children with dilated cardiomyopathy, and the work comes to us from Dr. Stephanie Dimmeler from Goethe University in Frankfurt. So Carolyn, Stephanie's team performed single nuclei RNA sequencing with heart tissues from six children with dilated cardiomyopathy. One was age 0.5, 1.75 and another at 5, 6, 12, and then 13 years of age. And they did this to gain insight into age and disease-related pathophysiology, pathology, and molecular fingerprints. And the goal was to gain further insight into dilated cardiomyopathy, which is a leading cause of death in children with heart failure. Dr Carolyn Lam: Cool. So what did they find Greg? Dr. Greg Hundley: Right, Carolyn. So, the number of nuclei in fibroblast clusters increased with age in dilated cardiomyopathy patients, a finding that was consistent with an age-related increase in cardiac fibrosis quantified by cardiovascular magnetic resonance imaging. Dr. Greg Hundley: Now Carolyn, fibroblast of the dilated cardiomyopathy patients over six years of age showed a profoundly altered gene expression pattern with enrichment of genes encoding fibrillary collagens, modulation of proteoglycans and a switch in thrombospondin isoforms and signatures for fibroblast activation. Additionally, Carolyn, a population of cardiomyocytes with a high pro-regenerative profile was identified in infant dilated cardiomyopathy patients, but was absent in those children that were greater than six years old. And this cluster in these infants showed high expression of cell cycle activators, such cyclin D family members increased glycolytic metabolism and any oxidative genes and alterations in beta adrenergic signaling genes. Dr Carolyn Lam: Wow. That sounds like a magnificent and elegant study. Could you boil it down to the take home messages? Dr. Greg Hundley: You bet. Carolyn. Great question. So two points first, infants with a predominantly regenerative cardiomyocyte profile, may preferentially receive treatment strategies to support cardiac regeneration while patients with a pattern associable with cardiac fibrosis may benefit from an early anti-fibrotic therapy to avoid diastolic dysfunction. And second, despite the impracticality of performing these large cohort studies in children with dilated cardiomyopathies, tailored pharmacological treatment is possibly realistic. For example, based on the expression of beta adrenergic signaling genes. Dr Carolyn Lam: Oh wow. That is super cool. That's Circulation for you, publishing these amazing basic science papers with very big clinical implications. Well, I've got another basic science paper for you and this time I've learned a new word actually. It's called O-GlcNAcylation. I should get you to say it after me. I had to get our editor-in-chief Joe Hill to teach me to say that, O-GlcNAcylation. So, cardiomyopathy from diverse causes is marked by increased O-GlcNAcylation. Now, in this paper, co-corresponding authors, Dr. Anderson and Umapathi from Johns Hopkins University provide a new genetic mouse model to control myocardial O-GlcNAcylation independent of pathological stress. Their data actually provided evidence that excessive O-GlcNAcylation caused cardiomyopathy, at least in part due to defective energetics. Enhanced O-GlcNAcase activity was well-tolerated. And conversely, attenuation of O-GlcNAcylation was beneficial against pressure overload induced pathological remodeling in heart failure. Dr. Greg Hundley: Interesting, Carolyn. So what are the clinical implications of these findings? Dr Carolyn Lam: Well, the data really provide new proof of concept that excessive O-GlcNAcylation is sufficient to cause cardiomyopathy, and they also suggest that attenuation of this excessive O-GlcNAcylation may represent a novel therapeutic approach for cardiomyopathy. Dr Carolyn Lam: Shall we go on and sort of wrap up on what else is in this issue? Because I'd like to talk about highlights from the Circulation family of journals that Sarah O’Brien really beautifully summarizes, talking about everything from Circulation: Arrhythmia & Electrophysiology, to [Circulation:] Cardiovascular Quality & Outcomes. It's just a beautiful piece where we get all the highlights. Must read. There's also a Perspective piece by Dr. Gillis on Rhythm Control in Atrial Fibrillation: Is Earlier the Better?, and that discusses the EAST-AFNET 4 and early AF trials. Dr. Greg Hundley: Very good, Carolyn. Well, from the mailbox, professors Pan and Liu exchange letters regarding a prior response to a letter regarding the article Genetic Architecture of Abdominal Aortic Aneurysm in the Million Veteran Program. Also, Dr. Arbus-Redondo has an EKG challenge entitled, Dual Chamber Pacemaker after Sinus Node Dysfunction and an Enlarged Right Atrium. Is it what it seems? Dr. Greg Hundley: And then finally, Dr. Corrado has a very nice Research Letter, entitled, Serial versus Single Cardiovascular Screening of Adolescent Athletes. Dr. Greg Hundley: Well, Carolyn, I'm dying to hear about fruits and vegetables. How about we get onto those featured discussions? Dr Carolyn Lam: Cheeky, cheeky, Greg. Here we go. Dr Carolyn Lam: Oh, I'm so excited about today's featured discussion because it's about my favorite thing, fruits and vegetables. Okay, wait a minute, everybody. Before you start rolling your eyes, this is a really important one. Have you ever asked yourself, what is the optimal intake levels of fruit and vegetables for maintaining long-term health? Well, guess what? We're about to find out and I'm so pleased to have the first author of today's feature paper, Dr. Wang Dong, and he's from Harvard medical school and Brigham Women's Hospital. We also have our Associate Editor, Dr. Mercedes Carnethon from Northwestern University and our Associate Editor who is also the editorialist to this paper, Dr. Naveed Sattar from University of Glasgow. So welcome, everyone. Dr. Wang, please tell us what you did in this study and what were your main results? Dr. Wang Dong: Thank you, Carolyn. So, basically, in this study, we analyzed the data from two long running cohort study. That is the Nurses' Health Study and Health Professional Follow-Up Study. So these two study includes more than 100,000 participants who had been followed for up to 30 years. And we also include a meta-analysis that includes in total 26 studies and about two million participant from 29 countries, and had countries around the world. So, basically, the major finding from this study is, of course, the intake of fruits, vegetable is inversely associated with the risk of death from all cause and the different kinds of cause-specific mortality. And we have a very interesting finding that is intake of about five servings per day, that can be translated into two serving of fruits and three servings of vegetables per day, was associated with the lowest risk of total mortality. So that's an optimal intake level for fruits and vegetable. Dr. Wang Dong: And another important finding from this study is, not all foods that some people consider to be fruits and vegetables can offer the same health benefits. For example, in this study, we found that starch vegetables such as peas and corn, and some fruits juice and potatoes are actually not associated with any benefit in terms of longevity. On the other hand, if you look at green living vegetables such as spinach, kale, and fruits that's orange color fruits and vegetables, that's rich in beta-carotene and vitamin C such as citrus fruits and berries, carrots they're associated with a substantial reduction in the risk of total mortality. That's a major finding from this paper. Dr Carolyn Lam: Oh, I just love it. I mean, just like such wholesome, beautiful findings from a wonderful study. Now, if I could ask you, cause I think the first thing everyone's going to say is, okay, these are associations. I mean, what'd you do about the residual risks? Could you maybe describe how you try to address some of these things like, is taking in fruits and vegetables just a surrogate for people who, I don't know, exercise more, for example? Dr. Wang Dong: Yeah. So in original data analysis, we actually have extensive data collection of all kinds of foods, lifestyle, risk factors, medication use, any health-related variables. So we carefully adjust for a large number of confounding factors. So actually another thing I want to point out, most all of these health-related lifestyle factors actually are inverse confounding factors in this kind of analysis. So when you adjust for other confounding factors, it's tend to attenuated your inverse association. So the review from confounding actually wouldn't be a major explanation for this association. Dr Carolyn Lam: Oh, that's great. And by the way, I think I misspoke. I'm not sure if I said residual confounding or residual risk just now, but you absolutely read me right, that I meant residual confounding. So thanks. Now that we've got that out of the way, if I could ask Mercedes, please. I mean, ah, another fruits and vegetables paper, I mean, what made this one different that we said we have to have it at Circulation. Dr Mercedes Carnethon: Well, thanks so much, Carolyn. And thank you Dong, for your team's outstanding work. I know what excited me about it was the demonstration of something that we have adopted into our lexicon, that one needs five fruits and vegetables. So I was excited to see you quantify it. In particular, the question I have for you is, did you see that these patterns of association of fresh fruit and vegetable intake were consistent across the age range and in both sexes? Dr. Wang Dong: Yes, of course. In total, this acts as a stratification variable. So basically, in our original data analysis, we did the analysis in the Nurses' Health Study, which all the participants are women, and in the Health Professional Follow-Up study, in which all the participants are men, would be analyzed separately and we found very consistent results in both cohorts. Then will be the meta-analysis to meta-analyze the results from these two cohorts. It comes out age, actually if you look at the paper, I think in one of the supplemental table, with the age stratified analysis, to look at the a better association if it still holds in different age group. And we did found that the results is pretty consistent in different age groups. And also, I would point out this meta-analysis provides further support to show that this results is generalizable in different people with different social economic status, demographics status also from different background. Dr Mercedes Carnethon: Thank you so much, Dong. it brings me to what Naveed wrote about in his editorial, that food is medicine and I just really loved that and loved the implications of that. So, I don't know, Naveed, if you've got some comments to make? Questions? Dr Naveed Sattar: Yeah, thanks Mercedes. No, I really love this as well because clearly the cardiovascular community, we do lots of trials. Lots of us are nihilists and just look at trials, but actually it's hard to do trials in the food and the dietary area, but these data are very consistent. I think there are multiple potential mechanisms that may explain this. We all have to eat every day, so it's a big part of our lives. Increase fiber intake, increase potassium, micronutrients, food displacement, the more fruit and veggies you eat, the less you'll eat of other things that perhaps are not as protective. And actually, part of the motivation to write an editorial was to put all that into context in terms of mechanisms. And particularly fiber, I think we underestimate the importance of fiber, but then it was also to discuss, well, if this is true, how do we help people make the changes? Dr Naveed Sattar: And at the level of policy, at the level of high risk groups, and my own particular favorite is really communicating dietary change in the clinic. And one of the things I often try, and we put this in a kind of headline figure in the editorial, was actually getting people to try to undergo the palate test or the retraining their palates. I have lots of patients, who, would you believe, in the west of Scotland, never really eat fruit and veg, and I really pushed them to say, "Look, would you please try? And it might take a few weeks for you to retrain your palate". And lots of people come back saying, "Ah, you're correct. And my God, now I like banana and I now like salad." Dr Naveed Sattar: So actually, there's lots of tips that we can do to help people increase from their average of two to three intake, which is the vast majority of population, to four to five, but it's a gradual process and it requires good communication with our patients and to compel them that these changes might take time, but that if they make these changes, they can get to a point where they really enjoy eating fruit and veg and all the multiple health benefits that come, which this paper has now showed, Mercedes. Dr Naveed Sattar: I think for me, that was the real nub of this. Dr Carolyn Lam: Naveed, I just love the way you express it. And indeed, everyone take up that editorial and look at that beautiful figure. I love the colorful fruits and vegetables on top because it also reminds us, and this paper shows, we are not talking about potato chips, and was it those, corn and peas. But, you know, we're talking about nutrition and fiber and the good stuff. Oh, this is just amazing. I wish we could go on forever, but we have a double feature this issue. And I just want to end by saying, thank you, thank you all of you, for being on the show today. It was such an important topic and I really loved the discussion as I'm sure the audience did. Thank you. Dr Mercedes Carnethon: Thank You. Dr Naveed Sattar: Thanks very much. Dr. Wang Dong: Thank you so much. Dr Carolyn Lam: I am so pleased to have with us today, a friend, a deeply admired colleague and the corresponding author of today's feature discussion, Dr. Mikhail Kosiborod from Saint Luke's Mid America Heart Institute. Dr Carolyn Lam: Welcome, Mikhail. And thank you for publishing this beautiful paper on EMBRACE heart failure with us. I know that this was presented as a late-breaking trial at the Heart Failure Society of America meeting, and it's a very much anticipated paper, but maybe I could start with it's all about SGLT2 inhibitors these days. So please tell us how does EMBRACE add to this accumulating knowledge that we have on SGLT2 inhibitors and heart failure? Dr. Mikhail Kosiborod: Well, first of all, Carolyn, thanks so much for publishing our trial in Circulation. And you're right, SGLT2 inhibitors have been taking the world of cardiometabolic medicine and heart failure by storm over the past few years. EMBRACE is a very unique trial because it really, took this world of rapidly developing technology in heart failure and heart failure monitoring, and coupled it with one of the hottest topics in heart failure today in terms of drug management, which is the advent of SGLT2 inhibitors and the emergence SGLT2 inhibitors as a efficacious therapy, not just for prevention of heart failure, but also treatment of heart failure. Because as you know, pulmonary artery pressure and hemodynamic status are one of the strongest predictors of patient outcomes, both in terms of symptoms, hospitalizations, and deaths in heart failure. And we know actually that monitoring and intervening on elevated pulmonary pressure in this patient population may lead to hospitalizations and possibly even death. Dr. Mikhail Kosiborod: But up until recently, it's been very difficult to monitor pulmonary pressures and to use them as an outcome in heart failure trials, because you will have to use invasive monitoring, essentially a right heart catheterization to get that data. Well, now we can actually have this implanted sensors like CardioMEMS, which are the sensors that we use in EMBRACE-HF trial. So, the question we wanted to ask is, we know SGLT2 inhibitors in DAPA-HF and EMPEROR-Reduced trials, clearly reduce the risk of cardiovascular death and hospitalization for heart failure, worsening heart failure, but the mechanisms have been hotly debated. Is there a possibility these agents can actually have an impact on hemodynamic status and pulmonary pressures? And that's the key central question that we tried to address and EMBRACE-HF trial by using this novel technology at the time, now it's been around for a few years, to noninvasively measure pulmonary pressures and use it as a primary outcome in our trial. Dr Carolyn Lam: Mikhail, first of all, hats off, it was a very, very clever idea to look at these patient populations who already have CardioMEMS right, and then perform this randomized trial. I mean, when I saw this, I was like, "Aw, man, how come I didn't think of that? That's just like so clever, but it's just so Mikhail to be ahead of the curve." But I'd like to remind the audience, this was a prospective randomized trial, the pre-specified outcomes, right? So maybe you could describe that in a greater detail and then the results. Yeah. Dr. Mikhail Kosiborod: Absolutely. Well, Carolyn, first of all, once again, thank you very much. You're being very kind. We do think it was a very novel clever idea and that you're absolutely correct, as this was very rigorously designed, randomized, double blind placebo controlled investigating trial within this study and 10 sites in United States. And the patients had to have heart failure, either with reduced or preserved ejection fraction, about half-and-half actually, as it turned out to be once it's all said and done with the trial. Because they had to have implanted CardioMEMS for clinical indication previously, they were quite advanced in terms of their heart failure. So more than half of the patients were in NYHA class III or IV, they had elevated brain natriuretic peptide levels, they had hybrid symptoms as you would expect. And essentially the patients were screened, and if they were eligible, randomized to use a empagliflozin-placebo in a double-blind fashion. Dr. Mikhail Kosiborod: And they were monitored actually for a couple of weeks prior to randomization to get a baseline pulmonary artery diastolic pressure. They were then treated for 12 weeks with empagliflozin, 10 milligrams a day, or a matching placebo. And we were measuring pulmonary pressure twice a day, every day for the 12 week treatment period, and then at the end of the treatment period, the treatment was stopped, but we actually continued to measure pulmonary pressure for one additional week again, twice a day, every day. So we actually saw what happened for one week after the treatment was stopped. And, as I mentioned before, the patient population was quite advanced from a heart failure standpoint. These were patients that were adequately managed with guideline-directed medical therapy for heart failure. Of course, about half of those patients have, have HFpEF. Did I mention before was the standard of care is not a thoroughly defined? Dr. Mikhail Kosiborod: And essentially what we observed was quite remarkable, which is average pulmonary artery diastolic pressure at baseline was about 22 millimeters of mercury across the patient population, and in patients treated with empagliflozin, there was quite a rapid reduction in pulmonary artery diastolic pressure that we saw almost immediately within one week as compared with placebo. And that divergence of curves in terms of pulmonary artery diastolic pressure continued over the entire 12-week treatment period. And by the end of the treatment period, there was nearly two millimeter of mercury difference in favor of empagliflozin, with lower pulmonary artery diastolic pressure in patients with empagliflozin compared with placebo. And also interestingly, even after the treatment was stopped for an additional week, those curves continued to diverge, with even greater lowering of pulmonary artery diastolic pressure in patients that received empagliflozin. So, I think to our knowledge, this is the first evidence from a randomized clinical trial, randomized double blind placebo controlled clinical trial, that SGLT2 inhibitors, in this case, empagliflozin, have essentially direct the congestion effect towards a lower pulmonary artery pressure rapidly and with effect amplified over time. Dr Carolyn Lam: Yes. Congratulations and beautifully present it there. Now, if I could ask a few more questions now, because the things will come up there. What happened to the diuretic dose? Is this depend on diuretic dose? Are there any subgroups that appeared to benefit more? Dr. Mikhail Kosiborod: No, excellent question, Carolyn. So first of all, we monitored average daily furosemide equivalent dose continuously throughout the trial, and what we observed was that there was no difference in diuretic dose, essentially, between the two groups from a loop diuretic management standpoint. Now, remember this patients are getting frequent pulmonary pressures with diuretics being adjusted all the time. But if you look at what happens over time, that's one of the figures in the paper you see essentially the flat lines in both groups. And coupling that with the fact that pulmonary pressures continue to diverge for another week after the treatment was stopped, at least in my mind, suggests that this hemodynamic benefits as we observed with empagliflozin as compared with placebo was lowering of pulmonary pressures is likely not simply due to diuretic effect. It just cannot be explained only by diuretic effect. I think these findings are very much in line with the analysis that we had in DAPA-HF trial with the analysis that recently were published from EMPEROR-Reduced, showing that you just can't explain what you see with heart failure benefits with SGLT2 inhibitors simply by diuresis. Dr Carolyn Lam: Fascinating. Well, how about the question of diabetes? Dr. Mikhail Kosiborod: Yes. So in terms of subgroups, that you mentioned, we did do subgroup analysis. Now I will say that the subgroup analysis have to be interpreted with a great deal of caution in this trial, because the entire trial had about 65 patients, so it's a small trial. It was really powered to look at the entire patient population and look at the primary end point of the diastolic pressure. Nevertheless, as I mentioned before, we had half-and-half reduced and preserved EF and we did not see a statistically significant heterogeneity in the treatment effect when we look at patients with reduced to preserved EF, so that hopefully both for outcome trials in preserved EF heart failure, we'll see, of course, what happens with that. And in terms of diabetes we saw a bit greater effect in patients with diabetes as compared to patients without diabetes, in terms of pulmonary artery pressure reduction. Dr. Mikhail Kosiborod: But again, I would just strongly caution interpretation of those subgroups because certainly when we look at clinical outcomes in those DAPA-HF and EMPEROR-Reduced, we see no such difference. We see that the benefits, right, the hard clinical outcomes, benefits, are quite consistent regardless of diabetes status. I will say one other thing, which I think is really important. If you look at the pulmonary artery pressure trajectory in patients treated with placebo in EMBRACE-HF, you see that they actually go up over time. And this is in patients that have frequent monitoring of blood pressures, our own guideline-directed medical therapy are closely watched by predominantly heart failure cardiologists and their teams to make sure that they're well-managed. And despite that, you see this increase in pulmonary pressure over time, and that's just another reminder to us that heart failure is a progressive disease despite best available therapy. Dr. Mikhail Kosiborod: These patients deteriorate over time, which is why treatment, novel advancements, treatments like SGLT2 inhibitors and their effective implementation is just so important because we know the benefits occur very early. We saw one week here, when we start seeing separation of curves, certainly see a significant difference by 12 weeks with pulmonary pressure. But of course we know with clinical outcomes, we see within a few weeks of randomization, already a significant benefit in reducing CV death and hospitalization for heart failure, both in DAPA-HF and EMPEROR-Reduced trials. So I think that's a critical point for clinicians to keep in mind at the time of the death. Dr Carolyn Lam: Mikhail, those are just such important and practical take-home messages. Thank you again. In the last minute though, I just really, really have to go back to that very clever method. Could I just pick your brain? I mean, it's like a very clever population. This CardioMEMS population that maybe what's in the future plans? Give us a sneak peek! Dr. Mikhail Kosiborod: Well, Carolyn, very insightful as always. I really think of it as a novel platform for drug development and heart failure. I think this is the proof of concept. This is really the first time we did something in the heart failure space was with monitoring of pulmonary pressures that shows that drugs that work for hard clinical outcomes actually do something meaningful on hemodynamics. We've struggled for such a long time in heart failure to have a good surrogate endpoints that would be reflective of clinical outcomes. This may be it. It may be one of them. And I think EMBRACE-HF is a good concept proving study that can say, if you have a compound and you think that compound may be effective for heart failure. So of course the congestion is so important that we know correlates so well with clinical outcomes Dr. Mikhail Kosiborod: When we started to trial all the way back to late 2015, very few patients had this device. It's not lots of patients have this device. And testing novel treatments to try to understand will there promise in heart failure, and even making go-no-go decisions, in terms of drug development, I think is starting to become a potential future development, which we should at least seriously consider in the heart failure space. Dr Carolyn Lam: Wow, Bravo. And Mikhail, I mean. Okay, audience, listen, you heard it right here. This is amazing. Thank you once again for publishing with us and congratulations on the beautiful paper. Dr Carolyn Lam: And from Greg and I, thank you audience for joining us again today, you've been listening to Circulation on the run. Tune in again next week. Dr. Greg Hundley: This program is copyright of the American Heart Association 2021.  

In this episode of More Life, Hartford HealthCare’s Steve Coates talks to Jim Mason, a 67-year-old heart failure patient who was faced with repeat hospitalizations. His cardiologist, Dr. Howard L. Haronian, who saw Mason as the perfect candidate for the outpatient CardioMEMS procedure. It involves implanting a wireless sensor in the pulmonary artery and can significantly reduce heart failure hospital admissions and vastly improve quality of life. Learn more about the CardioMEMS procedure at Hartford HealthCareRemember to subscribe, rate and share the health!

Monique Tanna, MD discusses CardioMEMS™ technology at Penn Medicine. She shares the benefits and cost effectiveness that has been shown with the CardioMEMS™ Heart Failure System and how it helps to monitor a patient and possibly ward off issues before they become problematic and end up with hospital readmission.

We review the inpatient management in HFrEF, role of GDMT initiation & HF exacerbating drugs. We end the episode with a discussion on HFpEF & device therapies with Professor Carolyn Lam, a Senior Consultant of the National Heart Centre, Singapore and Professor of Duke-NUS Cardiovascular Academic Clinical Program. Listen, Like, Subscribe, and give us a rating!

In this week's View, guest host Dr. Deepak Bhatt offers a preview of some of the hottest trials at ACC.19, taking place March 16-18 in New Orleans, including the Apple Heart study, results of the open-label extension of the PIONEER-HF trial, the HoT-PE study, results of the PARTNER 3 trial, Self-Expanding TAVR or SAVR in Patients at Low Risk of Surgical Mortality, echocardiographic outcomes from the COAPT trial, primary results of the AUGUSTUS trial, MOMENTUM 3, 1-year outcomes from the CardioMEMS post-approval study, the First Randomized Human Experience with a Ticagrelor Reversal Agent, the DEFINE PCI trial, MRUSMI, primary results of the GLOBAL LEADERS adjudication sub-study, the CLEAR Wisdom Trial, the CREOLE Study, DECLARE, REDUCE-IT, the STOPDAPT-2 trial, SMART-CHOICE, ODYSSEY OUTCOMES, and IRAD.

After a webchat on heart failure treatments, Dr. Maria Mountis, heart failure cardiologist and Dr. Edward Soltesz, Surgical Director of the Kaufman Center for Heart Failure and Recovery discussed topics that were addressed during the chat including heart failure medications, cardioMEMs monitoring, when patients are considered for advanced therapies, what patients should know about heart transplant or ventricular assist devices, and high risk heart surgery for patients with heart failure.

  Dr Carolyn Lam:                Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center, and Duke National University of Singapore. And I am joined today by our Editor of Digital Strategies, Dr. Amit Khera from UT Southwestern, as well as three wonderful fellows in training. Yes, you've guessed it, it's our FIT Podcast and I'm just so thrilled to be here again. Dr Carolyn Lam:                Amit, any words of introduction before we start? Dr Amit Khera:                  Thank you Carolyn. I think, for both of us, this is our favorite podcast, or two podcasts, that we do, a year. It reminds us of how bright the future is, with superb cardiology fellows in training around the country, and it really is a testament to how important we find fellows in training, to Circulation, to our mission, and how much we learn from them.                                                 So we're really excited about this group, today, and thank them for participating. Dr Carolyn Lam:                Absolutely. So, why don't we start, now, with ladies first? Let's hear from Dr. Elizabeth Hill. Dr Elizabeth Hill:                Thanks for having me today. My name is Beth Hill, and I'm a first year cardiology fellow at Scripps Clinic, in La Jolla, California. I've a particular interest in sports and exercise cardiology, which brings me to the article I picked today about sudden cardiac death and hypertrophic cardiomyopathy, hot topics in the field and in general.                                                 And so, today, I'm excited to be discussing the EVIDENCE HCM study, looking at the hypertrophic cardiomyopathy of risk, sudden cardiac death model. Dr Carolyn Lam:                Nice. So tell us a little bit about what really struck you about the paper and, perhaps, how that may apply to where you practice? Dr Elizabeth Hill:                What I really liked about the paper is that, when I see patients in clinic with hypertrophic cardiomyopathy, prior to having this risk stratification tool, we didn't really have a way to objectively risk stratify our patients with hypertrophic cardiomyopathy and really guide the discussion about who may benefit from an implantable cardiac defibrillator or ICD. And so, I've been using this a little bit with my patients. While it hasn't made it fully into the AHA or ACC guidelines yet, I'm using it as a tool. Dr Carolyn Lam:                Great. You know, these are seven risk factors, isn't it? I'm always struck by that survival curve that really shows that those with a predicted 6% risk stand out. Is that what you use, as well, to guide your decisions? Dr Elizabeth Hill:                Yeah. I think, as the authors noted, they picked this somewhat arbitrarily so that they could study their risk model. But I think what they found is that it seemed to fit well with the observed high risk of sudden cardiac death cohort, such that those that were seen and observed, about 9% risk of sudden cardiac death in five years, were in that greater than 6% cohort. So I think that population should receive ICDs, and that is one factor that I used to guide my decision making as well. Dr Amit Khera:                  Beth, this sort of interest that you've had for a long time, in sports cardiology, I've noted you've done some prior work in EKG screening and other screenings. In terms of this article specifically, as you pointed out, this is a really helpful tool because I still remember back when I was a fellow in training, there was, sort of, this thought that everyone was high risk with hypertrophic cardiomyopathy, and I think we realized that's not true at all. The overall incidence of sudden death was only 2.4% in this cohort.                                                 The question I have for you, in terms of application, is, as Carolyn pointed out, these are reasonably simple variables, but as we sometimes are now using cardiac MRI and genetics and other more advanced tools, where do you think they fit in, in the current paradigm, since this is a bit of a more simplistic score? Dr Elizabeth Hill:                The seven risk factors they put into this tool were noted to be independently associated with an increased risk of sudden cardiac death, and those are well known factors, entricular tachycardia, maximum wall thickness. But I really do think that other factors will come into play soon and are part of my discussion, and colleagues' discussions, including the late gadolinium enhancement on MRI, genetic factors, and I really think this may be a place for tools like machine learning. These authors, O'Mahoney and colleagues, they really did, kind of a tour-de-force, going back to the 1970s, but there is still a decent amount of data missing. So maybe we can partner with the machines and help them go back into these records, a little bit more effortlessly, and look at genetics, maybe some wearable device data, and really refine our risk stratification tool moving forward. But that's definitely something I use in risk stratification in some of my intermediate risk patients. Dr Amit Khera:                  Those are great points. I think your point about machine learning and novel algorithms will definitely take foot in the future.                                                 Maybe a follow-up, again, given your background interest, I think it's a trade-off where we're trying to, of course, avoid sudden death, but you also don't want to overtreat. Especially, when you think about athletes getting ICDs and how that changes, or anyone, for that matter, about maybe telling someone they're at high risk, or giving them an ICD when perhaps they don't need it. I guess that comes to, what's the threshold? Here they use 6%, but that ends up being a bit arbitrary, in terms of what threshold we use. And how do we decide, when we talk to our patients, about what threshold's a right threshold to apply an ICD? Dr Elizabeth Hill:                Yeah. That's a great question. Like you mentioned, these devices come with inherent risks, such as unnecessary shocks, increased risks for infection, and sometimes there's restrictions with athletic sport, although that's been changing recently.                                                 But, I think that's where the shared decision-making process comes into play, where you put current data on the table with the patients and, perhaps, their families as well, and have a risk-benefit discussion. Perhaps gather a little bit more data about the patient, maybe follow them over time, but I guess I wouldn't jump to put an ICD in, in every patient and, especially, the lower-risk cohort. And what number that is, I'm not quite sure. Here they say maybe less than 4%, but, again, somewhat arbitrary, I think. Dr Carolyn Lam:                Thanks Beth. I mean, as Amit said, it's just so inspiring to see how the papers are being used in practice. Really loved those perspectives.                                                 Now, from sunny San Diego all the way to snowy New Zealand. We have Dr. Mesfer Alfadhel. And Mesfer, tell us a little bit about yourself, and the paper that you've chosen? Dr Mesfer Alfadhel:        Thank you very much. I'm thrilled to be part of this podcast. I'm a second-year cardiology fellow-in-training at the Needham Hospital, in Needham City, New Zealand, where it's snowing at the moment. I'm also a clinical lecturer at the University of Otago School of Medicine. I do have great interest in general cardiology, as the rest of my colleagues, but also am passionate about interventional cardiology and structural heart disease.                                                 The paper I've chosen is really quite relevant to everyone in cardiology, and perhaps extends to other colleagues in other health professions impacted by automated external defibrillator use on survival and functional outcomes in shockable observed public cardiac arrest. The aim of the study was to determine the association of bystander automated external defibrillator use, the survival and function of outcomes in shockable observed out of hospital cardiac arrests. The study was from 2011 to 2015 and the Resuscitation Consortium prospectively collected detailed information on all cardiac arrests at nine regional centers, six in the United States and three in Canada.                                                 They also found that among nearly 50,000 out of hospital cardiac arrests, 8% were observed public out of hospital cardiac arrest, of which 61% were shockable. Overall, a remarkable one in five of shockable observed public out of hospital cardiac arrest were bystander shocked. Now the bystander automated external defibrillator observed, shockable observed public out of hospital arrests were associated with increased odds of survival and full or near full functional recovery almost 2.6 and 2.7 odds ratio than when compared to emergency medical service defibrillation. What's also interesting is that the longer the wait for the emergency services, the higher the benefits from a bystander observed shock. Dr Carolyn Lam:                You know, Mesfer, I appreciate that you chose this one as well. What struck out to me immediately was that more than 60% of out of hospital cardiac arrests were shockable. And when we think about the number of lives that could potentially be saved, therefore, that's quite astounding, isn't it? But can I ask you something? So these are in the US and Canada, how applicable do you think this is to New Zealand? Dr Mesfer Alfadhel:        We do have a small population, just over four million. The number of cardiac arrests here is around 2,000 out of hospital cardiac arrests. And I think probably half of them in the latest reports were shockable. The emergency response time in the urban areas is around six minutes, which I think is acceptable, but we have about 20% of population living in rural areas. And the emergency response time exceeds 10 minutes almost all the time. I think that probably a group that we need to direct intervention to in New Zealand. Dr Amit Khera:                  It's really an important article. I should say that June for the American Heart Association is AED and CPR month so great choice to remind us of the value of these and especially, the one thing that was amazing, obviously this is an observational study, but the absolute change, not relative, was about 14% meaningful recovery and so that's quite impressive in terms of the number needed to treat if you will. Maybe an adjunct to Carolyn's question is, when we think about strategies to enhance bystander AED use for strategies, essentially get the AED there faster. As you know if the EMT time was not delayed it wasn't necessarily better for the bystander.                                                 We had a paper in Circ sometime last year looking at drones and then also geocoding and other people in some countries have looked at apps where you essentially can train a group of people and then they can be texted for a sudden cardiac arrest in their area. I'm curious about any creative things, there's always training and AEDs, I think in this place it was public areas in industry, but what do you think are some creative things or things that we need to be doing to help enhance the ability for bystander or early AED use. Dr Mesfer Alfadhel:        I think this is one area in medicine in general that where technology is really going to advance how we deal with this problem. There's an app that's available, it was launched in the UK a few years ago and it's become available in New Zealand in the last two weeks called, the Good SAM. SAM stands for smartphone activated medics. And it's become available in New Zealand two weeks ago and I downloaded it and still yet wait for it to be activated. And the way it works is you can activate a medical emergency using the app and it dials the emergency response but what it also does is it activates the nearest three people with CPR training nearest to you and it tells you how far they are from the emergency. Now if you don't have the app and you call 911 or the equivalent, the operator can activate it to the nearby personnel who have that experience. And I think it's going to reduce the time markedly.                                                 Now the other end of the question where some of what strategies could be used I think we had a good report from Denmark where they made changes in 2007 in Denmark and then followed by the rest of the country in 2010 where they made CPR or resuscitation education as compulsory at school but also when getting a driving license they made courses available for free that increased the number of defibrillators available in public places and they shared that information with public. They've redone, audited their work, and compared to prior to intervention prior to 2007 and after that and they found an increase number of using the AEDs increased from somewhere around 2% to 15%, which is really encouraging. I think we are following Denmark in that regard probably at slower rate. Dr Amit Khera:                  Thank you those are excellent insights. Dr Carolyn Lam:                Amit, don't you see that I just love learning from these fellows during these podcasts. We should do more of these. This is awesome. Dr Amit Khera:                  I completely agree. Dr Carolyn Lam:                Thank you Mesfer, enjoy the skiing. But now from snowy New Zealand we're going all the way to Nashville Tennessee. Welcome Dr. Vineet Agrawal. So tell us a bit about yourself and your paper. Dr Mesfer Alfadhel:        So my name is Vineet Agrawal. I'm a second-year cardiology fellow at the Vanderbilt University Medical Center. My background is as a physician scientist and as a general cardiologist. My long-term goals are in understanding mechanisms underlying heart failure with preserved ejection fraction.                                                 With that in mind I was really taken by an article that was recently by Margaret Redfield's group from the Mayo Clinic in Circulation, titled “Global Pulmonary Vascular Remodeling and Pulmonary Hypertension Associated with Heart Failure and Preserved or Reduced Ejection Fraction.” I found this article to be a very interesting, hypothesis-generating article.                                                 In a nutshell what they did was they took an autopsy cohort of patients in the Mayo Registry and those who had heart failure with both preserved and reduced ejection fraction, normal controls, and those who had a primary pulmonary venous occlusive disease, and looked at the lung specimens of these patients. And interestingly what they found was there was a significant amount of pulmonary venous remodeling that had occurred in patients who had both preserved and reduced ejection fraction. This correlated not only with their right heart cath findings, so those who had elevated pulmonary pressures and elevated transpulmonary gradients, but also differed from the primary pulmonary venous occlusive disease in the sense that the histologic appearance of these vessels was quite different.                                                 And while as an autopsy study this is not necessarily an article that would immediately change practice, what I think it does do though is it forces us to think about these conditions in a different context and particularly with an eye towards future therapeutics. Heart failure with preserved EF as a disease, as I'm sure we all know, is sorely missing therapies that could alter the disease progression and potentially even alter mortality in these patients. And this article in my opinion really sheds light on at least anatomically a new location for us to think about as a therapeutic target when we try to better understand this disease and find therapies for these patients. Dr Carolyn Lam:                Vineet, can I just say you're singing to the choir here. I'm such a fan of this work as well for obvious reasons. But hey, could I ask you, in your clinical practice, do you see a lot of these patients with HFpEF and pulmonary hypertension and wonder how to treat them? And along those lines, how has this paper helped you think about these patients more? Dr Mesfer Alfadhel:        I would say when I first started residency as a medical student this was not necessarily a condition that was really something that I had learned much about or felt like I had been exposed to; however, as a resident I felt like most of the patients, or at least half of the patients, I was seeing with heart failure had a component of diastolic heart failure or they had a preserved EF but very symptomatic from the standpoint of heart failure. And I struggled to treat them, particularly in some part due to the fact that many of the risk factors that contribute to HFpEF, diabetes, uncontrolled hypertension, obesity, are chronic problems that are difficult to manage as a clinician regardless.                                                 And second because I feel that there just weren't any data to support any treatments that we were pursuing at the time and so we would try and apply what we had learned in other types of heart failure to these patients with limited results. If I could talk about what I think this article may change in terms of my practice today, one thing that we've always thought about in terms of pulmonary vascular remodeling in heart failure is that it's just a passive process that as fluid builds up you back up into the lungs and as the fluid builds up and backs up into the lungs you get remodeling.                                                 I think one thing that this article shows is that it may actually be a bidirectional process, which would suggest that perhaps we may need to reconsider looking at pulmonary-specific therapies in this population. But more importantly I think it does confirm that chronic elevating filling pressures do have an effect and a deleterious effect on the pulmonary vasculature. Particularly when you look at other trials such as the CardioMEMS trial, the CHAMPION trial in which the data pretty convincingly showed that as clinicians we don't do the best job of reducing left-sided filling pressures in our patients with heart failure as much as we think we do. This article really drives home the point to me that I really need to make sure that when I see these patients that I'm doing everything I can to reduce their left-sided filling pressures because the consequences of not doing so can affect the lungs, which can then in turn affect the heart as well. Dr Carolyn Lam:                Vineet, that's really words of wisdom. Couldn't agree more. And these are the first sort of autopsy, histological evidence that we have, which is so important. I think if I could just add a couple of perspectives too, it makes me think about making sure that I rule out PVOD in these patients sometimes. We now keep thinking about HFpEF we forget that we need to also rule out PVOD and the other thing much as we now think about not just the filling pressures but the remodeling it's good to note that they found it more in the venous than the arterial system, which also comes therefore with a warning message that we can't just extrapolate I suppose all the PAH therapies that we know about. What do you think about that? Dr Mesfer Alfadhel:        I absolutely agree with that. It's really interesting that all of our therapies from heart failure standpoint and from a PAH standpoint have focused on the myocardium, the neural hormonal cascade, and then the arterials. The pulmonary main artery and arterials. I don't think anyone really understands the biology of pulmonary veins and yet they're actually a pretty significant part of our everyday practice in cardiology. Pulmonary veins are thought to be the source of atrial fibrillation. We look at pulmonary vein inflow when we evaluate patients with echoes. And yet we understand so little about the biology and the mechanisms by which pulmonary veins are affected in both diseased and healthy patients.                                                 I think this article for that reason raises a number of very interesting questions and may potentially change the way we think about these patients. Dr Carolyn Lam:                I keep learning, Amit, this is awesome. I could go on forever so you better stop me. Dr Amit Khera:                  I should probably just be a fly on the wall. You must know Carolyn is a HFpEF, HFrEF aficionado and you guys should have a side call for another hour after this. But I do have one, maybe orthogonal question which is, it's interesting because if you look at how insights were made, they're made off areas I would argue at least that we don't, modern environment uses much which is the autopsy and probably to a large degree hemodynamics as much as probably in the old days although that's changing. I'm curious in a fellowship training program your exposure to autopsy and kind of current in-depth hemodynamic-type training, what's your experience? Dr Mesfer Alfadhel:        Our experience with looking at pathological slides, getting under the microscope, seeing tissue first hand, is somewhat limited in our fellowship training program. I would say in certain subspecialties like our heart failure, advanced heart failure subspecialties we do get a chance to see more myocardial biopsy specimens, but I think increasingly the focus has been on noninvasive methods by which we can assess some of these same things that we used to do, use the microscope for. Invasive hemodynamics I think similarly we get a lot of experience in terms of spending time in the cath lab but I do kind of wonder if we don't have the same in-depth training that we used to have in understanding all the nuances of hemodynamics that used to exist in the past.                                                 Certainly, I think that while that's partially a reflection of the way and the direction in which medicine is heading, there is a little bit that's potentially lost there. That said, while we have the benefit of manuscripts like this that does do in-depth hemodynamics and looks at autopsy samples from a clinical standpoint, if we were to ever try and understand this in a larger population I think we would be required to try and find a way to noninvasively or maybe through potentially invasive hemodynamics better study this in live patients. Dr Amit Khera:                  Appreciate that answer and I'm just for all of you, this has been outstanding. You all have served as incredible expert discussants. I know Carolyn already said it multiple times but we've learned a ton about each of these articles and great to see how they come alive and are used in practice and how they're applied in your own thinking and specifically as fellows in training with these have meant to you. We thank you all for joining us and it's really been a fantastic experience. Dr Carolyn Lam:                Amit, I can only echo your thanks and thank you listeners for joining us today. Fellows out there you are so important to us. Please, please apply to join us on the next FIT podcast as you can see it's really fun.                                                 Don't forget to join us again next week.

Dr Carolyn Lam:                Welcome to Circulation On the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center, and Duke National University of Singapore. Our feature paper this week discusses the very important patient group with myocardial infarction and non-obstructive coronary artery disease, a paper that we will be digging deep into right after these summaries.                                                 The first paper identifies a novel therapeutic target in pulmonary arterial hypertension, and that is nicotinamide phosphoribosyltransferase, a cytozyme which regulates intracellular NAD levels and cellular redox state, regulates histone deacetylases, promotes cell proliferation, and inhibits apoptosis.                                                 This is a paper from first author Dr. Chen and co-corresponding authors Dr. Machado from University of Illinois Chicago and Dr. Garcia from the University of Arizona. The authors found that plasma and mRNA and protein levels of  nicotinamide phosphoribosyltransferase  were all increased in the lungs and the isolated pulmonary arterial endothelial cells from patients with pulmonary arterial hypertension.                                                 They were also increased in the lungs of rodent models of pulmonary hypertension. Nicotinamide phosphoribosyltransferase deficient mice were protected from hypoxia mediated pulmonary hypertension; whereas, enhanced activity promoted human arterial smooth muscle cell proliferation via paracrine effect and inhibition of activity attenuated pulmonary hypertension in rats.                                                 This paper, therefore, provides evidence that nicotinamide phosphoribosyltransferase plays a role in pulmonary vascular remodeling and its inhibition could be a potential therapeutic target for pulmonary arterial hypertension.                                                 The next study suggests that high sensitivity cardiac troponin T may be an early biochemical signature for clinical and subclinical heart failure. In this study from first author Dr. Seliger, corresponding author Dr. deFilippi, and colleagues from Inova Heart and Vascular Institute, the authors measured high sensitivity cardiac troponin T at baseline among almost five thousand participants in the multi-ethnic study of atherosclerosis MESA cohort, who were initially free of overt cardiovascular disease.                                                 Cardiac magnetic resonance imaging was performed at baseline and repeated 10 years later among 2,831 participants who remain free of interim cardiovascular disease events, among whom 1,723 also received gadolinium enhanced cardiac magnetic resonance for characterization of replacement fibrosis by late gadolinium enhancement. Results showed that a mild elevation of high sensitivity cardiac troponin T identified subjects at highest risk for an increase in left ventricular mass and end diastolic volume over the next 10 years.                                                 Higher levels also associated with an increased incidence of replacement fibrosis, but with no differentiation between ischemic or non-ischemic fibrosis patterns. For the more high levels remained an independent predictor for incident heart failure, coronary heart disease events and cardiovascular events, independent of underlying left ventricular hypertrophy or ejection faction.                                                 The implications are that myocyte injury, measured with a highly sensitive cardiac specific troponin assay may ultimately be an important early signal used to target therapy to prevent or delay left ventricular remodeling and progression to heart failure.                                                 Does maintenance of cardiovascular risk factors at target eliminate the excess risk of mortality in cardiovascular diseases associated with type 1 diabetes? Well, this question was addressed in the next paper by Dr. Rawshani and colleagues of the Swedish National Diabetes Register in Gothenburg Sweden. The authors compared more than 33,300 patients with type 1 diabetes to more than 166,500 match controls without diabetes from the Swedish National Diabetes Register. They found that patients with type 1 diabetes, with five selected cardiovascular risk factors at target, demonstrated a non-significant access risk of death compared to controls.                                                 These five risk factors included glycated hemoglobin, blood pressure, albuminuria, smoking, and LDL cholesterol. Nonetheless, despite having all risk factors at target, persons with type 1 diabetes still had 82% to 97% elevated risk of myocardial infarction and heart failure respectively. For every incremental risk factor not at target, the excess risk of death in cardiovascular outcomes increased in a graded fashion.                                                 In conclusion, there was a steep graded association between decreasing number of cardiovascular risk factors at target and major adverse cardiovascular outcomes with patients with type 1 diabetes. While achievement of current evidence based target levels of five cardiovascular risk factors markedly reduced or even potentially eliminated the excess mortality risk, these patients remained at higher risk of myocardial infarction and heart failure compared with controls.                                                 The final paper suggests that hemodynamic guided heart failure management may be beneficial in general clinical practice and not just in the context of controlled trials. In this study by Dr. Heywood and colleagues from Scripps Clinic Torrey Pines in La Jolla, California, the authors examined the first 2,000 patients implanted with the novel Pulmonary Artery Pressure Sensor, CardioMEMS, in the general cardiology practice setting.                                                 They found that patients uploaded information an average of every 1.2 days, and that pressures were significantly reduced by remote monitoring using the Pulmonary Artery Sensor where patients with the highest mean pulmonary artery pressures had the highest reduction in pressures. Furthermore, they found that these general use patients experienced a greater reduction in pulmonary artery pressure over time compared to those in the pivotal CHAMPION clinical trial.                                                 The results from this large observational study, therefore, demonstrates hemodynamic heart failure management may be effective in U.S. clinical practice with high rates of patient adherence and effective pressure management.                                                 This paper is accompanied by an excellent editorial by Drs. Gorter, Rienstra, and van Veldhuisen from University Medical Center, Groningen, Netherlands, which really places this paper in the clinical context of heart failure and particularly patients with heart failure and preserved ejection faction                                                 Well that wraps it up for your summaries. Now for our feature discussion.                                                 We're discussing a hugely important emerging issue today. And it's MINOCA, a myocardial infarction with non-obstructive coronary arteries, and a very important paper in today's issue, which really provides the first insight into potential long-term medical therapy in the management of MINOCA.                                                 However, now this issue of MINOCA is quite new and I'm sure new to many of those listening on the line. So, I am with the first and corresponding author of the paper, Dr. Bertil Lindahl from Uppsala Clinical Research Center in Sweden. Welcome. Dr Bertil Lindahl:               Thank You. Dr Carolyn Lam:                And also the associate editor who managed this paper, Dr. Gabriel Steg from Hospital Bichat in Paris, France. Welcome back. Dr Gabriel Steg:                Hello. Dr Carolyn Lam:                Now, we need to start by first understanding what we're talking about. MINOCA ... give us a good definition of what you mean by MINOCA. And does it include the non-coronary causes of AMI, or non-obstructive disease? Does it include myocarditis? Does it include the non-cardiac causes, like pulmonary embolism? Dr Bertil Lindahl:               Our definition of MINOCA used in this paper is that you received the ICD code for acute myocardial infarction. If you have a clinically clear case of myocarditis or Takotsubo and were not included in this analysis. But we know if we look into patients that have got the diagnosis of myocardial infarction ... if you performed, for instance, MRI afterward, you can see that a portion of the patients experience ... between 10 and 30 percent of the MINOCA patients, have evidence of myocarditis, although it was not clinically expected.                                                 So this is a heterogeneous population ... initial diagnosis was myocardial infarction. Dr Carolyn Lam:                Thank you for clarifying what you used in your study. Gabriel, could I just, you know, bring you in on this because you invited an excellent editorial that accompanies this paper. And, basically, it helps to get us past all this terminology you know, MINOCA now. Could you maybe just clarify the overall perspective of what it means? Dr Gabriel Steg:                Yeah. This area is fairly new and we still have a major nomenclature problem. Clearly it's been recognized for many years that patients who have a clinical syndrome of myocardial infarction do not necessarily have obstructive coronary artery disease. At least severe obstructive coronary artery disease. Many patients have mild lesions and some patients apparently have no lesion at all.                                                 Now, over the last few years we've understood that this is really a syndrome. And that under that big umbrella, there are patients who have non-cardiac causes of troponin elevation and chest pain. These should be excluded from MINOCA. If you have pulmonary embolism, this is not MINOCA. This is pulmonary embolism.                                                 The second aspect is there are more subtle distinctions to be made with fairly new entities such as Takotsubo. When this study was started, Takotsubo was an emerging disease concept. And so the authors were not able to properly rule out the Takotsubos and probably a few myocarditis from their data set. We now have learned over the past few years that MRI is an excellent tool to screen MINOCA patients and flush out patients who have myocarditis or Takotsubo, which are not rare. Actually it's a substantial portion of that entity.                                                 And then we're left with what I call the true MINOCA. Now what's fascinating in the study here is really that ... first of all I want to say this is another great study from our Swedish colleagues leveraging their data collection tools, which are remarkable. Really an example to the world.                                                 The second thing is they have collected ten years of data on MINOCA. And they're able to tease out which are the agents that should be using secondary prevention in that population. Elegantly demonstrating with sensitivity analysis and positive and negative controls what are the agents associated with improved outcomes and what are the agents that apparently do not impact outcomes.                                                 So even though at the time they were not able to rule out myocarditis and Takotsubo properly, still the sheer size of their study, long term follow up, and the careful statistical analysis that they've done are remarkable. Dr Carolyn Lam:                I couldn't agree more. And more so in an area that is really emerging in importance. And for which we don't have any prospective clinical trials. I'm correct in saying that, right ? So Bertil, this would be a great point for you to let us know what are the main findings from your study please. Dr Bertil Lindahl:               The main findings are that statins are associated with a beneficial effect on the cardiac event. And also, ACE inhibitors or ARBs , while we were not able to show statistically things you can affect with beta blockers and similarly not with dual anti-platelet treatment. So that's basically the main findings of the study. Dr Carolyn Lam:                May I ask how have these findings personally impacted your clinical practice or do you think the next steps are gaps that need to be addressed first? Dr Bertil Lindahl:               I think that's an ongoing discussion in Sweden now and in our hospital on how this should be applied to clinical practice. Nothing. It will have an effect that statins and ACE Inhibitors or ARBs will be used. I'm not sure whether we still can say that we should not use beta blockers or dual antiplatelet treatment. But I think also that we are now discussing we should do a randomized clinical trial to really tease out whether we should use beta blockers or not or also verifying the findings regarding ACE Inhibitors and ARBs.                                                 So, I think there's always a discussion whether we can really use observation studies for treatment decision. But I think since we don't have any better trials so far I think that this is the best that we can get. So I think it will be used and applied in clinical practice. Dr Carolyn Lam:                Indeed. I really agree with what Gabriel said this is the best available evidence we have now. And my personal take home message was to pay more attention to the statins and the ACE Inhibitors. So congratulations on this great study.                                                 Gabriel, what do you think? What are next steps? I mean, MINOCA's not even in the guidelines now. Our guidelines talk about type 1, type 2, AMI ...how does it all fit in? Dr Gabriel Steg:                Well, we've seen a sea change in the concepts regarding myocardial infarction over the last fifteen years with the advent of troponin and the ability to diagnose new patients that previously we wouldn't even label as an MI.                                                 The second aspect is we've recognized over the years that there are some genuine MI's that don't have severe obstructive coronary artery disease. Now what's interesting is that some of them may have apparently mild obstructive disease. Which presumably is related to coronary dissections, embolism, plaque rupture with thrombosis that disappeared in the interim. And some of them may have actually "clean" coronary arteries and have myocardial infarction related to other mechanisms such as micro vascular mechanisms. What's interesting, and I'd like to ask the opinion of Dr. Lindahl is, these three types of diseases; mildly obstructive disease, coronary dissection, and microvascular angina are all more frequent among women. And I wonder whether you have any insights regarding gender differences in your registry. Dr Bertil Lindahl:               In this study, in the sub-group analysis we saw no significant interaction between gender and the effects. But unfortunately we don't have the registry information between , let's say completely "normal coronary arteries" versus "mildly obstructed coronary arteries". And that's a clear limitation of this study. It will be very interesting to see whether these effects are similar in these two sub-groups.                                                 It seems from other studies that approximately fifty percent of the MINOCA patients that have normal coronary arteries and fifty percent that have mild aortic disease. So this is a limitation of this study and I think that's just something we have to look for in the future. And I hope that we will have in the registry onwards, data on whether this normal or mild coronary artery disease. Dr Carolyn Lam:                Really appreciate that and really appreciate the insights you gentlemen have shared. Any final words or concluding remarks, Gabriel? Dr Gabriel Steg:                Well, again congratulations on the great study. I would refer our readers to the excellent editorial of John Beltrame that accompanies this paper, which reviews the concepts of MINOCA, the nomenclature, and some of the remaining and lingering questions that plague the field. And delineates way forward for studies.                                                 I think it's a fascinating area. I'm sure we're going to hear a lot more, both from the Swedish Heart Registry as well as other data sources. I think we all need to stay tuned to this important area. The prognosis of these patients is not so good, so we need to pay attention to that entity. Dr Carolyn Lam:                Wonderfully put. Well, thank you listeners for joining us this week. Please share this episode with all of your friends. So thank you and join us next week.  

The CardioMEMS™ is a permanently implantable system designed to wirelessly measure and monitor cardiac activity in patients with congestive heart failure.The CardioMEMS™ HF System is the first and only FDA-approved heart failure (HF) monitoring system proven to significantly reduce heart failure hospital admissions and improve quality of life in NYHA class III patients.Listen in as Scott Feitell, DO explains this new life saving procedure.

CardioMEMS™ is the first and only FDA-approved heart failure monitoring solution that provides physicians with vital real-time measurements from inside a person’s body. CardioMEMS consists of a small sensor that is permanently implanted into a person’s pulmonary artery via a catheter during a minimally-invasive procedure. Once in place, it provides real-time, on-demand access to data like pulmonary artery pressure and heart rate that allows physicians to more effectively manage patients with heart failure. Patients use a wireless electronics system to transmit the data to a secure website, which can be accessed remotely in a doctor’s office. With access to this data, physicians can make time-sensitive treatment decisions that can help keep patients out of the hospital. In trials, the use of CardioMEMS reduced hospital admissions for heart failure patients by 37 percent.Paul A Luetmer MD, FACC is here to discuss CardioMEMS™.

Doctors of the USA welcomes William T. Abraham, MD, FACP, FACC, FAHA, FESC, director of the Division of Cardiovascular Medicine and a professor of internal medicine, physiology and cell biology at the Ohio State University Medical Center to talk about the first FDA approved wireless device with remote monitoring to measure pulmonary artery pressure in certain heart failure patients. Listen in as he shares about the safety and efficacy of the device and how it allows health care professionals to monitor the condition of their patients remotely.Dr. William Abraham is the lead investigator for the CardioMEMS clinical trials and also serves as deputy director of Ohio State’s Dorothy M. Davis Heart and Lung Research Institute. He has been recognized as one of the “Best Doctors in America” for eight consecutive years. Also in 2009 he was named inaugural designated Chair of Excellence in Cardiovascular Medicine at Ohio State’s College of Medicine. Dr. Abraham earned his medical degree from Harvard Medical School in Boston, Mass., and completed his residency in internal medicine and fellowships in cardiology and heart failure/cardiac transplantation at the University of Colorado Health Sciences Center.Dr. Abraham is an internationally known researcher in heart failure. He has received grants from the National Institutes of Health, the American College of Cardiology and the Aetna Quality Care Foundation and has participated as principal investigator in more than 100 multicenter clinical drug and device trials.In addition to authoring more than 600 original papers, abstracts, book chapters and review articles, Dr. Abraham also co-edited Heart Failure: A Practical Approach to Treatment, a leading textbook on heart failure.Check out the Ohio State University Wexner Medical Center website.

Doctors of the USA welcomes William T. Abraham, MD, FACP, FACC, FAHA, FESC, director of the Division of Cardiovascular Medicine and a professor of internal medicine, physiology and cell biology at the Ohio State University Medical Center to talk about the first FDA approved wireless device with remote monitoring to measure pulmonary artery pressure in certain heart failure patients. Listen in as he shares about the safety and efficacy of the device and how it allows health care professionals to monitor the condition of their patients remotely.Dr. William Abraham is the lead investigator for the CardioMEMS clinical trials and also serves as deputy director of Ohio State’s Dorothy M. Davis Heart and Lung Research Institute. He has been recognized as one of the “Best Doctors in America” for eight consecutive years. Also in 2009 he was named inaugural designated Chair of Excellence in Cardiovascular Medicine at Ohio State’s College of Medicine. Dr. Abraham earned his medical degree from Harvard Medical School in Boston, Mass., and completed his residency in internal medicine and fellowships in cardiology and heart failure/cardiac transplantation at the University of Colorado Health Sciences Center.Dr. Abraham is an internationally known researcher in heart failure. He has received grants from the National Institutes of Health, the American College of Cardiology and the Aetna Quality Care Foundation and has participated as principal investigator in more than 100 multicenter clinical drug and device trials.In addition to authoring more than 600 original papers, abstracts, book chapters and review articles, Dr. Abraham also co-edited Heart Failure: A Practical Approach to Treatment, a leading textbook on heart failure.Check out the Ohio State University Wexner Medical Center website.