Podcasts about minneapolis heart institute foundation

Join Paul Batz and Kevin Sensenig on the Good Leadership Podcast as they recall the May 2024 Good Leadership Breakfast, featuring Kristine Fortman, CEO of the Minneapolis Heart Institute Foundation. In this episode, learn how she blended her love of science with a desire to uplift the voices of those leading her teams. She leads by honoring the differing and unique talents of each leader, adapting her leadership style to match the needs of each unique situation, and by honoring questions – both asking and answering – to make sure her teams are aligned. 

Do you think Facebook ads are challenging and confusing? Cassie Turczyn from the Minneapolis Heart Institute Foundation is here to guide us through her journey of conquering the complexity of paid ads, resulting in over 21,000 impressions and 200+ new emails for their list!The last round of my Grow Your List Ads Challenge paved the way for MHIF to expand their reach and attract potential donors, so today, we're sharing their tactical case study.Cassie walks us through the entire $375 ad campaign, the audiences they targeted, how they used Canva for ad graphics, and how they harnessed the power of Facebook Ads to capture the attention of 250+ new email leads.She also shares all the details around their email welcome sequence, and how they target and engage new subscribers. P.S. Do you want to grow your email list with 100+ new email subscribers…in JUST 7 days?! Click here to join my Grow Your List March Challenge!Resources & LinksCassie would love to connect with you on LinkedIn and you can learn more about the Minneapolis Heart Institute Foundation on their website.Want to make Missions to Movements even better? Take a screenshot of this episode and share it on Instagram. Be sure to tag @positivequation so I can connect with you. Are you ready to grow your email list with social ads in just seven days? Join the next round of my Grow Your List Ads Challenge where we'll create your lead magnet and ad copy and make sure that we're setting up your ads for success. Limited spots are left and we start the week of March 11th! Click here to register.Let's Connect! Send a DM on Instagram or LinkedIn and let us know what you think of the show! Head to YouTube for helpful digital marketing how-to videos and podcast teasers Want to book Dana as a speaker for your event? Click here!

Guest: Paul Sorajja, MD TRILUMINATE was the first trial to take a look at the impact of tricuspid regurgitation (TR) reduction on patients, and its results may lead to significant improvements in care and quality of life. To learn more about this trial, Dr. Paul Sorajja from the Minneapolis Heart Institute Foundation details the key findings from this trial and explores their impact.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania, from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode:Welcome to our Episode about a 14-year-old male who collapsed on the baseball field.Here's the case presented by Rahul:A 14-year-old male athlete was playing in a high school baseball tournament when he was hit in the chest with a pitched ball. The impact caused him to collapse on the field. Bystander CPR was begun given his unresponsiveness and emergency medical services were immediately called. The patient was transported to the hospital. Upon arrival, he was unresponsive and had no pulse. An electrocardiogram (ECG) showed ventricular fibrillation, and advanced cardiac life support was initiated. After several shocks and cardiac compressions, the patient regained a pulse and was transferred to the pediatric intensive care unit for further evaluation and management.To summarize key elements from this case, this patient has:Been struck by a high-velocity object in the chestSuffered a cardiac arrest, likely due to an arrhythmia from the blunt chest traumaThe presentation brings up a concern for Commotio Cordis, our topic of discussion today!We wanted to create this educational episode in light of the recent medical event experienced by the Buffalo Bill's safety Damar Hamlin. His blunt chest trauma, which led to cardiac arrest, has been postulated to be due to commotio cordis. At the date of this record, we are glad that Damar Hamlin is on the road to recovery.Absolutely, let's dive in more into this topic, Let's start with a short multiple-choice question:The 14-year-old described in our case suffered cardiac arrest after blunt chest trauma. Based on the working diagnosis of comottio cordis, what is the most likely EKG finding which may be seen in this patient?A. Ventricular fibrillationB. Ventricular tachycardiaC. Complete heart blockD. AsystoleThe correct answer is A. In a study published in JAMA (2002; 287(9):1142-1146) which used data from the US Commotio Cordis registry maintained by the Minneapolis Heart Institute Foundation, reported that the most common arrhythmia out of the 128 confirmed cases, 82 of which had EKGs which could be analyzed was ventricular fibrillation. Three patients had Vtach, 3 had Bradyarrhythmia and 1 had complete heart block. Although 40 patients had asystole, this was unlikely to be the initial rhythm after impact. Interestingly, the majority of these rhythms were recorded at the scene.Rahul, What is the definition of Commotio...

How's your heart, physically and emotionally? February is American Heart Month and this year the focus is on empowering Black adults to reduce their risks of heart problems.  That's because the CDC says Black Americans ages 35 to 54 are two times more likely to die from heart disease than white adults. MPR News host Angela Davis digs into why that is and what you can do about it, beyond eating healthy and exercising. Listen back to some of our Wednesday wellness shows that cover how to sleep better and how to forgive someone and ease that emotional and physical agony. Hear from two Black cardiologists who will tell us how to improve the heart health of Black Minnesotans. Guests: Mary Hayes Grieco is the author of the book: “Unconditional Forgiveness: A Simple and Proven Method to Forgive Everyone and Everything.” She's also the director of The Midwest Institute for Forgiveness Training in Minneapolis.   Dr. Michael Howell is a neurologist who specializes in sleep disorders. He's program director of the Clinical Sleep Medicine Fellowship at Hennepin Healthcare and the University of Minnesota, as well as medical director of the Fairview Sleep Center in Edina. Dr. Virend Somers is a Mayo Clinic cardiologist with expertise in the metabolic and cardiovascular aspects of sleep. Dr. LaPrincess Brewer is a cardiologist and assistant professor at the Mayo Clinic in Rochester. Her research focuses on heart disease prevention and testing new public health approaches to eliminating the racial disparities in cardiovascular disease.  Dr. Courtney Jordan Baechler is medical director of health equity and health promotion at Minneapolis Heart Institute Foundation at Allina Health. She's also a cardiologist practicing with Allina Health. Subscribe to the MPR News with Angela Davis podcast on: Apple Podcasts, Google Podcasts, Spotify or RSS.  Use the audio player above to listen to the full conversation.   

Heart attack, stroke and other kinds of heart disease are the leading cause of death for men and women in the United States. The risk of heart disease is even higher among Black Americans, who are two to three times as likely as whites to die from cardiovascular diseases.  The reasons for the vast disparity are complicated and include the toll of generational trauma and chronic stress. The good news is that most heart disease is preventable.    MPR News host Angela Davis talks with two cardiologists about addressing disparities and improving heart health in Black communities in Minnesota.   Guests: Dr. LaPrincess Brewer is a cardiologist and assistant professor at the Mayo Clinic in Rochester. Her research focuses on heart disease prevention and testing new public health approaches to eliminating the racial disparities in cardiovascular disease.  Dr. Courtney Jordan Baechler is a cardiologist and medical director of health equity and health promotion at Minneapolis Heart Institute Foundation at Allina Health. Subscribe to the MPR News with Angela Davis podcast on: Apple Podcasts, Google Podcasts, Spotify or RSS. Use the audio player above to listen to the full conversation.

This week, please join authors John McMurray and David Cherney, editorialist Kausik Umanath, as well as Associate Editors Ian Neeland and Brendan Everett as they discuss the original research articles "Initial Decline (Dip) in Estimated Glomerular Filtration Rate After Initiation of Dapagliflozin in Patients With Heart Failure and Reduced Ejection Fraction: Insights from DAPA-HF" and "Renal and Vascular Effects of Combined SGLT2 and Angiotensin-Converting Enzyme Inhibition" and editorial ""Dip" in eGFR: Stay the Course With SGLT-2 Inhibition." 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 Centre and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Associate Editor and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, it's the season of double features. Except this time, we're having a forum discussion of two related articles and an editorial that discusses both. What is it on? SGLT2 inhibitors. In the first paper, an analysis from the DAPA-HF trial, looking specifically at that initial dip in GFR that follows initiation of dapagliflozin in patients with HFrEF. Then we will discuss further, in a mechanistic way, the renal and vascular effects of combining SGLT2 inhibition on top of ACE inhibition. Lots and lots of good learning and insights, but let's go on first to the other papers in today's issue. Shall we? Dr. Greg Hundley: You bet, Carolyn, and I'm going to grab a cup of coffee. Carolyn, in this issue, wow, so many exciting original articles. In fact, there are two more articles that were going to pair together, both clinical and pertaining to TAVR procedures. In the first one, it was a group of authors led by Dr. Duk-Woo Park from the Asan Medical Center at the University of Ulsan College of Medicine. They conducted a multicenter, open-label randomized trial comparing edoxaban with dual antiplatelet therapy or DAPT, aspirin plus clopidogrel, in patients who had undergone successful TAVR and did not have an indication for anticoagulation. Now in this study, Carolyn, the primary endpoint was an incidence of leaflet thrombosis on four-dimensional computed tomography, CT, performed at six months after the TAVR procedure. Key secondary endpoints were the number and volume of new cerebral lesions on brain magnetic resonance imaging or MRI and the serial changes of neurological and neurocognitive function between six months and that time immediately post the TAVR procedure. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. In patients without an indication for long-term anticoagulation after successful TAVR, the incidence of leaflet thrombosis was numerically lower with edoxaban than with dual antiplatelet therapy, but this was not statistically significant. The effect on new cerebral thromboembolism and neurological or neurocognitive function were also not different between the two groups. Now because the study was underpowered, the results should be considered really as hypothesis generating, but do highlight the need for further research. Dr. Greg Hundley: Carolyn, there's a second paper pertaining to transcatheter aortic valve prosthesis. It's led by a group directed by Dr. Paul Sorajja from the Minneapolis Heart Institute Foundation and Abbott Northwestern Hospital. Carolyn, these authors prospectively examined 565 patients with cardiac CT screening for HALT, or what we would define as hypoattenuating leaflet thickening, at 30 days following balloon-expandable and self-expanding TAVR. Now, deformation of the TAVR prosthesis, asymmetric prosthesis leaflet expansion, prosthesis sinus volumes, and commissural alignment were analyzed on the post-procedural CT. For descriptive purposes, an index of prosthesis deformation was calculated, with values greater than 1 representing relative midsegment underexpansion. A time-to-event model was also performed to evaluate the association of HALT with the clinical outcomes. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. Nonuniform expansion of TAVR prosthesis resulting in frame deformation, asymmetric leaflet, and smaller neosinus volume was related to the occurrence of HALT in patients who underwent TAVR. What's the take home here, Carolyn? These data may have implications for both prosthesis valve design and deployment techniques to improve clinical outcomes in these patients. Now, Carolyn, both of these articles are accompanied by an editorial from Dr. Raj Makkar from the Smidt Heart Institute at Cedars-Sinai's Medical Center. It's a very lovely piece entitled Missing Pieces of the TAVR Subclinical Leaflet Thrombosis Puzzle. Well, how about we check what else is in this issue? My goodness, this was a packed issue. First, Carolyn, there are three letters to the editor from Professors Ennezat, Dweck, and then a response from Dr. Banovic pertaining to a follow-up from a previously published study, the AVATAR study, in evaluating valve replacement in asymptomatic aortic stenosis. There's also a Perspective piece from Dr. Wells entitled “Treatment of Chronic Hypertension in Pregnancy: Is It Time For A Change?” There's a Global Rounds piece from Professor Berwanger entitled “Cardiovascular Care in Brazil: Current Status, Challenges, and Opportunities.” Then there's also a Research Letter from Professor Eikelboom entitled “Rivaroxaban 2.5 mg Twice Daily Plus Aspirin Reduces Venous Thromboembolism in Patients With Chronic Atherosclerosis.” Dr. Carolyn Lam: There's another Research letter by Dr. Borlaug on longitudinal evolution of cardiac dysfunction in heart failure with normal natriuretic peptide levels. There's also a beautiful Cardiology News piece by Bridget Kuehn on the post-COVID return to play guidelines and how they're evolving. Well, that was a great summary of today's issue. Let's hop on to our feature forum. Shall we? Dr. Greg Hundley: You bet, Carolyn. Can't wait. Dr. Carolyn Lam: Today's feature discussion is actually a forum because we have two feature papers in today's issue. They all surround the cardiorenal interaction, should I say, of the SGLT2 inhibitors. For the first paper, discussing that initial decline or that dip in the GFR following initiation of dapagliflozin would be Dr. John McMurray, who's the corresponding author of this paper from DAPA-HF. Dr. John McMurray's from the University of Glasgow. Now next, we have also the corresponding author of another paper, really going into the mechanistic insights of the renal and vascular effects of combined SGLT2 and ACE inhibition. Dr. David Cherney is from Toronto General Hospital, University of Toronto. Dr. Carolyn Lam: We have the editorial list of these two wonderful papers, Dr. Kausik Umanath from Henry Ford Health in Michigan. Finally, our beloved associate editors, Dr. Ian Neeland from Case Western Reserve and Dr. Brendan Everett from Brigham and Women's Hospital, Harvard Medical School. Thank you, gentlemen. Now with all of that, what an exciting forum we have in front of us. Could I start by asking, of course, the respective authors to talk a little bit about your papers? I think a good place to start would be with Dr. McMurray. John, please. Dr. John McMurray: Thanks, Carolyn. I think our paper had three key messages. The early dip in eGFR that we saw was, on average, very small in patients with heart failure, about 3 mLs/min or about 5%. Very few patients had a large reduction in the eGFR. It was around 3%. Dapagliflozin-treated patients had a 30% or greater decline compared to about 1% of placebo patients. Finally, very few of those patients had a decline in the eGFR below a critical threshold, which for cardiologists might be around 20 mLs/min. We saw that in only five patients; that's 0.2% of the dapagliflozin-treated patients. Second message was that that early decline partially reverses. The nadir in our study was about 14 days. But by 60 days, on average, eGFR had increased again. Hold your nerve if you see an early decline in eGFR.   Dr. John McMurray: Maybe the most important message was that that decline in the eGFR is not associated with worse cardiovascular or renal outcomes. In fact, if anything, the opposite. If you look at the patients in the dapagliflozin group with a 10% or greater decline in eGFR, then compare it to patients who didn't have that decline, these individuals were about 27% less likely to experience the primary composite outcome of worsening heart failure and cardiovascular death. If you look at the placebo group, we saw exactly the opposite. Amongst those who had a greater than 10% decline in eGFR compared to those who didn't, those people with the early decline in eGFR were 45% more likely to experience the primary composite endpoint. The same is true for other cardiovascular outcomes for worsening kidney function. In the dapagliflozin group, decline in eGFR was not associated with more adverse events, not associated with more treatment discontinuation. That small decline in the eGFR is not a bad prognostic sign. If anything, it might be the opposite. Dr. Carolyn Lam: Thank you so much. That was really clear. David, are you going to tell us why this decline occurs? Dr. David Cherney: Yeah. Perhaps the paper that we published gives some insights into the mechanisms that are responsible for some of those changes in GFR that are thought to be acute hemodynamic effects. In the between trial, which is the trial that we published examining the effect of ACE inhibition followed by SGLT2 inhibition in patients with type 1 diabetes, we also saw that there was an expected effect of adding SGLT2 inhibition on top of an ACE inhibitor in people with uncomplicated type 1 diabetes. This acute dip in GFR was seen in this cohort of patients. We included only 30 patients in this small mechanistic study. At the same time, along with that dip in GFR, we also saw an increase in measures of proximal natriuresis. That proximal sodium loss is linked with changes in sodium handling in the kidney, which then causes changes in both probably afferent and efferent tone, which causes this dip in GFR primarily through natriuresis in this phenomenon called tubuloglomerular feedback. That was one major observation that gives insight into what we see in larger trials around the dip in GFR. Dr. David Cherney: In our mechanistic study, we also saw an additive effect on blood pressure. Blood pressure went down further with the addition of empagliflozin on top of an ACE inhibitor. In terms of the mechanisms that are responsible for the reduction in blood pressure, natriuresis certainly may be in part responsible, but we also saw a novel observation whereby there was a reduction in peripheral vascular resistance using noninvasive measures. There are likely several mechanisms that are responsible for the reduction in blood pressure. Then finally, we also saw reductions in markers of oxidative stress, which may also account for some of the effects that we see in blood pressure, as well as potentially some of the anti-inflammatory and anti-fibrotic effects that we see at least in experimental models that may have some clinical translatability to humans as well around the clinical benefits. I think the blood pressure, the renal hemodynamic effects, and some of the neurohormonal mechanisms are the major observations that we saw that may in part explain some of the really nice changes that were seen in Dr. McMurray's study. Dr. Carolyn Lam: Right. Thanks, David. But these were patients with type 1 diabetes and no heart failure. John, do you have any reflections or questions about how that may apply? By the way, what a beautiful study. Thank you, David. Dr. David Cherney: Pleasure. Thank you. Dr. John McMurray: Yes, David. I really enjoyed your study. In fact, I think, Carolyn, it does shed some insights perhaps to what's going on. As David pointed out, the reduction in peripheral arterial resistance, reduction in blood pressure, that may play some role in that early dip in eGFR as well as autoregulation in the kidney. Then the other interesting thing is that the distal nephron seems to adapt to that effect in the proximal tubule. Again, that may account for some of that recovery in eGFR, that reversal in the early dip that I spoke about, and which I think is very clinically important because, of course, physicians should make sure that they recheck eGFR if they see that early dip. Because they may find that few weeks later that that dip is much smaller and of much less concern. Dr. Carolyn Lam: Thank you, John. In fact, you're saying, stay the course, right- Dr. John McMurray: I have. Dr. Carolyn Lam: ... with the SGLT2 inhibitors. I'm actually stealing the words of the title of the editorial, a beautiful editorial by Kausik. I love that. Stay the course. Kausik, please, could you frame both papers and then with an important clinical take home message for our audience? Dr. Kausik Umanath: Sure. I think the analysis by John and his group was really relevant with the large sample size. What's impressive? Similar to a lot of these other SGLT2 studies that have come out, both in heart failure and in kidney disease progression and so on, it's remarkable how the other analysis, like the analysis of EMPA-REG and CREDENCE and so on, of similar dips. All show more or less the same magnitude, the same relative proportions of this GFR trajectory. I think the mechanistic study only highlights that though it's working with a slightly different population of type 1 patients and much earlier in their course in terms of where their GFRs are. Dr. Kausik Umanath: The other piece is that ultimately we need to understand this dip and know to monitor for it and so on. But I think the general clinician should really understand that a dip of greater than 10% really occurs in less than half the population that takes these agents. That dip, if it occurs, certainly doesn't do any harm. That said, if they see a bigger dip in the 30% range, monitor more closely and consider making sure that there aren't any other renal issues out there for that patient because they are a much smaller proportion of patients in these large trials that generate that level of dip. They should be monitored. Dr. Kausik Umanath: The other thought that we had, and thinking through this in a practical sense, is because you expect this dip, many of our cardiologists or even the nephrologists when we titrate these drugs, they're on a suite of other drugs. It's probably best to not adjust their Lasix or their loop diuretic, or their RAAS inhibitor at the same time as you're adjusting the SGLT2 inhibitor or starting it because then you may just introduce more noise into the GFR changes that you see over the next several weeks. It may be a sequential piece or at least holding those other agents constant while this gets titrated and introduced is a prudent course of action, so you don't misattribute changes. Dr. Carolyn Lam: Thanks so much. What clinically relevant points. In fact, that point about the diuretic especially applies in our heart failure world. You see the dip. Well, first, make sure the patient's not overdiuresed. Remember, there's more that the patient's taking. Thank you. That was a really great point. Brendan and Ian, I have to get you guys to share your views and questions right now. But before that, can I take a pause with you and just say, aren't you just so proud to be AEs of Circulation when we see papers like these and we just realize how incredible the data are and the clinical implications are? I just really had to say that. All right. But with that, please, what are your thoughts, Brendan? Dr. Brendan Everett: Yeah, sure. Thank you, Carolyn. Hats off to all three of our authors today for doing some amazing science. Thank you for sending it to Circulation. I think, in particular, I handled David's paper. I'm not a nephrologist and I'm probably the furthest thing from a nephrologist. Had to do my best to try and understand these concepts that I'm not sure I ever even was exposed to in medical school many years ago. I think it shows the breadth of the interest in our readership. The fact that these changes in eGFR have become a primary focus for our cardiovascular patients and that the clinical implications are really important. I guess my question, David, is... In your paper, you talked a little bit about this hypothesis of hyperfiltration and the role that hyperfiltration plays in setting patients with diabetes up for kidney disease. Is that playing a role in John's observation or not? Again, as a non-nephrologist, I have trouble connecting the dots in terms of that hypothesis and John's observation of the clinical benefit for patients that have a reduction in eGFR as opposed to no change. Dr. David Cherney: Yeah. It's a great question. It's very difficult to know with certainty in a human cohort because we can't measure the critical parameter, which is intraglomerular pressure, which we think these changes in GFR are a surrogate for. But if we go along with that train of thought, along reductions in glomerular hypertension, it very much makes sense that the patients who dip are those who have the... They're taking their medication, number one. Number two, they respond physiologically in the way that you expect them to, which is that their GFR dips at least transiently and then goes back up again through some of the compensatory mechanisms that John mentioned earlier. As was mentioned not only in this paper, but also in previous analyses from CREDENCE and previous analyses from VERTIS CV and others have shown that indeed that dip in GFR is linked with longer term renal benefits, at least. That is reflected in a reduction in the loss of kidney function over time. Dr. David Cherney: The patients who are on an SGLT2 inhibitor and those who dip by around 10% or less, those patients tend to do the best over time in terms of preserving GFR, not losing kidney function compared to patients who are on an SGLT2 inhibitor but do not dip, or those patients who actually have an increase in GFR. That is consistent with this idea that there may be a reduction in glomerular pressure, which is protective over the long term. That ties back into your question around hyperfiltration that this may indeed be due to a reduction in glomerular pressure, which is linked with risk over the long term. Dr. Carolyn Lam: Ian? Dr. Ian Neeland: I wanted to echo Brendan's comments about the excellent science. When I read these papers, it really speaks to the existential struggle that cardiologists have between kidney function and these medications that we know have cardiovascular benefits. How do we manage that practically? It's so clinically relevant, both the observation that John's paper made about the dip in the DAPA-HF trial as well as, David, your mechanistic insights. Dr. Ian Neeland: I wanted to ask John potentially about the most fascinating aspect to me of this paper was that patients with a dip of 10% or more actually ended up doing better in terms of cardiovascular outcomes, specifically hospital heart failure and hospitalizations than people on placebo with a greater than 10% dip. It speaks to the fact that... Is the physiology going on here different between those individuals whose GFR went down on placebo versus those who are on SGLT2 inhibitors? All the mechanistic insight that David's paper had in terms of blood pressure and intraglomerular pressure, how does that feedback and speak to why heart failure is strongly linked to this mechanism? We see this not just with SGLT2 inhibitors, but there are other medications now coming out showing that there's a relationship between this dip in GFR and heart failure. Can you speak to why this heart failure-kidney connection is so important and becoming greater and greater in terms of our understanding? Dr. John McMurray: Well, thank you for asking me the hardest question and one that I truly don't think I have a good answer to. I think it's obvious to all of us that the kidney is central in heart failure and perhaps cardiologists have neglected that fact, focusing more on the other organ. But by definition, almost the fluid retention that characterizes heart failure in terms of signs, and probably is the primary cause of symptoms, that clearly is a renally-mediated phenomenon. The kidney must be central to all of this. I think David right. I think the decline in eGFR that you see with this drug is simply a marker that the drug is having its physiological effect or effects. Whatever those are, they're beneficial. Clearly, patients who have an eGFR decline on placebo are different and they reflect, again, the patients that we see all the time. As our patients with heart failure deteriorate, one of the things that we commonly see, in fact becomes one of the biggest problems that we have to deal with, is that their kidney function declines. As their symptoms get worse, as their cardiac function gets worse, their kidney function also declines. Dr. John McMurray: I think you're seeing two contrasting effects here. One is the background change in eGFR, which is the placebo patients, and we've always known that that's a bad thing. Then we're seeing that early within 14 days marker of the pharmacological or physiological action of the drug. I hope you don't ask me how SGLT2 inhibitors work in heart failure. That's the other most difficult question I can think of, but I think this is just a marker of the fact that they are working. Dr. David Cherney: Yeah. Just to add to that briefly, there is this difficulty in sorting out the mechanisms that are relevant around the acute effects in the kidney that the dip in GFR reflects natriuresis that could keep patients out of heart failure; that the reduction in glomerular pressure reduces albuminuria. Albuminuria reduction is linked with kidney protection. It's linked with heart failure and ASCVD protection. Then there's also this concept of if you dip and then you stay stable afterwards, your GFR stays stable afterwards, those patients with stable kidney function that's not declining, the dippers in other words, those patients are probably able to maintain salt and water homeostasis better than someone who's declining more rapidly. All these things probably tie together in order to reflect, of course, there's a renal protective effect, but that some of those mechanisms may also tie into the heart failure mechanisms that John was mentioning. Dr. John McMurray: But, David, it's hard to imagine if we don't protect the kidney, we won't protect patients with heart failure given how fundamental, as I said, the kidney is, and how fundamentally important worsening kidney function is. Not only because it is a marker of things going badly, but also because it often results in discontinuation or reduction in dose of other life-saving treatments. To Kausik's point, it was very important about the risk of changing background life-saving disease modifying therapy. Actually, we didn't see that in DAPA-HF, which was very intriguing. There was no reduction in use of renin-angiotensin system blockers or mineralocorticoid receptor antagonists. Dr. Carolyn Lam: Thank you so much, gentlemen. Unfortunately, we are running out of time, but I would really like to ask one last question to the guests, if possible. Where do you think the field is heading? What next? What's the next most important thing we need to know? David, do you want to start? Then John, then Kausik. Dr. David Cherney: I think one of the aspects that we need to know in the future is where else can we extend these therapies into novel indications and extend the boundaries of where we currently work with these therapies. People with type 1 diabetes, for example, with either heart failure or with significant kidney disease, patients with kidney transplantation, is there a renal or cardiovascular protective effect? Then another high risk cohorts who have not been included in trials, those on immunosuppressants, for example, who were excluded from the trials. I think those are some of the areas that we need to extend into now that we understand how these therapies work in even very sick patients and that we also know that they likely have at least some benefit through suppressing inflammation, and possibly reducing infectious risks. That would provide a rationale for extending into some of these new areas. I think that's certainly, hopefully on the horizon for us. Dr. Carolyn Lam: John? Dr. John McMurray: Carolyn, obviously I think looking at post myocardial infarction population, that's an obvious place to go. There are a couple of trials there. I suppose the trial that I would love to see, and which I think would address the core question that we've been discussing today, which is: Is this all about the effect in the kidney and how important is the diuretic and natriuretic action of these drugs in heart failure? I think the key study that would address this would be doing a study in patients on dialysis. Because in those patients we could, I think, separate the issue of natriuresis, diuresis, and maybe even the dip in EGR that we've been talking about. If these drugs prove to be effective in end-stage kidney disease, patients on dialysis, that would be really fascinating. Dr. Carolyn Lam: Kausik? Dr. Kausik Umanath: That is a very interesting point. I don't know that we know necessarily outcomes, but I think from working with the DAPA-CKD, we do have a little bit of the safety data because we did continue it. I was the US MLI for that study and we did continue the SGLT2 passed into renal failure. There is a little bit of safety data there. But I don't think once you've declared an outcome, you're not collecting outcomes data after that point. That's a very interesting area to look into. Dr. Kausik Umanath: I also think the other place where this field's heading is trying to better tier and layer the multitude of agents. I think we've been waiting for about 20 to 30 years, at least in the kidney field, for something new to affect the progression of kidney disease after the ACE/ARB trials and so on. This one we've got SGLT2 inhibitors. We've got the new MRA, finerenone, and so on, which also have very beneficial cardiovascular effects. The question becomes: How do we layer these therapies? Which sequence to go in? Some of the others that are in pipeline as well that are out there that have very beneficial cardiovascular effects that may indeed also help kidney function and diabetes control, which do you go with first and so on? Dr. Carolyn Lam: Wow! Thank you so much. We really could go on forever on this topic, but it has been tremendous. Thank you once again. On behalf of Brendan, Ian, Greg, thank you so much for joining us today in the audience. You've been listening to Circulation On the Run. Don't forget to tune in again next week. Dr. Greg Hundley: This program is copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.

In this podcast, Dr. Scott Sharkey, senior consulting cardiologist with Minneapolis Heart Institute, provides a discussion on cardiomyopathy and more specifically Takotsubo syndrome. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: Describe how Takotsubo cardiomyopathy was discovered. Differentiate the diagnostic criteria for Takotsubo cardiomyopathy from other cardiology related conditions. Identify treatment options for Takotsubo cardiomyopathy. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "Achin' Breaking Hearts: Takotsubo Syndrome w/Dr. Scott Sharkey" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  DISCLOSURE ANNOUNCEMENT  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: CHAPTER 1: Cardiomyopathy. According to Dr. Sharkey, it is a general term for cardiac muscle disease, often times of unknown cause. Usually it refers to a dilated, poorly, contracting heart. Though it's also been called stress cardiomyopathy, Takotsubo does not behave like most cardiomyopathies. It's a microcirculatory disease, causing a stunned myocardium similar to an acute myocardial infarction, but with non-obstructive epicardial coronary arteries. Dr. Sharkey and his colleagues first noticed this phenomenon in patients with myocardial infarction that showed deep T wave inversions on EKG, and initial ECHOs with ejection fractions of 25-30%. Weeks later, these injuries would resolve, findings they attributed to a stunned myocardium. This phenomenon was then seen in a patient with a TBI, who again had a deep T wave inversion, and a large left ventricular regional wall motion abnormality with normal coronary arteries. The regional wall motion abnormality, again, resolved. These findings were noted in 20 similar cases that were then published in 1998. Though to note, this same syndrome was also present in the Japanese literature at this time. Later, it was noted patients were developing these symptoms not just from severe illness or trauma, but also from deeply emotional situations. This led to a write-up in Circulation in 2005, which received the 'Paper of the Year' award. From the early days to now, Dr. Sharkey went from seeing three to four patients per year with Takotsubo, to present day, one to two patients per week. The Minneapolis Heart Institute Foundation has done, and continues to do robust research on Takotsubo, noting that there is a subset of vulnerable patients that actually have recurrences of Takotsubo., They have also been able to study specific triggers for Takotsubo, like drug use, pheochromocytoma and critical illness in general. CHAPTER 2: Triggers for Takotsubo. As mentioned before, drug use, pheochromocytoma or critical illness are causes, but really any physical illness as well as any emotional stress are triggers for this syndrome. Death of a spouse is a good example of an emotional trigger, though as exemplified in the discussion, it can be any emotional situation. Teasing out the patient's history and the specific precipitation event is an art form. The autonomic nervous system is implicated here. Catecholamine levels are very elevated in these patients, as opposed to lower levels seen in acute MI patients. Pheochromocytoma and accidental overdose of epinephrine will cause this as well. The pathophysiology of the event is still being researched. It's postulated that this is all caused by vasospasms of the circulation or direct myocardial injury due to the catecholamine excess. It's presumed that effects occur on micro-circulatory level, and any disruption in blood flow is brief, less than 15-20 minutes, enough to raise serum troponins and cause wall motion abnormality. The involvement is circumferential, so the ECG findings are more diffuse. EKG changes include ST segment elevation in about 40% of patients. Otherwise T wave inversion is often seen, but is a later development. ST depression is not generally seen in Takotsubo, and would instead indicate a coronary artery occlusion. Echo findings show a classic, distinctive finding: poor contractility or akineses from the mid-heart to the apex, while the base of the heart is hypercontractile. Also called apical ballooning, the apex can be seen ballooning outward on echocardiograms. This is what is reminiscent of a Japanese clay pot, octopus trap, aka Takotsubo. And yes, the name is most certainly credited to the Japanese. CHAPTER 3: When a patient presents with an acute cardiac event that looks like Takotsubo, the patients still must undergo coronary angiogram to exclude a coronary occlusion. Cardiac echo and cardiac MRI are used to help diagnose this disease. Beta blockers and ACE inhibitors are used early on in treatment, but Dr. Sharkey suspects that patients would probably recover without them. The reality is, most of these patients get better. The myocardium, in the setting to Takotsubo, should recover. A process that usually takes one to two weeks. Anti-platelets do not play a role here, but anticoagulants are often given until the myocardium has recovered to prevent a small risk of left ventricular thrombus. Left ventricular outflow tract obstruction is a complicating factor in Takotsubo. Many of these patients are middle aged to older women, and have basal septal hypertrophy. This exacerbates, the outflow obstruction, which causes hypotension and shock in Takotsubo, 15-20% of the time. The left ventricular outflow obstruction should resolve with the resolution of Takotsubo. As mentioned, Takotsubo can have a recurrent phenomenon, and remarkably, these patients all recover their heart function. Curiously, the precipitating cause for these patients tends to be emotional. Though used in the initial treatment, beta blockers are not prescribed long-term for Takotsubo patients. In fact, Dr. Sharkey found that 30% of patients with a Takotsubo event were already on beta blockers, and 80% of those who have had recurrent Takotsubo were already on beta blockers and ACE inhibitors. CHAPTER 4: Patient presentation: Patients can present with chest discomfort and/or shortness of breath, much like an acute MI patient. They can also present with an acute concern of another nature. Dr. Sharkey gave the example of a patient presenting with a pasteurella multocida infection causing an airway obstruction. The patient's ongoing hypotension led to further work up and diagnosis of Takotsubo. Takotsubo patients can also be discovered during inpatient stays when incidental ECG wave form changes, troponin elevation, tachycardia, and/or hypotension are noted. About 10% of Takotsubo patient's develop cardiogenic shock. Most survive their ICU stay, even if advanced treatment, like intra-aortic balloon pumps or ECMO are required. For the critically ill, where beta blocker use is contraindicated in the light hypotension, Dr. Sharkey preferred choice of vasopressin followed by phenylephrine. Fortunately, patients recover from Takotsubo. However, malignant arrhythmias and cardiac arrest can happen. Patients are counseled to present to emergency care if their symptoms ever return. Thank-you for listening.

Dr. Courtney Baechler is a Cardiologist at the Minneapolis Heart Institute Foundation. She joins Roshini to talk about why women's heart research lags behind what doctors know about men. Mary Albright is the President of Starbird Association. She joins Roshini to discuss STEM. At the bottom of the hour, Roshini is joined by Sasha Cotten. Sasha is the Director of the Office of Violence Prevention in Minneapolis. The city is launching a new effort called "Cure Violence" and Sasha tells us all about it.   See omnystudio.com/policies/listener for privacy information.

Dr. Courtney Jordan Baechler is a board certified internist and cardiologist who focuses on the prevention of heart disease and behavioural change that supports overall well-being.   She recently joined the Minneapolis Heart Institute Foundation as their Program Director of the Emerging Science Centers in addition to seeing patients in their clinic.   Prior to this new role, Dr Baechler served as the assistant commissioner of health improvement for the MN Health Improvement Bureau.  She also served as vice president of the Penny George Institute for Health and Healing, Allina Health's prevention, wellness and clinical service line.  Courtney has an extensive background in the medical field, serving in many leadership roles in her community. In this episode Courtney shares her passion and inspiration about helping individuals, families, and communities to find their highest state of well-being—body, mind and spirit.  Courtney shares with us her advice based on her personal and professional experience for turning tragedy into something positive and the tools that you can use to help you persevere when life throws you a curveball.  We discuss how our mind, body and spirit impact our ability to heal on a physical and emotional level.  She talks about several holistic modalities for healing, including massage (and the power of touch), Qigong (pronounced chee-gong) and acupuncture. Courtney also talks about how nutrition helps align your body during periods of grief and anxiety. Courtney's tips are relevant for everyone and you'll leave this episode inspired to think of yourself first. You can find Dr. Courtney Jordan Baechler on:  FB: https://www.facebook.com/courtney.baechler IG: @courtjb03 Relevant links and resources: Penny George Institute for Health and Healing Don't forget to subscribe to our podcast so that you can uncover strategies, tips and resources from a variety of experts and our own banks of knowledge as you progress on your journey to living well.  Please share this podcast with a friend or anyone who you think could benefit from this information. Join our private Art of Living Well Podcast Facebook Community: This is a community where you can directly interact with us and ask us questions and suggest topics for future episodes. Upcoming Art of Living Well Programs: 10 Ways to Create a Healthy Relationship with Sugar - Online workshop - February 26th 7 Day Community Functional Medicine Liver Detox - April 5, 2020 Start date Clean Beauty 101 Online Workshop - April 15th, 12-1:15 PM Shop our Favorite Products:   https://www.theartoflivingwell.us/products Instagram: @theartofliving_well FB: theartoflivingwell Sign-up for our Art of Living Well Podcast email list. (We promise not to bombard you with email). Marnie Dachis Marmet's Website (Zenful Life Coaching) Stephanie May Potter's Website

Dr Mario Goessl of the Minneapolis Heart Institute Foundation. 22 thousand Americans die each year from Heart Valve disease. Dr Goessl talks about what research is being done to find new treatment strategies, and how you can get involved. Louis King President & CEO of Summit Academy. Summit Academy President Louis King will share some exciting stats about the number of students getting their GED. Also, they played a key role getting employees to construct and staff US Bank Stadium as they helped many people of color get good jobs at the home of this year’s Super Bowl. WCCO NFL expert & Host, Eric Nelson. After last weeks “Minneapolis Miracle” the Vikings are now just one win away from playing the Super Bowl in their own stadium. With kickoff in Philadelphia just hours away Eric Nelson helps preview today’s NFC Championship game.

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 journal this week features an in-depth review on transcatheter therapy for mitral regurgitation, a very, very hot and interesting topic. You have to listen on, coming up right after these summaries.                                                 Our first original paper this week sheds light on the influence of aging on aldosterone secretion and physiology. First author Dr. Nanba, corresponding author Dr. Rainey and colleagues from the University of Michigan in United States, examine the relationship between age and adrenal aldosterone synthase in 127 normal adrenals from deceased kidney donors. The donors' ages ranged from nine months to 68 years. The authors found that adrenals from older individuals displayed less normal aldosterone synthase expression and zona glomerulosa, and greater content of abnormal foci of aldosterone synthase expressing cells.                                                 Furthermore, older age was independently associated with dysregulated and autonomous aldosterone physiology, in an ancillary clinical study of subjects without primary aldosteronism. This study therefore suggests that aging may be associated with a sub-clinical form of aldosterone excess and provides at least one potential explanation for age related cardiovascular risk.                                                 The next study shows, for the first time, that the chemokine receptor, CXCR4, in vascular cells, limits atherosclerosis. The CXCL12 and CXCR4 chemokine ligand receptor axis is known to control cell homeostasis and trafficking. However, its specific in atheroprotection has thus far been unclear. This is addressed in today's study by first author Dr. During, corresponding author Dr. Weber, and colleagues of The Institute for Cardiovascular Prevention in Munich, Germany. In hyperlipidemic mice, the authors showed that cell-specific deletion of CXCR4 in arterial endothelial cells, or smooth muscle cells, marked the increase atherosclerotic lesion formation. Mechanistically, CXCR4 axis promoted endothelial barrier function through VE-cadherin expression and a stabilization of junctional VE-cadherin complexes. In arterial smooth muscle cells, CXCR4 sustained vascular reactivity responses, and a contractile smooth muscle cell phenotype. Whereas, CXCR4 deficiency favored the occurrence of macrophage-like smooth muscle cells in atherosclerotic plaques and impaired cholesterol efflux.                                                 Finally, in humans, the authors identified a common allele variant within the CXCR4 locus that was associated with reduced CXCR4 expression in carotid RG plaques, and increased risk for coronary heart disease. Thus, the study suggests that enhancing the atheroprotective effect of arterial CXCR4 by selective modulators may open normal therapeutic options in atherosclerosis.                                                 The next paper is the first to study the effects of rosuvastatin on carotid intima-media thickness in children, with heterozygous familial hypercholesterolemia. First author Dr. Braamskamp, corresponding author Dr. Hutten, and colleagues from Academic Medical Center Amsterdam in the Netherlands, study children with heterozygous familial hypercholesterolemia aged 6 to less than 18 years, with LDL cholesterol more than 4.9, or more than 4.1 millimoles per liter in combination with other risk factors, who received rosuvastatin for 2 years, starting at 5 milligrams once daily, with uptitration to 10 milligrams for children aged 6 to 10 years old, or 20 milligrams daily for those aged 10 to 18 years old.                                                 Carotid intima-media thickness was assessed by ultrasonography at baseline, 12 months and 24 months in all patients and in age-matched, unaffected siblings. Carotid intima-media thickness was measured at 3 locations, the common carotid artery, the carotid ball, and the internal carotid artery in both the left and right carotid arteries. At baseline, the mean carotid intima-media thickness was significantly greater for the 197 children with heterozygous familial hypercholesterolemia compared with the 65 unaffected siblings. Rosuvastatin treatment for 2 years resulted in significantly less progression of increased carotid intima-media thickness in children with heterozygous familial hypercholesterolemia than in the untreated, or unaffected siblings. As a result, there was no difference in carotid intima-media thickness between the two groups after two years of rosuvastatin. These findings, therefore, support the value of early initiation of statin treatment for LDL cholesterol reduction in children with heterozygous familial hypercholesterolemia.                                                 The final study highlights the therapeutic potential of a novel alpha calcitonin gene-related peptide for the treatment of heart failure. First author Dr. Aubdool, corresponding author Dr. Brain, and colleagues from King's College London in United Kingdom, tested the stable alpha analog of calcitonin gene-related peptide in 2 models ... First, an angiotensin 2 infused mouse, and secondly, pressure overload cardiac hypertrophy mouse model using suprarenal aortic ligation. They showed that systemic colon injection of the alpha analog blunted the angiotensin 2 induced rise in blood pressure, as well as the vascular and cardiac remodeling, changes in water consumption, and renal injury, that are normally associated with angiotensin 2 infusion. Furthermore, protective effects were also seen when starting the alpha analog treatment, only during the last week of the 2-week angiotensin 2 infusion, in other words, when hypertension was already established. Finally, the alpha analog preserved heart function, and diminished the degree of hypertrophy and fibrosis in the aortic ligation model.                                                 Thus, these results demonstrate the therapeutic potential of the alpha calcitonin gene-related peptide pathway, and the possibility that this injectable alpha analog may be effective in cardiac disease.                                                 Well, that wraps it up for this week's summaries! Now, for our featured discussion.                                                 For our feature discussion this week, we're talking about trans-catheter therapy for mitral regurgitation, a very hot field and a field in which there have been a lot of advances. To help us break it down, and get right into the insights, the challenges, and potential solutions, I am so pleased to have the first author of this in-depth review paper, Dr. Paul Sorajja from Minneapolis Heart Institute Foundation and Abbott Northwestern Hospital, as well as Dr. Manos Brilakis, associate editor from UT Southwestern, here with us today!                                                 Paul, could I start with you, and just ask you first to give us an idea of what we're talking about here when we talk about mitral regurgitation ... There are different kinds, which are we referring to, and what are the challenges involved in a trans-catheter therapy for mitral regurgitation? Dr. Paul Sorajja:                I think there are a number of challenges, I think the first thing is that MR is often thought of as one disease, but it's really an incredibly heterogeneous disease ... Broadly, we talk about primary versus secondary MR, but the mitral valve is so complex, with multiple different components, any one of which can disrupt and cause MR. When we're talking about trans-catheter therapy, it's often very easy, again, to think we could have one therapy that could treat a simply insufficient valve, but it's way more complex than that, and as a result, there have been many different approaches that have been developed, adding to the complexity of how we manage these patients. Dr. Carolyn Lam:               Right, and in your paper, I loved the way you grouped them, very logically, under those from mitral valve repair, and that for mitral valve replacement ... And then, under repair, you grouped it into leaflet versus targeting the LV ... Could you maybe give us some top-line insights on these techniques? Dr. Paul Sorajja:                Yeah, there are a number of different approaches that have mechanistically gone after the different components through the pathophysiology of MR, where there is leaflets, where there's analysts, cords, or ventricular approach ... I think it's somewhat simplistic to think of it that way, but as catheter-based technology, we are technically limited by what we can do from a catheter standpoint. I think it's inevitable to think about these catheter technologies as eventually being combined, rather than singular, in order to approach what surgeons do in the OR. Dr. Carolyn Lam:               Right, but then even going further, you spent quite a bit of the paper talking about trans-catheter mitral valve implantation ... So, replacing the mitral valve, that's really cool, could you tell us a bit about that, and about that important issue brought up about patient selection. Dr. Paul Sorajja:                Yes, it's a very good point, I think in terms of trans-catheter mitral replacement, I think that that's really where the future is going to go ... The simple analogy is that people think that it will follow the route of TAVR, but I think it will follow the route of TAVR more quickly so, because when you look at how the mitral valve is currently treated in the OR, sometimes, a lot of the times, patients can end up worse. Whereas, a trans-catheter solution actually, I think in terms of the safety margin, actually will equate a degree of safety relative to surgery, if it's done and developed correctly, as opposed to how TAVR's done. I think for TAVR, it's been a number of years for our field to be equivalent or superior to surgery, whereas I think with mitral, I think there's a lot of potential for mitral to have equated a degree of safety. As an example, in the Tendine Feasibility Study, it was published this past January ... A high-risk population, there was not a single procedure death, out of 30 patients ... And for these patients who would go to the OR with an eject fraction of 30 to 40 percent, I think that's quite remarkable. Dr. Carolyn Lam:               Wow, that's really exciting indeed! Manos, you handled this paper, and it's just so beautifully laid out ... That flow chart, I just want to refer all our listeners to the flow chart in Figure 7, that talks about maybe an approach that can be considered. Manos, could you share some thoughts on how this developed? Dr. Manos Brilakis:           Yeah, absolutely, and obviously Paul is the expert on this, but I think it's very important about this paper, and through discussions with Paul and through the development of the paper, is that there's more of a collaboration between the surgeons and the interventionists. So instead, if it's additional style of ... Or the interventionists are doing one thing and the surgeon is doing another, I think the key to success in the mitral field is working very closely together ... Many of those valves right now, the percutaneous valves, are done through a cut down and a typical approach, so working very closely to addressing the anatomic components of the mitral valve problem is a big plus.                                                 The other thing I think that is very important is the new emergence of imaging, trying to understand whether the new mitral valve is going to create issues with LVOT obstruction or not. I think that's leading to a whole new understanding of when and how patients are even candidates for this approach, and I think Paul can elaborate more on this, but as things evolve, fewer and fewer patients are going to be excluded from these new technologies. Dr. Carolyn Lam:               Paul, would you like to take that? What do you think is happening and will happen with patient selection? Dr. Paul Sorajja:                There has been a challenge in current feasibility studies, in terms of getting patients in, the anatomical restraints are exactly what Dr. Brilakis has outlined. There's a certain bulkiness and size to the valve, which essentially poses risk for LVOT obstruction if the valve is too big ... As a feasibility study that's still early, or a field that's still early in its development, there's been a really conservative approach in terms of patient selection to ensure that LVOT obstruction doesn't happen. I think we're pushing the boundaries for that, and I think we've learned a lot from CT imaging, in terms of predicting LVOT obstruction, and I think the valves are also getting to be shorter in profile, which makes it less likely ... But that is definitely one of the limitations, and it's a limitation that exists, not just for trans-cat therapy but also for surgical therapy. Dr. Carolyn Lam:               Right, and then maybe a question for both of you ... What do you think the future is going to hold? What do we need to make this more mainstream, and where do you think this will leave surgical approaches? I know you said a combined approach, but maybe you could elaborate a little bit more? Dr. Paul Sorajja:                I do think, and I agree, I think Manos' point is spot on about that ... This will have to be multidisciplinary, the surgeons and cardiologists absolutely need to continue to work together, that's what's led to the successful development of TAVR, and I think that will be even more so for mitral, because the mitral valve is just infinitely more complex, and we have a lot to learn from the surgeons. But I think going forward, the collaboration is going to be a requirement, and then the training is also going to be a significant portion ... Putting in a mitral valve is much more complex than putting in an aortic valve ... I think if there's a safety margin that's demonstrated, I still think that it will be more appealing and more rapidly adopted than aortic disease. Dr. Carolyn Lam:               Well, Manos? Dr. Manos Brilakis:           No, I completely agree with Paul on that respect. I think, in my mind, at least, an again, this is from an early standpoint, the next big step would be to make it completely percutaneous, right now, you still have to do the cut down, and it's a little more invasive, although still safer than the completely open surgery, but maybe having a complete percutaneous system would be the next big step ... There's no question in my mind, as well ... And watching very closely how Paul and the surgical team are handling this, I think this is definitely the way for the future. Sometimes, in TAVR, it's not as technically demanding, and you don't really need to have too many people in the room, but for this procedure, it's definitely more important to have everyone in the room, and benefit from everyone's expertise. Dr. Carolyn Lam:               Manos, could I switch tracks for a moment now, and ask you to comment on the question that I get a lot ... You're an Interventionist, you handle a lot of the interventional papers for Circulation, and a lot of people are wondering, what makes papers like Paul's ... What makes interventional papers something that we would want to publish in Circulation? Could you share some thoughts? Dr. Manos Brilakis:           Absolutely, thanks Carolyn ... That's a big part, I think, of the appeal of Circulation right now. We're really trying to communicate to people that cutting-edge, clinical science is actually at the heart and the core of Circulation, and clinical content is what drives a lot of editorial ... Especially in intervention, where particularly interesting and new, cutting-edge technologies, new trials, observational studies ... But essentially, things that are cutting-edge, and are going to have a specific implication and impact in the way the field is going ... And this is part of Dr. Sorajja's paper, showing where the future lies in terms of trans-catheter mitral technologies, but along the same lines, we love to have cutting-edge papers on various aspects ... Coronary, peripheral, all aspects of interventional cardiologies, as well as interventional imaging ... The goal, again is to make the submission easy, there are not many honors requirements for submitting the papers, it's very simple to submit, and there's an answer going out very quick, so we're looking forward to receiving more and more interventional papers on cutting-edge science. Dr. Carolyn Lam:               Thank you so much for joining us today, and don't forget to tune in again next week.  

Dr. Timothy Henry, Director of Research at the Minneapolis Heart Institute Foundation, and Dr. Jay Traverse, Senior Consulting Cardiologist at the Minneapolis Heart Institute at Abbott Northwestern Hospital, review the results of the LateTIME, SCIPIO and CADUCEUS trials.

Host: Janet Wright, MD Guest: Scott Sharkey, MD Takotsubo, or stress-induced cardiomyopathy (also known as 'broken heart syndrome'), was first recognized in Japan in the 1990s. Acute emotional or physical stress trigger the condition, which mimics the symptoms of a myocardial infarction (or MI). How can physicians differentiate between stress-induced cardiomyopathy and a more conventional MI, and how is stress-induced cardiomyopathy treated? What characteristics might make a patient more susceptible to developing this condition? Our guest is Dr. Scott Sharkey, senior consulting cardiologist at Minneapolis Heart Institute and director of the Takotsubo cardiomyopathy research program at the Minneapolis Heart Institute Foundation in Minnesota, shares some of the key diagnostic tests for differentiating between stress-induced cardiomyopathy and conventional MI. How common is this condition, and how can we limit the effects of stress-induced cardiomyopathy? Dr. Janet Wright hosts. Produced in Cooperation with

Host: Janet Wright, MD Guest: Scott Sharkey, MD Takotsubo, or stress-induced cardiomyopathy (also known as 'broken heart syndrome'), was first recognized in Japan in the 1990s. Acute emotional or physical stress trigger the condition, which mimics the symptoms of a myocardial infarction (or MI). How can physicians differentiate between stress-induced cardiomyopathy and a more conventional MI, and how is stress-induced cardiomyopathy treated? What characteristics might make a patient more susceptible to developing this condition? Our guest is Dr. Scott Sharkey, senior consulting cardiologist at Minneapolis Heart Institute and director of the Takotsubo cardiomyopathy research program at the Minneapolis Heart Institute Foundation in Minnesota, shares some of the key diagnostic tests for differentiating between stress-induced cardiomyopathy and conventional MI. How common is this condition, and how can we limit the effects of stress-induced cardiomyopathy? Dr. Janet Wright hosts. Produced in Cooperation with

Host: Janet Wright, MD Guest: Scott Sharkey, MD Takotsubo, or stress-induced cardiomyopathy (also known as 'broken heart syndrome'), was first recognized in Japan in the 1990s. Acute emotional or physical stress trigger the condition, which mimics the symptoms of a myocardial infarction (or MI). How can physicians differentiate between stress-induced cardiomyopathy and a more conventional MI, and how is stress-induced cardiomyopathy treated? What characteristics might make a patient more susceptible to developing this condition? Our guest is Dr. Scott Sharkey, senior consulting cardiologist at Minneapolis Heart Institute and director of the Takotsubo cardiomyopathy research program at the Minneapolis Heart Institute Foundation in Minnesota, shares some of the key diagnostic tests for differentiating between stress-induced cardiomyopathy and conventional MI. How common is this condition, and how can we limit the effects of stress-induced cardiomyopathy? Dr. Janet Wright hosts. Produced in Cooperation with

Host: Janet Wright, MD Guest: Scott Sharkey, MD Takotsubo, or stress-induced cardiomyopathy (also known as 'broken heart syndrome'), was first recognized in Japan in the 1990s. Acute emotional or physical stress trigger the condition, which mimics the symptoms of a myocardial infarction (or MI). How can physicians differentiate between stress-induced cardiomyopathy and a more conventional MI, and how is stress-induced cardiomyopathy treated? What characteristics might make a patient more susceptible to developing this condition? Our guest is Dr. Scott Sharkey, senior consulting cardiologist at Minneapolis Heart Institute and director of the Takotsubo cardiomyopathy research program at the Minneapolis Heart Institute Foundation in Minnesota, shares some of the key diagnostic tests for differentiating between stress-induced cardiomyopathy and conventional MI. How common is this condition, and how can we limit the effects of stress-induced cardiomyopathy? Dr. Janet Wright hosts. Produced in Cooperation with

Screening young athletes for heart disease; interview with Barry Maron, MD, of the Minneapolis Heart Institute Foundation; plus a summary of all articles in the issue.

Guest: Timothy Henry, MD Host: Larry Kaskel, MD Not all hospitals are equipped with staff or equipment to perform percutaneous coronary intervention on an emergency basis. However, in an emergency situation, critical decisions must be made: Take a patient to the nearest medical center that can provide fibrinoloysis or take the extra time to get them to a medical center who can perform PCI. What are the current protocols in place to make this often times life/death decision? Join host, Dr. Larry Kaskel talk with Dr. Tim Henry, Director of Research at the Minneapolis Heart Institute Foundation about his recent paper entitled, 'Design of a Standardized System For Transfer of Patients with ST-elevation Myocardial Infarction for Percutaneous Coronary Intervention.'