Podcasts about cedars sinai heart institute

Forty-four percent of U.S. women now live with some form of heart disease, a number that's been climbing steadily over the past decade. And although it's the leading cause of death among women, just 14 percent of cardiologists are women. This week on The Dose podcast, host Joel Bervell interviews cardiologist Martha Gulati, M.D., associate director of the Barbra Streisand Women's Heart Center at Cedars-Sinai Heart Institute in Los Angeles and president of the American Society for Preventive Cardiology. She talks about women's historical exclusion from clinical trials for heart disease, why sex and gender matter in the search for better treatments, and the persistent gaps in women's cardiology care and research — especially related to women of color. “In cardiology, we are still thinking about men more than we are about women,” Dr. Gulati says.

Join Dr. Danielle Belardo and her expert of the week, past Chief of Cardiology, author and women's health advocate Dr. Martha Gulati. Martha is an expert in women's heart health and an influential voice for women's empowerment in the medical field. On today's episode she sheds light on whether the health claims on your Instagram are fact or fiction and how guidelines are working to keep this from being detrimental to your health and wellness.     Danielle and Martha debunk myths and misconceptions surrounding:    The rigorous process of creating guidelines  How unbiased committees are created  Why medical guidelines are (always) better than anecdotal advise  How, even as a layman, you can use guidelines to ensure the credibility of your healthcare    Martha Gulati, MD is the President-Elect of the American Society for Preventive Cardiology. She was a Professor of Medicine and the inaugural Chief of Cardiology at the University of Arizona. She is the author of the best-seller, “Saving Women's Hearts”. She served as the chair of the national chest pain guidelines that were released in late 2021. She recently joined the Cedars-Sinai Heart Institute as a professor of cardiology and is the director of prevention, the associate director of the Barbra Streisand Women's Heart Center and holds the Anita Dann Friedman Endowed Chair in Women's Cardiovascular Medicine and Research.   Check out Martha's book - Saving Women's Hearts HERE!     Thank you so much for taking the time to contribute to a generation that values fact over fiction! Be sure to rate, review, and follow on your favorite podcast app and let us know which not-so-wellness trend you'd like to hear debunked. Follow your host on Instagram @daniellebelardomd and the podcast @wellnessfactvsfiction. Follow Martha @drmarthagulati.      Thank you to our sponsors for making this episode possible. Check out these deals just for you:  COZY EARTH - Go to cozyearth.com and enter WELLNESS at checkout to SAVE thirty-five  Percent.  TALKSPACE - visit talkspace.com and get $100 off your first month when you use promo code drdanielle at sign-up.  DIPSEA - go to dipseastories.com/drdanielle for a free 30 day trial. 

In this episode of the Heart podcast, Digital Media Editor, Dr James Rudd, is joined by Dr Michelle Kittleson from Cedars Sinai Heart Institute. They discuss her review on remote monitoring for heart failure. If you enjoy the show, please subscribe to the podcast to get episodes automatically downloaded to your phone and computer. Also, please consider leaving us a review at https://itunes.apple.com/gb/podcast/heart-podcast/id445358212?mt=2 Link to published paper: https://heart.bmj.com/content/107/5/366

Dr. Shufelt blows our minds with information on the research that is going on around hormones levels and cardiovascular health. Our menstrual cycle is an indicator of our overall health and we need to be paying more attention to our cycles!                 Our menstrual cycle is a strong indicator of our overall health, but we are not talking about it. Dr. Shufelt discusses more about low estrogen levels and how it can impact our health and specifically heart health. Heart disease kills more women than men every year, and it is starting to go up in women ages of 35-44 years of age. Dr. Shufelt shares how we can be proactive about our heart health. Women have novel indicators have cardiovascular issues, such as pregnancy. Pregnancy is our first natural stress test on our heart. We discuss further risk factors. Women get so busy with their lives that making appointments for themselves go out the window but we need to take time for ourselves and our checkups!   So you know she’s legit: Dr. Chrisandra Shufelt is the Director of the Women’s Hormone and Menopause Program at the Barbara Streisand Women’s Heart Center at the Cedars-Sinai Heart Institute. She is also Associate Professor at Cedars-Sinai Medical Center and the David Geffen School of Medicine at UCLA. Dr. Shufelt earned her bachelor's degree from the University of California, Irvine and her medical degree from the Keck School of Medicine at the University of Southern California (USC). She completed her internal medicine residency in Santa Barbara and a Women's Heart Disease and Health Fellowship at Cedars-Sinai Medical Center. Dr. Shufelt received a master's degree in epidemiology and biostatistics from the University of Southern California. Dr. Shufelt is a women’s health expert and board certified in internal medicine with advanced training in preventive cardiology and women's health. She has several leadership roles in the American College of Physicians, the North American Menopause Society and is a certified menopause practitioner. Her research is NIH-funded and focuses on premenopausal women with amenorrhea due to low estrogen and the impact of hormones on the immune system and heart disease. She has over 100 publications in the area of women’s health and is involved in several large studies including the Women’s Ischemia Syndrome Evaluation, the Women’s Health Initiative and the Los Angeles Atherosclerosis Study.     To Find out more about Dr. Shufelt’s work and ongoing research: https://giving.cedars-sinai.edu/barbra-streisand-womens-heart-center/our-leadership/chrisandra-shufelt    

Wow the crowd with your knowledge of pulmonary embolism! What are the red flags? What tools are available to guide you? How on Earth do you triage a patient with pulmonary embolism (PE)? What exactly is the RV spiral & how do PEs really cause morbidity and mortality?! Get schooled by pulmonary embolism expert, Dr. Oren Friedman, associate director of the Cardiac-Surgical Intensive care unit at the Cedars-Sinai Heart Institute. Doctors Cyrus Askin and Chris Chiu join as co-hosts. Test Yo’ Self Pulmonary embolism quiz Written by Cyrus Askin, MD, Justin Berk, MD, MBA, MPH. Figure by Cyrus Askin, MD. Edited by Matthew Watto, MD Full show notes available at http://thecurbsiders.com/podcast Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com.  Time Stamps 5:10 - Start of Interview / Introduction 10:00 - Case Presentation - Introduction of DVT / PE Spectrum and Pathophysiology 16:18 - How to Triage and Work-Up Pulmonary Embolism (CT, Echo, troponins, “eyeball”) 23:30 - Other ways to risk-stratify (Other CT findings, clot burden) 28:45 - What does a low-risk patient look like? 30:35 - When to consider treatment modalities other than general anticoagulation 35:12 - Anticoagulation treatment options 36:38 - Next step intensive interventions after anticoagulation 42:00 - Evidence behind catheter-directed lysis 44:05 - IVC Filter discussion 47:22 - Discharge criteria for PE 50:00 - Incidental PEs 52:40 - Interdisciplinary PERT Team Tags: pulmonary, embolism, thrombolysis, heparin, anticoagulation, right, ventricle, RV, left ventricle, LV, circulation, hypotension, shock, IVC, vena, cava, filter, catheter, TPA, echocardiogram, CT, scan, computed, tomography, shock, bleed, clot, deep, vein, thrombosis, vte, venous, embolism, assistant, care, doctor, education, family, foam, foamed, health, hospitalist, hospital, internal, internist, meded, medical, medicine, nurse, practitioner, professional, primary, physician, resident, student

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. This week's journal features novel results from the NCDR IMPACT Registry that informs us on risk prediction in patients with congenital heart disease undergoing cardiac catheterization. We'll be taking a deep dive into this right after these summaries.                                                 The first original paper provides pre-clinical data showing that delayed repolarization may underlie ventricular arrhythmias in heart failure with preserved ejection fraction or HFpEF. First author Dr. Cho, co-corresponding authors Dr. Marban, and Cingolani from Cedars-Sinai Heart Institute and their colleagues, induced HFpEF in Dahl salt-sensitive rats by feeding them a high-salt diet from seven weeks of age. They showed that susceptibility to ventricular arrhythmias was markedly increased in rats with HFpEF.                                                 Underlying abnormalities included QTc prolongation, delayed repolarization from down-regulation of potassium currents, and multiple re-entry circuits during ventricular arrhythmias. These findings are consistent with the hypothesis that potassium current down-regulation may lead to abnormal repolarization in HFpEF, which in turn predisposes to ventricular arrhythmias and sudden cardiac death.                                                 The next paper shows that genetic testing can help to identify patients with pulmonary veno-occlusive disease who were misclassified as pulmonary arterial hypertension. Now, heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type II or BMPR2 are the commonest genetic cause of pulmonary arterial hypertension. Whereas biallelic mutations in the eukaryotic translation initiation factor 2 alpha kinase 4 gene or EIF2AK4 gene are described in pulmonary veno-occlusive disease and pulmonary capillary hemangiomatosis.                                                 In the current study, first author Dr. Hadinnapola, corresponding author Dr. Morrell, and colleagues from University of Cambridge performed whole genome sequencing on the DNA from 864 patients with pulmonary arterial hypertension, as well as 16 patients with pulmonary veno-occlusive disease all recruited to the NIHR BioResource – Rare Diseases study. They found that 1% of patients with a clinical diagnosis of pulmonary arterial hypertension actually carry the biallelic EIF2AK4 mutations. Patients who are diagnosed clinically with pulmonary arterial hypertension, but who had a transfer coefficient for carbon monoxide of less than 50% predicted and an age of diagnosis of less than 50 years were much more likely to carry these biallelic EIF2AK4 mutation. In fact, the diagnostic yield for genetic testing in this group was 53%.                                                 Radiological assessment alone was unable to distinguish reliably between these patients and those with idiopathic pulmonary arterial hypertension. Importantly, these patients with biallelic EIF2AK4 mutations had a worst prognosis compared to other patients with pulmonary arterial hypertension. Thus in summary, younger patients diagnosed with idiopathic pulmonary arterial hypertension but with a low transfer coefficient for carbon monoxide, have a high frequency of biallelic EIF2AK4 mutations and should be reclassified as pulmonary veno-occlusive disease or pulmonary capillary hemangiomatosis. They have a poor prognosis and genetic testing can therefore identify these misclassified patients allowing appropriate management and early referral for lung transplantation.                                                 The next study identifies a novel molecular target for the treatment of pathological cardiac hypertrophy. This target is SIRT2 [inaudible 00:04:33] poorly characterized member of the Sirtuin family of proteins, which is a family of class III NAD-dependent deacetylases that regulate metabolism and age-related diseases including diabetes and cardiovascular diseases. In the current study, first authors Dr. Tang and Chen, corresponding authors Dr. Chen and Liu from the Chinese Academy of Medical Sciences in Peking Union Medical College used wild-type and Sirt2 knockout mice, and showed that SIRT2 protein levels and activity were reduced during pathological cardiac hypertrophy.                                                 SIRT2 deficiency promoted aging and angiotensin II induced pathological cardiac hypertrophy, and blunted metformin-mediated cardioprotective effects. On the other hand, SIRT2 overexpression repressed pathological cardiac hypertrophy. The molecular pathway involved deacetylation of liver kinase B1 at lysine 48 by SIRT2 to activate AMP-activated protein kinase sickling, which prevented hypertrophy of cardiomyocytes. Thus, SIRT2 is a potential target for therapeutic interventions in aging and stress-induced cardiac hypertrophy.                                                 The next study is the largest comparison of the prognostic value of coronary artery calcium with functional stress testing in patients with stable chest pain. In this study from first and corresponding author Dr. Budoff from Los Angeles Biomedical Research Institute and colleagues, authors looked at the PROMISE trial where patients with stable chest pain or dyspnea, and intermediate pre-test probability for obstructive coronary artery disease were randomized to functional testing or anatomic testing.                                                 Their main finding was that these chest pain populations referred for testing had a low event rate and both tests had different strengths. Coronary artery calcium had a high sensitivity for future cardiovascular events whereas functional testing had a high specificity. The clinical implications are that a normal coronary artery calcium score has a very low event rate and perhaps maybe used to avoid further cardiac testing in a stable chest pain population. On the other hand, an abnormal functional test result including information on exercise and symptoms has a moderate prognostic value.                                                 Of note, coronary CT angiography provided better prognostic and discriminatory power than either coronary artery calcium or functional testing. The implications of these important results are discussed in an accompanying editorial by Dr. David Newby from Edinburgh entitled, Can I Have My Cake and Eat It? On that intriguing note, we've come to the end of today's summaries, now for our feature discussion.                                                 For today's feature discussion, we are talking about an increasingly important population that is pediatric and adult patients with congenital heart disease undergoing cardiac catheterization. A little bit out of my usual comfort zone, but then you see, I'm with two spectacular experts today, Dr. Gerard Martin from Children's National Health System in Washington DC, one of the authors of today's feature paper; and Dr. Gerald Greil, Associate Editor from UT Southwestern. Welcome gentlemen. Dr. Gerard Martin:           Thank you Carolyn. Dr. Gerald Greil:                Thank you Carol. Dr. Carolyn Lam:               Gerard, no that would be Dr. Martin. Enlighten people like me who don't think about this every day, why the importance of looking at cardiac catheterization, and adverse outcomes in this particular population? Dr. Gerard Martin:           Carolyn, that's because of the tremendous advances in medicine, and particularly medicine that's dealing with children with congenital heart defects. Cardiac catheterization was once purely a diagnostic study. Now, it's a less invasive definitive treatment option for many of our pediatric and adult patients with congenital heart defects. As you may or may not know, congenital heart defects are the most common birth defects that impact nearly one out of every hundred live births.                                                 As I mentioned, we have these tremendous advances. As a result of that, there are now over a million children living with congenital heart defects. In the USA alone, improvements in care over the past 50 years, there are now more adults than children living with congenital heart defects. Dr. Carolyn Lam:               Wow. Now, I understand. I mean, cardiac catheterization not just meeting diagnostic but therapeutic, and such an important patient population. Tell us about your study? Dr. Gerard Martin:           As we said, cardiac catheterization is now replacing surgery for some of our defects. For some of the more complex defects, catheterization is providing treatments that make the surgery easier. Now in surgery, we've had registries for many years. These registries provided measurement of survival that allow comparison of programs, and we didn't have that ability with cardiac catheterization. The American College of Cardiology developed the IMPACT Registry. That was to solely provide measurements of the outcomes of catheterization procedures in the children and adults with congenital heart disease.                                                 Now, one aspect of the quality of the program is your rate of adverse outcomes; but simply measuring the number of adverse outcomes does not provide enough discrimination to compare programs. I think you can probably imagine that adverse outcomes will increase based upon the complexity of the type of patients you see, or the types of procedures that you might be performing. What we wanted to do was to create a risk standardization tool for our population where we can measure variation and performance between programs. If we can do that, then we can learn from the best performers to improve all the others. Dr. Carolyn Lam:               That's beautifully put. Could you tell us what you found? Dr. Gerard Martin:           Sure. The IMPACT Registry began on about 2011 and has grown from 50 sites to 111 sites in 2017. That's the majority of the sites in the United States that perform cardiac catheterization on children. We have now over 115,000 procedures. What we wanted to do with this is to look at some of the early procedures that were included and to see how adverse events were occurring. When we created the registry though, we used data variables from a previous research study in Boston called the CHARM.                                                 They created a tool to risk standardized outcomes during procedures. They did it by coming up with four categories of procedures, and some four markers of hemodynamic vulnerability. We tested their methodology with IMPACT, and it didn't really performed particularly well. In this study, what we did was to increase the number of risk categories. We took the nearly 200 types of procedures we do in the cath lab and divided them into six categories. We also increased the indicators of hemodynamic vulnerability from four to six.                                                 Now, what I mean by hemodynamic vulnerability? What is the patient's oxygen level when they go into the procedure? What is their blood pressure when they're in the procedure? Do they have one ventricle, or do they have two ventricles? What is the resistance in the lung vessels? All these are critically important. Lastly, we looked at some baseline patient characteristics. In other words, was age important? Sex, genetic conditions, or other comorbid conditions like the level of mechanical support that the patients were on. Then we put all that into our model to see if we could come up with a risk score. Dr. Carolyn Lam:               Right. The final adjustment model? Which factors that they include in the end? Dr. Gerard Martin:           We did find that there are lot of adverse events that do occur. We found major adverse events occurring in about same 7% of our patients. Most common adverse events were bleeding, or rhythm disturbances that require some medicine, or cardioversion during the procedure, or death during the hospitalizations. We did find that these major events were more common in the youngest patients or neonates, children under a month of age, or in patients with genetic disorders, or single ventricle physiology, and also patients that went to the cath lab with their kidneys not working very well.                                                 In the end, we did create a risk adjustment model that included the type of procedure that was done, the number of hemodynamic vulnerability indicators, and whether or not the patient had renal insufficiency, or single ventricle physiology, or coagulation, and we found really good discrimination. Our discrimination had a C-stat of 0.76 in the derivation cohort, and 0.75 in the validation cohort. The slope of the curve was excellent, so we really think we have something now that we can use as a tool. Dr. Carolyn Lam:               Gerald, you're a pediatric cardiologist. Could you give us your perspective on how important these results are? Dr. Gerald Greil:                I think it's the largest and the first study, which kinds of give us a calibration in our field how successful interventions are. How we can make centers better without finger pointing on specific centers, and how to advance the field as a whole? From that perspective, I'm quite excited that the group offered us to publish this paper in circulation. I was kind of asking a question to Dr. Martin because obviously, all essentials are closely monitored. There's obviously data publicly available. Do you think there's a risk that this way to monitor centers within the United States or probably worldwide, that it's potentially preventing innovation or risky procedures? Dr. Gerard Martin:           I think that, that's a good question. I think it's one thing that whenever we talk about transparency or public reporting, it's an argument against it. I think that having a model like this, actually levels the playing field. In other words, centers that are risk averse who aren't particularly innovative, you'll be able to look at those centers, see what type of patients they're doing and look at their adverse events for a low-risk population. Then, you can also look and see some other centers that are doing more complicated procedures, higher risk, and you can see what their adverse event rate is.                                                 Certainly, this is only talking about the adverse events. This has to be put together with the outcome of the procedure. In other words, if you're trying to relieve an obstruction, did you relieve it? Did you meet the intended goal of the procedure? This is only half of the story. The other part of it is, did you get the intended goal of the procedure? When you put the two of them together, perhaps some of those centers that are risk averse have lower complications, but maybe their success rate is lower. This will be able to tell the public everything they know, and they'll be able to tell their providers what they need to know to get better. Dr. Carolyn Lam:               I have to agree. Your paper does highlight, I think. Gerard, just one other question. What do you think our next steps? Dr. Gerard Martin:           The next step is to test the data. We have a new version of IMPACT that has rolled out, version 2 that has new procedures in it. Now, we have to test the data and we actually have to look for variability. Can we see a variation between the programs? Then, once we see if there's variation, if we see there is best performers and those performers that could improve, a question then is how do we take from what the best performers are doing to try and lift those that need to improve up. That's going to be the true hard work for this registry. Dr. Carolyn Lam:               Thank you so much for publishing it with us. Thank you so much audience for listening with us today. Don't forget to tune in 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 Youth National University of Singapore. Coming right up, we will be discussing fascinating new data on the prevalence of subclinical coronary artery disease in masters endurance athletes but first, here's your summary of this week's journal. The first paper provides insight into ischemic cellular post conditioning. Now, we know that cardiosphere derived cell therapy has been utilized as a strategy to treat ischemic heart disease and reduce chronic scar burden when administered months after myocardial infarction. In the current study, by first author Dr. de Couto, corresponding authors Dr. Marban and Berman from Cedars-Sinai Heart Institute in Los Angeles, California, the authors used rat and pig models of myocardial infarction to show that exosomes, which are nanosize lipid bi-layer vesicles, actually mediate the cardio protective effects of cardiosphere derived cells when administered after reperfusion of myocardial infarction.                                                 They further show that treatment with either cardiosphere-derived cells or their secreted exosomes reduce infarct size and improved functional recovery. Using RNA sequencing to determine exosome content and alterations in gene expression profiles on macrophages from cardiac tissue or bone marrow, they found that a specific micro RNA species miR 181-B within the exosomes, acted on macrophages and was implicated as a key mediator of the cardio-protective benefits. Thus, this study gives new reason to test the idea that allogeneic cardiosphere-derived cells may be efficacious in preventing scar formation and improving cardiac function, when given in the earlier reperfusion period. The data further support that exosomal transfer of miR 181-B from these cardiospheric-derived cells into macrophages underlie the cardio-protective effects after reperfusion.                                                 The next study describes a potential new therapeutic strategy for vasoproliferative retinopathy which can underlie age-related macular degeneration, the leading cause of blindness in industrialized nations. First author, Dr. Bucher, corresponding authors Dr. Yea and Friedlander, from the Scripps Research Institute in La Jolla, California used rodent models of retinal neo-vascular disease to show that Tspan-12, beta-catenin signaling plays an important role in the development of vasoproliferative retinopathy. As background, Tspan-12 belongs to the Tetraspanin family, which mainly includes cell surface proteins characterized by four transmembrane domains and two extra cellular domains.                                                 Members of the Tspan family participate in a diverse cellular processes and act as signaling platforms by forming Tspan-enriched micro domains in plasma membranes. The authors went further to use a novel phage display combinatorial antibody library to specifically design a Tspan-12 blocking antibody which is capable of interacting with human and mouse Tspan-12 antigen. They then provided strong evidence that the Tspan-12 blocking antibody prevents developmental pathological neovascularization in  murine models of vasoproliferative retinopathy. Combination therapy with a known anti-VEGF agent demonstrated significant synergy supporting the potential clinical use of the anti-Tspan-12 antibody as a novel angiomodulatory agent.                                                 The next study addresses the paradox that blacks have higher coronary heart disease mortality compared with whites, but non-fatal coronary heart disease risks may be lower for black versus white men. To address this paradox, first author Dr. Colantonio, corresponding author, Dr. Safford and colleagues from Weill Cornell Medical College in New York, compared fatal and non-fatal coronary heart disease incidents and case fatality among blacks and whites in three studies. The Atherosclerosis Risk in Communities or ARIC study, cardiovascular health study, and reasons for geographic and racial differences in stroke or regards study, all stratified by gender.                                                 They found that the incidents of non-fatal coronary heart disease was consistently lower among black versus white men, although black men have a higher burden of unfavorable social determinants of health and cardiovascular risk factors and a higher fatal coronary heart disease incidents. Following adjustment for social determinants of health and cardiovascular risk factors, black men and women had a similar risk of fatal coronary heart disease, but a lower risk of non-fatal coronary heart disease compared with white men and women respectively. Finally, blacks with incident coronary heart disease had a higher case fatality compared with whites and the difference remained similar after adjustment for social determinants of health and risk factors. Thus, there is an apparent lower risk for non-fatal coronary heart disease among black versus white men and women, which needs to be further studied. Blacks have a higher risk of their initial coronary heart disease event being fatal compared with whites, highlighting the need for reinforcing primary prevention in this population.                                                 The next study provides important information on the burden of re-admissions after hospitalization for critical limb ischemia. First author, Dr. Kolte, corresponding Dr. Aronow and colleagues from Brown University in Providence, Rhode Island, used the 2013/2014 nationwide re-admissions databases to identify almost 61,0000 hospitalizations for primary diagnosis of critical limb ischemia during which patients underwent endovascular or surgical therapy. They found a 30-day re-admission rate of 20.4%. Independent predictors of 30-day re-admission included presentation with an ulcer or gangrene, age above 65 years, females, large hospital size teaching hospital status, known coronary artery disease, heart failure, chronic kidney disease, anemia, coagulopathy, obesity, major bleeding, acute myocardial infarction, vascular complications, and sepsis. Interestingly, mode of revascularization was not independently associated with re-admissions.                                                 The most common reasons for re-admissions included infections, persistent or recurrent manifestations of peripheral artery disease, cardiac conditions, procedural complications, and endocrine issues. Finally, the costs of 30-day re-admissions for critical limb ischemia during the study period were 624 million U.S. dollars. Thus, this study provide knowledge of independent predictors and reasons for re-admissions that will help clinicians and hospitals to identify, develop, and implement strategies to reduce re-hospitalizations and healthcare costs associated with critical limb ischemia. The final study tells us that there may be a direct relationship between life-long exercise volume, and coronary atherosclerosis in athletes. Dr. Aengevaeren and colleagues from Radboud University Medical Center in the Netherlands, studied 284 middle-aged men engaged in competitive or recreational leisure supports, using contrast enhanced CT to assess coronary artery calcification and plaque characteristics.                                                 Participants also reported life-long exercise history patterns and exercise volumes were quantified as metabolic equivalent of task or met minutes per week. They found that participants in the more than 2,000 met minutes per week group had a higher prevalence of coronary artery calcification and atherosclerotic plaques. The most active group did, however, have a more benign composition of plaques with fewer mixed plaques and more often, only calcified plaques. These observations may explain the increased longevity typical of endurance athletes, despite the presence of more coronary atherosclerotic plaques in the most active participants. Well, that wraps it up for your summaries. Now for our featured discussion.                                                 Our current physical activity guidelines recommend 150 minutes of moderate exercise and that's supposed to protect against cardiovascular disease and increase longevity. However, what do we really know about the dose response relationships and the effects of exercises doses that exceed current recommendations. Well, recent data, including a paper in this week's issue, suggests that long-term, high volume endurance exercise may actually accelerate, rather than reduce coronary atherosclerosis. To discuss this exciting paper, we have the corresponding author, Dr. Sanjay Sharma, from Saint George's University of London, as well as editor of digital strategies and associate editor at UT Southwestern who handled this paper, Dr. Amit Khera. Welcome, gentleman. Dr. Amit Khera:                 Good morning. Dr. Sanjay Sharma:          Thanks for having us. Dr. Carolyn Lam:               First, Sanjay, oh yikes! As a runner and as a person who strongly advocates regular exercise, please, please, put us out of our misery. Tell us what you've found and what you think are the possible explanations. Dr. Sanjay Sharma:          I'm a runner too, and I don't think anyone would argue that the benefits of exercise on the cardiovascular system are unrivaled. People who exercise regularly do reduce their risk of an adverse event from a heart attack by 50% when they're in their 5th and 6th decade and they live around three years longer than people who don't exercise at all. Now as you rightly point out, the current recommendation suggests 2 1/2 hours of moderate physical activity per week and by that I would mean, at maximum, a 15-minute mile pace. Clearly, our endurance athletes exercise much, much more than that. They exercise 10 to 20 times greater than that volume and in parallel with this has been the emergence of a large number of people participating in marathon runs. For example, in Europe, there were two million marathon runs per annum and that figure's going up by about 5%.                                                 Coinciding with this burgeoning increase in endurance exercise, is the development of several reports that show that exercise may cause release of biomarkers of cardiac damage. Animal experiments have shown that exercise may cause scaring in the heart and human studies have shown that some marathon runners have more calcium in their coronary arteries compared to relatively sedentary individuals. One of the problems with these studies is firstly, the biomarker release is very transient, it goes away after about two days. Animal experiments cannot really reflect what goes on in human beings because they're artificial and animals are forced to exercise with electrical shocks, et cetera. The studies in human beings have been conducted in runners who have been former smokers.                                                 In fact, the most commonly reported study or cited study, contained individuals of whom 50% had risk factors for coronary artery disease. What we decided to do was to do a clean study, where we took 150 individuals who had none of the risk factors for coronary artery disease and 92 relatively sedentary controls who exercise within the normal limits. We have to exclude a lot of people because we have to exclude anyone that had ever smoked, anyone that had high blood pressure, high cholesterol, or a family history of permanent cardiac disease. We actually subjected them to all sorts of investigations and we found that a small number of male runners had more calcium in their arteries compared to sedentary individuals. Dr. Carolyn Lam:               Wow! Please tell us that there's something good that you can say about that. First of all, I really want to congratulate you on this most elegant study and Amit, I'm sure you put in what the editor's thought but we're just so proud to be publishing such a high quality study here. Amit, is there anything you might want to add of what the editors thought? Dr. Amit Khera:                 Sure, I first want to congratulate Dr. Sharma and his colleagues. This was a carefully done study and we've talked a bit about the coronary calcium but there was extensive investigation and I really think this advanced the field. Sounds like all three of us are runners, so this hit home to all of us and as he mentioned, this has been a very hot area and one that's been very controversial. I think here what we have is a manuscript that really helped move the field forward, helped us better understand the biology. The one thing I'll comment on that we found very interesting was the observation that those that were the masters athletes actually had more of a calcific phenotype, where as those that were not looked like a soft plaque phenotype, if you will. Actually, if you look, we have a companion article in circulation looking at sort of dose dependent finding a similar finding. My question, now turned back to Dr. Sharma is, what do you counsel your patients now with these findings? Has it changed now how you recommend exercise or your thoughts on how you counsel them? Dr. Sanjay Sharma:          Well, we examined 152 different athletes, or masters athletes in 92 controls. These athletes were aged 56 years old, who'd been training for 36 years and had immediate marathon number of 13. Now, what we've found in these individuals is that a small number of males, that's 11%, had a coronary artery calcium score of more than 300. Some men had more plaques than sedentary individuals and these plaques were distributed throughout all three coronary arteries. When we looked at the pathology of the plaques very carefully, we found that the plaques in the athletes were calcified. Indeed, 72% of athletes had very calcified plaques. We know that such calcified plaques are stable, they're less likely to fissure and are less likely to cause coronary thrombosis and therefore, acute myocardial infarction.                                                 This led us to propose that although exercise may be causing some atherosclerosis through the sheering and stressful source during exercise of the bending and kicking of vessels, we believe that the repair mechanism here is different to that seen in people who smoke or who have high cholesterol or high blood pressure. The repair mechanism results in very calcified and stable plaques in athletes and this may actually mitigate the risk of acute myocardial infarction and may explain why the number of people who actually suffer an acute myocardial infarction during a marathon run is very small, around 1 in 50,000, and no different to the number of people who suffer a sudden cardiac arrest playing football or basketball, due to congenital or inherited abnormalities of the heart.  Dr. Carolyn Lam:               Sanjay, those are just such important points to keep in mind as we read your paper. It did strike me as a significant minority, actually, of these long term endurance athletes who develop significant coronary artery calcification and it could potentially be a clinically benign phenotype. At the end of the day, this is a cross-sectional study, isn't it? We can't, I suppose, extrapolate into the clinical events. What are your postulations there and what could be future work that you're planning? Dr. Sanjay Sharma:          Well, you make a good point. This is a cross-sectional study and the demonstration of an increased cardiopathy calcium does not necessarily reflect future cardiac events. We have followed these individuals up for the last 18 months. These masters athletes and have not demonstrated a single one to develop an acute event that would last 18 months. We really don't know what the meaning of these plaques is. I think the only thing to do now, being we've got the liberty of having so many people that do marathon runs and so many people who've been exercising for three or four decades, we can actually do a prolonged follow up study, so the answers will be a while coming. To follow these people up with high calcium, just to see whether they do go on to develop adverse events in the future. All our study has shown is that some male athletes who've exercised lifelong get an increasing number of plaques. These plaques appear to be calcified and stable and the long term effects of such  plaques is unknown. Dr. Carolyn Lam:               Sanjay, just circling back to Amit's question earlier and maybe Amit, you could take it to after this. What do we recommend to our athletes who come in and have a high coronary artery calcium score? Do we tell them to stop? Dr. Sanjay Sharma:          I certainly wouldn't and I'm much less worried about an increase coronary calcium score in a lifelong runner or cyclist than I was 10 years ago. It appears that these plaques are there in some individuals, they are calcified, they appear stable. Given the fact that we know that coronary events during marathon running in experienced runners are very, very low indeed. I don't think I would be keen to do anything about it, not even consider stacking therapy based on our findings at present. As I said before, we do need longitudinal follow up to really identify all ascertain the precise implications of these plaques in masters athletes. Dr. Carolyn Lam:               Right, and this is again recognizing that your particular population was free of traditional cardiovascular disease. Of course, if we were to find these risk factors in our athletes, we would most certainly treat the traditional risk factors. Amit, anything to add there? Dr. Amit Khera:                 I think that was an excellent point about his approach to counseling patients. I will mention on the editorial staff, we felt like this was such an interesting area with emerging data and fast moving, that it was warranting of an editorial. I recommend people to look at the one by Aaron Baggish and Ben Levine. I think they had a very similar conclusion and that was that they don't necessarily proscribe exercise in patients with high coronary calcium but rather, focus on risk mitigation strategy, focusing on risk factors as we normally would do. I think the conclusions are similar and the thoughts in that editorial were insightful, pairing both of these papers and helping us make sense out of this really evolving field. Dr. Carolyn Lam:               Well, thank you Sanjay and Amit for this wonderful discussion. I learned so much as I'm sure our listeners did. You've been listening to Circulation On The Run. Tune in next week. 

Guest: Prediman Shah, MD Host: Janet Wright, MD It is apparent to most physicians that patients at high risk for having a cardiovascular event should be screened, but what about those patients who fall into the intermediate risk category (classified using the Framingham risk score)? Dr. Prediman Shah, director of the division of cardiology at Cedars-Sinai Heart Institute in Los Angeles, suggests that screening asymptomatic, intermediate-risk patients for subclinical atherosclerosis using non-invasive imaging might be beneficial. Dr. Shah also discusses the limitations of relying solely on the Framingham risk score, and recommends additional ways to classify a patient's risk for developing a cardiovascular event. What specific screening tests are best for detecting subclinical atherosclerosis? Dr. Janet Wright hosts. Produced in Cooperation with

Guest: Prediman Shah, MD Host: Janet Wright, MD It is apparent to most physicians that patients at high risk for having a cardiovascular event should be screened, but what about those patients who fall into the intermediate risk category (classified using the Framingham risk score)? Dr. Prediman Shah, director of the division of cardiology at Cedars-Sinai Heart Institute in Los Angeles, suggests that screening asymptomatic, intermediate-risk patients for subclinical atherosclerosis using non-invasive imaging might be beneficial. Dr. Shah also discusses the limitations of relying solely on the Framingham risk score, and recommends additional ways to classify a patient's risk for developing a cardiovascular event. What specific screening tests are best for detecting subclinical atherosclerosis? Dr. Janet Wright hosts. Produced in Cooperation with

Host: Janet Wright, MD Guest: Eduardo Marbán, MD, PhD Stem cell therapies across multiple disciplines continue to demonstrate promising results. How successful are autologous cardiac stem cell treatments proving to be at regenerating cardiac tissue after a heart attack? Which patients would be the best candidates for this procedure, and when might this treatment move from clinical trials into the clinic? Dr. Eduardo Marbán, director of the Cedars-Sinai Heart Institute, developed this procedure, and joins host Dr. Janet Wright to discuss its exciting applications.

Host: Janet Wright, MD Guest: Eduardo Marbán, MD, PhD Stem cell therapies across multiple disciplines continue to demonstrate promising results. How successful are autologous cardiac stem cell treatments proving to be at regenerating cardiac tissue after a heart attack? Which patients would be the best candidates for this procedure, and when might this treatment move from clinical trials into the clinic? Dr. Eduardo Marbán, director of the Cedars-Sinai Heart Institute, developed this procedure, and joins host Dr. Janet Wright to discuss its exciting applications.