Podcasts about minneapolis heart institute

In this thought-provoking episode of Parallax, Dr Ankur Kalra explores the unexpected intersection of cardiology and popular culture with Dr Kristen Shaw and Dr Kevin Harris from the Minneapolis Heart Institute. Their conversation centers around their recently published systematic analysis, "Portrayal of Acute Myocardial Infarction in Popular Film: A Review of Gender, Race, and Ethnicity". Through examination of 100 popular films, our guests unpack striking statistics: 90% of on-screen heart attacks occur in men, and symptom presentation is dramatically overplayed compared to clinical reality. The conversation delves into how these media portrayals potentially shape both patient behavior and public health outcomes, particularly for underrepresented populations. From exploring the stark disconnect between cinematic drama and clinical presentation to discussing practical solutions for improving public health messaging, this episode offers crucial insights for healthcare providers working to bridge the gap between media perception and medical reality. The discussion extends into broader themes of healthcare mistrust in the post-pandemic era, offering valuable perspectives on how improved representation could enhance patient education and emergency response outcomes. Essential listening for cardiologists, healthcare educators, and anyone interested in how media shapes public understanding of cardiovascular disease.

In this episode, Dr. Mario Gössl, Director of Transcatheter Valve Therapies at Allina Health Minneapolis Heart Institute and a registered yoga teacher, discusses the evolving landscape of cardiology, the challenges of talent retention, and the importance of addressing physician burnout.

In this episode, Dr. Mario Gössl, Director of Transcatheter Valve Therapies at Allina Health Minneapolis Heart Institute and a registered yoga teacher, discusses the evolving landscape of cardiology, the challenges of talent retention, and the importance of addressing physician burnout.

In this podcast, Dr. Nedaa Skeik, a vascular surgeon with Minneapolis Heart Institute, brings his knowledge and experience in regards to vascular insufficiency, and the importance of a timely diagnosis and management options. *Disclosure note: Dr. Nedaa Skeik, speaker for this educational event, has disclosed that he received honorarium from Medtronic.  All relevant financial relationships for Dr. Skeik have been mitigated. Enjoy the podcast. Objectives:Upon completion of this podcast, participants should be able to: Summarize the pathophysiology of different venous disorders. Recognize and confidently diagnose venous insufficiency. Identify the risks and benefits of different interventions for venous conditions. Differentiate medical management (conservative and interventional) for venous insufficiency. This activity has been planned and implemented in accordance with the accreditation criteria, standards and policies of the Minnesota Medical Association (MMA). Ridgeview is accredited by the Minnesota Medical Association (MMA) to provide continuing medical education for physicians.  CME credit is only offered to Ridgeview Providers & Allied Health staff for this podcast activity. After listening to the podcast, complete and submit the online evaluation form. 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 Education@ridgeviewmedical.org. Click the link below, to complete the activity's evaluation. CME Evaluation (**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.  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. None of Ridgeview's CME planning committee members have relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.  All of the relevant financial relationships for the individuals listed above have been mitigated. Thank-you for listening to the podcast. SHOW NOTES:   *See the attachment for additional information.  PODCAST OVERVIEW Wide Range of Venous Disorders and Presentations - Morphologic (spider, reticular, varicose), skin discoloration, ulceration - Functional (venous reflux +/- loss of pumping mechanism - Anatomic (thrombosis, congenital anomalies) - Presentation (asymptomatic vs symptomatic)Anatomy PathophysiologyEpidemiology - Chronic vein abnormalities- Prevalence (venous insufficiency) - Varicose veins & prevalence- Presence of symptoms Risk factors - Family component- Other  Clinical features - Correlation - severity of venous reflux, age- Asymptomatic - General symptoms - Vein appearance - Severity Disease Severity - Classification Scales - CEAP calssification scale- Venous Clinial Severity Score  Disease Progression - Correlation- pregression of disease not well understoodDiagnosis - History - Symptoms - Exam findings - including venous ultrasound - Differential diagnoses (edema, skin manifestations, vein engorgement) - Pre-management considerations (severity, superficial and/or deep, proximal/distal, multiple or single, comorbidities) ManagementAsymptomatic - visual sclerotherapy- surface laser therapy - complications Symptomatic- compression therapy - exercise - leg elevation - skin care Conserative Therapy- leg elevation - exercise - compression stockings Pharmacologic Therapy and Skin Care- vasoactive drugs - rheologic agents - skin care Interventional Options - Preintervention measures (venous anatomy, preop medications, anesthesia) - Sclerotherapy (visual, US guided)- Vein closure procedures (thermal - RFA/EVLA, chemical, MOCA, PEM, EHIT) - Surgical (phlebectomy, ligation, stripping) Post Intervention Care - pain management - ambulation - leg elevation - compression - return to normal activity/work - post procedural US - follow up appointment Thanks to Dr. Nedaa Skeik for his expert knowledge and contribution to this podcast. Please check out the additional show notes for more information/resources.

In this podcast, Dr. Robert Steffen, a cardiac surgeon with Minneapolis Heart Institute. Dr. Steffen brings his knowledge and experience regarding the prevalence of aortic valve disease, advancements in technology, as well as treatment modalities for patients who suffer with this problematic disorder. Enjoy the podcast. Objectives:Upon completion of this podcast, participants should be able to: State the prevalence of aortic valve disease. Identify when patients with aortic valve disease need intervention. Describe the different therapeutic options for patients with aortic valve disease and when to use them. This activity has been planned and implemented in accordance with the accreditation criteria, standards and policies of the Minnesota Medical Association (MMA). Ridgeview is accredited by the Minnesota Medical Association (MMA) to provide continuing medical education for physicians.  CME credit is only offered to Ridgeview Providers & Allied Health staff for this podcast activity. After listening to the podcast, complete and submit the online evaluation form. 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 Education@ridgeviewmedical.org. Click the link below, to complete the activity's evaluation. CME Evaluation (**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.  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. Thank-you for listening to the podcast.

This podcast, Dr. Peter Eckman, a cardiologist and heart failure specialist, with Minneapolis Heart Institute, discusses heart failure and why it is an extensive medical issue. Enjoy the podcast. Objectives:Upon completion of this podcast, participants should be able to: Recognize heart failure as a problematic clinical disease and its morbidity and mortality that leads to comprehensive medical management. Identify and describe optimal contemporary medical therapy for heart failure. Describe novel options for heart failure. CME credit is only offered to Ridgeview Providers & Allied Health staff for this podcast activity. After listening to the podcast, complete and submit the online evaluation form.  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 Education@ridgeviewmedical.org. Click the link below, to complete the activity's evaluation. CME Evaluation (**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. Thank-you for listening to the podcast. SHOW NOTES:  *See the attachment for additional information.  Heart Failure (HF)- Can occur without congestion or fluid retention - Characterized by fatigue, fluid retention, SOB, PND, orthopnea - We should consider the same urgency for heart failure as patients with CAD and CA. Heart Failure Preserved/Reduced Ejection Fraction (HFpEF/HFrEF)- HFpEF is a Preserved Ejcetion Fraction over about 50% - HFpEF - congestive phenotype more of a fluid retention       - an exercise intolerant phenotupe where the patient becomes intolerant of exercise induced dyspnea.       - Pulm HTN phenotype       - Increased pressure in the heart that gets transmitted to the lungs - HRrEF is Reduced EF is usually below 40% Medications- 4 classes of medications (MRAs, BB, SGLT2, ARNIs) - Treatment with mineralocorticoid receptor antagonists (MRAs) has been demonstrated to improve clinical outcomes in patients with HFrEF with mild to severe symptoms and also in patients with left ventricular dysfunciton after myocardial infarction. - SGLT2 inhibitors reduced the risk of cardiovascular death and hospitalizations for heart failure in a broad range of patients with heart failure, supporting their role as a foundational therapy for heart failure, irrespective of ejection fraction or care setting. - ARNI (angiotensin receptor/neprilysin inhibitor) medication is a newer treatment for heart failure. The combination of sacubitril and valsartan has helped people live longer and have a better quality of life. - Comprehensive EF therapy involves BB, ARNI, MRAs, angiotensin receptor/neprilysin inhibitors. Spironolactone, SGLT2 inhibitors. Treatment- Traditional therapy usually involves a BB and ACE inhibitor. - Currently we should be looking at comprehensive therapy when it comes to HF treatment.       - STOP USING LISINOPRIL.- SGLT2 inhibitors contraindicated ketoacidosis, amputation UTI, weight loss       - (SGLT2 inhibitors) DAPA-HF trial showed that dapagliflozin was superior to placebo at preventing cardiovascular deaths and heart failure events among patients with heart failure.  (Source: https://www.nejm.org/doi/full/10.1056/NEJMoa1911303#article_citing_articles ) - Catheterization - a vast majority of HF patients will need a right heart catheterization. - Cardiac pulmonary pressure monitoring Cardio MEMS - same day outpatient surgery which helps with medication adjustments and hospitalization in half. Works regardless of EF. - CardioVere laser spectroscopy which uses different wavelengths to detect light characteristics to determine the level of edema/fluid present wihin someone's tissues. Currently in development. - Casana is a toilet seat with certain sensors that detect and monitor impedance that check levels between different tissues, monitors HR and weight. - Cardiac contractility modulation causing electrical stumulation during a particular contraction of the myocyets it will augment potential (like a pacemeaker). -CORCHINCH - HF trial catheter based device that cinches up the heart, thereby making it smaller. It works more efficiently.  (Source: Clinical Evaluation of the AccuCinch® Ventricular Restoration System in Patients Who Present With Symptomatic Heart Failure With Reduced Ejection Fraction (HFrEF): The CORCINCH-HF Study) Novel Treatments- Atrial shunting procedure is investigational trials. Potentially impactful in exercise capacity and pressures but stay tuned as the verdict is not out. HfPEF exercise induced intolerance may be the best candidate. - SVC trial feasibility trial more durable effects of cardiac output.  Stay tuned. - LVAD for advanced therapies. Sometimes a bridge for candidacy as well as recovery. - Biventricular pacing has shown promise. *Heart failure is a problematic clinical disease entity with significant morbidity and mortality often leading to comprehensive medical management. It is often beneficial to enlist the help of our heart failure colleagues for these complicated patients.  Thanks to Dr. Peter Eckman - MHI heart failure specialist for his knowledge and contribution to this podcast. Please check out the additonal show notes for additional information/resources.

In this podcast, Dr. Joseph Karam, a vascular surgeon with Minneapolis Heart Institute leads the discussion on everything related to vascular disease from head to toe. Enjoy the podcast. Objectives:Upon completion of this podcast, participants should be able to: Define vascular disease. Identify vascular disease and differentiate the treatment modalities available. Describe clinical entities related to vascular disease such as peripheral artery disease (PAD), aortic aneurysms, carotid artery disease (CAD), and venous disease. Recognize when a referral to a vascular specialist is warranted. 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. To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation. CME Evaluation (**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. Thank-you for listening to the podcast. SHOW NOTES: *See the attachment for additional show information.  Vascular Medicine  - Evolving profession & essential to any healthcare     system Risk Factors   - Prevention    - Reducing risk factors    - Social determinants Carotid Disease    - Asymptomatic CAD    - Work up (ultrasound, CTA)    - Treatment options Thoracic/Abdominal Aortic Disease       - Thoracic aortic aneurysm (Type A, Type B)    - Abdominal aneurysm    - Infra renal aneurysms     - Aortic dissections    - Post-op complications (TVAR, abdominal aortic       aneurysm) Peripheral Vascular Disease       - Studies of natural history    - Critical limb ischemia    - Acute limb ischemia    - Treatment   Thanks for listening.

In this podcast, Dr. Jim Kolbeck, interventional and structural cardiologist with Minneapolis Heart Institute at United Hospital, discusses ECMO (extracorporeal membrane oxygenation) and the various aspects of this procedure. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: Explain the history and purpose for extra corporeal membrane oxygenation (ECMO). Assess when ECMO CPR (ECPR) is warranted. Identify and define inclusion criteria for ECMO and contraindications to ECMO. 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. To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation. CME Evaluation (**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. Thank-you for listening to the podcast. SHOW NOTES:  *See the attachment for the full chapter summaries.  Chapter 1: Definitions- History of ECMO- Extracorporeal membrane oxygenation (ECMO):       - V-A Veno-Arterial       - V-V Veno-Venous- Who gets ECMO        - V-A: Shock states        - V-V        - ECPR: V-A            - Out-of-hospital cardiac arrests            - ARREST Trial            - Refractory Cardiac Arrest            - Criteria Chapter 2: Cannulation- V-A ECMO       - Bifemoral- V-V ECMO       - Bifemoral or Femoral/Jugular       - Dual Lumen: Jugular vein        - Anticoagulation       - V-V to V-A       - Discussions of care Chapter 3:- Cannulate and Ship Model- Who's Involved- The Machine: Cardiohelp (portable ECMO machine)- Physiology of ECMO- Monitoring the Results Chapter 4: - Who Gets ECMO- Contraindications- The Future / Next steps

Heart disease in women is under recognized under treated, and under researched compared to men; although it is the number one killer of women in the world. In this podcast, Dr. Retu Sexena, a cardiologist with Minneapolis Heart Institute, discusses the epidemiology, symptoms and pathology of heart disease as it relates to women and cardio-obstetrics. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: Summarize the historical nature of heart disease in women. Recognize the cardiovascular risks in women. Identify signs/symptoms of heart disease in women. Review prevention efforts for heart disease in women. 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. To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation. CME Evaluation (**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. Thank-you for listening to the podcast. SHOW NOTES:  *See the attachment for the full chapter summaries.  Chapter 1:- History of cardiovascular disease in women - Symptoms - Risk factors Chapter 2:- Cardio-Obstetrics (CV-Ob) - Cardiomyopathies in pregnancy Chapter 3: - Treatment/Therapies and concerns - Hypertension - ICD guidelines, ASCVD risk scores, AHA guidelines, recommendations * For journal articles cited, and web links - see attached "Show Notes".

This week is a Double Feature Circulation on the Run. Please join author Patrick Serruys, editorialist Shamir Mehta, and Associate Editor Emmanouil Brilakis as they discuss their article "Ten-Year All-Cause Death According to Completeness of Revascularization in Patients with Three-Vessel Disease or Left Main Coronary Artery Disease: Insights from the SYNTAX Extended Survival Study" and editorial "Achieving complete revascularization for multi-vessel coronary artery disease." Then, please join author G. Michael Felker, and Associate Editor Mark Link as they discuss the Research Letter "Implantable-Cardioverter-Defibrillator Eligibility after Initiation of Sacubitril/valsartan in Chronic Heart Failure: Insights from PROVE-HF." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke-National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: So guess what, Greg, we have another double feature this week. First, we need to talk about completeness of revascularization in patients with three-vessel disease or left main coronary artery disease. Always a question, and this time we've got insights from the SYNTAX Extended Survival Study. And then, the next feature talks about implantable cardioverter defibrillator eligibility after initiation of sacubitril/valsartan in heart failure, and these are insights from PROVE-HF. But before we get to that, I suggest, as I pick up my coffee, could you tell us what some of the papers you've spotted? Dr. Greg Hundley: Thanks so much, Carolyn. Sure. So I'm going to start from the world of preclinical science, and the paper comes to us from Dr. Vadim Fedorov from The Ohio State University Wexner Medical Center. Carolyn, up to 50% of the adult human sinoatrial node is composed of dense connective tissue, and cardiac diseases, including heart failure might further increase fibrosis within the sinoatrial node pacemaker complex, leading to impaired automaticity and conduction of electrical activity to the atrium. However, unlike the role of cardiac fibroblasts in pathological fibrotic remodeling and tissue repair, nothing is known about fibroblasts that maintain the inheritantly fibrotic sinoatrial node environment. Dr. Carolyn Lam: That's true. So what did these authors do? Dr. Greg Hundley: Right, Carolyn. So these authors found that increased sinoatrial node-specific fibrosis, with presence of myofibroblasts and CILP-1, and periostin-positive interstitial fibrosis only in heart failure versus non-heart failure human hearts. And comprehensive proteo-transcriptomic profiles of sinoatrial node fibroblasts identified up-regulation of genes and proteins promoting stiffer sinoatrial node extracellular matrix in heart failure hearts. Dr. Greg Hundley: And next, fibroblast specific profiles generated by the team's proteo-transcriptomic analyses of the human sinoatrial node provided a comprehensive framework for future studies to investigate the role of sinoatrial node-specific fibrosis in cardiac rhythm regulation and arrhythmias. So really very interesting preclinical science, Carolyn. Dr. Carolyn Lam: Yeah. Makes me think of arrhythmias and heart failure very differently, too. Thanks Greg. Well, for my next paper, we know that dietary high salt is bad for us. It's associated with mortality and morbidity. Serum sodium can accumulate at sites of inflammation and affect the function of both innate and adaptive immune cells. But how do changes in extracellular sodium actually affect mononuclear phagocytes? Dr. Greg Hundley: Ah. Carolyn, this is really an interesting question, but how would you even set this up or go about investigating this? Dr. Carolyn Lam: Ah, good question, Greg, and these investigators are really smart. So first, let me tell you about the co-corresponding authors, Dr. Kempa from Berlin Institute of Medical Systems Biology at Max Delbrück Center for Molecular Medicine in the Helmholtz Association, and Dr. Müller from the Experimental and Clinical Research Center in Berlin, Germany. Now, guess what they did? They used sea horse technology, pulsed stable isotope-resolved metabolomics and enzyme activity assays to characterize the central carbon metabolism and mitochondrial function of human and murine mononuclear phagocytes under high salt, in vitro. Dr. Carolyn Lam: And what they found was a disturbance of mitochondrial respiration as the initial step by which high salt mechanistically influenced immune cell function. While these functional changes may help to resolve bacterial infections, a shift towards pro-inflammation could accelerate inflammatory cardiovascular disease. A further potential implication is that mitochondrial functional analysis in monocytes and other immune cells upon a high-salt challenge, could serve as a test for salt sensitivity of immune cells in future. Dr. Greg Hundley: Oh wow, Carolyn. We don't often think about salt sensitivity in immune cells. Really informative research. Well, my next paper comes to us from the world of clinical science, and it's from Professor Derek Chew, from the school of medicine, at Flinders University, the Department of Cardiovascular Medicine at Flinders Medical Center. Dr. Greg Hundley: Carolyn, this paper reports results from a multicenter prospective, patient-level, randomized comparison of care informed by unmasked zero to one-hour, high-sensitivity troponin-T protocol, reported as less than five nanograms per liter versus standard-practice, masked high-sensitivity, cardiac troponin T-testing, reported at a value of less than 29 nanograms per liter, assessed at zero to three hours, and followed participants for 12 months. Participants included were those presenting to metropolitan emergency departments with suspected acute coronary syndromes, without ECG evidence of coronary ischemia. And the primary endpoint was timed to all-cause death or myocardial infarction. Dr. Carolyn Lam: Interesting experiment there. So what did they find, Greg? Dr. Greg Hundley: Right, Carolyn. So, while the use of the zero to one-hour, high-sensitivity, cardiac troponin T-protocol expedited discharge of patients presenting to the emergency department, with a low-event rate at 30 days, an increase in death or myocardial infarction was observed at one year in those with unmasked, high-sensitivity, cardiac troponin T-concentrations. Next, among those with intermediate cardiac troponin concentrations, where care was informed by zero to one-hour unmasked, high-sensitivity, cardiac troponin T-protocols, increases in revascularization and reductions in noninvasive cardiac investigation were observed. Dr. Greg Hundley: So these changes in practice that result from the use of rapid-discharge protocols, may be potentially associated with an increase in all-cause death or MI, by 12 months among those low-level troponin elevations. So in summary, Carolyn, this research found that unmasked, high-sensitivity, cardiac troponin T-reporting, deployed within a zero to one hour protocol, did not reduce ischemic events over a 12-month followup, and changes in practice associated with the implementation of this protocol may be associated with an increase in death in MI among those with newly-identified troponin elevations. Dr. Carolyn Lam: Wow, that's very, very interesting and clinically important. Thanks, Greg. Well, let's do a little bit of a tour around what else is available in this week's issue, shall we? I want to talk about a Special Report that I was so privileged to contribute to and was led by Dr. Gemma Figtree. And it's a Call to Action for new global approaches to cardiovascular disease drug solutions. There's also a Research Letter by Dr. Solomon on the prognostic value of natriuretic peptides and cardiac troponins in COVID-19. Dr. Greg Hundley: Great, Carolyn. So I'm going to tell you about an exchange of letters between Professors Correia and Chaitman regarding a prior published article, entitled “Myocardial Infarction in the ISCHEMIA Trial: Impact of Different Definitions on Incidence, Prognosis, and Treatment Comparisons.” Also, there's a very nice Case Series from Professor Shapira entitled, “In the Heart of the Ancient Silk Road: Fever of Unknown Origin, Right Ventricular Mass, and Systemic Vasculitis. And then, finally, Dr. de Boer has a very nice On My Mind piece From Studying Heart Disease and Cancer Simultaneously to Reverse Cardio Oncology. Dr. Carolyn Lam: So interesting. Well, let's get onto our double feature, Greg. Dr. Greg Hundley: Absolutely. Well, listeners, we are here for our first feature discussion today and we have with us really, an very interesting panel. First, Dr. Patrick Serruys from National University-Ireland, Galway, Dr. Shamir Mehta from McMaster University in Ontario, and our own associate editor, Dr. Manos Brilakis, from Minneapolis Heart Institute. Welcome gentlemen. Patrick, we're going to start with you. Could you describe for us the hypothesis that you wanted to test. Dr. Patrick Serruys: Yeah. The hypothesis was that if the surgeon and the interventional cardiologist doesn't achieve a complete revascularization, there will be a penalty. The penalty is we look at the all-cause mortality because that's really a unbiased assessment. Dr. Greg Hundley: And then, tell us the design of your study for us. Dr. Patrick Serruys: So SYNTAXES, which is the extension of the SYNTAX study up to 10 years, had 1,800 patient, and then basically, we took a threshold of eight. If you have a residual SYNTAX for more than eight, you have an incomplete revascularization. We stratify for less than four, four to eight, and above eight. And clearly, the group above eight has a bad outcome, not only with PCI, but also with surgery. The score is a little bit more difficult to establish in surgery, because you don't have an angiography immediately after the procedure. Dr. Patrick Serruys: And then as I said, if you do a complete revascularization by PCI, and that's basically a residual SYNTAX score of zero, then you have an outcome which is comparable to the surgical outcome. What is interesting, if you have above eight, you have to think twice and maybe refer that patient to surgery. It's difficult to anticipate, but of course, bifurcation, total chronic occlusion, small vessel, is the three major reason to have a residual SYNTAX score. Dr. Greg Hundley: Very good. So Shamir, could you help us put these results in context with other studies that have been performed in this sphere of research? Dr. Shamir Mehta: Yeah, sure. I would be happy to. So the SYNTAX study was unique in that they were able to look at the degree of revascularization, and the key finding that PCI was comparable to CABG surgery in terms of outcomes, when complete revascularization was able to be achieved, is a very intriguing finding. In cases where PCI was not able to achieve complete revascularization, it was clear superiority of CABG surgery. And so the question is in this study, this comparison, which is a non-randomized comparison, whether or not there's any type of external validity for these findings. Dr. Shamir Mehta: And, in fact there is. It's a timely publication, because recently we had the 4,000-patient multinational COMPLETE trial, which looked at the issue of complete revascularization versus incomplete revascularization in patients with STEMI, and found that complete revascularization with multi-vessel PCI, in appropriately-chosen patients, reduced hard clinical outcomes, including the composite of cardiac mortality and/or current myocardial infarction. And it reduces it quite substantially, by about 26%, and it's a highly-significant benefit. Dr. Shamir Mehta: I think the caveats to this finding are important, though. Because in the COMPLETE trial, patients were not eligible for recruitment, unless the interventional cardiologists felt that all of the lesions were amenable to PCI. So complete revascularization had to be achieved in the trial. And in fact, over 90% of patients in the trial were able to achieve complete revascularization. So that's absolutely key, and that brings up the importance of having a heart team in evaluating these patients. Dr. Shamir Mehta: The second point is that the SYNTAX score, Patrick had referred to was relatively low in the trial, it was only 4.6. Meaning that the lesions that were attempted were relatively straightforward, meaning that there was a high probability of achieving complete revascularization. So again, I think we're starting to see from the randomized trials and from the observational studies, the types of patients that may be suitable for PCI versus suitable for CABG surgery. Dr. Greg Hundley: Very nice. Well, Manos, Shamir, what an outstanding description in helping us put this paper in context with other research in this space. Manos, I know you see a number of papers come across your desk. Also, for you, what attracted you to this particular study? Dr. Emmanouil (Manos) Brilakis: Yeah, thank you, Greg. And again, congratulations to Patrick for a phenomenal study. I think the main strength of this analysis is the clinical relevance. I think everyone is still debating this question, is complete revascularization the goal in every patient? And all of the data, as mentioned already, have several limitations. Nevertheless, they move us a little bit closer to understanding better on whom complete revascularization should be used. Dr. Emmanouil (Manos) Brilakis: So the clinical relevance is one key. I think this paper does set the stage well for a randomized trial. End of the day, we are still not hundred percent sure if COMPLETE is the best for everyone, because COMPLETE counts as a risk, and the risk is going to be higher in those patients who have more complex anatomy. But that study will give us the definitive answer about which is the best way to go for each individual base. Dr. Greg Hundley: Very nice, Manos. So that's a great segue. So I'll turn to both Shamir and Patrick, and ask them also, as well, what do you think is the next study to be performed in this particular space? Shamir, you first and then we'll finish with Patrick. Dr. Shamir Mehta: Well, I think the concept of complete revascularization has now essentially been proven in multiple trials. And don't forget, if you go back several decades, really the first proof was in the context of CABG surgery. So really, this should be the goal in patients with multi-vessel disease. The next large randomized trial that is going to be starting very soon is the COMPLETE 2 trial where we are actually looking at the lesions physiologically to see whether or not we need to revascularize lesions that are physiologically significant versus anatomically severe. Dr. Shamir Mehta: This is an important question because what it does is it has the potential to reduce the number of lesions that we perform PCI in, by about 50%. We are also looking at plaque composition in that trial with optical coherence tomography. A very, very large number of patients will be receiving that. So that will be trying to target PCI to the actual pathophysiology of the disease, by targeting unstable plaques to perform PCI on. I think this is the whole next era of coronary intervention, where we are now beginning to target our therapies to the actual pathophysiology of the disease, which is a very, very exciting idea. Dr. Greg Hundley: And Patrick, do you have anything to add? Dr. Patrick Serruys: Yeah. I think, that obviously, you have to convert the anatomical SYNTAX Score in a functional SYNTAX Score. You could do that with the pressure wire and hyperemia of diastolic resting gradient. You can also do that by QFR or FFR CT. So we are going in that direction since a few years. The second point is that we have been working on machine learning that, at some point, the segmentation of the coronary segment, the assessment of the narrowing is done. And then, the next step that we are doing right now to is to convert that to the multi-slice CT scan. Dr. Greg Hundley: Very nice. Well, listeners, we want to thank Dr. Patrick Serruys, from National University-Ireland, Galway, Dr. Shamir Mehta from McMaster university in Ontario, and our own associate editor, Dr. Manos Brilakis, from Minneapolis Heart Institute, really bringing to us this paper that, in patients with complex coronary artery disease, incomplete revascularization can be common after PCI. And the degree of incompleteness can be associated with 10-year mortality. And therefore, if it's unlikely that complete or nearly complete revascularization can be achieved with PCI in patient with three-vessel disease, maybe we should be considering coronary artery bypass grafting. Dr. Greg Hundley: Well, again, let's get on now to that second feature discussion. Well, listeners, we are now here for our second feature discussion today, and we have with us Dr. Michael Felker from Duke University, and our own associate editor, Dr. Mark Link, from UT Southwestern. Welcome, gentlemen. And Mike, we'll start with you. Tell us a little bit about the background pertaining to your study and what hypothesis did you want to address? Dr. G. Michael Felker: Great. Thanks, Greg. So I think everybody's very familiar with the concept of favorable ventricular remodeling in patients with heart failure, that we know is something that happens when we treat our patients with guideline-directed medical therapy, like beta blockers, ACE inhibitors, MRAs. Interestingly, with the introduction of sacubitril/valsartan and the landmark PARADIGM trial, we had a drug where we had clearly a major outcome benefit, but we actually had very little understanding about whether that was mediated by remodeling. Dr. G. Michael Felker: And those questions led us to design the PROVE trial, which was a single-arm trial of 794 patients, looking at whether or not patients with heart failure and reduced ejection fraction who met the FDA label for sacubitril/valsartan, the initiation of that therapy will be associated with favorable changes in ventricular structure and function, as well as favorable changes in natriuretic peptide. The current paper's really trying to put those results in a clinical context around some of the things that we make clinical decisions about, in taking care of heart failure patients in this case, whether and when patients qualify for a primary prevention ICD. Dr. Greg Hundley: Fantastic, Mike. And so you've told us a little bit about the study design, and did you have exactly the same number of patients, or what was the study population for this sort of substudy, if you will? Dr. G. Michael Felker: Yeah. So in PROVE, we enrolled people who had chronic heart failure in the EF, less than 40%, because that's the FDA label for sacubitril/valsartan. In this analysis, because we were interested in patients who qualified for ICD therapy, we limited our analysis to those who an EF plus or equal to 35%. Because, as you all know, the guideline for primary prevention ICD is people who have a EF less or equal to 35% after at least three months of optimized heart failure therapy. Dr. G. Michael Felker: And so, one of our questions was in some patients start on sacubitril/valsartan, what happens to their ventricle and how many patients might favorably remodel? This is, obviously, a question that comes up a lot clinically as more and more we're switching people from ACE inhibitors, or ARBs, to sacubitril/valsartan in line with the recommendation that's 1A from the AHA guidelines. Dr. Greg Hundley: Fantastic. ell, we're all listeners waiting to hear your results, Mike. This is very exciting. So what did you find? Dr. G. Michael Felker: I think our results were quite interesting. I mean, for one thing, the patients that were enrolled PROVE were incredibly well-treated at baseline, and they had had heart failure for quite some time, and a average median time of over six years. So this is not patients who are just recently diagnosed. A lot of these are people that you might think, clinically, we're unlikely to go on and have much favorable ventricular modeling, but that's not what we found. We actually found that after the initiation of sacubitril/valsartan, after six months, on average, we had a five point increase in injection faction. Dr. G. Michael Felker: And by 12 months, on average, that was almost 10 points. So quite a bit of favorable remodeling, even in these patients you might think were less likely to do that. And we put that in the context of ICD decision-making. By six months, 32% of the patients who would initially have been eligible based on the guidelines for primary prevention ICD, no longer met those criteria because their EF had risen to greater than 35, and by 12 months, it was up to 62% of those patients. So as we're thinking about decision-making around ICDs, I think these data have some pretty obvious direct clinical relevance to decisions we now make in the care of our patients. Dr. Greg Hundley: Really interesting. So Mark, I know you get several papers coming across your desk, and as associate editor, boy, I think I can see why this paper was attractive to you. Tell us a little bit, how do we put these results from this study into the context of how we decide whether a patient should receive an ICD? Dr. Mark Link: Yeah. The current guidelines are to wait three months after guideline-directed medical therapy, and then repeat the ECHO and see if they still qualify. I think what this study shows us is that patients can continue to improve after three months, and that improvement is somewhat continuous, actually. Because at six months, the improvement in EF was five percent, and at 12 months, it was 10%. So I think that's what this shows, the context is, if you have a patient who has a low EF and they are improving, but still haven't quite made it to 35, let's say when they went from 25 to 30 in three months, I'd probably hold off and wait another three months and repeat the ECHO again. Dr. Greg Hundley: Excellent. Well, Mike, Mark, I'm going to ask you question. And we'll start with you Mike, and then go to Mark. What study would you perform next in this space? Mike, you first. Dr. G. Michael Felker: So, I think it's important to recognize some of the limitations of any study you do, including this one. So this was not a randomized trial. PROVE was a single-arm trial, there wasn't a control group. And the question about the ICD per se was not pre-specified. It was really a post-hoc analysis. So as is often the case, I think these are intriguing and highly-suggestive results, but I think there's clearly an opportunity to confirm them in perspective studies designed to answer this specific question. Dr. G. Michael Felker: So you could imagine a trial where patients who are starting on sacubitril/valsartan who don't have ICDs, get randomized to waiting three months or waiting six months, or 12 months or whatever the interval would be. So I think these are intriguing, and that there definitely opportunities to develop confirmatory results. Dr. Greg Hundley: Excellent. Mark, do you have anything to add to that? Dr. Mark Link: I think the big thing we would really like to know are predictors, predictors of response and predictors of non-response. And that would take a larger trial perspective, and that would be very, very valuable. Because if you could have a predictor of a non-responder, they would get an ICD earlier, and predictors of responders, you might wait a while. Dr. Greg Hundley: Very nice. Well, listeners, we get rate studies here in circulation, and you'll find this one as a research letter, highlighting that in the substudy of the PROVE heart failure study, that in patients with an EF less than or equal to 35%, the introduction of sacubitril/valsartan improved EF to greater than 35%, at 62% of subjects at 12 months. Really an interesting finding, and perhaps further randomized clinical trials as suggested by both Mike and Mark here, are maybe warranted in the future. Dr. Greg Hundley: Well, on behalf of Carolyn and myself, we want to A, thank Dr. Mike Felker and also our associate editor, Mark Link, and wish you, as listeners, a great week, and we will catch you next week On the Run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021. 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, 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.

This week’s episode features author Karolina Szummer and Associate Editor Emmanouil Brilakis as they discuss the article "Comparison Between Ticagrelor and Clopidogrel in Elderly Patients with an Acute Coronary Syndrome: Insights from the SWEDEHEART Registry." TRANSCRIPT BELOW 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. Dr Greg Hundley: And I'm Dr Greg Hundley, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Carolyn, this week's feature article, we're going to investigate antiplatelet therapy use, but in older patients, as opposed to those that are middle-aged, and have sustained a prior acute myocardial infarction. But, before we get to that, how about we grab a cup of coffee and jump into the other papers in the issue? Dr Carolyn Lam: Absolutely, Greg. I've got my coffee right here, and I really want to start with a paper that adds to our understanding of, guess what, the sodium=glucose cotransporter 2 inhibitors, SGLT2 inhibitors, and their diuretic and natriuretic effects in combination with loop diuretics. Of course, a clinically really important question since now we know that SGLT2 inhibitors improve outcomes in patients with heart failure in whom they are likely to be co-prescribed with a loop diuretic. So, Professor Chim Lang from University of Dundee and his colleagues performed the RECEDE-CHF trial, which was a randomized double-blind placebo-controlled crossover trial of 23 patients with type 2 diabetes and HF REF taking regular loop diuretics who were randomized to the SGLT2 inhibitor empagliflozin 25 milligrams once daily or placebo for 6 weeks with a 2-week washout period. The primary outcome was change in 24-hour urine volume from baseline at week 6. Dr Greg Hundley: So, empa versus placebo. What did they find? Dr Carolyn Lam: In patients with heart failure and type 2 diabetes taking a regular loop diuretic, empagliflozin caused a significant increase in urine volume at both day 3 and week 6, compared to placebo, as well as empa also caused a significant increase in electrolyte-free water clearance. Though there was a small non-significant increase in natural uresis with empagliflozin at day 3, this was absent by week 6. These results suggest that empagliflozin may have an advantageous diabetic profile in patients with type 2 diabetes and heart failure in addition to loop diuretics, with only a short transient natriuresis. Dr Greg Hundley: Very nice, Carolyn. Great information. Diuretics, heart failure reduced ejection fraction, and empagliflozin. Well, my clinical paper comes from Dr Renato Lopes from Duke University Medical Center, and this is a sub study from the ISCHEMIA trial that evaluates whether an initial invasive strategy in patients with stable ischemic heart disease and at least moderate ischemia improves outcomes in patients with a history of heart failure or left ventricular dysfunction when the EF is greater than 35%, but less than 45%. Dr Carolyn Lam: Aw, that mid-range ejection fraction. Favorite topic. So, Greg, what did they find? Dr Greg Hundley: Those with heart failure and left ventricular dysfunction randomized to the invasive versus the conservative strategy had a lower rate of the primary outcome, 17% versus 29%. Whereas those without heart failure and left ventricular dysfunction did not, 13% versus 14%. A similar differential effect was seen for the primary outcome, all-cause mortality and cardiovascular mortality, when invasive versus conservative strategy associated outcomes were analyzed with LVF as a continuous variable for those with and without prior heart failure. Dr Carolyn Lam: Wow, that is clinically important, Greg. So, can you summarize our take home message? Dr Greg Hundley: Well, Carolyn, ischemia trial participants with stable ischemic heart disease and at least moderate ischemia with a history of heart failure or LV dysfunction, were at increased risk for the primary outcome. And in this small high-risk subgroup with heart failure and an ETF between 35% and 45%, an initial invasive approach was associated with a better event free survival. This result should really be considered for hypothesis generation and future studies. Dr Carolyn Lam: Greg, for the next paper, do you remember hydrogen sulfide? The stuff we learned about in school. It's the gas with that characteristic foul odor of rotten eggs. Well, guess what? This whole paper is about hydrogen sulfide, and in the body, it actually has antihypertensive and anti-inflammatory effects, and its endogenous generation key enzyme is cystathionine gamma lyase, or CSE, and that's expressed in CD4+ T cells. So today's paper provides insights into how all of these players work together in the development of hypertension. To investigate the pathophysiological relevance of this CSE hydrogen sulfide system, co-corresponding authors, Doctors Geng and Cai from Fuwai hospital and Chinese Academy of Medical Sciences, Peking University Medical College, as well as Dr Xu from Peking University Health Science Center in Beijing. Well, they and their coauthors performed elegant experiments involving peripheral blood lymphocytes, isolated from hypertensive patients or spontaneously hypertensive rats. They also looked at mice with CSE-specific knockout in T cells, and CD4 null mice. Dr Greg Hundley: Well, Carolyn, what did they find? Dr Carolyn Lam: Well, they found that endogenous cystathionine gamma lyase, or CSE, and hydrogen sulfide, but not cystathionine beta-synthase, in lymphocytes, responded to blood pressure changes. Deleting CSE in CD4+ T cells exacerbated angiotensin II-induced hypertension by reducing circulatory and renal T regulatory numbers. Hydrogen sulfide from CSE self-hydrates, liver kinase 1, thereby activating the AMP kinase energy pathway to promote TReg differentiation and proliferation, which then attenuates the vascular and renal immune inflammation, and thus, prevents hypertension. Dr Greg Hundley: Carolyn, this sounds like a very thorough study. What are the clinical implications? Dr Carolyn Lam: Endogenous CSE hydrogen sulfide in lymphocytes may be both a potential biomarker of hypertension, or its complications, or hydrogen sulfide donor may be a therapeutic approach to lower hypertension. Dr Greg Hundley: Great, Carolyn. Well, my next paper comes from Professor Goo Taeg Oh from Ewha Women's University, and it really involves the world of inflammation. So Carolyn, as you know, macrophages produce many inflammation-associated molecules released by matrix metalloproteinases, such as adhesion molecules, as well as cytokines, which play a crucial role in atherosclerosis. In this paper, the authors investigated the relationship between Ninjurin-1, or nerve injury-induced protein 1, a novel MMP9 substrate expression, and atherosclerosis progression. Dr Carolyn Lam: Ninjurin-1? Interesting. So, what were the results? Dr Greg Hundley: Well, Carolyn, Ninj1 expression and atherosclerosis progression were assessed in atherosclerotic aortic tissue and serum samples from coronary artery disease patients and healthy controls, as well as athero-prone, apolipoprotein E-deficient, or APOE -/- wild type mice. Two important findings, Carolyn. First, the authors in vivo results conclusively showed a correlation between Ninj1 expression in aortic macrophages and the extent of human and mouse atherosclerotic lesions. Ninj1-deficient macrophages promoted pro-inflammatory gene expression by activating mitogene-activated protein kinase, or MAP kinase, and inhibiting the phosphoinositide 3-kinase signaling pathway. Whole-body and BM-specific Ninj1 deficiencies significantly increase monocyte recruitment and macrophage accumulation in atherosclerotic lesions through elevated macrophage-mediated inflammation. Now, in addition and secondly, macrophage Ninj1 was directly cleaved by MMP9 to generate a soluble form that exhibited anti-atherosclerotic effects, as assessed both in vitro and in vivo. Treatment with the sNinj1-mimetic peptides, ML56 and PN12, reduced proinflammatory gene expression in human and mouse classically activated macrophages, thereby attenuating monocyte transendothelial migration. Moreover, continuous administration of mPN12 alleviated atherosclerosis by inhibiting the enhanced monocyte recruitment and inflammation characteristics of the disorder in mice, regardless of the presence of Ninj1. So in summary, Carolyn, Ninj1 is a novel MMP9 substrate in macrophages, and sNinj1 is a secreted athero-protective protein that regulates macrophage inflammation and monocyte recruitment in atherosclerosis. Dr Carolyn Lam: Wow, Greg, that was incredibly summarized. Thank you. Let's go through what else there is in today's issue. In cardiology news, Bridget Kuhn talks about how the pandemic intensifies the push for home-based cardiac rehabilitation options. There's a white paper by Dr Ho and colleagues, including me, describing the diagnostic dilemma of HFpEF. There's a Research Letter by Dr Gill talking about the cardiometabolic trait sepsis and severe COVID-19, a Mendelian randomization investigation. There's also a Research Letter by Dr Wu on the atlas of exosomes microRNAs secreted from human iPSC-derived cardiac cell type. Dr Greg Hundley: Carolyn, this issue is just packed with articles, because I've got five more to tell our listeners about. First, it's a research letter from Professor G. Hovingh, entitled, Inclisiran Durably Lowers LDLC and PCSK9 Expression in Homozygous Familial Hypercholesterolemia, The ORION-2 Pilot Study. Next, there's an ECG challenge from Dr Jason Gilge relating to AV conduction during atrial flutter. Next, Dr Keith Churchwell has a nice piece related to the importance of those involved in cardiovascular care and participating in their civic duties, including voting. Next, Professor Karthikeyan has nice On My Mind related to overestimation of stroke risk and rheumatic mitral stenosis and the implications for oral anticoagulation. And finally, Carolyn, another research letter, from Dr Pieter van Paassen, entitled, Neutrophils and Contact Activation of Coagulation as Potential Drivers of COVID-19. Well, Carolyn, how about we get on to our feature discussion and review in older patients, which antiplatelet therapy may be safest? Dr Carolyn Lam: Let's go! Dr Greg Hundley: Well, listeners, now we're turning to our feature discussion, and today we'll talk about antiplatelet therapy. And then we have with us, Dr Karolina Szummer from Karolinska Institutet, and our own Associate Editor, Dr Manos Brilakis from the Minneapolis Heart Institute. Welcome to you both, and Karolina, let's start with you. Could you describe for us your hypothesis and some of the background information that led you to perform this study? Dr Karolina Szummer: Thank you so much for having me here and for sharing the ideas behind our study. Current recommendations recommend that we use high-potent antiplatelet agents for treating myocardial infarctions, and in particular, elderly patients are not included. So we decided to do an observational study to look at patients in our Swedish registries treated for myocardial infarctions who were 80 years and older. Dr Greg Hundley: Very nice. Can you tell us a little bit more about your study design? And also the study population? Dr Karolina Szummer: The startup populations are all patients who were admitted to an acute coronary care unit for treatment of myocardial infarctions, and they were all 80 years and older, and they were included from 2010 to 2017. So this encompasses the period during which treatment with ticagrelor was introduced. So we are comparing to ticagrelor versus clopidogrel for the outcomes during the year, following the myocardial infarction. Dr Greg Hundley: And how many patients did you enroll in the study? And what were your study results? Dr Karolina Szummer: We enrolled, in total, 14,000 patients, and these consisted of non-STEMI and of STEMI patients. The majority, about two thirds, were non-STEMI patients. We show, in this study, elderly patients have a lower risk of readmission for myocardial infarction or stroke, but they have a higher risk of having readmission for bleeding and death. So the risk-benefit ratio seems to be skewed towards having, probably, more harm with ticagrelor being more risky than clopidogrel in this study population of elderly. Dr Greg Hundley: And was this true for both men and for women? Dr Karolina Szummer: Yes. So this was true for both men and women. And we did a sensitivity analysis. We looked closer at those who are younger than 80 years old, and in this patient population, the results selected in the same way as for our cohort of elderly, they actually did have the same benefit with a low risk of MI, stroke, and death, and high risk of bleeding. But in the elderly, we noticed a signal towards harm with an increased risk of death. Dr Greg Hundley: It sounds like with ticagrelor, did we have a lower risk of death and a slightly lower risk of myocardial infarction and stroke, but a higher risk of bleeding? Was that the findings? Dr Karolina Szummer: So for the elderly, there was a high-risk of death and bleeding with ticagrelor compared to clopidogrel, but a lower risk of ischemic component of MI and stroke. Dr Greg Hundley: And then with those under 80, those were the ones that had the lower risk of death, lower risk of MI and stroke, but the higher risk of bleeding? Dr Karolina Szummer: Yes, that's correct. So really the end point that differs most is that there is sustainment towards higher mortality in the elderly, because in both younger and elderly, the risk of readmission for bleeding was elevated in both. Dr Greg Hundley: Now, let's turn to our own Associate Editor, Manos Brilakis. Manos, can you help us put these results into perspective, relative to other studies that evaluate the efficacy of antiplatelet therapy, post myocardial infarction? Dr Emmanouil (Manos) Brilakis: I would like to start by congratulating Dr Szummer. It's a wonderful paper, and, I think, provide some new insights on how to use the medications in the ACS patients. And going on the background, if we look at the guidelines, both the European guidelines, as well as the American guidelines, what they say is that both ticagrelor, as well as prasugrel, are preferred and recommended for patients with ACS, both non-ST elevation ACS, as well as ST segment elevation myocardial infarction. And actually, European guidelines say that clopidogrel should only be used when prasugrel or ticagrelor are not available or are contraindicated. And this is based on two trials. One is the PLATO trial, and the other is the TRITON-TIMI 38, that both showed, actually, more benefit with the more intensive P2Y12 inhibitors. And this is what is extrapolated to all patient populations. But as you've heard before, there was only a minority of elderly patients that were included in those trials, about 13% to 15%, and that is why the present study is important, because it suggests that maybe we should look more carefully into the patient's age and potentially other characteristics like frailty or other comorbidities, that might actually alter the risk-benefit ratio. And maybe those medications should not be routinely given to all patients, but perhaps, elderly patients, or at least some of them, might not require, and actually be better off with clopidogrel. Dr Greg Hundley: Let's turn back to Karolina. Karolina, the study was observational. What do you see as, perhaps, a next study to follow up the results that you've brought to us with this study? Dr Karolina Szummer: So the next step would definitely be to do a randomized control trial in the elderly to explore this topic further, to really know for sure what the safety and efficacy is, and what's the best treatment would be for these patients. Dr Greg Hundley: Very good. And Manos, do you have anything to add? Dr Emmanouil (Manos) Brilakis: One more thing. So, there was actually a trial that compared ticagrelor as well as prasugrel with clopidogrel in elderly patients that was called the POPUlar AGE trial that was published last year. And actually this one, published earlier this year, and actually this trial randomized a thousand patients who were more than 70 years old, to either more-intensive or less-intensive. And the results were actually very similar to the findings from Dr Szummer's study from SWEDEHEART, showing that there was more bleeding without any ischemic benefit. And didn't show actually higher mortality but didn't show any significant benefit. So that actually adds to the data that maybe the elderly patients, the selection of antiplatelet agent should be taken into account. And I think for me, this also extrapolates the high bleed risk, higher risk of bleeding, based on criteria, which we currently use mainly for duration. We say, for example, if you're precise DAPT score, which is a score for determining risk of bleeding, is high, you should consider shorter duration of DAPT, but it doesn't say anything about the type of DAPT. And for me, this makes sense that the high bleeding risk, and age is one of the main risk factors for high bleeding risk, should be taken into account also for determining the type of P2Y12 inhibitor. Dr Greg Hundley: Well listeners, we've had a great discussion with Karolina Szummer from Karolinska Institutet, and our own Manos Brilakis from the Minneapolis Heart Institute, really reviewing the utility of ticagrelor versus clopidogrel in older individuals, above the age of 80, that have sustained myocardial infarction, and identifying that ticagrelor is associated with a higher risk of death and bleeding, as opposed to clopidogrel, opening the question up as to whether further studies in older individuals need to be performed to examine the efficacy of antiplatelet therapy. So, on behalf of Carolyn and myself, we wish you a great week and look forward to catching you On the Run next week. This program is copyright the American Heart Association, 2020.

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. Dr Greg Hundley: And I'm Greg Hundley, associate editor from the Pauley Heart Center at VCU health in Richmond, Virginia. Well Carolyn, our feature this week really examines long-term efficacy of drug eluting stents versus coronary artery bypass grafting in those patients with left main disease. Really looking at long-term extended follow up from the PRECOMBAT trial but before we get to that, how about we grab a cup of coffee and jump into some of the other articles in the issue? And I'll start off. My first article is a basic science paper looking at catecholamine sensitive and ventricular tachycardia in ARVC. And it comes from Dr Long-Sheng Song from the University of Iowa Carver College of Medicine. So, the study from Dr Song used protein mass spectrometry analyses and that identified integrin beta one is downregulated in those patients with arrhythmogenic right ventricular cardiomyopathy hearts without changes to calcium handling proteins as adult cardiomyocytes express only the beta-1 D isoform, they generated a cardiac specific beta-1 D knockout mouse model and perform functional imaging and biochemical analyses to determine the consequences from integrin beta-1 D loss of function in hearts in vivo and in vitro. Dr Carolyn Lam: Nice, very elegant design. So what were the results Greg? Dr Greg Hundley: Well Carolyn, the authors found that integrin beta- 1D deficiency and RyR2 serine 2030 hyper phosphorylation were detected by Western blotting in left ventricular tissues from patients with ARVC but not in patients with ischemic or hypertrophic cardiomyopathy. And in the mouse experiments, beta-1 D negative or knockout mice exhibited normal cardiac function and morphology, but presented with catacholamines sensitive polymorphic ventricular tachycardia consistent with increased RyR2 serine 2030 phosphorylation and apparent calcium handling in beta-1 D knockout cardiomyocytes. So Carolyn, in conclusion, the authors found their data suggest that integrin beta-1D deficiency represents a novel mechanism underlying the increased risk of ventricular arrhythmias in patients with ARVC. Dr Carolyn Lam: Okay. You told us about integrin beta-1 D and I'm going to tell you about apolipoprotein M. So Greg, what do you know about apolipoprotein M? Dr Greg Hundley: Well, Carolyn, at seven o'clock the morning, I seem to have forgotten a little bit about that. Can you remind me what apolipoprotein M is? Dr Carolyn Lam: Sure Greg, very happy to. So apolipoprotein M or apoM mediates the physical interaction between high density lipoprotein particles and sphingosine 1-phosphate and exerts an anti-inflammatory and cardio-protective effects in animal models. Now listen on, listen on. So authors, Dr Chirinos from Perelman Center for Advanced Medicine, University of Pennsylvania and Dr Javaheri from Washington University School of Medicine and co-authors hypothesized that reduced levels of apoM would be associated with worse outcomes in human heart failure. Specifically, they tested the hypothesis that reduced circulating apoM would be associated with the risk of death, a composite of death, ventricular assist, device implantation or heart transplantation and a composite of death, heart failure related hospitalization among adults with heart failure and rolled in a large multicenter Penn heart failure study. They did stratified analysis in patients with heart failure with reduced and preserved ejection fraction and even replicated these findings in two independent cohorts, the Washington University heart failure registry and a subset of the TOPCAT trial. What they found was that reduced apoM plasma protein levels indeed were associated with adverse outcomes in heart failure including both HFpF and HFrF. The relationship between reduced apoM and outcomes and heart failure was particularly pronounced when concentrations of its binding partner sphingosine 1-phosphate were also reduced. ApoM protein levels were associated with inflammation in human heart failure and thus the conclusion being that apoM represents a risk marker in human heart failure. Further studies are of course needed to assess whether it could be a therapeutic target as well. Dr Greg Hundley: Very good. Carolyn. So more information for the world of heart failure isn't it. I'm going to sort of switch over to coronary artery disease and talk about low attenuation non-calcified plaques that are sometimes appreciated on cardiac computed tomography scans. And in this study, Dr Michelle Williams from the University of Edinburg evaluated the results from the multi-center SCOT-HEART trial or the Scottish computed tomography of the heart. So Carolyn, the future risk of myocardial infarction is commonly assessed using cardiovascular risk scores, coronary artery calcium score or coronary artery stenosis severity and the authors assessed in 1,769 patients about 56% men and the average age 58 years and they followed them up for a median of 4.7 years and looked at whether noncalcified low attenuation plaque burden on coronary CT angiography might be a better predictor of the future risk of myocardial infarction. Dr Carolyn Lam: Interesting. So what did they find? Dr Greg Hundley: Well, low attenuation plaque burden was the strongest predictor of myocardial infarction irrespective of cardiovascular risk score, coronary artery calcium score or coronary artery area stenosis. And patients with low attenuation plaque burden greater than 4% were nearly five times more likely to have subsequent myocardial infarction and the hazard ratio was 4.65 with a confidence interval of two to more than 10 and a half. So in conclusion, Carolyn in patients presenting with stable chest pain, low attenuation plaque burden is the strongest predictor of fatal or nonfatal myocardial infarction and these findings may add to classical risk predictors of myocardial infarction. Dr Carolyn Lam: Wow. Important findings. Okay, let's go onto what else is in this week's journal issue. There's an online mind by Dr Jaffe. It's on the universal definition of myocardial infarction. It talks about both present and future considerations. There's an ECG challenge by Dr Arias and what's described as spontaneous wide QRS complex rhythm in a patient with wide QRS complex tachycardia. Dr Greg Hundley: Very good, Carolyn. Well, I've got two other articles. Another on my mind piece from Professor Peter Nagele from the University of Chicago Medicine and it discusses a simplified proposal to redefine acute MI versus acute myocardial injury. Looking at that troponin question. And then finally Dr Fabian Hoffman from the Heart Center and University of Cologne has a research letter on providing new data regarding the evolution of pulmonary hypertension during severe sustained hypoxia. Well Carolyn, how about we get onto that feature discussion looking at left main disease and whether we should place an intercoronary stent or undergo coronary artery bypass grafting. Dr Carolyn Lam: Important question. Let's go, Greg. Dr Greg Hundley: Welcome everyone to our feature discussion today that really pertains to interventional cardiology and we're very fortunate to have Duk-Woo Park from Asian Medical Center in Seoul, South Korea and our own associate editor, Dr Manos Brilakis from the Minneapolis Heart Institute. Well Duk-Woo, we'd like to get started with you and could you tell us a little bit about the background data and the hypothesis related to your research study? Dr Duk-Woo Park: Our research, it was the 10-year report of the PRECOMBAT trial. If I'm going to first introduce the background over the last half of a century bypass surgery, it was a mainstream, the number one choice of on protecting the main disease. Yeah. Did you know unprotected left main disease, the one were very high risk of coronary artery disease and owing two and the supply, the large burden of myocardium. But the last two decades, 20 years. Their remarkable evolution in PCI field including development adaption of a drug eluting stent and the adaption of intravascular ultrasound as well as experience of intervention or catalyst expertise. So on the basis of such evolution, many interventional cardiologists think about that, a PCI with a drug eluting stent. Will it be non-inferior to a standard type A surgery? Sometime for single region PCI could be very nice alternative option for unprotected left main disease that the reason why we're going to start quick on the trial. This trial already done 15 years ago at the time. We designed this PRECOMBAT trial on the basis of that background. Dr Greg Hundley: Very good. Well can you tell us a little bit about the study population of this trial and what was your study design? Dr Duk-Woo Park: This is a open library trial design and we at first time we evaluated the noble unprotected left main disease and the for considerable for clinical and ethic eligibility, initially assessed by intervention or cardiologists as you as a cardiac surgeon and the reason why we try to pick up the post treatment eligible population and then at the screening initial re-screen the nearly 1,400 patient and then finally 600 of patient who was our individuation one arm is drug eluting stent, first-generation ciphers 10 versus another arm is convention or a coronary artery bypass stent grafting. Dr Greg Hundley: What were you looking for your outcome measures and how long did you follow these patients? Dr Duk-Woo Park: Initially and the BDN two year follow and are published in England, the journal of medicine nearly eight years ago. And then we did five year follow-up at the publish the JAG in five years ago and the this time is a, we did complete that 10 year follow up all the render mutation population and the median follow-up duration is nearly more than 11 years and we complete 10 year follow-up and the key outcome was PCI is a comparable apart from surgery for treatment of left main disease. Dr Greg Hundley: And were there other outcomes that you were looking for? Dr Duk-Woo Park: We evaluated several important clinical outcomes. We primary end the point we select competent outcome compass of all cause of mortality by myocardial infarction, stroke, or ischemia-driven target vessel revascularization. Secondary outcome was each component of a primary outcome all-cause mortality as you raise the harder clinical and the point like compost outcome like this am I sure. So finally we did not any statistical difference with the regard to primary composite outcome as well as a hard clinical compost outcome as death or stroke. Finally, we did not detect all-cause mortality. One exception or difference was a target vascularization as well as a repeat rebase collateralization was a much higher after PCI than after bypass surgery. Dr Greg Hundley: So overall, in this more lengthy follow up of 10 years. The primary outcomes were similar between the two interventional arms, but there was a difference in target vessel revascularization. With that being more frequent after PCI as compared to bypass, were there any other subgroups that tended to have distinctions or discrepancies between your primary outcome? Dr Duk-Woo Park: As the sensitive to analysis, in circulation we supply the subgroup analysis or more, we did not find any differential treatment. IPEC according to subgroup in age group, diabetes and clean-cut presentation or in environmental coronary embolism shock versus application. We didn't find any interaction effect, just the except the extent of disease vessel, left or main. We the three best three digit bypass surgery was better than PCI. However we did not do any P value. Adjust them on. So interpretation is should it be cautious. Dr Greg Hundley: Well you know as an interventional cardiologist, what new information does this bring and how do you interpret the results of this study relative to other studies that have been published in the past? Dr Emmanouil Brilakis:  I think this is a very timely study, especially since about a year ago we did have the five-year outcomes from two other similar trials, the Excel file and the Nobel trial which say randomized patients with unprotected left main disease to either PCI or bypass. And actually those studies had some differences which are also relevant to the present study. So for example, Excel overall the outcomes were similar. There was a higher all-cause mortality in the PCI where normal had better outcomes in terms of death, MIT VR, but there was no difference in mortality. So I think the natural question that comes up from the studies was whether mortality is different with PCI versus coronary bypass and you know the PRECOMBAT, the 10 years. It's really suiting in that respect because it doesn't show any difference in the overall mortality. So I think this comes very timely and the answers a lot of questions. Of course there's limitations with the sample size and the number of patients treated, but I think although it's a very timely result. Dr Greg Hundley: Maybe I'll start first with you, Manos and then I'll circle back to you. Duk-Woo. Manos what do you see is the next important study to perform in this field? Dr Emmanouil Brilakis:  I think the natural question here is these outcomes which are similar but use first generation drug eluting stents, which we no longer use. He did use high proportion of five which is an excellent feature in, again congratulate Duk-Woo and the other co-investigators for doing such a high rate of follow-up. But we now know that the techniques, for example, for bifurcations, maybe the DK crush or double DK crush might be a better technique to do. So in my mind, the next question would be if who use the current, a much improved the drug eluting stent and state of the art bifurcation techniques. For example, DK crush where the double-kiss crush bifurcation would, the outcomes have been different and perhaps PCI will be similar, even better than bypass in long-term outcomes. So for me this next study will be state of the art techniques, state of the art materials and long-term for follow-up as in frequently. Dr Greg Hundley: Duk-Woo. How about from your perspective? Dr Duk-Woo Park: You know, a future perspective is a very difficult to expect. Our trial is the longest to follow-up trial. We have the nation are insurance support and we nearly a hundred percent pop picked up fighters status, but I think most of them interventional cardiologists as well as a cardiac surgeon. One true additional longest follow-up Excel and Noble trial. The reason why we didn't do additional random trial using additional second generation drug eluting stent. We already do exit trial approximately 2000 and noble trial and more than thousand patients we already do and the two trial a complete five-year follow and most of the trial is as well as the clinician want to extend the follow-up of Excel and Noble trial but I don't know how much that extended of a follow-up would be possible. Dr Duk-Woo Park: The next step as you know the intervention or cardiac surgeon still debate about the long-term mortality issue after release of exited five-year-old research and the data peak issue, European association cardiac thoracic group. We did draw the endorsement of a guideline so I think an additional stem we require the individual patient level data analysis involving, Excel, Nobel, Syntech and PRECOMBAT trial would be required to provide the more definite compelling evidence for mortality difference as well as the have the end point and including or so some end point to repeat revascularization. We do allow individual patient data analysis. That would be next. The short step, next the long step, we definitely require extended follow-up, Excel and Noble trial. Dr Greg Hundley: Very good. Well listeners, this has been another very informative feature discussion where we've compared PCI and coronary artery bypass grafting in those with left main disease. And now from this PRECOMBAT trial, 10 years of follow up showing very similar outcomes related to death, myocardial infarction and stroke in the two randomized arms. We want to thank Dr Duk-Woo Park and Dr Manos Brilakis for presenting this information and as we move forward, their insights as to next studies with newer technologies and different examinations of stents. More long-term follow-up from ongoing trials and then individualized patient assessments. Listeners, we hope you have a great week and hope everyone is staying safe in this COVID crisis. Take care. This program is copyright of the American Heart Association 2020.  

Majority Leader Senator Paul Gazelka joins Roshini to share the latest in COVID-19 testing and also, why he's not always in agreement with Governor Walz about next steps for Minnesota. NBC News Correspondent Joe Fryer joins to share the realities of covering current events during the COVID-19 times. Dr. Courtney Boechler of the Minneapolis Heart Institute follows Joe to address the rumors that heart attacks and strokes are down which is leading people to not go to see their doctors for serious problems. 

In this Live Friday CME Series recap, Dr. Todd Holcomb, an Internist and hospitalist with Lakeview Clinic and Ridgeview Medical Center, presents an interesting Internal Medicine case that is sure to scratch some heads, and remind us of the need to go back to the beginning, if it's not making sense after several attempts. Dr. Holcomb is accompanied by cardiologist Dr. Joshua Buckler, with Minneapolis Heart Institute, Dr. Jonathan Larson, family physician at Lakeview Clinic, Dr. Carl Dean, nephrologist with Kidney Specialists of Minnesota, and Dr. David Gross, radiologist with Consulting Radiologists.  So put on your thinking caps, listen closely and ask yourself what you would do as Dr. Holcomb guides us through this interesting case. Enjoy the podcast! OBJECTIVES:    Upon completion of this podcast, participants should be able to: Identify secondary causes of hypertension. Identify when further testing is warranted. Discuss newer treatments available for cholesterol related conditions. CME credit is only offered to Ridgeview Providers 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 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: "2019 Internal Medicine Case Conference" (**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.)  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.   FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. 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: PART 1: Alright, let's break down the first portion of this case discussion. This is a 60 yo male with chest pain for over a year. Intermittent aching and burning in right anterior chest, worse with activity and lately has worsened overall with a stressful job and strong family hx of heart disease. General exam ins unremarkable. ECG normal. HDL is 60 and LDL slightly up at 137. PFTs and CXR are normal.  Stress echo is normal.  Cardiology referral results in a low Ca++ score but some plaque in the LAD. Dr. Buckler, the cardiologist, feels this is ischemic heart disease until proven otherwise. Therefore, a coronary angiogram is necessary. Imaging has its limitations, as do stress tests. When the history still doesn't point in another explicable direction, we must follow the logic and most likely etiology, which is till coronary artery disease and ACS. One of the problems with stress tests in general, is there are limitations inherent. It's hard to miss the big stuff, but the more minor findings can be missed. With a high pretest probability, he could have perhaps gone straight to angio. In this case, though, he was started on a statin and aspirin. Per Dr. Buckler, Imdur could also have been given. Two year later, he comes in with headaches in the same area of the head since his wife recently passed away. He takes Advil for this. BP has been elevated at home. Dr. Jonathan Larson, family physician, questions the type of headache, it's location and possible etiologies. Is the Advil causing rebound headaches or contributing to the headaches? The elevated home blood pressures also need further investigation. His kidney function is temporarily normal. NSAIDs are d/c'd and Lisinopril is started. A month later, the headaches have improved. BP improved, but not tremendously. In addition, his chest pain has gone away. A new antihypertensive, a combo HCTZ/Lisinopril regimen is started. Although Amlodipine would have been a reasonable choice. A year later, he returns with the same chest pain on exertion. Normal ECG. Normal renal function too. He now goes back to a CT angiogram showing multi-vessel disease. Per Dr. Buckler, one of the reasons he has worsened on a statin is that we may have limited understanding of his pathology, or potentially the CTA was not accurate the first time. Virtual FFT now can show the flow and how significant the lesion is, which is an advancement in this technology. Unfortunately, despite aggressive lipid therapy, sometimes people progress. A few days after the CTA, his Creatinine goes up a bit and GFR goes to 43. This is also after years of Lisinopril. Dr. Carl Dean comments on this alteration in renal function. He feels this is not entirely unexpected, but the data doesn't really reflect CIN (contrast induced nephropathy). Yet intuitively and experientially, we sometimes see this. The amount of contrast used is significantly more on a CTA than on an invasive angio. At this point, the ACE inhibitor is held and Amlodipine is started. Renal function now has improved. The angiogram demonstrates significant 3 vessel disease, with good downstream targets. The SYNTAX surgical risk score directs the cardiologist toward CABG instead of PCI. Post angio, he develops some lower extremity edema, and he is discontinues on Amlodipine, resumed on the HCTZ, Lisinopril. The creatinine is now 2.4. Did he receive enough fluids for the angiogram? Or was the few hundred cc's he obtained during the angio okay? Again, hindsight is 20/20, but the data doesn't support a causality for AKI due to CIN, nor is there a true preventable measure, including n-acetylcysteine or bicarbonate. Perhaps, in this case, CIN as a possibility in the past as discussed, that many would not argue with overhydrating. Ultimately it was felt the ACE and contrast contributed to his creatinine elevation. The ACE combo is now stopped and he is started on Hydralazine and Metoprolol. Creatinine improves, and he goes into CABG surgery. He is discharged and he continues on aspirin and Plavix for 3 months, and Carvedilol and Hydralazine. Atorvastatin is increased to 80 mg daily, a more aggressive dose. EF is normal on echo.  Do statins affect kidney function positively or negatively? According to Dr. Dean, there is no trial that supports either. His BP starts to increase, and Lisinopril is once again added, along with an increase of creatinine, and the ACE is again d/c'd. HCTZ was added. Then spironolactone for ongoing HTN. He's still running high though. Labetalol is replacing carvedilol now. And the pressure is still running high. What is happening here? What to do next? Do we try Lisinopril again? It is attempted, and he once again fails the creatinine test. It goes up again. PART 2: What we do now for this patient? It seems he can only improve on Lisinopril for blood pressure, but his creatinine continues to go up. According to Dr. Dean, in this patient, Lisinopril may not be a great option going forward, not only due to creatinine increase, but it will not help him in terms of mortality outcome. renal artery stenosis is a concern in this case. Dr. Tara McMichael interjects the question, could a loop diuretic have been tried? With a creatinine of 2.3, a loop diuretic could have been an option, since volume and sodium retention could be contributing to the hypertension. Isosorbide with hydralazine is also an option if more meds were to be added. Per Dr. Buckler, however, a four drug regimen that is poorly controlling blood pressure doesn't necessarily indicate adding a fifth drug. We need to know if there is a secondary cause of HTN. Sometimes, even in the setting of renal artery stenosis, patients still require significant anti-HTN drug regimens. Also, per Dr. Dean, the pretest probability in this type of patient for renal artery disease is high. And will an intervention be desirable if it is found? The ASTRAL trial demonstrated no improvement in outcomes. The CORAL trial was also done and considered to be a negative trial. One of the trial criticisms though was that it didn't include patients with severe enough disease. According to Dr. Dean, refractory hypertension should cause screening for this and an intervention should be done if it is seen.  Our patient has a renal u/s that shows bilateral RAS. Dr. David Gross, radiologist discussed the results of the MRA. The aorta, SMA and celiac trunk show atherosclerosis. The renal arteries are paired bilaterally. They have moderate to high grade narrowing of the arteries. Dr. Buckler asks the question of the safety of gadolinium in renal disease. In the setting of low GFR, in other words, less than 30, the risk for nephrogenic systemic fibrosis exists, although very rare. This is usually fatal, though. Basically, he has 4 out of 4 arteries occluded. Dr. Dean feels referral to a center of excellence for this unique issue is best for the patient. He undergoes transaortic endarterectomy, as his creatinine is rapidly going up. A significant plaque is resected from the aorta which was extending into the renal arteries. Post-procedure, he is placed on metoprolol, requiring nothing further. Rosuvastatin, Zetia and baby aspirin is started. Basically, unclogging the pipes resulted in a cure. And a while later, he's no longer on any antihypertensives. Blood pressures are great now. LDL now 57 on the new cholesterol meds. Zetia has limited data, but the PcsK9 inhibitor and his LDL is now 1. Dr. Buckler states there is a lot of unknowns about the LDL levels and whether there is a point of diminishing returns, but the science is not there yet. In this case, Dr. Buckler feels that stopping the Zetia and continuing the pcksk9 inhibitor makes sense. PART 3: Renovascular HTN is more commonly found in the setting of acute, severe, refractory, very high blood pressure. Work-up is needed when there is a strong possibility of secondary cause, and in the absence of another secondary cause, like pheochromocytoma or hyperaldosteronism. Also in an acute rise in BP, a young age, elevated Cr after starting an ace inhibitor, etc. Renal asymmetry on imaging and flash pulmonary edema are other clues. If Cr and BP are stable in the setting of stenosis, no intervention is indicated. Testing can potentially worsen function, as can the interventions performed to treat the disease. Who benefits most? People with short term hx of HTN, people who fail optimal medical therapy, not tolerating medical therapy and progressive renal failure. Ultrasound and CTA or MRA are the options for work-up. US is cheaper, but time consuming and operator dependent, with modest sensitivity/specificity. CTA is accurate for atherosclerosis. Highly sensitive and better if GFR below 30. MRA is highly sens/spec. Gadolinium complications can ensue in low GFR situations. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9) will lower LDL up to 60%. 50% decease in stroke and MI risk. The PCSK9 enzyme binds to liver LDL receptors and thereby increases plasma LDL levels. so inhibiting this enzyme leads to a lower LDL level. These inhibitors also can decrease triglycerides, increase HDL somewhat and decrease the volume of atheroma. Low adverse effects are noted with the med as well. Regarding renovascular HTN, Dr. Dean also reminds us that someone who is significantly older with chronic renal ischemia in the setting of this disease, may not have improvement in renal function even after intervention. Therefore, some of these patients who suddenly reperfuse a chronically ischemic kidney may actually worsen. Renal artery stenosis is also not an absolute contraindication for ACE. Such as in low EF heart failure. If the creatinine markedly rises, it can be discontinued again. Fibromuscular dysplasia patients, unlike atherosclerosis patients, should all receive an intervention. This is more commonly found in younger patients. Dr. Buckler addresses the ease of use and cost of the PCSK9 inhibitors. It turns out the cost is high at this point, up to $14k/year. But coverage has shown promise in FH and refractory high LDL. As it was alluded to by Dr. Holcomb, the patient really doesn't exercise and has a very stressful job, as it turns out. His dies wasn't discussed. Was he managing his risk factors very well? What does that mean nowadays? We have potent medications and skillful intervention options for reacting to this sort of pathology nowadays, but where are we at with prevention? Hopefully a conversation for another day.

She became CEO of Minneapolis Heart Institute to change lives. Now, she's pushing a legacy of equality. On a quest to challenge the media, backward medical notions, and the public to move women's heart research up 35 years to equal men's heart research, Fortman is overseeing a movement she hopes goes viral- #ResearchHer. Her world routinely mixes business, healthcare, and philanthropy. She keeps her own heart healthy by hiking new terrain with her husband and three sons.  See omnystudio.com/listener for privacy information.

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. Dr Greg Hundley: And this is Dr Greg Hundley from VCU health, the Poly Heart Center in Richmond, Virginia. Well, Carolyn, this week's feature analyzed a pool cohort of all patients in partner one and partner two, both the trials and registries. Patients had severe aortic stenosis and were treated with TAVR or SAVR and then were analyzed with respect to the development of prosthetic valve endocarditis. But more to come on that later. Dr Carolyn Lam: Let me start by telling you about my picks from this week's journal. So the first one is a really interesting natural experiment. First, do you think that a short term visit to a location with severe air pollution increases the risk of cardiovascular disease? Dr Greg Hundley: Well, Carolyn, I would say yes. Dr Carolyn Lam: Greg, you're too smart. But let me tell you what these investigators did. So their co-corresponding authors, Dr Araujo from David Geffen School of Medicine and UCLA, Dr Zhu from UCLA Fielding School of Public Health, and Dr Qiu from College of Environmental Sciences and Engineering in Peking University. These co-corresponding authors and their colleagues did a natural experiment by collecting urine and blood samples from 26 healthy adult residents of Los Angeles before, during, and after they spent 10 weeks in Beijing during the summer of 2014 and 2015. Dr Greg Hundley: I am really excited to hear this. Carolyn, what did they find? Dr Carolyn Lam: So traveling from less polluted Los Angeles to more polluted Beijing induced pro oxidative and pro inflammatory effects, which reversed after returning to Los Angeles. This is also the first human study associating exposures to polycyclic aromatic hydrocarbons with changes in paraoxonase 1, enzymatic activity, and circulating levels of hydroxyeicosatetraenoic and hydroxyoctadecadienoic acids. Cool, huh? Dr Greg Hundley: Absolutely. Carolyn, you did an awesome job. Very nice. Well, my article comes from the world of basic science and it's from Dr Philip Shaul at the University of Texas Southwestern medical Center. So Carolyn, in recent studies of obesity induced insulin resistance in mice with corroborating findings in human type 2 diabetics, this group, Shaul’s group, previously made the surprising discovery that the insulin resistance is driven by an altered post-translational modification in IgG that leads to enhanced activation of FCYR2B in endothelial cells. And as a result, there is an attenuation of insulin transcytosis across endothelial cells and delivery to skeletal muscle myocytes where up to 80% of glucose disposal usually occurs. Dr Carolyn Lam: Oh. Interesting, Greg. So what did the authors find in the study and how did these findings equate with obesity and hypertension? Dr Greg Hundley: Well, they found that hyposialyation of the Fc glycan on IgG is identified as a key contributing factor in obesity induced hypertension. And therefore low levels of IgG Fc glycan sialylation may identify individuals at greater risk of developing hypertension. In addition, the degree of sialylation of IgG may predict the relative response of an individual to any hypertensive therapy. Dr Carolyn Lam: Nice. So my next paper is from Dr Al-Lamee from Imperial College, London, and colleagues who studied the ability of a pre-randomization stress echocardiographic score to predict the placebo-controlled efficacy of PCI within the ORBITA trial. Now as a reminder, the primary results of the ORBITA trial showed us smaller than expected effect size of PCI in comparison with placebo in single vessel stable coronary artery disease on the primary end point of change in treadmill exercise time. Now in the current study, 183 patients underwent dobutamine stress echo cardiography before randomization, and they found that the degree of ischemia assessed by dobutamine stress echo cardiography predicted the placebo-controlled efficacy of PCI on patient reported angina frequency. Dr Greg Hundley: Hmm. Very interesting. So help me out again, Carolyn. What's the clinical importance of this? Dr Carolyn Lam: Ah, so this study really provides the first placebo-controlled evidence of an association between stress echo cardiography, ischemia, and the magnitude of placebo-controlled benefit attributable to PCI. And the greater the downstream stress echo cardiography abnormality caused by the stenosis, the greater the reduction in symptoms from PCI. That's the take home. Dr Greg Hundley: Oh wow. Very interesting. You know, especially we perform so many stress echo cardiograms. What a great relationship to unfold and present. Well, Carolyn, I'm going to walk through several other important publications in this issue of the journal. The first is from Dr Peter Eckman from the Minneapolis Heart Institute, and he provides an In-Depth review of veno-arterial extra corporal membrane oxygenation, or VA-ECMO, for cardiogenic shock and it's beautifully written for the busy clinician. Robert Platt, PhD, and colleagues discuss in an On My Mind piece the fact that those with adverse cardiovascular sequelae during pregnancy may require development of new cardiovascular risk prediction models. The hypertension or the diabetes that occurs during pregnancy, perhaps we need to incorporate that into our prediction models. Next. Our own associate editor Torbjørn Omland provides results in a research letter from the peace trial relating the relationship between smoking and high sensitivity troponin T levels. Dr Allen Sniderman from McGill University Health Center writes a letter to Welsh and Associates regarding their study of the UK bio bank database and measures of HDLC. A paper we discussed just a few weeks ago. Dr Derek Chew from the DCRI and Durham North Carolina has another EKG challenge for us. And Dr Tracy Hampton provides an updated news report regarding cardiovascular disease from several recently published articles in the world of basic science. And then finally Dr Thomas Krieg from the University of Cambridge has a nice piece regarding clinical implications of targeting succinate metabolism in ischemia reperfusion injury. Well, Carolyn, what a great slate, but I can't wait to get to that feature discussion related to prosthetic valve endocarditis. Dr Carolyn Lam: Me too. Let's go. Our feature discussion today is really the first paper that describes adjudicated evaluation of prosthetic valve endocarditis in patients with transcatheter and surgical aortic valve replacement. Very unique and valuable data from the partner's trial. I'm so pleased to have with us the corresponding author, Dr Wael Jaber from Cleveland Clinic as well as our associate editor, Dr Manos Brilakis from UT Southwestern. So Wael, very unique question. Could you please tell us how you went about doing this? And I suppose in this setting, the first question on everyone's mind is how did you make this diagnosis of prosthetic valve endocarditis? Dr Wael Jaber: Actually we saw this as an opportunity that probably we should never miss. I think this is one of the rarer instances where we can objectively not only look at SAVR data but also TAVR data. And over the past maybe seven years, eight years, we started getting here as a referral center patients with TAVR endocarditis for surgery. And we never thought we'd start seeing these weird organisms, different bugs. Of course this is a population that's frail or elderly, but we never had any idea if they behave similarly to SAVR or differently than SAVR in our previous experience with SAVR endocarditis. So we planned this actually about maybe five years ago, but we didn't have the data because you know the partner trials were undergoing another evolution by going to lower and lower risk population. So we pose this question about a year and a half ago to CRS by asking them, can you provide us with the data on all the endocarditis in partner. The idea was not only to answer one question but to answer multiple questions. So the first question was in the modern era, what happens in SAVR? All the SAVR endocarditis information we have so far as you will know has been from mainly single center studies or even when we learn about it from multiple centers sites, usually IN European studies, the Swedish registry, the Danish registry, and these are usually limited by the fact that there are a multicenter. The adjudication is at the site what endocarditis happened. So that was the first question. Then the second issue for us was, does TAVR, because of the unusual access to the heart and the fact that we dilate the valve, post dilate the valve, their paravalvular AI, they could be micro-fractures of the refis. This is provide a different opportunity for these bugs to form on the valve, and do they behave differently? And the third question was, is there any difference between SAVR and TAVR incidence of endocarditis? And bugs. And the final question was what happens to patients when they develop endocarditis in the current decade. Do they do well? Especially for septic endocarditis or do they succumb to their illness? And also this is how we came up with a strategy to answer all these questions. Dr Carolyn Lam: Very nice. So Wael, could you just expand a little bit more about how the diagnosis or adjudication of prosthetic valve endocarditis was done? And then tell us please, what did you find? Dr Wael Jaber: All the partner patients, the records were sent to a central place. So the ECHOS first were educated at central places. We were one of those centers. Other places were Columbia University, MedStar and Quebec, the group in Quebec. So all the ECHOS were adjudicated centrally. So that's first, as far as from the echo side of calling it endocarditis or not. On the clinical side, again, all the records and the forms were sent to a central adjudication committee, CDC group. We served at the Cleveland Clinic as the CDC for most of these trials and actually even for the current trials. So they were sent and they were adjudicated according to the Duke criteria. Which is, you know, the most, probably, reliable way still today to adjudicate these. And then there was the CDC and the echo core labs were separate. So the people who have information from the CDC did not have access to what's going on in the core lab and vice versa. So these were independently adjudicated as far as echocardiographic evidence and clinical evidence. And then they were fed into it. So by the end, when you hold it on a Duke criteria endocarditis, the echo was fed after the fact, not before. So this is in general how it happened. So all the events were educated centrally, not at the site. And the ECHOS, the same thing, were adjudicated centrally. Dr Carolyn Lam: Fantastic. And I would love to hear the results. Dr Wael Jaber: The first question was, what's the incidence of endocarditis? And we decided because of the way these trials were done, to report the incidents as you would see in the results section, to report the incidents of endocarditis per 1000 person year because of the imbalances in follow up and the competing risk for death from other reasons. So we found in general that the incidents of endocarditis was 5.2 endocarditis events per 1000 patients per year in the TAVR side and 4.1 in the SAVR side with a non statistically significant difference. More importantly, we found out that once you develop endocarditis, unfortunately most of these patients succumb to the illness and are dead after the diagnosis. So the risk of dying after developing endocarditis is 4.4 times higher than patients who did not have endocarditis in the trials. In all the trials. Now there's some caveats here. First, these are trials with different patient populations, as you well know. Starting with partner with the inoperable patients moving on to the most modern S3 trial, which was on the lowest kind of side of population. So we have totally different population groups. Some of them had prolonged hospitalizations before and after, so this should be taken with a little bit of caution. However, if you look at some of the individual trial data, we found that incidents of endocarditis at least have a trend towards a reduction of incidence of endocarditis over time going from partner, the initial experience with partner, all the way to the modern era. Dr Carolyn Lam: That is so great. Manos, you know, as an interventional cardiologist yourself, could you tell us how important these results are? Does it affect your practice? Dr Emmanouil Brilakis: Thanks again, Carolyn. I would like to congratulate Wael for a phenomenal paper. I think it's a very timely study and addresses one of the common concerns there is about whether TAVR does predispose people to more risk for endocarditis. Although again, the opposite grade was kind of low at 0.5% a year. I think this may be a little more than people are commonly seeing in the setting of TAVR, and I think the paper is a good reminder that this is something we should always be mindful and watching. Although typically we'll discuss with the patient about the risk of stroke or access complications, but the risk of infection may not be as well emphasized. And based on this one question I would have is about what can we do if there is something that could potentially lower that risk? I understand the limitations of retrospective study, but are there any recommendations that you have based on the study? Should give more aggressive antimicrobial therapy? Any other biotic prophylaxis or anything else that can be done to reduce the risk of endocarditis in those patients? Dr Wael Jaber: Actually this is the question we raised. Unfortunately we did not. So the guidelines did not catch up with what we know. So if you look right now, like I was reviewing this paper that came up last month from the Swedish Registry for Endocarditis, it came out in Europe in the European Heart Journal, and one of the questions they raised is how to address, in the editorial, how to address the risk of endocarditis and prophylaxis in this population. There are no standards for that. This is one aspect of it. We need first an update of the guidelines of how to address this issue. The second question is we do not have any idea, unfortunately, about duration of antibiotics. How the antibiotics prophylaxis were given before the procedure, like as we do right now commonly in surgery, and after the procedure in these patients. We do not know that. Like right now, at least at our center, if you go in for aortic or mitral valve surgery or any valve surgery, you have to have a dental clearance before you start, before you go to surgery. I don't know if this was rigorously applied in the setting of TAVR, and I think it would be a good idea to apply it to make sure that there are no dental, phosphide or potential infections and things like that. So I think it's a multi-front battle to get these patients to the lowest risk possible. I don't think there's one single silver bullet here. Dr Emmanouil Brilakis: So thanks again, Wael for addressing this. I agree that there's a lot of information to be gained understanding the intricacies of endocarditis prophylaxis. And building on this, let's say another patient develops endocarditis as you've shown in your 170 patients in the study. It was fascinating that staph aureus was actually less common than it was for surgical valves, which has been shown in other studies as well. So you think this affects the choice of the biotic prophylaxis? And then also if the patient develops endocarditis, I understand many people who are not candidates for surgery, but from the ones who did actually undergo surgery, what are the outcomes encouraging? Dr Wael Jaber: This is a fascinating question actually. This is one of the reasons we had... There was a delay for us in getting the paper out from when we presented it as an abstract at TCT a year and a half ago, is we didn't know. We wanted to answer that question. The second part of the question is how many patients went to surgery? And unfortunately, very few patients. So less than a handful of patients end up going to surgery. And we do not know why. So this is the dilemma here. Is why the rate of referral to surgery for redo surgery was very low. Was it because these patients were the sickest of the sick? Maybe it is because we waited too long and we did not treat them the same way. We should have treated prosthetic valve endocarditis, which is surgery to be offered as soon as possible because there's no really antibiotic cure for that. So we do not have the answer for that because these very few patients went to surgery and actually I think of those who went to surgery, even the mortality there even was similar to people who did not go to surgery. But we cannot speculate on that because the very few patients. As far as the bug involved, I think this could be a reflection of the antibiotics given at the time of the procedure, so probably we're covering that very well. But if you notice from the paper, most of the infections happen more than 30 days after the procedure. Whether this is something that was acquired because these patients are more likely to end up in the hospital again for other reasons, whether these patients had endocarditis because they have more instrumentation down the road... Remember this is a population in general above the age of 65 which would require colonoscopies, frequent urinary tract issues, and other procedures. So we know that we're covering very well, at least I can speculate, we're covering very well for the first 30 days because very few patients had endocarditis right after the procedure, but we're not covering probably after the 30 days. And that remains to be studied. And the worrisome thing is to try to treat these patients with prophylactic antibiotics for a long time and then end up with bug resistance and things like that. Now the CDC issued a big warning about this yesterday. I am not comfortable to speculate from this small number of patients on how to treat for prophylaxis, but I'm comfortable to say probably patients should be sent to surgery as soon as possible after developing endocarditis, especially prosthetic valve endocarditis because the outcomes are dismal. Dr Emmanouil Brilakis: And do you think... Let's say patient is not a candidate for surgery and gets endocarditis, and I presume they get into prolonged therapy. There were some patients like this that did okay, right? So there is some hope even for those patients. Dr Wael Jaber: I feel like I'm the cup half full here because if you look at the mortality curves here, we're talking about north of 95% death in this population. So the people who survive this must be very few people survive. So probably about seven patients who survive. So the mortality was 96% at six months versus 46%. So there are very few people who survived that event. Maybe I should go back now and figure out what was the quality of life after survival. So I don't think the picture we have right now is very rosy as far as the way we're managing endocarditis. Dr Carolyn Lam: Manos, I'm going to give you the final parting words from this very interesting discussion. I mean what do you think are the take home messages and future directions from here? Dr Emmanouil Brilakis: I agree that this is a phenomenal landmark study and my key takeaways are the same ones that Dr Jaber presented before. But the main thing is, on the consent process, who can tell the patients there is about 0.5% per year. So it's not zero, but it's very high either. The second thing is that this choice between TAVR versus SAVR, that should not have to do with the risk of infection because as it was shown very convincingly, it was very similar to the two groups. And number three that everything possible should be done to prevent this because if you do get infection, the outcomes are not very good. Dr Carolyn Lam: Thank you so much Manos, Wael. Thank you so much audience for joining us today. You've been listening to Circulation on the Run. Tune in again next week. This program is copyright American Heart Association 2019.  

In this Live Friday CME recap podcast, Dr. Santiago Garcia, a cardiologist with Minneapolis Heart Institute, provides an overview of percutaneous mitral valve repair; specifically the MitraClip. Objectives:    Upon completion of this podcast, participants should be able to: Recognize that mitral valve regurgitation is highly prevalent and detrimental to the quality of life and survival. Select the differences between functional and degenerative mitral regurgitation. Describe the mechanism of action of percutaneous repair and clinical data to support its clinical use. Identify indications for the determination of surgical mitral valve repair and replacement. CME credit is only offered to Ridgeview Providers 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 honoring you 1 CME/CEU credit in 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: "Percutaneous Mitral Valve Repair" - CME Internet Enduring Activity (**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.)  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.” -----  FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. Santiago Garcia, MD has received honoraria from Abbott Vascular. An independent review of his presentation confirms he is following EBM guidelines, as MitraClip is the only trans-catheter mitral valve repair (TMVr) therapy that delivers a treatment option for patients with significant symptomatic mitral regurgitation. Santiago Garcia, MD works with Abbott Vascular engineers and provides feedback on new MitraClip designs, and does not endorse Abbott Vascular. There is NO commercial tie to Abbott Vascular products, and NO impact on this specific Ridgeview CME presentation/podcast. Santiago Garcia, MD has received honoraria from Medtronic. An independent review of his presentation confirms he is following EBM guidelines. Santiago Garcia, MD provides training and consultation for chronic total occlusion devices (stents). He does NOT endorse Medtronic products and NO commercial tie to Medtronic products, therefore has NO impact on his Ridgeview Medical Center CME presentation. Santiago Garcia, MD has received honoraria from Edwards Lifesciences. An independent review of his presentation confirms he is following EBM guidelines. Santiago Garcia, MD is a speaker and proctor for Edwards Lifesciences. He does NOT endorse Edwards Lifesciences products. There is NO commercial tie to Edwards Lifesciences products, therefore there is NO impact on this CME presentation. All other planning committee members and presenters have disclosed they have no significant financial relationship with any cardiovascular device companies that have been disclosed and the NO conflict of interest exists with Santiago Garcia, MD’s presentation/educational event. ----- SHOW NOTES: Welcome back everyone to Ridgeview Podcast: CME Series! It's Live Friday CME recaps. Jason Hicks here, and it's my pleasure to host this episode. Thanks for joining us on this lovely fall day. In this episode, we are joined by Dr. Santiago Garcia, staff interventional cardiologist with Minneapolis Heart Institute. He is going to enlighten us on some of the particulars of percutaneous mitral valve repair. Most specifically, the Mitraclip, which is effectively the mitral clip procedure for the indication of mitral regurgitation. So pour a cup of coffee, and chill out on the porch; and get ready to take in some cutting edge cardiology here on Ridgeview Podcast CME Series with Dr. Santiago Garcia. CHAPTER 1: Alright all you stellar continuing educationalists. Yep, that's a real word. It's time to digest some of this excellent info. According to the study out of Mayo Clinic that Dr. Garcia discusses, the prevalence of mitral valve disease (MVD) is actually higher than aortic valve disease (AVD). Both increase with age. But by the age of 75, 1 in 10 will have MVD, and it is higher than AVD. About 4 million in the U.S. have mitral regurgitation (MR), and about half are eligible for therapy. However, there are a relatively small number that actually go on to get mitral valve surgical therapy, due to the fact that the guidelines are fairly stringent for this. Asymptomatic, severe mitral regurgitation, as well as patients with symptoms can benefit greatly by surgical therapy. Some definitions and quick discussion though, regarding mitral regurgitation. What is it? Mitral regurgitation is just that. Regurgitation through the mitral valve into the left atrium during systole. It results in a systolic murmur. Standard diagnosis is made by echocardiogram, usually transthoracic echo (TTE). This will tell us about the severity of the MR. Also, remember that many people are asymptomatic with this, even in the setting sometimes of severe MR. The guidelines for mitral valve open surgery are sort of complicated, but Dr. Garcia summarizes as follows: Primary, also known as degenerative mitral regurgitation (DMR) and secondary MR. Primary (or DMR) deals with pathology of the leaflets. Leaflets are attached to the muscle of the heart. These patients in general have more tissue than what they actually need. Secondary MR is, most commonly, due to previous MI. The scar on the wall of the heart pulls on the valve and the leaflet are therefore pulled down. Functional MR is also a form of secondary MR and has to do with LV dysfunction and no actual valve structure abnormality. There tends to be a different treatment algorithm for each type of MR.  There is no class, one indication for surgery for secondary MR. A large randomized trial concluded there was no benefit in surgery in patients also undergoing CABG. With primary MR, surgery has a class 1 indication, as long as there are symptoms and a EF of at least 30%. In asymptomatic patients, repair is recommended if A-fib is present, pulmonary hypertension, and a very experienced surgeon. There are only a few such surgeons in the country. The likelihood of surgical success must be >95% in order to proceed with surgical correction. Mitral valve (MV) surgical repair is the overall standard of care. The most pathology site is the P2 scallops, with excessive tissue and a flail posterior leaflet, as mentioned by Dr. Garcia. A resection and then reapproximation of this tissue is performed. A valve ring is often placed as well. About 50% of patients who may qualify for percutaneous therapy. Coming up next, Dr. Garcia will go into the background and some of the intricacies of the MitraClip procedure. CHAPTER 2: The MitraClip device is the only commercial available device in the United States for primary or degenerative MR.  The guidelines give percutaneous therapy a class 2B indication. These are high risk patients, who typically have had previous sternotomy or are older than 80. FMR (functional mitral regurgitation), which is discussed and defined in Cardiology Review, 2010, by Schmitto et.al, "as a systolic retrograde flow from the left ventricle into the left atrium due to reduction and/or elimination of the normal systolic coaptation of the mitral valve leaflets." The valve structure is essentially normal, but the function of the valves during systole is not, and therefore results in regurgitation. FMR did not previously have an indication for surgery until the COAPT, which was recently published in the New England Journal of Medicine, resulted in FDA approval. This trial took over a decade to perform, and the results were impressive, but another trial would be needed to have a class 1 indication. EVEREST 2 was another trial that helped lead to approval of the device. So, how are mitral regurgitation patients approached in general? A TEE (transesophageal echocardiogram) is performed. There are separate criteria for FMR and DMR. These criteria were used in the clinical trial mentioned. However, some of these criteria are now obsolete, given there are other devices, for instance the XTr, that can now be used, and more of these patients could now potentially be treated with percutaneous therapy. In addition, if the mitral valve area is small, this therapy can lead to iatrogenic mitral valve stenosis. Is this useful for CHF patients? Well, in the COAPT and EVEREST 2 trials, patients needed to be on optimal medical therapy. If patients' MR improved significantly with medical therapy alone, then they would not be procedural candidates. If their MR was no better in the setting of optimal medical therapy, then they would be candidates for the procedure. How is this procedure done? First, venous access is obtained; then the left atrium is accessed from the right atrium. The left atrium in navigated. With the clip opened, the catheter/device enters the left ventricle, then grabs valve tissue. The clip is closed and then the device is deployed. Basically, the device truly clips together the leaflets of the mitral valve in order to close the gap that results in severe regurgitation. This is obviously very visual, so please check out the presentation slides to Dr. Garcia's presentation. The posterior, superior quadrant of the atrial septum is where the puncture will take place. This allows for maneuverability down toward the ventricle. This is all done under TEE guidance. Therefore it is done under general anesthesia. The clip is best situated in A2 P2 (the anterior and posterior 2nd scallops of the valve). There are long and short clip arm device options, and the size of the leaflets and their degree of retraction will dictate which device is used. The leaflets are basically clipped together, creating two orifices from the original one. A +2 mitral regurg indicates good success post-procedure. And the goal is also not to cause mitral stenosis. Left atrial pressure reduction is also a goal here; such as a reduction of 10mmHg, as mentioned by Dr. Garcia. Stay tuned for the next segment where Dr. Garcia discusses the COAPT trial, and some of the other studies that led to approval of this innovative procedure. CHAPTER 3: COAPT was the pivotal trial for patients with FMR for a mitral clip device. Again, this is a class 2B indication for the procedure. It was hypothesized that by impacting mitral regurgitation, we could decrease preload and CHF readmissions. It (COAPT) compared to 300 pts in each study are, one with medical therapy and one with medical therapy and the clip. There was almost a 50% reduction in admissions. The NNT (number needed to treat) to prevent one hospital admission was 3. In addition, a mortality reduction of 40% was seen, with an NNT of 6. Overall, to prevent 1 event, either heart failure admission or death, the NNT is 4. This is unprecedented in terms of a device trial. The COAPT showed a complication rate of

In this podcast, Dr. Joshua Buckler, a cardiologist with Minneapolis Heart Institute at Ridgeview Heart Center, provides an overview of growing issue of atrial fibrillation, and the increased need for its awareness and the modalities to evaluate and treat it. Objectives:    Upon completion of this podcast, participants should be able to: Identify risk factors for atrial fibrillation. Express the importance of screening for atrial fibrillation. Recognize when a patient needs to be referred for atrial fibrillation. CME credit is only offered to Ridgeview Providers 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 honoring you 1.25 CME/CEU credits within 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: "Atrial Fibrillation (Podcast)" (**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.)  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.”   FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. Planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed no conflict of interest exists with the presentation/educational event. SHOW NOTES: CHAPTER 1: We understand around 10% about an Atrial Fibrillation (A-Fib or AF), which makes understanding it a challenge. The majority of AF starts in the left atrium likely due to left atrial stretch secondary to mitral regurgitation or hypertension. This then leads to loss of connectivity and communication of the atrial cells, leading to micro reentry circuits. A lot of the AF comes from the pulmonary vessels where they connect to the LA. Why does this happen? Currently, we are unsure. AF comes down to the irregularity of atrial contraction fighting to get through AV node, resulting in irregularities of the ventricular action. AF runs about 300-500 bpm. Those high irregular rates through the AV node can result in symptomatic patients trying to maintain cardiac function over prolonged periods of time. Second, is the loss of AV synchronization - which is how the atrium and ventricle work in concert together. Lastly, is stroke risk. AF is so important, because it is grossly under-recognized and the implications of stroke and heart failure (HF), which can be catastrophic. The literature seems to support that individuals with AF seem to have a lower quality of life.  The statistics are staggering, that a patient with AF has a 5x risk of stroke, 3x risk of heart failure, 3x risk of myocardial infarction or dementia. There has been a 5-6 fold increase in rates of AF since 1999. AF is commonly found with patients who are obese, diabetics, those who use alcohol and untreated obstructive sleep apnea.  Dr. Buckler believes that entry point into the healthcare system is crucial for the success of AF patients. Establishing a one call system with curbside to the cardiologist for patients experiencing new onset AF. Obesity is a direct risk factor for AF. The "Legacy trial" was performed in Adelaide, Australia. It looked at losing 10% of body weight dramatically reduces AF following cardiac ablation. Patients with smaller weight fluctuations, around 2% of body weight, did better post-ablation, than those with higher weight fluctuations of around 5% increase in body weight. CHAPTER 2: AF is similar to diabetes. It affects everything. It's affected by everything and no one wants to deal with it. There is a large multidisciplinary approach to the treatment of AF due to the complex nature of the disease process.  There is a large push to get the AF patient into the sleep clinic, as OSA and AD are closely intertwined. Furthermore, there is independent data that if OSA is treated, so is the patient's AF. Dr. Buckler believes in a team approach to the successful management of AF. He notes that is the PMD can start the workup by getting thyroid testing, sleep study, setting up the echo and placing the patient on anticoagulation as well as a rate limiting medication is a good start. Most cardiologists believe a rhythm control strategy is the way to go for treating most AF patients. The utilization patterns of AF patients is problematic. Most AF patients are costing the healthcare system around $8,700 per year/per patient. Dr. Buckler mentions a study that if some AF are ablated early in their disease state, the short-term cost far outweigh the costs downstream if they have recurrent AF. Addressing risk factor modifications, including OSA, obesity, ETOH, DM, smoking, are instrumental in the care of the AF patient. Believe it or not, endurance athletes have higher rates of AF. Whereas, high endurance women athletes actually have lower rates of AF. Something to chew on. Ablation has a high likelihood of success with initial treatment successful upwards of 90% of the time. The network of AF patient and how they enter the system is highly complex and intertwined coming down to primary care, emergency medicine, hospital medicine and cardiology. Building in pathways to the neurologist is critical for those individuals who may have experienced a cryptogenic stroke from undiagnosed AF. CHAPTER 3: How do we screen for AF?  Holter monitors are still being used which seem to be of low yield. The ZIO patches are also used as well, but for around 14 days - but what if the patient does not have an episode of AF? Even 30-day monitors are good, but not great, as the average time period a patient will have an episode is around 42-43 days. So maybe we should consider an implantable cardiac monitor or better yet, what about consumer wearable's. What are consumer wearable you may ask well they are the: apple watch which have been FDA cleared not approved for AF detection or another device called Kardia single lead EKG machine that can tell you if you are in AF or other dysrhythmias. Some non-western medicine approaches to the treatment of AF are yoga, acupuncture and biofeedback. Ultimately, Dr. Buckler believes that across the country no one has a truly good data set that documents the burden of AF patients. Furthermore, AF patient's generally have longer lengths of stay when hospitalized. Some interesting modalities not quite ready for prime-time at the ED entry point may be, TEE, cardio version, or CTA, evaluating for left atrial appendage clot then cardio version which might be promising. Dr. Buckler believes that every AF patient should be seen by cardiology, at least once. Cardiology should be the repository for AF. Optimally, the idea would be to offer that service within 48-hours. Also, would like the patient to get through risk factor management more efficiently. The check list once again -- everyone needs a sleep study, echo, thyroid testing, etc.

Listen to our first episode with two guests! Ankur spoke with Emmanouil S Brilakis, MD and Michael Megaly, MD from the Minneapolis Heart Institute, Abbott Northwestern Hospital about their article on the role of drug-coated balloons in small-vessel coronary artery disease (SVD) published in US Cardiology Review 13.1. Percutaneous coronary intervention of SVD remains challenging due to difficulties with device delivery and high restenosis rate, making drug-coated balloons an attractive emerging option in patients with SVD. In this brilliant conversation, Ankur, Emmanouil and Michael unravel the potential advantages, challenges and practical realities of using drug-coated balloons in SVD, and the findings of the latest randomised controlled trials studying this area. Hosted by @AnkurKalraMD. Produced by @RadcliffeCardiology. [Disclaimer: The use of drug-coated balloons in coronary intervention is still off-label; it has not been approved by the FDA.]

In this podcast Ty Harrison, a Physician Assistant with the Minneapolis Heart Institute at Ridgeview Heart Center, addresses which type of stress test for chest pain is correct - why and for whom. Ty will also discuss the issue of assigning the wrong test, and that it is largely multi factorial, secondary to associated risk factors.  Objectives:    Upon completion of this podcast, participants should be able to: Describe how various stress tests are employed. Select which provocative test(s) should be ordered for specific cohorts of patients. Recite the contraindications for stress testing. Identify when a CT coronary angiogram or CMR should be considered, and on which patient subtype(s). CME credit is only offered to Ridgeview Providers 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 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: "Don't Stress the Test" (**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.)  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.”   FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. 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: Before you send a patient over for a stress test, get a baseline EKG. Does the patient have a LBBB?  If so, then is the EKG really not interpretable? If the patient has a history of previous MI, or old Q waves via EKG a stress echo is not the appropriate test; as the patient will likely have wall motion abnormalities. The basics of adenosine testing is there are adenosine receptors on the vascular smooth muscle of cardiac vessels which causes healthy arteries to dilate and those vessels that are unhealthy will not dilate creating a perfusion mismatch. The nuclear portion of the stress test is where the radioisotope is given with the adenosine, which is taken up by healthy myocardium. If area has diminished perfusion, this will create a mismatch.  Dead tissue will not take up isotope - indicative of a previous infarct. The stress portion of the nuclear test will be to assess for a perfusion mismatch to evaluate for signs of ischemia. You want to compare rest vs. stress images. Lexiscan is an A2A agonist. Advantages do not require pharmacy, single injection, short acting. Lexiscan is the stress portion of the nuclear testing. By the way, the radionuclear isotope is about 10 mSv or equivalent to about 200 chest x-rays. Optimal patient for a Lexiscan is someone who cannot exercise, once again LBBB, paced, those who can walk on a treadmill. Specificity and sensitivity: 90% for Lexiscan, if selected correctly. Cons to Lexiscan are: cost, hospital based, radiation exposure, pregnancy. Pearl: things that buy you an angio on treadmill stress testing are EKG changes, redevelopment of chest sxs, image changes. 2 of those 3 criteria moves us to angio. CHAPTER 2 SUMMARY: The 2-main echos we are concerned with are stress echo, and Dobutamine or chemical echo. Unfortunately, the stress echo is not as sensitive as a nuclear test. The pros of a stress echo:  cost, no radiation. The echo process: patient will initially have a baseline-resting echo to look at the EF, and for wall motion abnormalities. Important to point out that this is not a valvular study. Although if Aortic Stenosis is visualized, this generally is a contraindication to stress echo. Sensitivity and specificity:  around 85%, not bad. For the stress portion of the test, you are shooting for about 85% of the patient maximum predicted heart rate. Unfortunately, if obese - a nuclear study is a 2-day test due to large amount of radiation required for the studies. An additional contraindication for stress echo would be morbid obesity, COPD, previous cardiac insult with wall motion abnormalities, LBBB, reduced EF. Dobutamine Echos have limited utility. They take a long time to perform. It makes people feel crummy. Physicians usually have to be present. Once caveat would be for the chronically wheezing asthmatic with bronchospasms or history of status asthmatics. Dobutamine is a B1 and B2 agonist, which will help with asthmatic sxs.  Dobutamine has inotropic properties and less chronotropic activity, which can occasionally require atropine to increase HR. Dobutamine has limited utility. Treadmill stress testing is used to "rule out" disease.  Stress echos are generally considered the appropriate test for women. Caffeine is an adenosine analog and can affect Lexiscan results.  Beta-blockers are typically held for about 36-hours. CHAPTER 3 SUMMARY: A treadmill stress test Bruce protocol is performed in 3-minute increments. Starts at a 10% grade, with a pace 1.8 miles per hour. Goal standard is about 10-minutes. Bruce protocol goes to 21- minutes. Predictive value of a significant coronary event if the patient meets the goals of a Bruce protocol is extremely low. Buzz words that make you stop the treadmill test are pretty self-explanatory, include: reproduced chest pain sxs, drop in BP, arrhythmias, EKG changes. The negative predictive value of a neg CT coronary angiogram - in upper 90% range. Elevated calcium scores can limit the efficacy of the CT coronary angio making it difficult to accurately interpret the test. Stress test is for revealing sxs. Stress tests are not for modifying outcomes.  If the patient can do 4 METS, usually you can clear them for surgery. Stress test should be a rule-out test. CTA FFR is Fractional Flow Reserve - is an assessment of flow across a coronary lesion. In addition, it tends to take the reader out of the equation.

Ankur is back with his second #AudioArticle! This week he spoke with Santiago Garcia from the Minneapolis Heart Institute about Santiago’s US Cardiology Review 13(1) article on the role of high-sensitivity cardiac troponin (hscTn) assays and their ability to rapidly rule in or rule out acute coronary syndrome (ACS) with improved sensitivity. Chest pain is one of the most common reasons for an emergency room visit in the US, with almost 6 million ER visits annually, yet there is no consensus on how to compare the results from various hscTn assays. Tune in to hear Santiago outline the advantages and limitations of using hscTn as a standard biomarket to evaluate patients with suspected ACS in the ER. Hosted by @AnkurKalraMD. Produced by @RadcliffeCardiology.

Dr. Mike Miedema, a preventive cardiologist with the Minneapolis Heart Institute, discusses cardiovascular disease (CVD) prevention, including current uses of aspirin and diabetic agents for primary CVD prevention.  Dr. Miedema also discusses current changes in recent cholesterol guidelines. Objectives: Upon completion of this CME event, program participants will be able to: Describe current optimal use of aspirin for primary cardiovascular disease prevention. Express their understanding of novel diabetic agents used for CVD prevention. Explain changes in the recent cholesterol guidelines. CME credit is only offered to Ridgeview Providers 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 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: A 2018 Cardiovascular Prevention Update - CME Enduring Activity (**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.)  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.”   FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. 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:   We were fortunate to be joined by Dr. Michael Miedema on December 14, 2018 to discuss cardiology updates and how they are about to impact our practice, if not already. He is a board certified cardiologist, and senior consulting cardiologist and principal investigator with MHI. He trained in medical school at U of M, then went on to an internal medicine residency at Abbott Northwestern, with his cardiology fellowship to follow at the University of Minnesota.  He went on then to another fellowship in cardiovascular prevention at Harvard, in addition to earning his Masters in Public Health. He happens to also be on the committee for the ACC/AHA 2019 Guidelines for the primary prevention of cardiovascular disease. And despite the fact that he grew up in rural Minnesota, this midwesterner speaks as fast as any east-coaster I’ve ever met! So whether you’re in your car,  operating your snowblower or starting that crossfit New Year's resolution , enjoy the knowledge that’s about to be dropped by our very esteemed colleague, Dr. Mike Miedema.   Aspirin: should people take aspirin for primary prevention of heart attack and stroke? We used to say, probably yes!  In the ASCEND trial (New England Journal) in the fall of 2018, Low dose aspirin was looked at and in 7.5 years there was approximately a 12% reduction in major CV events, however serious bleeding was increased by 29%. Not a simple nose bleed, but hospitalization type bleeding.    Another trial, ASPREE in the NEJM also in the fall of 2018, looked at older patients without CV disease, above age 70, taking low dose aspirin for 5 years. It showed no benefit again in overall CV risk, but bleeding risk was increased signficantly, by 38%. In fact all cause mortality showed an increase in cancer in this group, which is interesting. At the very least, the study showed no improvement in cancer risk.   Another trial published in Lancet, the ARRIVE study, consisted of 12000 patients. They were kept on ASA low dose for 5 years, and once again no improvement in the aspirin group was shown. However, the calculated risk was about twice what their actual risk was. The bleeding risk once again was higher.  Rates of MI actually demonstrated no change in the aspirin group.    The Physicians Health Study looked at a primary outcome of MI. It showed that ASA prevented the outcome of MI. Later the investigators tried to expand the outcomes of the study to include CV deaths in general. Unfortunately this now diluted the effect of aspirin and in other words, aspirin’s effect on preventing all cause CV death, like aortic dissection, etc., which makes aspirin look less effective. In addition, there is the issue of these trials looking at “intention to treat” which relates to an inherent bias toward the intervention arm, which didn’t account for the people who had to pull out the trial.  The double edged sword is that many people do in fact pull out of the trials and are still included in the trial results, which skews the results as well.    To conclude, aspirin is likely not helpful if you’re over age 70.  Essentially, if you’re at low CV risk or increased bleeding risk, you probably also shouldn’t take it. Between the ages of 40 and 70, patients may benefit from aspirin therapy, although not without risk of bleeding.      Cholesterol: One month ago, ACC/AHA updated the cholesterol guidelines from the 2013 version. In 2013, statins were recommended for primary and secondary prevention.  Secondary prevention includes lifestyle modifications.  There has been a movement to stratify people into not high risk and higher risk.    With regard to secondary prevention, the Improve-It trial was reanalyzed. The initial trial looked at ezetimibe with and without a statin.  Over 7 years and 18000 patients, there was  a 2% reduction in risk for CV disease. Cholesterol went down by 20%. Risk scores were calculated when the study was reanalyzed. Only half the trial had zero to 1 of the usual risk factors, and there was no benefit in this group. And in this group over the 7 years, there was no benefit from ezetimibe. In 25% of the trial, there was a benefit, but these people had 3 or more risk factors. Consequently, this group saw the most improvement and benefit. Essentially, if you’re not at high risk, a statin is sufficient. Ezetimibe can be considered in this group if the statin does not get you below an LDL of 70.  Otherwise, if you decide not to add ezetimibe, a maximally tolerated statin is appropriate. Older than age 75?  A statin can be offered but not mandatory. The very high risk group, however, meaning a major CV event (ACS, MI, Stroke or symptomatic PAD) history, along with at least one other risk factor, the LDL goal must be less than 70.  Statin therapy, along with ezetamibe is warranted, and if this doesn’t work, a PCSK9 inhibitor is indicated as well. These are expensive meds, though. Ezetimibe is not very expensive and tolerated well, so if that LDL can’t get below 70, it should really be added in this group.   Regarding primary prevention, familial hypercholesterolemia should be screeened for.  An LDL > 190 should be on a statin. No other risk factors are needed. People with type2 DM should be on a statin as well. Greater than age 75? Risks must be weighed, but statin is optional. Age 0-20, lifestyle, FH screening. 20-39, if LDL > 160 and/or a calculated greater lifetime risk, a statin can be offered. Plaque is much more regressable in earlier rather than later stages. A trial is currently under way looking at this concept, attempting to treat people in their 30s. This is the Cure Athero trial which is ongoing.  For age 40-75 with ldl between 70-190, if risk is less than 5%, no intervention besides lifestyle is indicated. With a calculated risk of >20% they should be on a statin.  If somewhere between low and high risk, there are other risk enhancers that should be looked at, i.e. family hx, inflammatory diseases, ethinicity, etc. If the calculated risk is 7.5 to 20%, a statin should be offered, but if there is uncertainty about whether to treat, a calcium score should be obtained. In fact, this is one of the major guideline changes, in that calcium scoring should be looked at. If the score is 0, then no therapy should be used. Scores between 1-99, statin should be offered, but 100 or greater, statin is indicated.  This concept was from a paper published in JACC in 2015.  Again, Ca++ scoring is best used in the group with intermediate risk between 7.5 and 20%.  Following the cholesterol is also advised. In fact, fasting lipid panels are not required. The panel can now be done non-fasting. Trial data has also shown that statins are very safe. Over 20 years, cancer, dementia and other theorized health risks were debunked.  Coenzyme Q10 use, and monitoring CPK, ALT/AST on asymptomatic patients are not indicated.  To summarize, people with known CV disease should be on a high intensity statin with goal LDL < 70, ezetimibe and PCSK9 added if at high risk. Also, if FH, consider adding ezetimibe and PCSK9, goal < 100. DM? Moderate intensity statin, higher if at high risk. Primary prevention? Moderate intensity statin, high intensity if high risk. If risk is uncertain, do a Calcium score.  Another trial is ongoing looking at fish oil (EPA and DHA).  EPA (vasepia) the purified variety ("fish oil on steroids"), is implemented in the mildly elevated TG population. Over 5 years, this medication along with statin therapy showed a reduced risk 25% reduction and 5% absolute risk reduction. Strangely, if your TG are in the 1000s, you are not at higher CV risk, but when they are mildly elevated, there is more atherogenicity. Essentially, if you have mildly elevated TG, you may benefit from this treatment. Expense and dosing is an issue, but this must be a considered therapy.    Diabetes: Cardiologists are becoming more engaged in DM care once again. The vast majority of DM is type 2. 1/3 of adults in this country are pre-diabetic. The risk of MI and stroke is significantly greater in diabetics and lifestyle really matters most with diabetics as well.  A recent paper in JACC demonstrated the significant benefit in lifestyle improvement.  The UKPDS trial looked at lifestyle vs. insulin vs. metformin.  Metformin showed substantial benefit in diabetes related events and diabetes related death. If metformin is started before insulin, a significantly lower Hgb A1C and lower BMI is seen. Type 2 DM is a disease of insulin sensitivity, not deficiency. Insulin is a storage hormone and does lead to weight gain. Metformin is recommended therefore as first line for type 2 DM, based on studies in the 90s and early 2000s. They showed improvement in Hgb A1C, but CV risks really weren’t shown to improve.  Based on 3 large trials in 2010 (ADvance trial, a VA trial and the Accord trial) no significant reduction in CV events was shown. In fact a slight increase in all cause mortality was shown. This was in people with more intense glucose control. Weight gain was a significant issue in aggresive Hgb a1c treatment group.   There a two relatively new medications: sglt2 inhibitors and the glp1 agonists. The sglt2s basically block the  pulling of glucose from the urine back into the blood stream. This lowers the HgbA1C. It also has a natriuretic/diuretic effect as well. There is very little risk of hypoglycemia with this drug as well. It is also a natriuretic. In 2015, a trial looking at this class of med revealed a 14% reduction in MACE.  CV death showed a 38% reduction. Most of the benefit was in patients with risk of heart failure.  Another trial also showed a 33% reduction in heart failure hospitalizations.  The largest trial though of 17000 patients was a primary and secondary prevention trial. Similar benefts were noted, but also a renal benefit. Ultimately, our type 2 DM patients should have these medications considered for both primary and secondary prevention. GLP1 receptor agonists or glutides, are also an option. This medication class causes less glucose production by the liver, more uptake by the muscles and delayed gastric emptying. Weight loss may occur with this med. CV effects include decreased inflammation and decreased risk for clotting in the smaller vessels. Overall reduction in Hgb a1c, weight loss, improved LDL, decrease in BP and decreased inflammation. 13 to 14 % reduction in MACE was noted with this, especially in stroke and atherosclerosis. Not so much with CHF due to an anti-atherosclerotic mechanism.  Glutides are given once weekly. Yeast infections are more common with the SGLT2s due to increased glucose in the urine.  ACC constructed a pathway for use of these various medications:  Essentially, For your DM pts with CHF, an SGLT2 should be given, and a GLP1 for DM pts with previous CV events. Cost is also an issue with these meds; however they can be used together.   CV genetics considerations and screenings is an up and coming topic.  The Framingham study said CV disease is due to multiple-factorial processes and risk factors. Therefore it is hypothesized that mutliple genes may lead to higher risk.  If your lifestyle is good, even if you have increased genetic risk, you can substantially lower your risk. In about 2% of the population, an FH gene can be found.  If you have this gene, your risk is higher than others at a similar cholesterol level, and for a longer period of your life of course. Therefore it is important for these patients to address this with medication and lifestyle.  Adding the genetic risk score to your overall basic CV risk factors will help to predict your actual CV risk.  This risk calculation and stratification is still being studied and looked at.   ACC/AHA Risk calculator link: cvriskcalculator.com   In summary:    ASA for primary prevention probably shouldn’t be used. Select high risk patients are okay, but avoid in the elderly.  Cholesterol:  Statin plus ezetemibe and pcsk9 for higher risk, and Ca score for  those uncertain about their risk.  DM: use the new meds with type 2 DM at high CV risk.  Genetics: not quite ready for prime time, but we need to look into this more and get ready for patients desiring this in the future.  Again, a big thanks to Dr. Miedema for joining us and for providing this cardiology update. Ridgeview appreciates his expertise, his ongoing dedication to his patients and to the cardiology specialty.

Dr. Joseph Karam, vascular surgeon and researcher with the Minneapolis Heart Institute, discusses arterial and venous diseases in a head to toe fashion, including cerebrovascular disease, aortic disease and several others.  Dr. Karam also addresses the many approaches the vascular surgeon will take to diagnose and treat these various conditions.  This talk applies to all of us working on the front lines in medicine today!  Enjoy this 1-hour CME episode at your leisure, as it is broken down into six segments, along with a brief summary at the end of each segment.  Objectives: Upon completion of this lecture/discussion, program participants will be able to: Identify various innovations in vascular surgery Recognize and discuss care continuum options for patients in need of vascular care. CME credit is only offered to Ridgeview Providers 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 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: Beyond the Heart: Recognizing and Treating Vascular Disease  (**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.)  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.”   FACULTY DISCLOSURE ANNOUNCEMENT  It is our 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. 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.

A computer tomography angiogram, otherwise known as a CT angiogram, is a mouthful to say, but this procedure can be a very useful tool for patients having heart problems. You may have heard of people getting CT angiograms, or regular angiograms, and wondered what this was, why it's done and if you need to have one. Dr. John Lesser, a cardiologist from Minneapolis Heart Institute®, is here today to tell us about this procedure, who makes a good candidate and what other options patients might have now and in the future.

Dr. Raed H. Abdelhadi, Cardiac Electrophysiologist at the Minneapolis Heart Institute at Abbott Northwestern Hospital, reviews the background for the Riata ICD recall and the available data on the Riata ICD lead, explains the preliminary results for the Riata Multicenter Study, discusses the challenges regarding screening and management and summarizes the Riata Summit.

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.

Dr. Thomas Knickelbine, Director of Preventive Cardiology at the Minneapolis Heart Institute at Abbott Northwestern Hospital discusses US population risk factors, explains how to approach patients with statin intolerance, describes the current approaches to treatment of non-HDL cholesterol and Metabolic Syndrome and outlines MHI prevention goals and future vision.

Dr. Benjamin Sun, Chair of Cardiac, Thoracic and Transplant Surgery at the Minneapolis Heart Institute at Abbott Northwestern Hospital, identifies which valves can be repaired, explains why we don't repair valves more frequently and describes when valve replacement is still preferred.

Dr. Nedaa Skeik, Vascular Medicine Consultant at the Minneapolis Heart Institute® atAbbott Northwestern Hospital, explains different treatment modalities for deep vein thrombosis (DVT), describes the history of inferior vena cava (IVC) filters, lists indications and complications (common and rare) of IVC filters, and explains identification and management of arterial pseudoaneurysm as a rare complication of IVC filters.

Dr. Barry J. Maron, Director of the Hypertrophic Cardiomyopathy Center at the Minneapolis Heart Institute at Abbott-Northwestern Hospital looks explains how to risk stratify hypertrophic cardiomyopathy (HCM) patients and describes the role of the implantable cardioverter defibrillator in HCM patients.

Senior Consulting Cardiologist at the Minneapolis Heart Institute at Abbott-Northwestern Hospital, Dr. Robert Hauser, summarizes pacing hemodynamics, describes the value of cardiac synchronization, and explains ICD reliability and patient longevity.

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

Host: Jack Lewin, MD Guest: Robert Hauser, MD Because new cardiac technologies are often rapidly integrated into clinical practice, we must be mindful that these innovations can contain a level of risk. Regrettably, we've seen examples of this before with previous generations of implantable cardioverter-defibrillators (ICD), and some experts say the latest advances in ICD technology could pose similar problems. Host Dr. Jack Lewin explores this issue with Dr. Robert Hauser, senior consulting cardiologist at the Minneapolis Heart Institute and a founder and past president of the Heart Rhythm Society.

Host: Jack Lewin, MD Guest: Robert Hauser, MD Because new cardiac technologies are often rapidly integrated into clinical practice, we must be mindful that these innovations can contain a level of risk. Regrettably, we've seen examples of this before with previous generations of implantable cardioverter-defibrillators (ICD), and some experts say the latest advances in ICD technology could pose similar problems. Host Dr. Jack Lewin explores this issue with Dr. Robert Hauser, senior consulting cardiologist at the Minneapolis Heart Institute and a founder and past president of the Heart Rhythm Society.