Podcasts about lvot

This week on The Beat, CTSNet Editor-in-Chief Joel Dunning speaks with Dr. Mario Castillo-Sang, the Surgical Director of Mitral Valve and Heart Failure Therapies at St. Elizabeth Healthcare, Edgewood, Kentucky, USA, about totally endoscopic cardiac surgery. Chapters 00:00 Intro 01:17 Minimal Access Bedside Cardiac 04:37 Lung Cancer, Histological Subtype 09:29 TAVR vs SAVR, AS & CAD 12:22 Biopros TVR Outcomes 15:48 Mitral Annular Disjunction, MVR 18:47 Ozaki Technique, AV Reconst 20:46 Redo LVOT Reconst for Endocarditis 22:33 Totally Endoscopic ASD Closure TVR 24:08 Dr. Castillo-Sang, MI Bedside Endoscopy 40:51 Closing They explore key highlights from Dr. Castillo-Sang's CTSNet series Endoscopic Cardiac Surgery Series: The Swiss Army Knife Approach, his journey in performing endoscopic surgeries, and how he learned the techniques. Dr. Castillo-Sang shares the advantages of endoscopic surgery, as well as tips and recommendations for those wanting to learn this approach. He emphasizes the importance of the instruments he has worked with, detailing how these have improved over time. Additionally, they explore Dr. Castillo-Sang's involvement with the Endoscopic Cardiac Surgeons Club, discussing how he got involved and providing details about the club's upcoming annual meeting.   Joel also highlights recent JANS articles on the estimated worldwide variation and trends in incidence of lung cancer by histological subtype in 2022 and over time, transcatheter vs surgical aortic valve replacement in Medicare beneficiaries with aortic stenosis and coronary artery disease, long-term outcomes after bioprosthetic tricuspid valve replacement, and outcomes of patients with mitral annular disjunction undergoing mitral valve repair.  In addition, Joel explores aortic valve reconstruction using the Ozaki technique, redo LVOT reconstruction for endocarditis, and totally endoscopic ASD closure with tricuspid valve repair. Before closing, he highlights upcoming events in CT surgery.   JANS Items Mentioned  1.) Estimated Worldwide Variation and Trends in Incidence of Lung Cancer by Histological Subtype in 2022 and Over Time: A Population-Based Study  2.) Transcatheter vs Surgical Aortic Valve Replacement in Medicare Beneficiaries With Aortic Stenosis and Coronary Artery Disease  3.) Long-Term Outcomes After Bioprosthetic Tricuspid Valve Replacement: A Multicenter Study  4.) Outcomes of Patients With Mitral Annular Disjunction Undergoing Mitral Valve Repair  CTSNET Content Mentioned  1.) Aortic Valve Reconstruction—The Ozaki Technique  2.) Redo LVOT Reconstruction for Endocarditis  3.) Totally Endoscopic ASD Closure With Tricuspid Valve Repair  Other Items Mentioned  1.) Endoscopic Cardiac Surgery Series: The Swiss Army Knife Approach  2.) Endoscopic Cardiac Surgeons Club  3.) Mini Heart Valves   4.) Aortic Valve Replacement Series     5.) Career Center 6.) CTSNet Events Calendar  Disclaimer The information and views presented on CTSNet.org represent the views of the authors and contributors of the material and not of CTSNet. Please review our full disclaimer page here.

JACC: Case Reports Associate Editor Maurizio Taramasso, MD, PhD, joins author Brinder S Kanda, MD, FACC to discuss their case presented at AHA and published in JACC: Case Reports. In this case, an 83-year-old female with decompensated heart failure was found to have HOCM with SAM of the mitral valve and a large P2 flail segment with ruptured cords. TEER was performed resulting in mild MR and resolution of the prior LVOT gradient. The case supports TEER for patients with medication-refractory HOCM.

JACC: Case Reports Associate Editor Maurizio Taramasso, MD, PhD, joins author Brinder S Kanda, MD, FACC to discuss their case presented at AHA and published in JACC: Case Reports. In this case, an 83-year-old female with decompensated heart failure was found to have HOCM with SAM of the mitral valve and a large P2 flail segment with ruptured cords. TEER was performed resulting in mild MR and resolution of the prior LVOT gradient. The case supports TEER for patients with medication-refractory HOCM.

CardioNerds (Dr. Yoav Karpenshif – Chair of the CardioNerds Critical Care Cardiology Council) join Dr. Munim Khan, Dr. Shravani Gangidi, and Dr. Rachel Goodman from Tufts Medical Center's general cardiology fellowship program for hot pot in China Town in Boston. They discuss a case involving a patient who presented with stress cardiomyopathy leading to cardiogenic shock. Expert commentary is provided by Dr. Michael Faulx from the Cleveland Clinic. Notes were drafted by Dr. Rachel Goodman. A young woman presents with de novo heart-failure cardiogenic shock requiring temporary mechanical circulatory support who is found to have basal variant takotsubo cardiomyopathy.  We review the definition and natural history of takotsubo cardiomyopathy, discuss initial evaluation and echocardiographic findings, and review theories regarding pathophysiology of the clinical syndrome. We also highlight complications of takotsubo cardiomyopathy, with a focus on left ventricular outflow obstruction, cardiogenic shock, and arrythmias. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Takotsubo cardiomyopathy is defined as a reversible systolic dysfunction with wall motion abnormalities that do not follow a coronary vascular distribution. Takotsubo cardiomyopathy is a diagnosis of exclusion; patients often undergo coronary angiography to rule out epicardial coronary artery disease given an overlap in presentation and symptoms with acute myocardial infarction. There are multiple echocardiographic variants of takotsubo. Apical ballooning is the classic finding, but mid-ventricular, basal, and biventricular variants exist as well. Patients with takotsubo cardiomyopathy generally recover, but there are important complications to be aware of.  These include arrhythmia, left ventricular outflow tract (LVOT) obstruction related to a hyperdynamic base in the context of apical ballooning, and cardiogenic shock. Patients with Impella devices are at risk of clot formation and stroke. Assessing the motor current can be a clue to what is happening at the level of the motor or screw. Notes What is Takotsubo Syndrome (TTS)? TTS is a syndrome characterized by acute heart failure without epicardial CAD with regional wall motion abnormalities seen on echocardiography that do not correspond to a coronary artery territory (see below).1 TTS classically develops following an acute stressor—this can be an emotional or physical stressor.1 An important feature of TTS is that the systolic dysfunction is reversible.  The time frame of reversibility is variable, though generally hours to weeks.2 Epidemiologically, TTS has a predilection for post-menopausal women, however anyone can develop this syndrome.1 TTS is a diagnosis of exclusion. Coronary artery disease (acute coronary syndrome, spontaneous coronary artery dissection, coronary embolus, etc) should be excluded when considering TTS. Myocarditis is on the differential diagnosis. What are the echocardiographic findings of takotsubo cardiomyopathy? The classic echocardiographic findings of TTS is “apical ballooning,” which is a way of descripting basal hyperkinesis with mid- and apical hypokinesis, akinesis, or dyskinesis.3 There are multiple variants of TTS. The four most common are listed below:3(1) Apical ballooning (classic TTS)(2) Mid-ventricular variant(3) Basal variant (4) Focal variant Less common variants include the biventricular variant and the isolated right ventricular  variant.3 Do patients with TTS generally have EKG changes or biomarker elevation? Patients often have elevated troponin, though the severity wall motion abnormalities seen on TTE i...

CardioNerds (Drs. Teodora Donisan, Jenna Skowronski, and Johnny Hourmozdi) discuss Cardiomyopathies with Dr. Steve Ommen. Through a case-based discussion, we review the diagnostic evaluation of suspected restrictive cardiomyopathy, and Dr. Ommen shares his expertise in the nuances of caring for patients with hypertrophic cardiomyopathy, from counseling to pharmacologic, device, and septal reduction therapies. We cover the foundations of diagnosis and management that will be helpful to CardioNerds preparing to encounter hypertrophic cardiomyopathy on the boards or on the wards. Dr. Johnny Hourmozdi drafted notes. The audio was engineered by Dr. Atefeh Ghorbanzadeh. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiomyopathies The presence of an S4 and a rapid y-descent in the jugular venous pulsation on exam should clue you to the presence of a restrictive filling pattern. Restrictive filling doesn't necessarily mean restrictive cardiomyopathy and is more commonly due to dilated or ischemic cardiomyopathy. The five main topics of counseling that every hypertrophic cardiomyopathy (HCM) patient should understand: (1) Prognosis, (2) Family Screening, (3) Risk of Sudden Death, (4) Treatments, and (5) Physical Activity. Remember 1/3: In clinical trials of cardiac myosin inhibitors for HCM (mavacamten), about a third of patients had a tremendous improvement in symptoms, another third had some improvement, and the final third had no improvement or had to discontinue the drug due to negative inotropy. When counseling patients about septal reduction therapy, consider the patient's age. For younger patients, surgical myectomy at an experienced center offers a higher success rate and greater durability with lower rates of pacemaker placement when compared to alcohol septal ablation. Historically, the conclusion that it was higher risk to be an athlete with HCM was unfortunately generalized to mean that it was high risk to exercise for patients with HCM. “And we turned a generation of HCM patients into HCM cardiometabolic syndrome patients, which is actually a worse combination.” Notes - Cardiomyopathies What is the initial approach to evaluating a patient with new or suspected cardiomyopathy, including hypertrophic cardiomyopathy (HCM)? A history and physical exam, including a thorough past medical and family history, is always the first step and helps determine the patient's risk for potential underlying etiologies, including genetic cardiomyopathies, hypertrophic cardiomyopathy, or those related to treatments of previous cancer. In terms of ECG findings, pay attention to QRS voltage (high or low) and the presence of any arrhythmias. TTE should be obtained in all patients and is often sufficient to diagnose many underlying cardiomyopathies, including HCM. Cardiac MRI (CMR) is helpful as an adjunct when TTE alone is inconclusive or imaging quality is poor. CMR can help provide a better idea of chamber sizes and wall thickness, and late gadolinium contrast enhancement (LGE) can also be helpful if present in a specific pattern, though often HCM patients may have non-specific patterns of LGE. Invasive hemodynamics assessment is reserved for patients with discordance between non-invasive testing and the clinical impression. It can also be useful to guide the management of heart failure, especially in advanced disease. How do you treat patients with hypertrophic obstructive cardiomyopathy (HOCM)? In patients with HCM and LVOT obstruction (defined a...

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

Go online to PeerView.com/UBM860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, with a mortality rate estimated to be about three times greater than that experienced by individuals of similar age without HCM. So far, the FDA has approved only one noninvasive treatment option indicated for the treatment of HCM—a first-in-class cardiac myosin inhibitor (CMI) called mavacamten. A second CMI, aficamten, is currently being studied. As timely diagnosis of patients with HCM may reduce or delay the need for invasive treatment, these treatment options are essential for cardiologists to understand. This PeerView activity covers what you need to know about diagnosing and managing HCM for optimal patient care. A patient case threads through each section and offers a window into real-world diagnostic and treatment challenges as our expert shares guidance and the latest evidence. By the end of this activity, you will be able to explain the underlying pathophysiology of HCM, apply your new knowledge for timely diagnosis and individualized treatment of HCM, and implement strategies for long-term patient safety and improved outcomes. Upon completion of this activity, participants should be better able to: Apply current guidance and the latest evidence to support accurate differential diagnosis and encourage early treatment in patients suspected of having HCM; Evaluate the efficacy and safety evidence supporting the ability of modern targeted strategies to address the underlying pathophysiology of HCM; Individualize treatment of HCM based on patients' personal preferences and goals of care and identify opportunities to reduce inequities; and Implement strategies that encourage and support regular assessment of clinical status, LVEF, and LVOT gradient in patients with HCM, consulting with specialty colleagues as needed.

The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Eldrin Lewis.Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #26 A 45-year-old man presents to cardiology clinic to establish care. He has had several months of progressive dyspnea on exertion while playing basketball. He also reports intermittent palpitations for the last month. Two weeks ago, he passed out while playing and attributed this to exertion and dehydration. He denies smoking and alcohol intake.   Family history is significant for sudden cardiac death in his father at the age of 50 years. Autopsy has shown a thick heart, but he is unaware of the exact diagnosis. He has two children, ages 12 and 15 years old, who are healthy.   Vitals signs are blood pressure of 124/84 mmHg, heart rate of 70 bpm, and normal respiratory rate. On auscultation, a systolic murmur is present at the left lower sternal border. A 12-lead ECG showed normal sinus rhythm with signs of LVH and associated repolarization abnormalities. Echocardiography reveals normal LV chamber volume, preserved LVEF, asymmetric septal hypertrophy with wall thickness up to 16mm, systolic anterior motion of the anterior mitral valve leaflet with 2+ eccentric posteriorly directed MR, and resting LVOT gradient of 30mmHg which increases to 60mmHg on Valsalva.   You discuss your concern for an inherited cardiomyopathy, namely hypertrophic cardiomyopathy. In addition to medical management of his symptoms and referral to electrophysiology for ICD evaluation, which of the following is appropriate at this time? A  Order blood work for genetic testing B  Referral for genetic counseling C  Cardiac MRI D  Coronary angiogram E  All of the above Answer #26 Explanation   The correct answer is B – referral for genetic counseling.  Several factors on clinical evaluation may indicate a possible underlying genetic cardiomyopathy. Clues may be found in: ·       Cardiac morphology – marked LV hypertrophy, LV noncompaction, RV thinning or fatty replacement on imaging or biopsy ·       12-lead ECG – abnormal high or low voltage or conduction, and repolarization, altered RV forces ·       Presence of arrhythmias – frequent NSVT or very frequent PVCs, sustained VT or VF, early onset AF, early onset conduction disease ·       Extracardiac features – skeletal myopathy, neuropathy, cutaneous stigmata, and other possible manifestations of specific syndromes In select patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). In first-degree relatives of selected patients with genetic or inherited cardiomyopathies, genetic screening and counseling are recommended to ...

Commentary by Dr. Julia Grapsa, Edoardo Zancanaro, and Sebastian Ludwig

In Whom Should LVOT/Aortic Root Enlargement Be Performed at the Time of AVR Guest: Juan A. Crestanello, M.D. Host: Kyle W. Klarich, M.D. (@KyleWKlarich) Whom should an LVOT and/or Root Enlargement be performed at the time of an aortic value replacement? You will learn what a root enlargement is, why and how it is done, things to avoid, what to allow for in the future. You will hear what the risks of performing a root enlargement are and if it can be done in a redo surgery as well as its alternatives.  Joining us today to discuss In Whom Should LVOT/Aortic Root Enlargement Be Performed at the Time of AVR is Juan A. Crestanello, M.D., Professor of Surgery, Chair of the Department of Cardiovascular Surgery at Mayo Clinic in Rochester, Minnesota. Specific topics discussed: What is an aortic root enlargement? How is it done? Why do a root enlargement? Avoid patient prosthesis mismatch, allow for ViV in the future, prevent structural valve deterioration What is the risk of performing a root enlargement? Can you do a root enlargement in a redo surgery? What are the alternatives to a root enlargement? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV. NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Being Dynamic is usally a great thing... but not when youre crushing the only good way out of the left ventrile.  In this episode we cover dynamic obstruction of the LVOT (specifically sub-valvular): what is it? who gets it? What to do about it. We missed ya'll, so come have alisten and brush up on a rare but important phenomena in our critically ill patients.

A first-in-class allosteric and reversible inhibitor selective for cardiac myosin approved based on the results of the EXPLORER-HCM trial, mavacamten was approved for the treatment of adults with symptomatic NYHA class 2-3 obstructive hypertrophic cardiomyopathy after their phase 3 data indicated use was with improved exercise capacity, LVOT obstruction, NYHA functional class, and health status patients with oHCM.  In the latest edition of Don't Miss a Beat, hosts Stephen Greene, MD, and Muthiah Vaduganathan, MD, MPH, are joined by special guest Anjali Owens, MD, of Penn Medicine. An assistant professor of medicine in the Division of Cardiology and medical director of the Center for Inherited Cardiac Disease at the Perelman School of Medicine, Owens is a leading researcher in oHCM with real-world clinical experience treating the disease. During the episode, Owens takes our hosts on a deep dive into the disease state from her perspective. 

CardioNerd (Amit Goyal) join Emory University School of Medicine cardiology fellows (Sonali Kumar, John Lisko, and John Ricketts) for a lovely stroll on the BeltLine in Atalanta, GA. They discuss an interesting case of severe mitral stenosis treated with Valve-in-MAC transcatheter mitral valve replacement (TMVR) with LAMPOON. Drs. Vasilis Babaliaros and Adam Greenbaum provide the E-CPR and program director Dr. B. Robinson Williams III provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media ABCDEFGHI JKClick to Enlarge A. CXRB. ECGC. TTE: Trasns-mitral PW Doppler D. Laceration in swineE-F: CT planningG. Transeptal catheters H. Trans-mitral PW Doppler (post procedure) I. LVOT gradients J-K. Post procedure CT TTE 1 TTE 2 TTE 3 TEE 1 TEE 2 Fluoroscopy 1 Fluoroscopy 2 Fluoroscopy 3 TEE 3 Fluoroscopy 4 TEE 4 TEE 5 Fluoroscopy 5 Fluoroscopy 6 Fluoroscopy 7 TEE 6 TEE 7 https://youtu.be/1gUyat6pg30 LAMPOON Procedure Episode Schematics & Teaching Coming soon! Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

CardioNerds (Amit Goyal & Daniel Ambinder) join Virginia Commonwealth University (VCU) cardiology fellows (Ajay Pillai, Amar Doshi, and Anna Tomdio) for a delicious skillet breakfast and amazing day in Richmond, VA! They discuss a fascinating case of a patient with Wolff-Parkinson-White (WPW) and hypertrophic cardiomyopathy (HCM). Dr. Keyur Shah provides the E-CPR and program director Dr. Gautham Kalahasty provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s presented to the ED after an episode of unwitnessed syncope while drinking. Patient had suddenly passed out from a seated position with no prodrome or post-ictal state. He had episodes like this in the past, which were thought to be seizures, but otherwise PMHx only notable for alcohol use disorder. He denied any FH of SCD or syncope. In the ED, exam was unremarkable. Labs notable for mild thrombocytopenia, mild hyponatremia with AKI, 2:1 AST/ALT ratio, elevated NT-proBNP, and a very high lactate that rapidly corrected with fluids. EKG was notable for sinus tachycardia, short PR interval, wide QRS, and delta waves consistent with Wolff-Parkinson-White (WPW) pattern. Echo showed preserved LVEF, thickened LV septum (1.6 cm) and posterior wall (1.3 cm) concerning for hypertrophic cardiomyopathy (HCM). No outflow tract gradient was noted at rest or with stress, and the strain pattern demonstrated apical sparing. Evaluation for cardiac amyloid, including plasma cell dyscrasia and PYP scan, was negative. Cardiac MRI confirmed severely thickened LV inferior and inferolateral walls at 1.7 cm with no LVOT obstruction. 25% of the myocardium demonstrated patchy LGE.   Due to concern for WPW syndrome, the patient underwent an EP study. This revealed a malignant septal accessory pathway that was successfully ablated with resolution of the WPW EKG features. Given large LGE burden in setting of HCM, patient underwent placement of primary prevention ICD. Genetic testing for PRKAG2 mutation is pending given comorbid WPW and HCM.  Case Media ABCDEFClick to Enlarge A. CXR: Slightly increased interstitial markings in the lung bases, an elevated right hemidiaphragm. No acute airspace disease or pulmonary edemaB. ECG: Sinus tachycardia rate 120bpm, PR interval 80ms, QRS 130ms, WPW pattern.  Arruda algorithm localizes to posterior septum.C. CMR:  Myocardium nulls before blood pool.D. CMR:  Delayed gadolinium enhancementE. Follow up ECG: NSR 78, repolarization abnormalities.  T wave memory inferior leads.F.

In this episode, we cover the presentation, clinical signs / symptoms and workup of takotsubo cardiomyopathy. Come take a listen so you'll never miss that octopus-trap of a clinical confounder, with juicy pearls around LVOT obstruction.

This week we delve into the world of cardiomyopathy and also stress echo to review a recent work from the team at Boston Children's on stress echo and its role in the assessment of the pediatric HCM patient. We speak with Assistant Professor of Pediatrics Ming Hui Chen of Harvard University about a recent work she co-authored on this modality in children with HCM. Are changes in the LVOT gradient with exercise associated with differences in medium term outcome? Dr. Chen provides the answers this week. doi: 10.1016/j.echo.2020.01.020

This week we delve into the world of cardiomyopathy and also stress echo to review a recent work from the team at Boston Children's on stress echo and its role in the assessment of the pediatric HCM patient. We speak with Assistant Professor of Pediatrics Ming Hui Chen of Harvard University about a recent work she co-authored on this modality in children with HCM. Are changes in the LVOT gradient with exercise associated with differences in medium term outcome? Dr. Chen provides the answers this week. doi: 10.1016/j.echo.2020.01.020

First, there are two proposed mechanisms of CPR, brilliantly summarized in this paper: Cardiac Pump Mechanism: “blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.” Thoracic Pump Mechanism: “With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.” It is likely that both mechanisms are at play: …In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory. Is there any evidence that M-CPR Devices improve outcomes – since they’re marketed as “life saving devices”? A Meta Analysis from Gates et. al. concluded: Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest. However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse. Gonzales et. al. compared “pit crew” resuscitation with “scripted” mCPR implementation and found: In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge. Why might this be the case? We know based off work by Hwang et. al. who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients! In another study, anderson et. al. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root.  All of these studies and more are explained in a wonderful video created by Felipe Teran: The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR: TEE to save lives, guide compressions, and guide interventions Pt 1. #FOAMED.  p.s. – checkout cabofest2018.com  But, how do we do we know that we’re compressing the LV without TEE? Well, we don’t exactly. However, Qvigstad E et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.” They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2. They found that there’s not “one superior hand position”, and that optimal positioning varies: How does this explain when we should place mCPR? It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle.  Are we applying mCPR too early? Poole et. al discuss this in a paper titled: Mechanical CPR: Who? When? How? In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5) The authors continue and note that… subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p 

Dr Paul Wang:                   Welcome to the monthly podcast On the Beat, for Circulation: Arrhythmia, and Electrophysiology. I'm Dr Paul Wang, editor-in-chief, with some of the key highlights from this month's issue.                                                 In our first paper, Elizabeth Saarel and associates describe the analysis of athletes in the ICD sports registry. The authors found that over a median follow-up of 42 months of 129 young athletes, and a mean age of 16 years, there were 35 athletes, or 27%, that received a total of 38 shocks. Long QT syndrome and hypertrophic cardiomyopathy were the most common diagnoses. While shocks related to competition and practice were not uncommon, there were no serious adverse sequelae. Lead malfunction rates were similar to previously reported in an unselected pediatric ICD populations. There were no occurrences of death, arrest, injury related to arrhythmia during sports. There was one ventricular tachycardia ventricular fibrillation storm during competition.                                                 In our next paper, Kedar K. Aras and associates theorize that the tissue volume to wavelength volume ratio is important in determining ventricular fibrillation sustainability. They perform panoramic optical mapping of coronary perfused human left ventricular wedge preparations, which were subjected to acts of potential duration changes produced by IK,ATP agonist pinacidil and antagonist glybenclamide. They found that pinacidil and escalating concentrations progressively decreased the volume wavelength in ventricular fibrillation became sustained when the tissue volume to wavelength ratio was above the safety factor, K equals 4.4. In addition, ventricular fibrillation was only sustained when the ventricular volume exceeded the critical wavelength volume defined by the product of pacing cycle wave length in the longitudinal transverse and transmural directions.                                                 In our next paper Thomas Deneke and associates examine the ability of a novel infrared thermal probe to predict endoscopically detected thermal esophageal lesions post atrial fibrillation ablation. They studied six patients undergoing their first pulmonary vein isolation, using radio frequency point by point catheter ablation in the HEAT-AF study; 12 or 19% of patients had endoscopically detected thermal esophageal lesions. The peak esophageal temperature Tpeak was significantly higher, 56.3 degrees Celsius versus 45.7 degrees Celsius. P less than 0.0001 in patients with endoscopically detected thermal esophageal lesions compared to those without lesions. Logistical regression analysis demonstrated Tpeak was a statistically significant predictor, P equals 0.0008 pf endoscopically detected thermal esophageal lesions with an odds ratio of 1.52.                                                 In our next paper Dian Cheng and associates examine a novel algorithm incorporating right precordial and posterior leads to discriminate between left ventricular outflow tract and right ventricular outflow tract foci. The V3R to V7 index was prospectively tested in consecutive patients at four centers. In 94 patients of the validation cohort with 79% RVOT foci, a QS pattern in lead V3R exclusively recorded in right ventricular outflow tract foci, while an S wave in V3 was exclusively recorded in left ventricular outflow tract foci. The V3R to V7 index of LVOT origin was significantly great than that of RVOT 1.05 versus 0.28 P, less than 0.001 with a V3R to V7 index of greater than equal to 0.85 predicting an LVOT origin with 87% sensitivity and 96% specificity. With the V3R to V7 index of 0.85 or greater RVOT origin could be excluded with 98.6% accuracy.                                                 In the next paper Jim Cheung and associates examine the in-hospital outcomes, cause, and thirty-day readmissions following catheter ablation of MI associated ventricular tachycardia. The authors use a nationwide readmissions database to evaluate 4109 admissions for catheter ablation of MI associated ventricular tachycardia occurring between 2010 and 2015. The index admission in-hospital mortality rate was 2.7% and the procedural complication rate after ventricular tachycardiablation was 11.5%. Pulmonary hypertension, lung disease, obesity and coagulopathy were independent predictors of mortality. Following discharge after VT ablation the thirty-day readmission rate was 19.2%. With the median time to readmission of 10.0 days, in an in-hospital mortality of 2.9%. Cardiac causes accounted for 74% of readmissions. With ventricular tachycardia accounting for 41% of admissions and congestive heart failure accounting for 14% of readmissions. Pulmonary hypertension, congestive heart failure, smoking, chronic pulmonary disease, and prolonged index hospitalization were significant independent predictors of thirty-day readmission. After adjustment thirty-day readmissions were associated with a 38.9% increase in cumulative hospitalization costs.                                                 In the next paper Tomofumi Nakamura and associates examine the relation of hemorrhagic and thromboembolic events with anticoagulations strategy in the setting of epicardial axis procedures for ventricular arrhythmia mapping and ablation. In 355 patients oral anticoagulants were stopped perioperatively in heparin administered prior to the procedure. The patients were divided to three groups per the anticoagulations strategy. Group 1, no heparin was administered before pericardial access, Group 2, heparin was administered in reverse before pericardial access, and Group 3 heparin was administered and not reversed. Significant pericardial bleeding defined is greater than 80 milliliter occurred in 46 cases or 13% and did not differ among the three groups. Unintentional cardiac puncture in left ventricular chest infraction less than [inaudible 00:07:32] 35% were independently associated with pericardial bleeding with an odd ratio of 16.4 or 2.28. Of 38 procedures with unintentional cardiac puncture there were no differences in pericardial bleeding for different anti-coagulant strategies. Thromboembolic events occur in 5 patients, 1 coronary embolism, 1 stroke, 2 deep vein thrombosis, and 1 fatal pulmonary embolism and 1 thrombus on a temporary ventricular assist device.                                                 In the next paper, Elisabeth Mouws and associates examine whether the combination of lines of conduction block with multiple wave fronts at the pulmonary vein area may result in increased arrhythmogenicity and susceptibility to atrial fibrillation. The author performed intra-operative high-density epicardial mapping of pulmonary vein area and is 450 sites with an intra-electrical distance of 2 milliliters which performed during sinus rhythm in 327 patients. With and without preoperative intra-fibrillation. Excitation of the pulmonary vein area occurred via multiple consecutive wave fronts in the vast majority, 81% of patients. In total 561 wave fronts were observed which propagated through the septal or paraseptal regions tore the pulmonary vein area in 82%. Substantial dissociation of consecutive wave fronts was observed with delta activation times of 10.6 milliseconds. No difference was observed in delta activation times of consecutive wave fronts during sinus rhythm between patients with and without atrial fibrillation. In excitation-based risk factor model including conduction delay of greater equal to 6 millimeters conduction block of greater than or equal to 6 millimeters and conduction delay conduction block of 16 millimeters or greater, wave fronts vie the posterior inferior and posterior superior in multiple opposing wave fronts demonstrated a 5-fold risk of atrial fibrillation when multiple risk factors were present.                                                 In our final paper Yoshitaka Kimura and associates examine the prognostics significance of PR interval prolongation on adverse cardiac events. They studied 176 patients with repaired tetralogy of flow with a median age of 17.4 years then they evaluated their correlation with right ventricular volume and function measured by cardiac magnetic resonance and the significance as a risk factor of adverse cardiac events were ventricular arrhythmias, atrial arrhythmias, heart failure, hospitalization, complete AV block, and all cause death. First degree AV block was noted 25 patients or 14% during a median follow-up of 10 years there was a progressive prolongation of PR interval 2.0 milliseconds per year. Importantly there were significant correlations between PR interval prolongation and right ventricular enlargement or right ventricular disfunction. In contrast, patients who underwent pulmonary valve replacement, N equal 23, significant shortening of PR interval was noted, 204 versus 176 milliseconds, P equals 0.007. Cox regression analysis showed that the first degree AV block was an independent risk factor for ventricular arrhythmias hazard ratio 5.479, in complete heart block, hazard ratio 27.67, and it had a tendency for heart failure hospitalization, hazard ratio 3.3. In addition PR interval prolongation greater than 2 millisecond per year was also a significant risk factor for ventricular arrhythmias regardless of the presence or absence of first degree AV block in enrollment.                                                 That's it for this month. We hope that you will find the journal to be the go to place for everyone interested in the field. See you next time.

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

Figuring out if your patient will benefit from more IV fluid is paramount. The ultrasound assessment of volume responsiveness is a topic that is always full of controversy.  Here, I talk about one of the many techniques: LVOT VTI. 

TSRA Podcast: Congenital - LVOT Obstruction (Charles Cole & Jim Jaggers) by TSRA

Augmentation by Echo. Deidre Murphy examines advanced aspects of bedside echocardiography, and the immense amount of information it provides in a critical care setting.