Cardionerds: A Cardiology Podcast

CardioNerds

Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!

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44 snips

Aug 23, 2022 • 42min

229. CardioNerds Rounds: Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins

It’s another session of CardioNerds Rounds! In these rounds, Dr. Stephanie Fuentes (EP FIT at Houston Methodist) joins Dr. Hugh Calkins (Professor of Medicine and Director of the Electrophysiology Laboratory and Arrhythmia Service at Johns Hopkins Hospital) to discuss the nuances of atrial fibrillation (AF) management through challenging cases. As an author of several guideline and expert consensus statements in the management of AF and renowned clinician, educator, and researcher, Dr. Calkins gives us many pearls on the management of AF, so don’t miss these #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Challenging Cases – Atrial Fibrillation with Dr. Hugh Calkins Case #1 Synopsis: A woman in her mid-60s presents with symptomatic paroxysmal atrial fibrillation (AF). An echocardiogram has demonstrated that she has a structurally normal heart. Her primary care doctor had started Metoprolol 50 mg twice a day but she has remained symptomatic. In office, an EKG confirms AF, but she converts to sinus while there. She is seeking advice to prevent further episodes and in general wants to avoid additional medications Case #2 Takeaways We discussed several potential options for treatment. Amongst the first things we discussed was amiodarone. In a patient of this nature without structural heart disease and under the age of 70, Dr. Calkins discussed that he would probably consider amiodarone as a 2nd line option. While amiodarone may be effective in maintaining sinus rhythm in comparison to other antiarrhythmic medications like sotalol, flecainide, and propafenone, it does have significant toxicity. If antiarrhythmic drugs (AAD) were to be considered, we also discussed the options of dofetilide versus sotalol. Dofetilide typically requires inpatient initiation due to the risk of QT prolongation and Torsades. Since women tend to have longer corrected QT (QTc) intervals, high dose dofetilide may be more proarrhythmogenic in women. Though, Dr. Calkins noted that many patients don’t tolerate sotalol due to fatigue and generally dofetilide is well tolerated. When it comes to the “pill in the pocket” approach, Dr. Calkins noted that its utility is more so in patients with persistent AF that is known to not stop on its own. For instance, an individual who has AF a few times a year that is persistent may benefit from flecainide or propafenone (“in the pocket”) instead of being brought in for an electrical cardioversion. In this scenario, the first time one of these agents is used, the patient ought to be closely monitored. For our patient, her episodes were too frequent and self-terminating for a “pill in the pocket” approach to be effective. Current guideline recommendations for catheter ablation include a Class IA recommendation for patients with paroxysmal AF refractory to AADs, and a Class IIA recommendation as first-line therapy for patients with paroxysmal AF. In the 2020 ESC Atrial Fibrillation Guidelines, catheter ablation is given a Class IA recommendation to improve symptoms of AF recurrences in patients who have failed or are intolerant of one Class I or III AADs. For patients who have failed or have been intolerant of beta blocker alone for rhythm control, catheter ablation is given a Class IIA recommendation. As first-line therapy in paroxysmal AF, catheter ablation is given a Class IIA recommendation as well. Of note, three recent trials have demonstrated catheter ablation as first line therapy is reasonable and newer guidelines will reflect this. Specifically, EARLY-AF compared ablation (cryoablation) vs AAD (mainly with flecainide/propafenone) as a first line therapy. The cryoablation arm showed significantly less recurrence of AF at one year The guidelines clearly state that aligning the treatment plan with the patient’s goals and risk tolerance are paramount. Catheter ablation does have potential complications such as pericardial effusion or access-related issues, though these are rare. Furthermore, as time has passed, catheter ablation success rates have improved. Up and coming techniques such as electroporation may be game-changing with regards to success rate and safety. Waiting times for a procedure may be an issue, so one could consider an AAD, such as flecainide, as a standing dose awaiting the procedure. Regarding predictors of success for catheter ablation, Dr. Calkins noted that the key factor was type of AF. With paroxysmal AF there is roughly 70-80% success rate with the 1st procedure, 50-70% with persistent AF, and 30-50% with longstanding persistent AF. Other predictors of success include BMI (higher BMI associated with a lower success rate and a higher rate of complications), left atrial size (with a linear dimension of ≥ 5.5 cm indicating less likelihood of success), age, and obstructive sleep apnea. One of the questions that was raised was screening for structural heart disease before starting flecainide/propafenone. Typically, an EKG and TTE are done, and if they are not suggestive of structural heart disease, Dr. Calkins noted it would be reasonable to use these agents. With increasing age, there’s increased risk of subclinical CAD, though it is not in the guidelines to perform functional testing or anatomic imaging prior to starting these agents. Finally, Dr. Calkins noted as an aside that in patients with sick sinus syndrome, management in the past has involved placing a permanent pacemaker (PPM) followed by AAD agents. However, catheter ablation may be a better option because it treats AF and improves the sinus rate because of its effect on the autonomic system, eliminating pauses that would have otherwise warranted a pacemaker. After ablation, the resting HR can improve 10-30 bpm and this can be a marker of successful catheter ablation. Case #2 Synopsis: A man in his mid-60s with a history of surgically placed bioprosthetic AVR, CAD with prior CABG, newly diagnosed ischemic cardiomyopathy with LVEF 20-25% with imaging revealing reversible ischemia in multiple coronary territories, presented to the clinic with dyspnea in the setting of persistent AF now 6 weeks after multi-vessel PCI. Other relevant information is that he appears congested in clinic and his EKG demonstrates a left bundle branck block (LBBB) with QRS at 172 ms. He seeks your opinion for management options. Case #2 Takeaways Dr. Calkins discussed that the only safe AAD in this circumstance would be Amiodarone, and that the risk of developing complete heart block (CHB) in a patient with LBBB placed on amiodarone is not high enough to preclude its use. One strategy would be to give this patient an amiodarone load followed by direct current cardioversion (DCCV). Following DCCV, if the patient maintains sinus rhythm, one could consider continuing with amiodarone at a lower dose or pursuing catheter ablation as a next strategy. Dr. Calkins emphasized understanding the temporal relationship between AF and HF in patients with reduced ejection fraction. In patients with new-onset AF and reduced EF, aggressive rhythm control with catheter ablation would be warranted because there is a higher likelihood of improving the cardiomyopathy. Another option to consider in patients with HFrEF and permanent atrial fibrillation that remain symptomatic or who have had hospitalizations with HF is AV node ablation with cardiac resynchronization therapy, though for a patient like this other viable treatment options remain to be tested. Regarding an ICD, the patient may recover their EF post-revascularization and implementation of guideline-directed therapy. Thus, with ischemic cardiomyopathy post revascularization, the decision to place an ICD should wait 90 days. Furthermore, the EF may improve with control of the AF. Case #3 Synopsis: A woman in her mid-80s with hypertension and recent COVID-19 pneumonia is admitted to the hospital with hypoxia, reduced LVEF and found to have AF with rapid ventricular response. The patient’s underlying conditions were treated and attempts at ventricular rate control were attempted but limited by blood pressure. A DCCV with amiodarone loading was also attempted but failed to maintain sinus rhythm. Case #3 Takeaways Some feasible options in this circumstance include further loading with amiodarone and reconsidering another DCCV versus an AV node ablation with permanent pacemaker implantation if medical therapies are limited or failing. Digoxin use for rate control alone in critically ill patients is typically discouraged. This is because we now know that its mechanism of action involves raising vagal tone and acutely ill patients typically have low vagal tone so it may not be helpful. However, in patients with rapid AF and HF, it is reasonable to use it. When used in combination with amiodarone, one may reduce the dose of digoxin in half given its drug-drug interaction Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Aug 17, 2022 • 54min

228. Narratives in Cardiology: Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni – New Jersey Chapter

In this episode, Daniel Ambinder (CardioNerds Co-Founder), Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital), Dr. Eunice Dugan (Cardiology fellow at Cleveland Clinic) and Dr. Zarina Sharalaya (Interventional and Structural Cardiologist at North Texas Heart) learn from the Dr. Sheila Sahni (Interventional Cardiologist and Director of The Women’s Heart Program at The Sahni Heart Center) regarding radiation safety in the cath lab and methods of reducing radiation exposure to the operator. She also discusses radiation safety for the pregnant interventional cardiologist and how to safely manage pregnancy during the gestational period. We hear her inspirational journey as a female interventional cardiologist and her experience in starting the Women’s Heart Program at Sahni Heart Center. Special message by Dr. Jeff Lander, New Jersey ACC Chapter Governor. Audio editing by CardioNerds Academy Intern, Pace Wetstein. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://youtu.be/iIwnsu6qJ4k Tweetorial – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://twitter.com/gurleen_kaur96/status/1563608232211296256?s=21&t=iay5zosSBDjPBLWJ4kWIAw Quoatables – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni “Having anyone who can believe in you when you are really passionate about something is really all you need… the passion is what’s going to carry you through. It’s not about being male or female or pregnant or not pregnant, it’s about what you love to do and how can you master it.” “Our careers can wait, but family planning cannot. If you are fortunate enough to have the opportunity to start a family even if it’s during your training, you should”. Notes – Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni What are procedural techniques to utilize during a heart catheterization to reduce radiation exposure to the operator? Decrease number and length of cine acquisitions and fluoroscopy time Decrease the frame rate – halving the frame rate reduces radiation dose by 50% Decrease the distance between the image intensifier and the patient Limit steep LAO angulations Apply collimation as much as possible which reduces overall patient dose and scatter radiation Limit digital magnification which can increase skin dose exposure by 50% What are the important dose limits to consider for a pregnant female and her fetus in the cath lab? The US Nuclear Regulatory Commission (NRC) regulatory equivalent dose limit is 5mSv during the entire pregnancy of the declared pregnant woman. The annual natural background radiation dose in the US is 3mSv. The average under-lead dose to a working pregnant interventionalist over the entire gestation is ~0.3mSv. The fetus of a working pregnant interventionalist is estimated to receive ~0.09mSv over an entire gestation. What are the ways in which pregnant women can protect themselves and the fetus from radiation exposure in the cath lab? Disclose (confidentially if desired) pregnancy to the radiation safety office to ensure fetal protection Wear an additional dosimeter underneath the lead apron at waist level to track fetal radiation dose Decrease occupational exposure via radiation protection measures as summarized below What are important considerations for lead apron use in the cath lab to maximize radiation protection? Make sure your lead fits! Do not sit in your lead- sitting in lead can lead to cracks which can decrease protection Hang up your lead when not being used Consider shoulder pads/arm sleeve addition to lead apron to protect breast tissue Ensure that your lead apron is undergoing periodic screening to monitor for defects Consider lead thickness – 0.5mm thickness attenuates 98-99.5% of scattered radiation, 0.35mm thickness attenuates 95-96% of scattered radiation References Sahni S, Chieffo A, Balter S. Women as one. Radiation Safety in the Practice of Cardiology. https://rad.womenasone.org/. Accessed March 31, 2022. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

4 snips

Aug 14, 2022 • 1h 6min

227. CCC: Positive Pressure Ventilation in the CICU with Dr. Sam Brusca, Dr. Chris Barnett, and Dr. Burton Lee

The modern CICU has evolved to include patients with complex pulmonary mechanics requiring more non-invasive and mechanical ventilation. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founder Dr. Amit Goyal were joined by FIT lead, Dr. Sam Brusca, who has completed his NIH Critical Care and UCSF Cardiology fellow and currently faculty at USCF. We were fortunate enough to have two expert discussants: Dr. Burton Lee, Head of Medical Education and Global Critical Care within the National Institutes of Health Critical Care Medicine Department and master clinician educator with the ATS Scholar’s Critical Care for Non-Intensivists program, and Dr. Chris Barnett, ACC Critical Care Cardiology council member and Section Chair of Critical Care Cardiology at UCSF. In this episode, these experts discuss the basics of mechanical ventilation, including the physiology/pathophysiology of negative and positive pressure breathing, a review of ventilator modes, and a framework for outlining the goals of mechanical ventilation. They proceed to apply these principles to patients in the CICU, specifically focusing on patients with RV predominant failure due to pulmonary hypertension and patients with LV predominant failure. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Positive Pressure Ventilation in the CICU Respiratory distress, during spontaneous negative pressure breathing can lead to high transpulmonary pressures and potentially large tidal volumes. This will increase both RV afterload (by increasing pulmonary vascular resistance) and LV afterload (by increasing LV wall stress). An analogy for the impact of negative pleural pressure during spontaneous respiration on LV function is that of a person jumping over a hurdle. The height of the hurdle does not increase, but the ground starts to sink, so it is still harder to jump over. Intubation in patients with right ventricular failure is a tenuous situation, especially in patients with chronic RV failure and remodeling (increased RV thickness, perfusion predominantly during diastole, RV pressure near or higher than systemic pressure). The key tenant to safe intubation is avoiding hypotension, utilizing induction agents such as ketamine or etomidate, infusing pressors, and potentially even performing awake intubations. Non-invasive positive pressure ventilation in HFrEF has hemodynamic effects similar to a cocktail of IV inotropes, dilators, and diuretics. CPAP decreases pulmonary capillary wedge pressure (LV preload), decreases systemic vascular resistance (afterload), and increases cardiac output. Airway pressure during mechanical ventilation is based on the “equation of motion”: Pressure = Volume/Compliance + Flow*Resistance + PEEP. Our goals of oxygenation on mechanical ventilation include achieving acceptable PaO2/Sat with the lowest FiO2 possible (avoiding oxygen toxicity) and optimal PEEP (which increases oxygenation but can have detrimental impact on cardiac output) Our goals of ventilation on mechanical ventilation include achieving acceptable pH and PaCO2 while preventing ventilator induced lung injury and avoiding auto-PEEP. We prevent lung injury by reducing tidal volume (ideally <8cc/kg, plateau pressure < 30 cmH20, driving pressure < 15 cmH20) and auto-peep by reducing respiratory rate (and allowing for full expiration). No ventilator mode is “superior” to the others. What is most important is that providers are comfortable with the applied mode and able to appropriately respond to active changes in patient effort and mechanics. Show notes – Positive Pressure Ventilation in the CICU 1. What are the hemodynamic effects of Negative Pressure breathing in the RV and LV? RV – Negative pleural pressure is transmitted to pericardium and RV – Negative pleural pressure is also transmitted to the pulmonary vasculature – Thus, the pressure drop is net neutral across the RV-PA circuit and does not affect afterload – However, large negative pleural pressure swings still lead to increased transpulmonary pressure, increased lung volumes, and associated increased PVR (RV afterload). LV – Negative pleural pressure is transmitted to the pericardium and LV – Negative pleural pressure is NOT transmitted to the extra-thoracic aorta – Transmural pressure across the LV increases and the gradient for flow from LV to distal aorta decreases (as LV pressure drops but distal aorta doesn’t) – Overall, this increases LV afterload What are the hemodynamic effects of Positive Pressure breathing on the RV and LV? RV – Positive pressure is transmitted to the pericardium and the RV – Positive pressure is transmitted to the pulmonary vasculature – Thus, the pressure increase is net neutral across the RV-PA circuit and does not affect afterload – However, positive pressure and increased transpulmonary pressure with instilled flow/volume increases PVR (RV afterload) – Notably, PVR and lung volume can graphically be illustrated as a U-shaped curve. PVR initially decreases as volume is instilled toward functional residual capacity (FRC), with traction of extra-alveolar vessels. As lung volume increases above FRC, PVR increases, with intra-alveolar vessel compression LV – Positive pressure is transmitted to the pericardium and the LV – Positive pressure is NOT transmitted to the extra-thoracic aorta – Transmural pressure across the LV decreases and the gradient for flow from LV to distal aorta increase (as LV pressure increases but distal aorta doesn’t) – Overall, this decreases LV afterload 2. Is NIPPV useful in in patients with heart failure? – Though studies have been inconsistent, there is likely a benefit (reducing intubation +/- mortality) for implementing NIPPV in acute decompensate heart failure – Given the hemodynamic benefits outlined above, positive pressure administered via modalities such as CPAP and Bi-PAP improve LV function – Preload decreases (positive pressure decreases inflow into the RA), Wedge pressure decreases, SVR decreases, and Cardiac output increases – CPAP is primarily needed for oxygenation; however, Bi-PAP can augment ventilation and of-set increased work of breathing – Importantly, NIPPV should not unnecessarily delay intubation in patients who are failing, as this delay likely increases mortality across patient populations. 3. What are the Oxygenation Goals of Mechanical Ventilation? – To achieve acceptable PaO2 and SaO2 (>65 mmHg, >92-94%), whilst avoiding inspired oxygen toxicity (FiO2 > 60%) – Oxygenation is primarily impacted by FiO2 and PEEP. PEEP can be titrated to aide in reducing FiO2, though can have negative impacts on cardiac output by reducing venous return 4. What are the Ventilation Goals of Mechanical Ventilation? – To achieve acceptable PCO2 and pH without causing harm (ventilator induced lung injury) – We avoid ventilator induced lung injury by reducing tidal volume (ideal < 8 cc/kg), reducing mechanical power (respiratory rate), reducing plateau pressure (< 30 cmH20), reducing driving pressure (< 15 cmH20), and reducing repeated alveolar opening/closing (by having adequate lung recruitment) – Ventilation is primarily impacted by TV and respiratory rate, which equate to minute ventilation 5. How can we calculate Airway Pressure using the Equation of Motion as related to Mechanical Ventilation? Airway Pressure = V/C + FxR + PEEP V/C = TV/Compliance and represents the alveolar pressure of the lung generated by a given TV at a given static lung compliance FxR = Flow x Resistance and is akin to Ohm’s law (V=IR), representing the pressure due to dynamic/resistive forces in the larger airways PEEP is the pressure stating point at the beginning of the inspiration 6. What considerations need to be taken when intubating a patient with RV Failure/Pulmonary Hypertension? – Intubation should be avoided if possible (though notably, respiratory distress and spontaneous breathing is not necessarily preferable, especially in the setting of respiratory acidosis or excessively low lung volumes) – Reliable vascular access and in-line pressors are key to avoiding hypotension during induction – Rapid sequence intubation (RSI) drugs such as etomidate and ketamine are preferred to propofol – Awake intubation is safest if feasible References – Positive Pressure Ventilation in the CICU 1. Alviar CL, Miller PE, McAreavey D, et al. Positive Pressure Ventilation in the Cardiac Intensive Care Unit. J Am Coll Cardiol. Sep 25 2018;72(13):1532-1553. doi:10.1016/j.jacc.2018.06.074 2. Barnett CF, O’Brien C, De Marco T. Critical care management of the patient with pulmonary hypertension. Eur Heart J Acute Cardiovasc Care. Jan 12 2022;11(1):77-83. doi:10.1093/ehjacc/zuab113 3. Bradley TD, Holloway RM, McLaughlin PR, Ross BL, Walters J, Liu PP. Cardiac output response to continuous positive airway pressure in congestive heart failure. Am Rev Respir Dis. Feb 1992;145(2 Pt 1):377-82. doi:10.1164/ajrccm/145.2_Pt_1.377 4. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positive-pressure ventilation for respiratory failure after extubation. N Engl J Med. Jun 10 2004;350(24):2452-60. doi:10.1056/NEJMoa032736 5. Girardis M, Busani S, Damiani E, et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. Oct 18 2016;316(15):1583-1589. doi:10.1001/jama.2016.11993 6. Investigators I-R, the A, New Zealand Intensive Care Society Clinical Trials G, et al. Conservative Oxygen Therapy during Mechanical Ventilation in the ICU. N Engl J Med. Mar 12 2020;382(11):989-998. doi:10.1056/NEJMoa1903297 7. Schjorring OL, Klitgaard TL, Perner A, et al. Lower or Higher Oxygenation Targets for Acute Hypoxemic Respiratory Failure. N Engl J Med. Apr 8 2021;384(14):1301-1311. doi:10.1056/NEJMoa2032510 CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

Aug 4, 2022 • 1h 7min

226. Case Report: Fall from Grace – A Case of Pulmonary Embolism – Massachusetts General Hospital

CardioNerds (Amit and Dan) join join Dr. Andrew Dicks (Vascular medicine physician at Prisma Health, former fellow at Mass General Vascular) and Dr. Prateek Sharma (Vascular interventional & medicine fellow at MGH) for an ice-cold drinks at the Esplanade in Boston, MA to discuss a case about a patient who developed a pulmonary embolism and masterfully discuss the diagnosis and management of of pulmonary emboli. Dr. Ido Weinberg (Director, Vascular Medicine Fellowship at MGH) provides the ECPR for this episode. Case Abstract: A 59-year-old Spanish-speaking man with no significant past medical history presents after falling 15-20 feet from a ladder and landing on his back. He was found to have an L1 fracture and left radial fracture and underwent T12-L2 fusion with neurosurgery on hospital day 1 and ORIF of left radial fracture with orthopedic surgery on hospital day 2. On hospital day 5, he develops acute onset tachycardia with HR in the 130s bpm with new O2 requirement associated with mild shortness of breath at rest without any chest discomfort. His labs were notable for an elevated troponin and proBNP. He underwent CTPA which demonstrated acute bilateral occlusive pulmonary emboli (PE) extending in the right and left main pulmonary arteries. TTE demonstrated right ventricle dilation. The patient was started on a heparin infusion and a PE response team (PERT) meeting was held to discuss treatment options. Given recent surgery, use of thrombolytic therapy was felt to be too risky and thus he was taken for percutaneous thrombectomy in the cath lab. PA pressure prior to intervention was 51/21 mmHg. The patient underwent suction thromboembelectomy with the Flow Triever device with extraction of thrombus and improvement in PA pressure to 19/11 mmHg. He was treated with anticoagulation thereafter and discharged home two days after the procedure. Jump to: Case media – Case teaching – References 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! Case Media Acute bilateral occlusive and nonocclusive pulmonary emboli extending from the right and left main pulmonary arteries to the lobar and segmental arteries of all the lobes. Moderate right heart strain including the right atrium and the right ventricle. RV/LV ratio > 1.0. Right ventricular cavity is dilated (RV size at the base measures to 45mm). Right ventricular systolic function is moderately decreased. Right ventricular free wall is hypokinetic with sparing of the right ventricular apex consistent with acute right ventricular strain Pulmonary angiography demonstrated extensive proximal bilateral PEs Caption: Post-procedure TTE demonstrated resolution of RV strain with normalization of RV size and function. Episode Schematics & Teaching Pearls While there are markers to suggest PE, such as ECG findings or evidence of RV dilatation, a PE cannot be confirmed without imaging. Elevation of cardiac biomarkers and evidence of RV dysfunction are used to risk stratify PE, not the degree of thrombus burden or locale of thrombus. Enoxaparin is the preferred anticoagulant to initiate at time of PE diagnosis if comorbidities allow. Optimal treatment of intermediate risk PE remains uncertain as there is little data about long-term outcomes. Aggressive treatment should be used judiciously and chosen on a case-by-case basis. PE response teams (PERT) allow for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. Notes 1. What is a PERT team and why is it helpful? We have several tools and approaches for the management of PE. There are also many subspecialities involved in the care of patients with PE, including vascular medicine, intervention cardiology, hematology, pulmonology, cardiac surgery, radiology, emergency department, intensive care, and more. As such, the best treatment plan for a given patient with PE can be challenging, especially if the services involved in treatment of the PE function in silos. PERT, or PE Response Team, was built to address this concern. It is a multidisciplinary team that originated at MGH whose goal is to coordinate care for high-risk PE patients and advance PE-related care in the institution. PERT allows for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. 2. How do we risk stratify patients with PE? Risk stratification is largely dependent on the hemodynamic significance caused by the PE. In addition to vital sign derangement, patients with PE should also be evaluated for evidence of cardiac strain due to PE by checking for evidence of RV dilatation on CT or TTE and for elevation of cardiac biomarkers. The combination of this information is used to risk stratify patients. Additionally, risk stratification tools, such as the PESI and sPESI scores, are used to guide risk stratification. Based on the ESC 2019 guidelines, PEs are stratified into high risk, intermediate-high risk, intermediate-low risk, or low risk. High risk: evidence of hemodynamic instability as defined by hypotension or shock. Intermediate-high risk: evidence of both RV dysfunction on imaging AND elevated cardiac biomarkers in the absence of HD instability Intermediate-low risk: evidence of either RV dysfunction on imaging OR elevated cardiac biomarkers in the absence of HD instability Low risk: no evidence of cardiac dysfunction on imaging or labs and no evidence of HD instability. Risk stratification is important as it helps guide medical management of patients. Important factors that have not been associated with PE severity include degree of thrombus burden and location of clot. 3. What do we know about optimal management of patients with intermediate risk PE? Unfortunately, data is fairly limited with regards to the optimal management strategy for patients with intermediate risk PE, namely whether anticoagulation alone is sufficient versus if a patient would benefit from more advanced therapies. All patients should be started on anticoagulation, preferably SQ enoxaparin if comorbidities allow, as soon as possible (if there are no contraindications to anticoagulation). However, choosing which patients would benefit from more advanced therapies remains limited. Thrombolysis has been associated with lower all-cause mortality in patients with intermediate-risk PE when compared to anticoagulation alone. However, not surprisingly, thrombolysis was also associated with more major bleeding, including intracranial hemorrhage. In the ULTIMA trial, catheter directed thrombolysis was shown to improve RV dysfunction more quickly compared to anticoagulation at 24 hours. However, at 90 days, there was no difference in degree of RV dysfunction between the two groups. Percutaneous thrombectomy devices have been shown to be safe and effective at reducing RV size. However, there are no head-to-head comparisons of these modalities versus anticoagulation or thrombolysis and data is limited regarding the long-term efficacy. Choosing the correct patient to proceed with advanced therapies remains challenging and the decision is often made on a case-by-case basis. There are ongoing randomized control trials that will hopefully assist in guiding this decision making. 4. What about management for those with high-risk PE? High risk PEs mandate aggressive and rapid treatment. Thrombolysis has been shown to have a mortality benefit compared to anticoagulation. Catheter directed thrombolysis can be considered in high-risk PE; however, rapid implementation needs to be available. VA-ECMO has also been demonstrated to reduce mortality in these patients. 5. What additional treatment options are available for patients with PE who are not improving on anticoagulation and have a contraindication to thrombolytic therapy? There are several contraindications to thrombolytic therapy, including recent surgery, CVA, or bleeding. Percutaneous and surgical thrombectomy should be considered in these patients. Surgical thrombectomy is effective but does require significant anticoagulation during the surgery while the patient is on cardiac bypass. For this reason, patients that have a contraindication to thrombolysis might not be able to tolerate the high levels of anticoagulation required for the surgery and thus a surgical thrombectomy might not be a feasible option. There are several percutaneous thrombectomy devices on the market currently which have been shown to be safe and effective at reducing the RV size in the acute period. Because these devices do not require thrombolytic agents, the risk of bleeding is lower and there is less ICU utilization. However, there have not been head-to-head comparisons between these devices and other treatment modalities. References Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405 Robertson L, Jones LE. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for the initial treatment of venous thromboembolism. Cochrane Database Syst Rev. 2017;2:CD001100. doi:10.1002/14651858.CD001100.pub4 Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411. doi:10.1056/NEJMoa1302097 Chatterjee S, Chakraborty A, Weinberg I, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA. 2014;311(23):2414-2421. doi:10.1001/jama.2014.5990 Kucher N, Boekstegers P, Müller OJ, et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation. 2014;129(4):479-486. doi:10.1161/CIRCULATIONAHA.113.005544 Subramaniam RM, Mandrekar J, Chang C, et al. Pulmonary embolism outcome: a prospective evaluation of CT pulmonary angiographic clot burden score and ECG score. AJR Am J Roentgenol. 2008;190(6):1599-1604. doi:10.2214/AJR.07.2858 Jain CC, Chang Y, Kabrhel C, et al. Impact of Pulmonary Arterial Clot Location on Pulmonary Embolism Treatment and Outcomes (90 Days). Am J Cardiol. 2017;119(5):802-807. doi:10.1016/j.amjcard.2016.11.018 Tu T, Toma C, Tapson VF, et al. A Prospective, Single-Arm, Multicenter Trial of Catheter-Directed Mechanical Thrombectomy for Intermediate-Risk Acute Pulmonary Embolism: The FLARE Study. JACC Cardiovasc Interv. 2019;12(9):859-869. doi:10.1016/j.jcin.2018.12.022

Jul 31, 2022 • 1h 10min

225. ACHD: Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients with Dr. Rafael Alonso-Gonzalez

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Jul 26, 2022 • 1h 15min

224. Atrial Fibrillation: Assessment of Stroke & Bleeding Risk with Dr. Elaine Hylek

CardioNerds (Amit Goyal), Dr. Colin Blumenthal (CardioNerds Academy House Faculty Leader and FIT at the University of Pennsylvania), and Dr. Anjali Wagle (CardioNerds Ambassador and FIT at Johns Hopkins University), discuss the baseline assessment of stroke and bleeding risk in patients with atrial fibrillation (AF) with Dr. Elaine Hylek. Dr. Hylek is a professor of medicine at the Boston University School of Medicine and is the Director of the Thrombosis and Anticoagulation Service at Boston Medical Center. Stroke is a potentially devastating and preventable complication of AF. Understanding the balance between stroke and bleeding risk is crucial in determining who should be on anticoagulation. Join us to discuss this topic! In the next episode of the series, we will discuss situational risk assessment in the context of peri-cardioversion, peri-procedural status, triggered atrial fibrillation, and more. Audio editing by CardioNerds Academy Intern, Pace Wetstein. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Hylek discloses grant and research support from Medtronic and Janssen, and honoraria and/or consulting fees from Boehringer Ingelheim, and Bayer. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Atrial Fibrillation: Assessment of Stroke & Bleeding Risk The CHA2DS2-VASc should be used to determine stroke risk in all patients. It was updated from the CHADS2 score to better separate patients into high and low risk and a score of 0 has a very low risk of a stroke. Understanding a given model’s derivation is key to application for any risk model. Understanding who was and was not included when a risk score was derived helps determine how to clinically use it. For example, mechanical valves, hypertrophic cardiomyopathy, cardiac amyloidosis, and moderate to severe MS were all excluded or poorly represented and should receive AC in AF regardless of CV. The HAS-BLED score should be used to identify modifiable risk factors for bleeding and address them. It is less useful to determine when we should stop AC. Factors that go into the score are dynamic and the intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). Fear the clot. Patients should be on AC unless there is a serious contraindication as embolic strokes can be devastating with a high mortality (~24% mortality at 30 days) “What am I saying by not writing the prescription… I am saying that it’s OK to have an ischemic stroke.” Survey data shows that patients are willing to experience 3.5 GI bleeds on average before 1 stroke, so favoring AC is often a patient centered approach Notes – Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Notes drafted by Dr. Anjali Wagle 1. Why do strokes happen in atrial fibrillation? Why is reducing stroke risk so important? Atrial fibrillation is associated with a significantly increased risk of stroke. The mortality of strokes related to AF have been estimated to be around 25% at 30 days in early studies which included either persistent or permanent AF, though of note, these studied were biased towards larger strokes since the diagnosis was based on physical exam and not high resolution imaging. AF promotes thrombogenesis through Virchow’s triad which includes: Abnormal blood flow Endothelial damage Hypercoagulability In atrial fibrillation, patients usually have a dilated left atrium and decreased blood flow through the atrial appendage which contribute to thrombogenesis. Multiple risk scores have been derived (i.e., CHA2DS2VASc) for estimation of stroke risk in patient with AF to identify whom to treat with anticoagulation to reduce the stroke risk. 2. How were CHADS2 and CHA2DS2VASc (CV) created and validated? The CHADS2 score was derived in 2001 by Gage et al from data including hospitalized patients with nonrheumatic AF who were not prescribed warfarin at hospitalized discharge. The CHADS2 score assigns one point to congestive heart failure, hypertension, age ≥ 75 years, and diabetes mellitus and two points to a previous history of stroke or transient ischemic attack (TIA) for a total of 6 points. Stroke rate per 100 patient-years rose by a factor of 1.5 for each 1-point increase in the CHADS2 score. However, it was found that there were several limitations associated with the CHADS2 score including that more than half of the patients were classified as moderate risk, making it unclear if antiplatelet or anticoagulation should be used in this population. Additionally, there were other “minor” risk factors (female sex, CAD, age 65-74) that were not included in the score. In 2010, Lip et al proposed the CHA2DS2VASc score that included these three additional factors: female gender, vascular events, and age 65-74. These additions to the original CHADS2 score allowed the CHA2DS2VASc score to reclassify patients in the moderate risk group into either the high or low risk groups (CV <1 or >2), making the decision of when to start anticoagulation easier. Some weaknesses of the CV score include that the individual factors are binary. For example, one point for diabetes does not discriminate risk based on if the patient’s A1c is 14 vs. 7. Similarly, the score is static and assumes the risk from each risk factor doesn’t change over time even though the endothelial dysfunction caused by a specific disease state isn’t fixed. Additionally, the C-statistic for the CV score is only 0.6 with newer scores that are more accurate including such as GARFIELD-AF (but these newer scores are less user friendly). That being said, the score still does a very good job of differentiating between high and low risk patients, which is the most important clinical question when deciding if someone needs anticoagulation. 3. Which populations were not studied in the validation of the CV score? Many of these studies have woefully low enrollment of racially diverse populations. Additionally, patients with amyloidosis, moderate-severe MS, and HOCM have a baseline higher risk of stroke were excluded from these studies. Patients with bioprosthetic valves were also excluded from the original derivation though there is now limited data showing use of the CV is reasonable. 4. How does AF burden affect stroke risk? Is there a temporal association between AF and stroke? Early trials did not find a temporal association between AF and stroke, though these trials often used physical exam definitions for stroke and current technology like implantable loop recorders (ILRs) didn’t exist to monitor 24/7. More modern studies like the TREND and KP-RHYTHM trials showed that stroke risk is related to AF burden. Longer episodes of AF seem to clearly be associated with stroke, but shorter episodes of AF aren’t as temporally related to stroke. In the LOOP trial use of ILRs to detect episodes of AF longer than 6 minutes led to a 3-fold increase in AF detection and initiation of AF, but did not reduce the number of strokes. This could indicate that there is some amount of AF that doesn’t require AC or that short runs of AF are associated with atrial myopathy that could be causing the strokes. It remains unclear what is the “chicken and egg” in this scenario. 5. How can we assess bleeding risk for patients with atrial fibrillation? How can we use these scores in our clinical practice? Developed and published in 2010 by Pisters et al., the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly [age >65], medication predisposing to bleeding, excessive alcohol use) score aimed to create an easy to calculate and clinically meaningful score to estimate bleeding risk. It was validated using 3,978 patients from the Euro Heart Survey on AF and had good predictive accuracy (C-statistic 0.72). Of note, the score uses the less severe ISTH definition for a major hemorrhage, which doesn’t require as severe bleeding as the TIMI major bleeding definition. Many of the factors that go into the score are dynamic (for example HTN is SBP > 160 and not a history of HTN). The intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). This would reduce the patients HAS-BLED score and therefore their bleeding risk. There is no absolute cutoff where anticoagulation in AF would be considered prohibitive. 6. What is the approach for patients with borderline stroke risk with a CV of 1 in men or 2 in women? Patients with a CV of 1 have between a 0.6% and a 0.9% risk of stroke/TIA/systemic embolism in a given year. That means even with a CV of 1 they have close to a 1/100 risk of an event in a given year. Given the high mortality and morbidity with embolic strokes and the lower incidence of major bleeding with modern DOACs, should have shared decision-making conversation with patients about starting AC at this risk level. One can consider other risk factors not in CV like LA function, appendage morphology, AF burden etc to help as tie breakers. References – Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010 Nov;138(5):1093-100. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of Clinical Classification Schemes for Predicting Stroke: Results From the National Registry of Atrial Fibrillation. JAMA. 2001;285(22):2864–2870. Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society. Journal of the American College of Cardiology. 2006;48(4):e149-e246. doi:10.1016/j.jacc.2006.07.018 Lip GY, Lim HS. Atrial fibrillation and stroke prevention. The Lancet Neurology. 2007;6(11):981-993. doi:10.1016/S1474-4422(07)70264-84. Hart RG, Pearce LA, Aguilar MI. Meta-analysis: Antithrombotic Therapy to Prevent Stroke in Patients Who Have Nonvalvular Atrial Fibrillation. Ann Intern Med. 2007;146(12):857-867. doi:10.7326/0003-4819-146-12-200706190-00007 van Doorn S, Debray TPA, Kaasenbrood F, et al. Predictive performance of the CHA2DS2-VASc rule in atrial fibrillation: a systematic review and meta-analysis. Journal of Thrombosis and Haemostasis. 2017;15(6):1065-1077. doi:10.1111/jth.13690 Lip GYH, Nieuwlaat R, Pisters R, Lane DA, Crijns HJGM. Refining Clinical Risk Stratification for Predicting Stroke and Thromboembolism in Atrial Fibrillation Using a Novel Risk Factor-Based Approach. Chest. 2010;137(2):263-272. doi:10.1378/chest.09-1584 Okumura K, Inoue H, Atarashi H, et al. Validation of CHA2DS2-VASc and HAS-BLED Scores in Japanese Patients With Nonvalvular Atrial Fibrillation: – An Analysis of the J-RHYTHM Registry –. Circ J. 2014;78(7):1593-1599. doi:10.1253/circj.CJ-14-0144

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Jul 17, 2022 • 48min

223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon

With the advent and rapid evolution of contemporary percutaneous coronary intervention (PCI), the early invasive management of acute myocardial infarction (AMI) has become a mainstay in therapy with significant impact on patient outcomes. However, despite modern advances in technology and system-based practices, AMI presenting with cardiogenic shock (CS) continues to portend a high risk of morbidity and mortality. Few randomized controlled clinical trials are available to guide decision-making in this uniquely challenging patient population. Understanding the pathophysiologic mechanism by which injury occurs and propagates the shock cycle can be instrumental in selecting an appropriate strategy for revascularization and left ventricular unloading. In this episode we are joined by Dr. Venu Menon, The Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine, section head of clinical cardiology, fellowship program director, and director of the Cardiac intensive care unit at the Cleveland Clinic. Dr. Menon shares his wealth of knowledge and experience to help us review the contemporary data available for AMI CS management in a case-based discussion. We are also joined by Dr. Priya Kothapalli, star chief fellow and future interventionalist from University of Texas at Austin, series co-chair Dr. Yoav Karpenshif, and CardioNerds Co-founders Amit Goyal and Daniel Ambinder. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. This episode is made possible with support from Medmastery. At Medmastery you can learn some of the most important clinical skills like echo, advanced EKG, coronary angiography, PCI basics, pacemaker- and ICD troubleshooting and so much more. CardioNerds listeners can get an exclusive 15% discount on a lifetime subscription. Click HERE for details. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon The H&P does matter! Age, location of infarction, heart rate, systolic blood pressure, and heart failure symptoms all carry weight in determining prognosis and risk of mortality. Define functional status, comorbid conditions, and life expectancy to help guide clinical decision-making. Do a quick bedside echocardiogram if possible to elucidate the predominant mechanism driving CS and rule out mechanical complications. Act with urgency! Get to the catheterization lab to characterize coronary anatomy and revascularize the culprit vessel as soon as possible. Minimize/avoid the use of vasopressors; if needed, wean as quickly as possible to avoid worsening myocardial ischemia. Consider mechanical circulatory support early! Despite dramatic advances in AMI management, data is limited in AMI CS management. Ask the important questions, get involved in the scientific inquiry as a trainee! Show notes – Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon 1. Why is it important to recognize AMI complicated by CS? AMI CS occurs in 7-10% of patients presenting with AMI and has a higher prevalence among elderly patients. The SHOCK trial (1999) showed significant survival benefit at 6 months with early revascularization with balloon angioplasty compared to medical therapy alone in AMI CS. Registry data suggests that early revascularization is beneficial in AMI CS even in elderly patients. Decision-making should be guided using a holistic view of the patient’s overall biology. Despite advances in revascularization techniques and availability of mechanical support, AMI CS portends a 40-45% risk of 30-day mortality in the modern era. Significant variation in management strategy exists between centers and data to guide decision-making is limited. The Society for Cardiovascular Angiography and Intervention (SCAI) classification system of shock stage may be helpful in characterizing patient risk and guiding clinical decision-making. 2. Which patients with AMI CS should undergo invasive monitoring and revascularization? What should be the timing of any intervention? In viable patients presenting with AMI CS, the primary goal should be to get to the catheterization laboratory to characterize the anatomy and revascularize the culprit vessel as soon as possible. Patient history, physical exam, laboratory exam, and echocardiography, if available, are critical pieces of information that should be obtained without delaying catheterization laboratory transfer. Patients presenting in SCAI shock stages C-E may require stabilization pre-procedure while minimizing delays to revascularization. Anticipating potential sequelae (such as acute pulmonary edema with respiratory failure requiring intubation) is crucial to minimizing delays. Maintain adequate perfusion pre-procedure (goal mean arterial blood pressure of >65mmHg). Minimize use and avoid escalation of vasopressor or inotropic therapy, as these agents worsen myocardial ischemia. The prevalence of multivessel disease, left main or proximal left anterior descending artery disease in AMI CS is high. Revascularization with restoration of TIMI 3 flow as soon as possible should be the primary goal, regardless of strategy. 3. When should mechanical circulatory support (MCS) be used in AMI CS? Immediate MCS may be beneficial in patients with persistent hemodynamic or electrical instability or patients at high risk for developing instability. MCS should be placed early and maintained until the shock cycle is reversed. If the primary mechanism for CS is left ventricular failure, an intra-aortic balloon pump (IABP) or transvalvular axial flow pump (Impella) may be considered. Additional strategies include venoarterial extracorporeal membrane oxygenation with left ventricular venting strategy or TandemHeart percutaneous assist device. There is limited data regarding the role of MCS in AMI; this is an area of active clinical investigation. Mechanistically, MCS provides the obvious benefits of supporting systemic perfusion while reducing cardiac workload; risks include bleeding, thrombosis, hemolysis, limb ischemia, and other vascular complications. MCS should be weaned slowly using multiple clinical and hemodynamic parameters, including Swan Ganz catheter data. If unable to wean MCS due to insufficient myocardial recovery despite support over a prolonged period in the setting of adequate revascularization, additional options such as durable MCS, heart transplantation, or palliative care should be considered. 4. What is the current evidence base for culprit-only vs. complete revascularization in AMI CS? The CULPRIT-SHOCK trial showed an increased 30-day and 1-year risk of a composite of all-cause mortality and need for renal replacement therapy in patients that underwent culprit and immediate non-culprit vessel revascularization in AMI CS. While there is no definitive data to support complete revascularization in AMI CS, this strategy may be considered in patients with multiple possible culprit lesions or subtotal non-culprit lesions with reduced TIMI grade flow corresponding with wall motion abnormality and normal wall thickness suggestive of viable myocardium. References – Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon Tehrani BN, Truesdell AG, Psotka MA, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Hear Fail. 2020;8(11):879-891. doi:10.1016/j.jchf.2020.09.005 Kapur NK, Davila CD. Timing, timing, timing: the emerging concept of the ‘door to support’ time for cardiogenic shock. Eur Heart J. 2017;38(47):3532-3534. doi:10.1093/eurheartj/ehx406 Hochman JS, Sleeper LA, Webb JG, et al. Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock. N Engl J Med. 1999;341(9):625-634. doi:10.1056/NEJM199908263410901 Ibanez B, Halvorsen S, Roffi M, et al. Integrating the results of the CULPRIT-SHOCK trial in the 2017 ESC ST-elevation myocardial infarction guidelines: viewpoint of the task force. Eur Heart J. 2018;39(48):4239-4242. doi:10.1093/eurheartj/ehy294 Shah AH, Puri R, Kalra A. Management of cardiogenic shock complicating acute myocardial infarction: A review. Clin Cardiol. 2019;42(4):484-493. doi:10.1002/clc.23168 Basir MB, Kapur NK, Patel K, et al. Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):ccd.28307. doi:10.1002/ccd.28307 Doll JA, Ohman EM, Patel MR, et al. A team-based approach to patients in cardiogenic shock. Catheter Cardiovasc Interv. 2016;88(3):424-433. doi:10.1002/ccd.26297 Thiele H, Ohman EM, de Waha-Thiele S, Zeymer U, Desch S. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019;40(32):2671-2683. doi:10.1093/eurheartj/ehz363 Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419-2432. http://www.nejm.org/doi/10.1056/NEJMoa1710261. Accessed April 10, 2021. Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525 Henry, Timothy D., et al. “Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement from the American Heart Association.” Circulation, vol. 143, no. 15, 2021, doi: 10.1161/cir.0000000000000959. Guest Profiles Dr. Venu Menon Dr. Venu Menon earned his medical degree from Jawaharlal Institute of Postgraduate Medical Education and Research in Pondicherry, India. He completed his internship and residency in internal medicine at St. Luke’s-Roosevelt Hospital in New York, NY, where he served as a Chief Resident. He continued at St. Luke’s-Roosevelt for his Cardovascular fellowship. Dr. Menon is currently the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He serves as the section head of clinical cardiology, fellowship program director, and director of the Cardiac intensive care unit at the Cleveland Clinic. He is the Chair of the AHA’s Acute Cardiac Care and General Cardiology Committee of the Council on Clinical Cardiology. Dr. Priya Kothapalli Dr. Priya Kothapalli completed her medical school at Temple University. She did her residency at Houston Methodist. She is currently the chief fellow and CardioNerds ambassador at University of Texas at Austin, and will soon become the institution’s first ever interventional cardiology fellow CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

Jul 14, 2022 • 43min

222. CardioNerds Rounds: Challenging Cases – Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford

It’s another session of CardioNerds Rounds! In these rounds, Co-Chair, Dr. Karan Desai (previous FIT at the University of Maryland Medical Center, and now faculty at Johns Hopkins) joins Dr. Ryan Tedford (Professor of Medicine and Chief of Heart Failure and Medical Directory of Cardiac Transplantation at the Medical University of South Carolina in Charleston, SC) to discuss the nuances of managing pulmonary hypertension in the setting of left-sided heart disease. Dr. Tedford is an internationally-recognized clinical researcher, educator, clinician and mentor, with research focuses that include the hemodynamic assessment of the right ventricle and its interaction with the pulmonary circulation and left heart. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Challenging Cases – Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Case #1 Synopsis: A woman in her late 30s presented to the hospital with 4 weeks of worsening dyspnea. Her history includes dilated non-ischemic cardiomyopathy diagnosed in the setting of a VT arrest around 10 years prior. Over the past 10 years she has been on guideline-directed medical therapy with symptoms that had been relatively controlled (characterized as NYHA Class II), but without objective improvement in her LV dimensions or ejection fraction (LVEF 15-20% by TTE and CMR and LVIDd at 6.8 cm). Over the past few months she had been noting decreased exercise tolerance, worsening orthopnea, and episodes of symptomatic hypotension at home. When she arrived to the hospital, she presented with BP 95/70 mmHg, increased respiratory effort, congestion and an overall profile consistent with SCAI Stage C-HF shock. In the case, we go through the hemodynamics at various points during her hospitalization and discuss options for management including medical therapy and mechanical support. The patient was eventually bridged to transplant with an Impella 5.5. Initial Hemodynamics Right Atrium (RA) Pressure Tracing: Right Ventricle (RV) Pressure Tracing: Pulmonary Artery (PA) Pressure Tracing: Pulmonary Capillary Wedge Pressure (PCWP) Tracing: Case 1 Rounding Pearls One of the first points that Dr. Tedford made was thinking about our classic frameworks of characterizing acute decompensated heart failure, specifically the “Stevenson” classification developed by Dr. Lynne Stevenson that phenotypes patients along two axes: congestion (wet or dry) and perfusion (warm or cold). Dr. Tedford cautioned that young patients may not fit into these classic boxes well, and that a normal lactate should not re-assure the clinician that perfusion is normal. In reviewing the waveforms, Dr. Tedford took a moment to note that besides just recording the absolute values of the pressures transduced in each chamber or vessel, it is critical to understand the morphology of the tracings themselves. For instance, with the RA pressure tracing above, there is no respiratory variation in the mean pressure. This is essentially a “resting Kussmaul’s sign,” which is typically indicative of significant RV dysfunction. Thus, even though our echocardiogram in this case did not necessarily show a significantly dilated RV with mildly reduced longitudinal function (TAPSE), hemodynamically the patient is demonstrating significant RV compromise. If we compare the RA pressure tracing to the PCWP, we see that there is respiratory variation in the PCWP tracing. We typically think of pronounced respiratory variation in the RA or PCWP tracing in the setting of obesity or lung disease, but loading conditions can also lead to significant respiratory variation. As was noted during the case discussion, irreversible pulmonary hypertension is considered an absolute contraindication to heart transplantation though there is variation on the absolute threshold above which transplantation is contraindicated. Generally, a pulmonary vascular resistance (PVR) of 3 Woods Units is considered a contraindication to isolated cardiac transplantation. Testing for reversibility of an elevated PVR with a vasodilator like nitroprusside is common in this patient population. In a study by Dr. Steven Hsu and colleagues, Pulmonary Artery Pulsatility Index (PAPi) was shown to be the hemodynamic factor that best correlated with intrinsic RV myocyte dysfunction in patients with advanced heart failure (using a cutoff of PAPi of 1.85). Dr. Tedford made note to remember that PAPi is highly influenced by RA pressure (the denominator in the ratio). Case #2 Synopsis: A woman in her late 40s presented to clinic for another opinion regarding her PH management. In regards to her history, in the 1990s she underwent a mechanical mitral valve replacement (MVR) for mixed mitral valve disease in the setting of rheumatic fever as well as a single vessel CABG (SVG to the RCA). In the early 2000s, she had developed severe and symptomatic tricuspid regurgitation (TR) and underwent redo sternotomy for TV repair (TVr). She had generally done well until the past year when she started developing dyspnea on light exertion, abdominal fullness, lower extremity edema and over the course of a year she had four hospitalizations for heart failure. Over her hospitalizations, she was also diagnosed with hemolytic anemia. Diagnostic work-up revealed pre and post-capillary PH. Dr. Tedford reviews the subsequent hemodynamic evaluation and provides insight on managing PH post valvular intervention. She was ultimately diagnosed with mitral paravalvular regurgitation treated with transcatheter PVL closure. Initial Hemodynamics RA Pressure Tracing RV Pressure Tracing PA Pressure Tracing PCW Pressure Tracing Left Ventricular (LV) Pressure Tracing PCW and LV Simultaneous Pressure Tracing Case 2 Rounding Pearls: The patient had been placed on sildenafil for persistent PH post-valve intervention. Dr. Tedford briefly mentioned the SIOVAC trial which was designed to evaluate treatment with sildenafil (40 mg TID) compared with placebo amongst patients with persistent PH (mean PA pressure ≥ 30 mmHg) 1 year after valvular replacement or repair (majority of whom were patients that had mitral valve intervention). In this study, sildenafil was associated with worse functional status, specifically heart failure or dyspnea compared to placebo (34% vs. 20%, p = 0.04). Dr. Tedford briefly touched upon the prognostic value of the diastolic pulmonary gradient (DPG, calculated as diastolic PA pressure subtracted by PCWP) in patients being considered for cardiac transplantation. We commonly use PVR and transpulmonary gradient (TPG) to characterize the degree of pre-capillary PH and suitability for transplantation. However, these markers are not ideal surrogates for pulmonary vascular remodeling and differentiating between fixed remodeling versus reversible changes. For instance, the TPG can be elevated not only as a result of pulmonary vascular remodeling but elevated LA pressures passively transmitted back to the pulmonary vasculature leading to elevations in the diastolic PA pressure. The DPG was thought to potentially define higher risk left heart failure patients with clinically significant pre-capillary PH. However, in Dr. Tedford’s 2014 analysis, the DPG did not delineate higher risk among patients with elevated TPG and PVR undergoing cardiac transplantation. There could be several explanations including that the cutoff for abnormal DPG is low (≥7) and thus small errors in measurement could have significant influence on what is characterized as abnormal. Furthermore, the diastolic PA pressure measurement is particularly prone to ringing artifact. References – Challenging Cases – Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Aslam MI, Jani V, Lin BL, et al. Pulmonary artery pulsatility index predicts right ventricular myofilament dysfunction in advanced human heart failure. Eur J Heart Fail. 2021 Feb;23(2):339-341. doi: 10.1002/ejhf.2084. Epub 2021 Jan 5. PMID: 33347674; PMCID: PMC8574988. Bermejo J, Yotti R, García-Orta R, et al., on behalf of the Sildenafil for Improving Outcomes after VAlvular Correction (SIOVAC) investigators. Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension: a multicenter, double-blind, randomized clinical trial. Mehra MR, Canter CE, Hannan MM, et al; International Society for Heart Lung Transplantation (ISHLT) Infectious Diseases, Pediatric and Heart Failure and Transplantation Councils. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update. J Heart Lung Transplant. 2016 Jan;35(1):1-23. doi: 10.1016/j.healun.2015.10.023. PMID: 26776864. Tedford RJ, Beaty CA, Mathai SC et al. Prognostic value of the pre-transplant diastolic pulmonary artery pressure-to-pulmonary capillary wedge pressure gradient in cardiac transplant recipients with pulmonary hypertension. J Heart Lung Transplant. 2014 Mar;33(3):289-97. doi: 10.1016/j.healun.2013.11.008. Epub 2013 Nov 28. Erratum in: J Heart Lung Transplant. 2019 Feb;38(2):233. PMID: 24462554; PMCID: PMC3955214. Thibodeau JT, Drazner MH. “The Role of the Clinical Examination in Patients With Heart Failure.” JACC Heart Failure (2018): 543-551. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Jul 12, 2022 • 7min

221. Guidelines: 2021 ESC Cardiovascular Prevention – Question #18 with Dr. Jaideep Patel

Dr. Jaideep Patel, a preventive cardiologist at Johns Hopkins Hospital, discusses the management of a 60-year-old Black woman with hypertension and heart failure, highlighting the importance of adding an SGLT2 inhibitor. The podcast also covers the four pillars of heart failure therapy and provides clinical pearls on the use of guanelade-cyclist emulator and I babredine for heart failure.

Jul 7, 2022 • 9min

220. Guidelines: 2021 ESC Cardiovascular Prevention – Question #17 with Dr. Melissa Tracy

Dr. Melissa Tracy, a preventive cardiologist, discusses the use of proton pump inhibitors (PPIs) to reduce gastrointestinal bleeding risk in high-risk patients on dual antiplatelet therapy. The podcast explores the findings of a meta-analysis on the combined use of clopidogrel and PPIs and highlights the discrepancies between ESC and AC guidelines regarding PPI use and interactions.

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