The following question refers to Section 7.7 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by St. George's University medical student and CardioNerds Intern Chelsea Tweneboah, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Michelle Kittleson.Dr. Kittleson is Director of Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute, Cedars-Sinai. She is Deputy Editor of the Journal of Heart and Lung Transplantation, on Guideline Writing Committees for the American College of Cardiology (ACC)/American Heart Association, is the Co Editor-in-Chief for the ACC Heart Failure Self-Assessment Program, and on the Board of Directors for the Heart Failure Society of America. Her Clinician’s Guide to the 2022 Heart Failure guidelines, published in the Journal of Cardiac Failure, are a must-read for everyone!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 #10 Ms. Heffpefner is a 54-year-old woman who comes to your office for a routine visit. She does report increased fatigue and dyspnea on exertion without new orthopnea or extremity edema. She was previously diagnosed with type 2 diabetes, morbid obesity, obstructive sleep apnea, and TIA. She is currently prescribed metformin 1000mg twice daily, aspirin 81mg daily, rosuvastatin 40mg nightly, and furosemide 40mg daily. In clinic, her BP is 140/85 mmHg, HR is 110/min (rhythm irregularly irregular, found to be atrial fibrillation on ECG), and BMI is 43 kg/m2. Transthoracic echo shows an LVEF of 60%, moderate LV hypertrophy, moderate LA enlargement, and grade 2 diastolic dysfunction with no significant valvulopathy. What is the best next step? A Provide reassurance B Refer for gastric bypass C Refer for atrial fibrillation ablation D Start metoprolol and apixaban Answer #10 ExplanationThe correct answer is D – start metoprolol and apixaban.Ms. Hefpeffner has a new diagnosis of atrial fibrillation (AF) and has a significantly elevated risk for embolic stroke based on her CHA2DS2-VASc score of 6 (hypertension, diabetes, heart failure, prior TIA, and female sex). The relationship between AF and HF is complex and the presence of either worsens the status of the other. Managing AF in patients with HFpEF can lead to symptom improvement (Class 2a, LOR C-EO). However, large, randomized trial data are unavailable to specifically guide therapy in patients with AF and HFpEF. Generally, management of AF involves stroke prevention, rate and/or rhythm control, and lifestyle / risk-factor modification. With regards to stroke prevention, patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women) should receive chronic anticoagulant therapy (Class 1, LOE A). When anticoagulation is used in chronic HF patients with AF, a DOAC is recommended over warfarin in eligible patients (Class 1, LOE A).The decision for rate versus rhythm control should be individualized and reflects both patient symptoms and the likelihood of better ventricular function with sinus rhythm. For patients with HF and symptoms caused by AF,

The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.  The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Nancy Sweitzer. Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series. 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 #9 Mr. Flo Zin is a 64-year-old man who comes to discuss persistent lower extremity edema and dyspnea with mild exertion. He takes amlodipine for hypertension but has no other known comorbidities. In the clinic, his heart rate is 52 bpm and blood pressure is 120/70 mmHg. Physical exam reveals mildly elevated jugular venous pulsations and 1+ bilateral lower extremity edema. Labs show an unremarkable CBC, normal renal function and electrolytes, a Hb A1c of 6.1%, and an NT-proBNP of 750 (no prior baseline available). On echocardiogram, his LVEF is 44% and nuclear stress testing was negative for inducible ischemia. What is the best next step in management? A Add furosemide BID and daily metolazone B Start empagliflozin and furosemide as needed C Start metoprolol succinate D No change to medical therapy Answer #9 Explanation The correct answer is B – start empagliflozin and furosemide as needed. The patient described here has heart failure with mildly reduced EF (HFmrEF), given LVEF in the range of 41-49%. In patients with HF who have fluid retention, diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF (Class 1, LOE B-NR). For patients with HF and congestive symptoms, addition of a thiazide (eg, metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate or high-dose loop diuretics to minimize electrolyte abnormalities (Class 1, LOE B-NR). Therefore, option A is not correct as he is only mildly congested on examination, and likely would not require such aggressive decongestive therapy, particularly with normal renal function. Adding a thiazide diuretic without first optimizing loop diuretic dosing would be premature. The EMPEROR-Preserved trial showed a significant benefit of the SGLT2i, empagliflozin, in patients with symptomatic HF, with LVEF >40% and elevated natriuretic peptides. The 21% reduction in the primary composite endpoint of time to HF hospitalization or cardiovascular death was driven mostly by a significant 29% reduction in time to HF hospitalization, with no benefit on all-cause mortality. Empagliflozin also resulted in a significant reduction in total HF hospitalizations, decrease in the slope of the eGFR decline, and a modest improvement in QOL at 52 weeks. Of note, the benefit was similar irrespective of the presence or absence of diabetes at baseline. In a subgroup of 1983 patients with LVEF 41% to 49% in EMPEROR-Preserved, empagliflozin, an SGLT2i, reduced the risk of the primary composite endpoint of cardiovascular death or hospitalization f...

The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Gregg Fonarow.Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA's Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA's Preventative Cardiology Program.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 #8 Ms. Flo Zinn is a 60-year-old woman seen in cardiology clinic for follow up of her chronic HFrEF management. She has a history of stable coronary artery disease, hypertension, hypothyroidism, and recurrent urinary tract infections. She does not have a history of diabetes and recent hemoglobin A1c is 5.0%. Her current medications include carvedilol, sacubitril-valsartan, eplerenone, and atorvastatin. Her friend was recently placed on an SGLT2 inhibitor and asks if she should be considered for one as well. Which of the following is the most important consideration when deciding to start this patient on an SGLT2 inhibitor? A The patient does not have a history of type 2 diabetes and so does not qualify for SGLT2 inhibitor therapy B While SGLT2 inhibitors improve hospitalization rates for HFrEF, there is no evidence that they improve cardiovascular mortality C Patients taking SGLT2 inhibitors tend to suffer a more rapid decline in renal function than patients not taking SGLT2 inhibitor therapy D Patients may be at a higher risk for genitourinary infections if an SGLT2 inhibitor is started Answer #8 Explanation   The correct answer is D – SGLT2 inhibitors have been associated with increased risk of genitourinary infections. Sodium-glucose co-transporter protein 2 (SGLT2) inhibitors have gathered a lot of press recently as the new kid on the block with respect to heart failure management. While they were initially developed as antihyperglycemic medications for treating diabetes, early cardiovascular outcomes trials showed reduced rates of heart failure hospitalization amongst study participants independent of glucose-lowering effects and irrespective of baseline heart failure status – only 10-14% of patients carried a heart failure diagnosis at baseline. This prompted trials to study the effects of SGLT2 inhibitors in patients with symptomatic chronic HFrEF who were already on guideline directed medical therapy irrespective of the presence of type 2 diabetes mellitus. The DAPA-HF and EMPEROR-Reduced trials showed that dapagliflozin and empagliflozin, respectively, both conferred statistically significant improvements in a composite of heart failure hospitalizations and cardiovascular death (Option B). Most interestingly, these effects were seen irrespective of diabetes history. In light of these findings, the 2022 HF guidelines recommend SGLT2 inhibitors in patients with chronic, symptomatic HFrEF with or without diabetes to reduce hospitalization for HF and cardiovascular mortality (Class I, LOE A). The benefits of SGLT2 inhibitors extend beyond cardiovascular health.

The following question refers to Section 7.3.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.  The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Robert Mentz.  Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very 2022 heart failure Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22. Welcome Dr. Mentz!  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 #7 Ms. Valarie Sartan is a 55-year-old woman with a history of HFrEF (EF 35%) and well controlled, non-insulin dependent diabetes mellitus who presents to heart failure clinic for routine follow up. She is currently being treated with metoprolol succinate 200mg daily, lisinopril 10mg daily, empagliflozin 10mg daily, and spironolactone 50mg daily. She notes stable dyspnea with moderate exertion, making it difficult to do her yardwork. On exam she is well appearing, and blood pressure is 115/70 mmHg with normal jugular venous pulsations and trace bilateral lower extremity edema. On labs, her potassium is 4.0 mmol/L and creatinine is 0.7 mg/dL with an eGFR > 60 mL/min/1.73m2. Which of the following options would be the most appropriate next step in heart failure therapy?  A  Increase lisinopril to 40mg daily  B  Increase spironolactone to 100mg daily  C  Add sacubitril-valsartan to her regimen  D  Discontinue lisinopril and start sacubitril-valsartan in 36 hours  E  No change  Answer #7 Explanation   The correct answer is D – transitioning from an ACEi to an ARNi is the most appropriate next step in management.   The renin-angiotensin aldosterone system (RAAS) is upregulated in patients with chronic heart failure with reduced ejection fraction (HFrEF). Blockade of the RAAS system with ACE inhibitors (ACEi), angiotensin receptor blockers (ARB), or angiotensin receptor neprilysin inhibitors (ARNi) have proven mortality benefit in these patients.   The PARADIGM-HF trial compared sacubitril-valsartan (an ARNi) with enalapril in symptomatic patients with HFrEF. Patients receiving ARNi incurred a 20% relative risk reduction in the composite primary endpoint of cardiovascular death or heart failure hospitalization. Based on these results, the 2022 heart failure guidelines recommend replacing an ACEi or ARB for an ARNi in patients with chronic symptomatic HFrEF with NYHA class II or III symptoms to further reduce morbidity and mortality (Option D). This is a class I recommendation with level of evidence of B-R and is also of high economic value. Making no changes at this time would be inappropriate (Option E).  While it would be reasonable to increase the dose of lisinopril to 40mg (Option A), this should be pursued only if ARNi therapy is not tolerated.   Mineralocorticoid receptor antagonists (MRAs) have a class I (LOE A...

CardioNerds co-founder Daniel Ambinder joins Cleveland Clinic cardiology fellows, Dr. Essa Hariri, Dr. Anna Scandinaro, and Dr. Beka Bekhdatze, Clinical pharmacist at Cleveland Clinic, Dr. Ashley Kasper, and Dr. Craig Parris from Ohio State University Medical Center for a walk at Edgewater Park in Cleveland, Ohio. Dr. Andrew Higgins (Crtitical Care Cardiology and Advanced HF / Transplant Cardiology at Cleveland Clinic) provides the ECPR for this episode. They discuss the following case involving a rare cause of non-ischemic cardiomyopathy. A young African American male was admitted for cardiogenic shock following an admission a month earlier for treatment resistant psychosis. He was diagnosed with medication-induced non-ischemic cardiomyopathy, which resolved with a remarkable recovery of his systolic function after discontinuation of the culprit medication, Clozapine. Episode notes were drafted by Dr. Essa Hariri. Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy. Enjoy this case report co-published in US Cardiology Review: Clozapine-induced Cardiomyopathy: A Case Report CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). 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 - An Unusual Case of Non-ischemic Cardiomyopathy The diagnosis of drug-induced non-ischemic cardiomyopathy is usually one of exclusion. High clinical suspicion is needed to diagnose drug-induced cardiomyopathy. Missing the culprit medication causing drug-induced cardiomyopathy could be detrimental as there is a high probability of reversing a systolic dysfunction after stopping the offending medication. Clozapine is an effective medication for the treatment-resistant schizophrenia and is associated with reduced suicide risk. Clozapine is reported to cause drug-induced cardiomyopathy and is more common with rapid drug titration. Clozapine is more commonly associated with myocarditis. Close monitoring and vigilance are critical to preventing cardiac complications associated with initiating clozapine. The management of clozapine-associated cardiomyopathy includes clozapine cessation and heart failure guideline-directed medical therapy. Show Notes - An Unusual Case of Non-ischemic Cardiomyopathy We treated a case of clozapine-associated cardiomyopathy presenting in cardiogenic shock. Drug-induced cardiomyopathy is a common yet under-recognized etiology of non-ischemic cardiomyopathy. Clozapine is an FDA-approved atypical antipsychotic medication frequently prescribed for treatment-resistant schizophrenia and the only antipsychotic agent that has been proven to significantly reduce suicide among this patient population. However, Clozapine is reported to be associated with several forms of cardiotoxicity, including myocarditis (most common), subclinical clozapine associated cardiotoxicity, and least commonly, drug-induced cardiomyopathy. Clozapine-associated cardiomyopathy should be considered as a differential diagnosis in schizophrenic patients presenting with signs of acute heart failure.  Rapid titration of clozapine is a risk factor for clozapine-associated cardiomyopathy and clozapine-associated myocarditis. To date, there is no evidence or consensus supporting preemptive screening. According to the American Psychiatric Association, whenever clozapine-induced myocarditis or cardiomyopathy is suspected, a cardiology consult is warranted.

Renal replacement therapy (RRT) is routinely utilized in the CICU. Series co-chairs Dr. Eunice Dugan and Dr Karan Desai along with CardioNerds Co-founder Dr. Daniel Ambinder were joined by FIT lead and CardioNerds Ambassador from University of Washington, Dr. Tomio Tran. Our episode expert is world-renowned nephrologist Dr. Joel Topf. Dr. Topf is Medical Director of Research at St. Clair Nephrology, and editor of the Handbook of Critical Care Nephrology. In this episode, we describe a case of cardiogenic shock due to acute myocardial infarction resulting in renal failure, ultimately requiring continuous RRT (CRRT). We discuss the most common causes of AKI within the cardiac ICU, indications for initiating RRT, evidence on the timing of RRT, different modes of RRT, basic management of the RRT circuit, and how to transition patients off of RRT during renal recovery. Episode notes were drafted by Dr. Tomio Tran. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. 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 - Approach to Renal Replacement Therapy in the CICU Do not commit “Renalism” - withholding lifesaving treatments from patients with renal impairment due to fear of causing renal injury. Shared decision making is key. In the ICU, most of the time, AKI is caused by ATN due to adverse hemodynamics. Nephrologists can help determine the cause if the patient has an atypical presentation. Late dialysis initiation is non-inferior to early dialysis initiation. Early initiation may lead to higher rates of prolonged time on dialysis. Slow low efficiency daily diafiltration (SLEDD) vs CRRT are equivalent in terms of outcomes and are the preferred methods among patients with hypotension. Intermittent Hemodialysis (iHD) can be used once patients are hemodynamically stable. A “Furosemide Stress Test” can be used to test intact renal function or renal recovery by challenging the nephron to make urine. Show notes - Approach to Renal Replacement Therapy in the CICU What are the risk factors and differential for AKI in the CICU? Start by using the pre-renal vs intrinsic renal vs post-renal framework. Additional considerations in cardiac patients include contrast induced nephropathy, pigment nephropathy, cardiorenal syndrome. Enjoy Episode 262. Management of Cardiorenal Syndrome in the CICU. In the ICU setting, intrinsic renal injury due to ATN is among the most common etiology of AKI. Many risk factors for AKI are not modifiable in the ICU. Optimize renal function by avoiding nephrotoxins, minimizing contrast usage, and keeping the MAP >65-75 mmHg. Contrast nephropathy as an etiology is questionable and may be a marker of a sicker patient population. Avoid “Renalism” - providing substandard care to patients with renal disease due to fear of worsening renal function. Most etiologies are treated with supportive care. What is the approach to timing of renal replacement therapy initiation? Definitions for early vs late vs very late initiation of RRT:Early – Worsening AKI without indications for RRTLate – Worsening AKI with relative indications for RRT Very late – Worsening AKI with strict indications for RRT Late initiation is noninferior in terms of mortality; early initiation is associated with higher rates of prolonged/permanent RRT.1,2,3 Very late initiation associated with worse outcomes.4 In general,

Join CardioNerds to learn about patent ducts arteriosus and Eisenmenger syndrome! Dr. Dan Ambinder (CardioNerds co-founder), ACHD series co-chair Dr. Dan Clark,  Dr. Tony Pastor (ACHD fellow, Harvard Medical School), and Dr. Kate Wilcox, Medicine/Pediatrics Resident, Medical College of Wisconsin join Dr. Candice Silversides (Editor-in-chief #JACCAdvances) for this terrific discussion. Notes were drafted by Dr. Kate Wilcox. .Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Patent Ductus Arteriosus & Eisenmenger Syndrome The ductus arteriosus, which is formed from the distal portion of the left sixth arch, is key to fetal circulation because it allows blood to bypass the high resistance pulmonary circuit present in utero. After birth there is a significant drop in pulmonary vascular resistance (PVR) which generally leads to functional ductal closure within 48 hours (permanent seal takes 2-3 weeks to form). Risk factors for having a PDA include birth before 37 weeks of gestation, trisomy 21, and congenital rubella. A PDA results in a left to right shunt (qP:qS >1) which over time overloads the left side of the heart and causes pulmonary vascular remodeling. The extra workload on the left side of the heart causes left atrial (can cause atrial arrhythmias) and left ventricular dilation. If left untreated you can eventually have shunt reversal due to very high PVR (Eisenmenger physiology). There are some treatment options at this point (pulmonary vasodilators, etc) but it’s definitely better to close the PDA before this point. One interesting physical exam finding that can stem from shunt reversal in a hemodynamically significant PDA is differential cyanosis (upper body or pre-ductal saturations will be higher than lower body/post-ductal saturations). You can also see clubbing in the toes but not the hands for the same reason. Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information.

The Cardiorenal Syndrome is commonly encountered, and frequently misunderstood. Join the CardioNerds team as we discuss the complex interplay between the heart and kidneys with Dr. Elliott Miller (Assistant Professor of Medicine at Yale University School of Medicine and Associate Medical Director of the Cardiac Intensive Care Unit of Yale New Haven Hospital), and Dr. Nayan Arora (Clinical Assistant Professor of Medicine and Nephrologist at the University of Washington Medical Center). We are hosted by FIT lead Dr. Matthew Delfiner (Cardiology Fellow at Temple University), Cardiac Critical Care Series Co-Chairs Dr. Mark Belkin (AHFTC faculty at University of Chicago) and Dr. Karan Desai (Cardiologist at Johns Hopkins Hospital), and CardioNerds Co-Found Dr. Dan Ambinder. In this episode we discuss the definition and pathophysiology of the cardiorenal syndrome, explore strategies for initial diuresis and diuretic resistance, and management of the common heart failure medications in this setting. Show notes were developed by Dr. Matthew Delfiner. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. 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 - Management of Cardiorenal Syndrome in the CICU Cardiorenal syndrome (CRS) represents a range of clinical entities in which there is both heart and kidney dysfunction, and can be driven by one, or both, of the organs. CRS is caused by reduced renal perfusion, elevated renal congestion, or a combination of the two. Treatment therefore focuses on increasing perfusion, by optimizing cardiac output and mean arterial pressure, and reducing congestion through diuresis. Patients should be monitored for an adequate response to the initial diuretic dose within 2 hours of administration. If the response is inadequate, the loop diuretic dose should be doubled. Diuretic resistance can be managed via sequential nephron blockade, most commonly with thiazide diuretics, but also with amiloride, high-dose spironolactone, or acetazolamide, as these target different regions of the nephron. In cases of refractory diuretic resistance, hypertonic saline can be considered with the help of an experienced clinician. Continuation or cessation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis. Show notes - Management of Cardiorenal Syndrome in the CICU 1. Cardiorenal syndrome (CRS) is a collection of signs/symptoms that indicate injury to both the heart and kidneys. Organ dysfunction in one can drive dysfunction in the other. Cardiorenal syndrome can be categorized as: Type 1 - Acute heart failure causing acute kidney injury Type 2 - Chronic heart failure causing chronic kidney injury Type 3 - Acute kidney injury causing acute heart failure Type 4 - Chronic kidney injury causing chronic heart failure Type 5 - Co-development of heart and kidney injury by another systemic process. These categories can be helpful for education, discussion, and research purposes, but they do not usually enter clinical practice on a regular basis since different categories of cardiorenal syndrome are not necessarily treated differently. 2. CRS is caused by either reduced renal perfusion, elevated renal congestion, or a combination of the two. When dealing with CRS, note that: CRS can be caused by poor kidney perfusion,

Dr. Filip Ionescu (hematology-oncology fellow at Moffitt Cancer Center in Tampa, FL), Dr. Teodora Donisan (cardiology fellow at the Mayo Clinic in Rochester, MN and CardioNerds House Thomas chief), Dr. Sarah Waliany (internal medicine chief resident at Stanford University in Palo Alto, CA), Dr. Dinu Balanescu (internal medicine chief resident at Beaumont Hospital in Royal Oak, MI) and Dr. Amit Goyal (structural interventional cardiology fellow at the Cleveland Clinic, in Cleveland, OH and CardioNerds Co-Founder), discuss the cardiotoxicities of common cancer treatments with Dr. Susan Dent, a medical oncologist and one of the founders of the field of Cardio-Oncology. Using the recently published ESC Guidelines on cardio-oncology, they cover cardiovascular risk stratification in oncology patients, pretreatment testing, as well as prevention and management of established cardiotoxicity resulting from anthracyclines, trastuzumab, and fluoropyrimidines. They touch on the unique aspects of cardio-oncology encountered in patients with breast cancer, rectal cancer, and lung cancer, who are frequently the recipients of multiple cardiotoxic treatments. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. Access the CardioNerds Cardiac Amyloidosis Series for a deep dive into this important topic. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology 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. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology 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 - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Oncologist Perspective with Dr. Susan Dent Formal cardiovascular risk stratification must be performed prior to initiating a potentially cardiotoxic anticancer treatment regimen. Considering both drug toxicity and patient-related factors (e.g., age, smoking, hypertension etc) is important.  Anthracyclines affect the cardiomyocyte in complex ways which lead to a largely irreversible cardiomyopathy. All patients should have a pretreatment echocardiogram and ECG.  Trastuzumab cardiotoxicity, by contrast, is more like stunning the myocardium, which manifests as a reversible decrease in left ventricular ejection fraction which generally normalizes upon discontinuation of the drug.  The treatment of chemotherapy-induced cardiomyopathy should involve interdisciplinary discussions and shared decision making with the patient. Beyond guideline-directed medical therapy of heart failure with reduced ejection fraction, management can include temporarily holding or permanently discontinuing the offending agent.  Fluoropyrimidine-associated cardiotoxicity manifests as cardiac ischemia from coronary vasospasm. A 5FU infusion is essentially a stress test as it tends to unmask clinically silent atherosclerosis.  Show notes What is the basic pretreatment assessment of any oncology patient who is to receive a potentially cardiotoxic regimen?  Awareness and management of the cardiovascular toxicity of oncology treatments are of paramount importance to be able to deliver treatment safely and to achieve maximal efficacy guided by an expert multidisciplinary team. Thanks to Dr. Dent and her colleagues’ work, this year we have seen the publication of the first Cardio-Oncology guideline (1). Perhaps the most important recommendation is that cancer patients about to start a cardiotoxic regimen should undergo formal cardiovascular risk stratification by considering both the adverse profile of the planned treatment...

CardioNerds Cofounder Dr. Amit Goyal join Dr. Usman Hasnie and Dr. Will Morgan from University of Alabama at Birmingham for a hike up Red Mountain. They discuss the following case: A 75-year-old woman with prior mitral valve ring annuloplasty presented with subacute, intermittent, self-limiting neurologic deficits. Brain MRI revealed multiple subacute embolic events consistent with cardioembolic phenomena. Transesophageal echochardiogram discovered a mobile mass on the mitral valve as the likely cause for cardioembolic stroke. She was taken for surgical repair of the mitral valve. Tissue biopsy confirmed that the mass was an IgG4-related pseudotumor. Expert commentary is provided by Dr. Neal Miller (Assistant Professor of Cardiology, University of Alabama at Birmingham). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares Check out this published case report here: IgG4-Related Disease Masquerading as Culture-Negative Endocarditis! 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 - Cardioembolic Stroke due to an IgG4-related pseudotumor Surgical indications for endocarditis include severe heart failure, valvular dysfunction with severe hemodynamic compromise, prosthetic valve infection, invasion beyond the valve leaflets, recurrent systemic embolization, large mobile vegetations, or persistent sepsis (in infective endocarditis) despite adequate antibiotic therapy. IgG4 related disease is rare, and likely underrecognized due to the lack of reliable biomarkers. Biopsy and histologic confirmation are imperative to clinch the diagnosis. Cardiac manifestations of IgG4-related disease are rare but are often related to aortopathies. Valvular disease is extremely rare as a manifestation of the disease. Treatment of IgG4 related disease includes steroids as the first line treatment. IgG4 related disease requires a multi-disciplinary approach to both diagnose and treat. Show Notes - Cardioembolic Stroke due to an IgG4-related pseudotumor Notes were drafted by Dr. Hasnie and Dr. Morgan IgG4-related disease has a very diverse presentation including mimicry of infection, malignancy and other autoimmune conditions. It is a fibroinflammatory condition that results in deposition of IgG4 positive plasma cells. It has been described in multiple organ systems including the pancreas, kidneys, lungs and salivary glands.  Cardiac manifestations are extremely rare and valvular disease even more so. There are thirteen cases of IgG4 related valvular disease, and of these only two had mitral valve involvement such as this case. The most commonly reported cardiovascular manifestations are related to aortopathies.  This disease remains poorly understood at this point. There are no true biomarkers that can be used to risk stratify the diagnosis for clinicians. Biopsy is imperative to the diagnosis. Even serum IgG4 levels are normal in 30% of cases despite meeting histologic criteria on biopsy making the diagnosis incredibly difficult to make.  While guidelines have not been developed to guide treatment of IgG4-related disease, steroids are considered the first line treatment option for patients. Often times dosing is 2-4 weeks with a prolonged taper. When looking for glucocorticoid sparing agents, azathioprine, mycophenolate mofetil, and methotrexate are considered alternatives.  References - Cardioembolic Stroke due to an IgG4-related pseudotumor 1. Kamisawa T, Funata N, Hayashi Y, et al. A new clinicopathological entity of IgG4- related autoimmune disease. J Gastroenterol 2003;38:982-4.  2. Deshpande V, Zen Y, Chan JK, et al. Consensus statement on the pathology of IgG4-related disease. Mod Pathol. 2012;25(9):1181-1192. doi:10.1038/modpathol.2012.72  3. Dahlgren M,