56. Case Report: Arrhythmogenic Desmoplakin Cardiomyopathy – Northwestern University Feinberg School of Medicine

CardioNerds (Amit Goyal & Daniel Ambinder) join Northwestern University cardiology fellows (Sarah Hale, Sarah Chuzi, and Graham Lohrmann) for burgers and a great case by the Chicago River! They discuss a fascinating case of arrhythmogenic desmoplakin cardiomyopathy. Dr. Lisa Wilsbacher provides the E-CPR and program director Dr. Benjamin Freed provides a message for applicants.  Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai

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CardioNerds (Amit Goyal & Daniel Ambinder) join Northwestern University cardiology fellows (Sarah Hale, Sarah Chuzi, and Graham Lohrmann) for burgers and a great case by the Chicago River! They discuss a fascinating case of desmoplakin dilated cardiomyopathy Desmoplakin (DSP) dilated cardiomyopathy with LMNA (lamin A/C) variant of uncertain significance. Dr. Lisa Wilsbacher provides the E-CPR and program director Dr. Benjamin Freed provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A male in his early 40s presented for second opinion regarding multiple ICD shocks. 10 years prior he was diagnosed with a “weak heart,” thought secondary to a viral illness and a dual-chamber ICD was placed at that time. He noted shocks occurring for the first time 5 years prior, at which time amiodarone was started. They recurred two years prior, when he was diagnosed with paroxysmal atrial fibrillation. Finally, he was hospitalized one month before presentation with multiple ICD shocks and was found to have high defibrillation thresholds (DFTs) and amiodarone was stopped. He  then presented for a second opinion from the Northwestern CardioNerds! 

The patient had been doing well on GDMT and had NYHA Class I symptoms (Enjoy Ep #13 – Approach to GDMT). He did note a family history of a cousin with “cardiac issues” and did not know his father’s family history. Physical exam demonstrated bradycardia and ECG demonstrated an a-paced, v-sensed rhythm at 50 bpm. TTE demonstrated a moderately dilated LV with LVEF 30%, globally reduced LV function and multiple wall motion abnormalities without a vascular distribution.  PET-CT was performed which showed diffuse uptake and high-intensity signal at the inferolateral and basal anterior walls. Cardiac MRI showed diffuse circumferential epicardial delayed enhancement with associated diffuse, enhancing thickening of the pericardium favoring inflammatory versus fibrotic process. Patient was initially diagnosed with cardiac sarcoid and started on prednisone and weekly methotrexate.  

On return of genetic testing, patient found to have a pathogenic variant for desmoplakin gene, and it was felt his cardiomyopathy was secondary to desmoplakin Left Dominant Arrhythmogenic Cardiomyopathy (LDAC, or left-dominant ARVC) presenting with inflammatory myocardial injury. On follow up the patient remained listed for transplant, and DFTs improved off amiodarone.  


Case Media


Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. We started the case talking about DFTs. What are DFTs?! 
    • Defibrillation Thresholds (DFTs) are the minimal amount of energy required to return a patient to sinus rhythm that is in a cardiac dysrhythmia.  
    • Most modern ICD leads have thresholds less than 15 joules and typically less than 10 joules with biphasic shocks. High DFT thresholds tend to be defined as >25J or a safety margin of <10J. 
    • DFT testing is not routinely recommended during implantation of left-sided transvenous devices; however, in patients undergoing right-sided transvenous ICD or ICD pulse generator changes, DFT testing is a reasonable approach. Patients undergoing subcutaneous ICD placement should generally have DFT testing. 
    • Contraindications to DFT testing include acute LV thrombus, atrial fibrillation/flutter without adequate anticoagulation, severe aortic stenosis, recent stroke or TIA, or hemodynamic compromise as DFT itself can cause hypotension and/or CVA.   
  2. What are the major causes of high DFTs? 
    • First there are myocardial factors. This includes pathology that affects the current density through the myocardium. Conditions like hypertrophic cardiomyopathy, inflammatory cardiomyopathy, or significant LV dilation can lead to high DFTs.    
    • The second set of factors are extra-cardiac causes that lead to increased impedance or resistance in the counter coil, such as high BMI or medications that lead to electrical imbalances such as amiodarone, which is a common cause of increased DFTs. However, the increase in DFT caused by amiodarone can be small and routine DFT testing in patients is not recommended.   
    • The last cause is a device factor, such as a lead fracture or a mal-positioned lead.  
  3. In the case, we used MRI and PET. What are their role in Cardiomyopathy? 
    • Cardiac MRI (CMR) has transformed our ability to assess cardiomyopathies, specifically by accurately defining chamber size & function, characterizing myocardial tissue, and determining ischemia & viability. The specific pattern of late gadolinium enhancement (LGE) can help us differentiate between ischemic and non-ischemic etiologies and specific cardiomyopathies have characteristic patterns on MRI. Further, MRI can reliably identify edema, inflammation, and fatty replacement. CMR can provide a wealth of information in a variety of disease processes. Enjoy Ep #33 – CMR!
    • When evaluating an unexplained cardiomyopathy, FDG-PET can be useful in identifying active myocardial inflammation. 18F-FDG is a glucose analogue that can differentiate activated macrophages in areas of inflammation from normal myocytes if there is appropriate suppression of normal physiologic myocardial glucose uptake (I.e., Ketogenic Diet). This can be especially useful in Cardiac Sarcoidosis. Note, if there is global myocardial uptake, without diffuse perfusion defects, it may be a false positive scan in the setting of inadequate prep!  
    • For more on evaluation of heart failure, enjoy Ep #12 – Eval of New Onset HF & CPS Ep #48 – HFrEF
  4. When should we consider a genetic cause to cardiomyopathy? 
    • If a family history suggests a genetic predisposition to cardiomyopathy, a cardiomyopathy seems out of proportion to an identified ischemic or non-ischemic cause, a patients presents with a cardiomyopathy at a young age, or if multi-modal imaging has not revealed a clear cause of a cardiomyopathy, genetic testing would be appropriate. 
    • Various studies have indicated that 30 to 50% of unexplained cases of (DCM) may have a genetic component. A detailed, at least three-generation family history should be obtained when initially evaluating a dilated CM, as most genetic cardiomyopathies are autosomal dominant with variable penetrance.  
    • Genetic counseling is key prior to genetic testing given complexities including interpretation of potentially confounding results and contextualizing results for relatives. 
  5. Our patient’s final diagnosis was “Arrhythmogenic Desmoplakin Cardiomyopathy”…what’s that?! 
    • Arrhythmogenic RV Cardiomyopathy is a familial cardiomyopathy which usually affects the RV via fibrous or fibro-fatty replacement of normal myocardium. This predisposes patients to sudden cardiac death (SCD), ventricular arrhythmias, and heart failure.  
    • ARVC classically displays autosomal dominant inheritance from mutations in genes encoding desmosomal proteins affecting the cell-to-cell junction: desmoplakin (DSP), plakophilin 2 (PKP2), desmoglein 2 (DSG2), and desmocollin 2 (DSC2). Rarely, genes unrelated to cell-to-cell junction may be involved.  
    • Clinically we have noted a “Left-Dominant Arrhythmogenic Cardiomyopathy” (LDAC), with similarities to classic ARVC, but affecting predominantly the LV.  
    • Genotype-phenotype studies are shedding light on these “Arrhythmogenic Cardiomyopathies”. DSP mutations affect predominantly the LV (causing LDAC) whereas PKP2 mutations affect predominantly the RV (causing ARVC); these are distinct entities with key differences in presentation, progression, and markers of SCD risk (see Smith et al., Circulation 2020 reference for more!). Pertinent to our case, a subset of patients with DSP cardiomyopathy will have evidence of myocardial inflammation on FDG-PET and will are initially misdiagnosed as a myocarditis or sarcoidosis. 

References


CardioNerds Case Reports: Recruitment Edition Series Production Team

50. Case Report: Hereditary Restrictive Cardiomyopathy – Duke University

CardioNerds (Amit Goyal & Dan Ambinder) discuss a case of hereditary restrictive cardiomyopathy with Duke University cardiology fellows Navid Nafissi and Sipa Yankey, and Marat Fudim, an advanced heart failure attending. E-CPR is provided by Dr. Richa Agarwal, fellowship program director of advanced heart failure and cardiac transplantation at Duke University with a final message by fellowship director Dr. Anna Lisa Crowley. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.  

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CardioNerds (Amit Goyal & Dan Ambinder) discuss a case of hereditary restrictive cardiomyopathy with Duke University cardiology fellows Navid Nafissi and Sipa Yankey, and Marat Fudim, an advanced heart failure attending at Duke University. E-CPR is  provided by Dr. Richa Agarwal, fellowship program director of advanced heart failure and cardiac transplantation at Duke University with a final message by fellowship director Dr. Anna Lisa Crowley. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A 69 yo M with history of atrial fibrillation presents with 5 months of progressive HF symptoms, now NYHA class IV. He was found to be grossly volume overloaded, tachycardic in atrial fibrillation, and hypoxic. CXR demonstrated significant cardiomegaly, and labs indicated new normocytic anemia with evidence of hepatic dysfunction and an elevated NT proBNP. TTE demonstrated massive bi-atrial enlargement, preserved ejection fraction, filling pattern consistent with grade III diastolic dysfunction, and torrential TR. The echocardiogram did not have evidence of constrictive pericarditis and agitated saline study showed Right to Left shunt through a likely PFO. MRI to evaluate for infiltrative cardiomyopathy did not show late gadolinium enhancement (LGE). RHC demonstrated findings consistent with restrictive cardiomyopathy including equalization of diastolic pressures, square root sign, and concordance of RV and LV pressures. PYP scan evaluating for TTR amyloid was negative and laboratory workup did not suggest AL amyloid, Fabry’s, Hemochromatosis, or storage disease. Patient’s symptoms remained refractory and thus eventually underwent successful OHT. Genetic testing eventually revealed missense mutation in MYBPC3 – revealing an inherited cause of restrictive CM for the patient! 


Case Media


Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. When thinking about the etiology of a restrictive cardiomyopathy, we can organize the causes into four major categories: 
    1. Infiltrative (e.g., amyloidosis, sarcoidosis) 
    2. Storage diseases (e.g., hemochromatosis, Fabry’s) 
    3. Non-infiltrative (e.g., idiopathic, diabetic cardiomyopathy, genetic causes) 
    4. Endomyocardial (e.g., endomyocardial fibrosis, hypereosinophilic syndrome) 
  2. On examination, patients with restrictive cardiomyopathy may have prominent right-sided symptoms, including hepatomegaly, ascites, and significant peripheral edema. On exam, neck veins may demonstrate a steep y descent, and cardiac auscultation may have a +S4, and murmurs of tricuspid and mitral regurgitation.
  3. A multimodal imaging workup is recommended for evaluating RCM.  
    1. TTE: Typically demonstrates normal LVEF, normal chamber volumes, biatrial enlargement, and restrictive diastolic filling patterns (.e.g, E/A > 2, E/e’ > 14, decreased mitral deceleration time < 150 ms). We can see increased wall thickness with infiltrative processes and storage diseases.
    2. cMRI: specific patterns of Late Gadolinium Enhancement may indicate certain pathology (e.g., amyloid may demonstrate diffuse subendocardial, heterogeneous, or transmural signal). T2 signal can identify inflammation and quantify iron. 
    3. PYP scan: It has a >99% sensitivity for cardiac ATTR amyloid. If monoclonal gammopathy excluded, PPV 100%. 
  4. Invasive hemodynamics can show physiology consistent with RCM. This includes square root sign, equalization of diastolic pressures, and concordance during respiration of LV/RV pressure changes. In contrast, constrictive physiology will yield discordant respirophasic LV/RV pressure changes. Endomyocardial biopsy may be necessary to identify etiology but the yield for patchy diseases, like sarcoid, can be low. 
  5. Patients with end-stage RCM can be difficult to manage medically, especially as they become refractory to diuretics. They poorly tolerate antihypertensive agents (due to inability to augment limited stroke volume), heart rate lowering medication (due to low SV, they are dependent on HR to maintain CO which is HR x SV), and have a very limited optimal preload window (need high filling pressures to fill the stiff ventricles but also have symptoms of fluid overload). Due to anatomic considerations, patients are rarely candidates for durable left ventricular assist devices and often require orthotopic heart transplant. However, patients with RCM have higher waitlist mortality and longer wait times, in part due to lower utilization of MCS.   

Educational Video

Produced by Dr. Karan Desai

References


CardioNerds Case Reports: Recruitment Edition Series Production Team

49. Case Report: Platypnea-Orthodeoxia secondary to a PFO – Allegheny Health Network

CardioNerds (Amit Goyal & Daniel Ambinder)  join Allegheny Health Network cardiology fellows (Adnan Khalif, Mahathi Indaram, Kushani Gajjar, and Michael Nestasie) for a lovely Pittsburgh hike and discuss a fascinating case of platypnea-orthodeoxia secondary to a PFO. Dr. Farhan Katchi provides the E-CPR and Program director Dr. Craig Alpert provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A 64 y/o female with a history of venous and arterial embolism on anticoagulation, known PFO, and obesity presented after a fall. There was no loss consciousness, pre-syncopal symptoms, chest pain, aura, weakness, or palpitations. She had no recent preceding illness. When she arrived in the ED she was hypoxic to 87% on ambulation on room air and required 4L of nasal cannula O2 supplementation. The AGH CardioNerds were consulted!  

On examination, the team noted that upon sitting up the patient would desaturate to the mid 80% but when lying down oxygen saturation would improve to 95%! Her ECG demonstrated a RBBB and no acute ST-T changes. TTE was obtained and showed normal LV and RV function and size, no valvular disease, and a likely PFO on an agitated saline study. Cardiac MRI revealed mild RV hypertrophy and Qp:Qs of 0.8 (right/pulm cardiac output < left/systemic cardiac output, indicating right to left shunting).  RHC showed normal right-sided pressures. A right femoral vein bubble study  was done showing torrential right to left shunting! She underwent PFO closure and her platypnea-orthodexia resolved; she was discharged on room air. 


Case Media


Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. Platypnea-orthodeoxia syndrome (POS) is when dyspnea (Platypnea) and hypoxia (Orthodeoxia) are present in the upright position, but improve upon lying flat. One cause is ARLIAS, or Acute Right-to-Left Inter-Atrial Shunting, which requires an anatomic component (I.e., ASD or PFO) and a functional component (I.e., PH, PE, RV failure) for Right-to-Left shunting to occur 
  2. A PFO, or patent foramen ovale is a common congenital defect and typically will not lead to hypoxia unless there is right to left shunting. Typically flow is left to right due to an LA to RA pressure gradient and lower compliance of the RV.  
  3. Remember when evaluating for a PFO with agitated saline, the timing of the appearance of bubbles is important!  Early appearance of bubbles (seen in less than 5 beats of the cardiac cycle, think about intra-cardiac shunt. Delayed opacification (> 5 to 6 beats) occurs when the bubbles slowly build in the LV with each successive beat as they circulate to the LV and suggests extra-cardiac shunt.  
  4. Cardiac MRI is helpful in quantifying the shunt fraction (Qp:Qs).  This is the ratio of pulmonary flow (Qp) to systemic flow (Qs), where hemodynamically significant Left-to-Right shunt is > 1.5, especially when we see RA/RV dilation. Qp/Qs < 1.1 indicates net R to L shunt. Other ways to measure a Qp:Qs are echocardiogram (less accurate) and right heart catheterization.  
  5. If there remains clinical concern for PFO with right to left shunting without evidence of a clear functional cause clinically or by catheterization (I.e., no evidence of high PA pressures, pericardial effusion, constrictive pericarditis), consider a right femoral vein bubble study. Upper extremity agitated saline enters the RA via the SVC; however, patients with prominent eustachian valve at the IVC can have blood flow directed towards the interatrial septum. This will be demonstrated on femoral vein bubble study! 

Educational Video

Produced by Dr. Karan Desai

References


CardioNerds Case Reports: Recruitment Edition Series Production Team

47. Case Report: Syphilitic Aortitis with Severe Aortic Regurgitation – UT Southwestern

CardioNerds (Amit & Dan) join UT Southwestern cardiology fellows (Shreya Rao, Sonia Shah, and Nick Hendren) for some delicious Dallas Tacos! They discuss a fascinating case of syphilitic aortitis with severe aortic regurgitation presenting as cardiogenic shock. Program director Dr. Gail Peterson provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. 

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

CardioNerds Cardiology Podcast: Episode 47: Syphilitic Aortitis with Severe Aortic Regurgitation - UT Southwestern
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

  • A 57 year old male presents with 3 months of progressive dyspnea on exertion, orthopnea and lower extremity edema. However, his symptoms suddenly worsened over the past few days. He has no other known medical history or prior surgeries. Further, he denies tobacco, alcohol or illicit drug use and reports a preference for male sexual partners.  
  • On presentation to the hospital, he had a markedly wide pulse pressure, a decrescendo diastolic murmur at the left upper sternal border and a water hammer pulse readily identifiable. TTE confirmed the clinical findings of severe aortic regurgitation with holodiastolic flow reversal in the thoracic, as well as the thoraco-abdominal aorta. Right heart catheterization was performed and showed equalization of the LVEDP and aortic diastolic pressure at 40 mmHg with Cardiac Output of 1.73 L/min. RPR was positive at a high titer (1:512). He was ultimately diagnosed with syphilitic aortitis with severe aortic regurgitation.  
  • He progressed to cardiogenic shock and was managed with nitroprusside, dobutamine, and furosemide infusion as well as IV penicillin for syphilitic aortitis and presumed neurosyphilis. The patient was stabilized and eventually underwent an uncomplicated prosthetic aortic valve replacement and aortic root resection and reconstruction and has done well post-operatively!  
  • Pathology was consistent with syphilitic aortitis: “lymphoplasmacytic inflammation, large foci of necrosis, and neovascularization” 

Case Media


Episode Schematics & Teaching

The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. When suspecting severe AR, first characterize the AR as either acute or chronic based on clinical evaluation and hemodynamics. From there, AR can further be characterized as primary (valve disorder) or secondary (disorder of the aortic root/aorta). 
  2. Chronic AR exposes the LV to volume overload (leading to increased LVEDV), afterload, and increased wall stress. Chronic severe AR has two phases: 
    • Compensated Phase: Responding to increased wall stress, eccentric hypertrophy occurs. LVEF is maintained during this stage, though LV dilation may begin to occur. Patients are typically asymptomatic.  
    • Decompensated Phase: Eventually, compensatory mechanisms are insufficient and significant LV dilation occurs and LVEF decreases. Patients will develop exertional dyspnea and CHF symptoms.   
  3. The physical exam of patients with chronic AR is full of classic findings and eponyms! Specifically, regarding murmurs of AR, there is the classic diastolic, blowing, decrescendo murmur heard in the LUSB. Typically, the severity of AR correlates with the duration of the murmur more than the intensity. 
  1. Some 2D echo findings of chronic, severe AR include pressure half-time less than 200 ms, holo-diastolic flow reversal in the proximal descending aorta and/or abdominal aorta, and a dilated LV due to remodeling. Other criteria include vena contracta > 0.6 cm, flail valve, regurgitant volume > 60 mL/beat, regurgitant fraction > 50%, and LVESD > 50 mm.  
  2. The goal of management of acute AR is temporary stabilization before proceeding with surgical intervention. This includes vasodilators to reduce afterload and potentially inotropy to support cardiac output. Avoid excessive negative chronotropy as it can prolong diastole and worsen acute AR. If patient is bradycardiac, can increase HR with beta agonists or temporary pacing to decrease time spent in diastole.  
Produced by Dr. Karan Desai, MD

References

CardioNerds Case Reports: Recruitment Edition Series Production Team

43. Introducing CardioNerds Case Reports – with Dr. Julia Grapsa

JACC: Case Reports Editor-in-Chief, Dr. Julia Grapsa joins Cardionerds, Amit and Dan, to introduce a new episode series: CardioNerds Case Reports (#CNCR)! We discuss the value of learning through cases, podcasts and other innovations in education, importance of promoting wellness in medicine, the editorial review process for case reports, and being an editor-in-chief as a woman in medicine.

The CardioNerds Case Reports series will shine light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert.

We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

Take me to the Cardionerds Case Report (CNCR) Series Page
Take me to the Cardionerds Episode Topics Page

43. Introducing CardioNerds Case Reports - with Dr. Julia Grapsa Editor-in-Chief of JACC: Case Reports
Episode graphic created by Dr. Carine Hamo

References

  1. Grapsa J (2019) Voices in Cardiology. JACC Case Reports.
  2. Grapsa J, Fuster V (2019) JACC: Case Reports: New Era of Clinical Cases, Bridging Patients With Guidelines. J Am Coll Cardiol.
  3. Grapsa J, Fuster V (2020) JACC: Case Reports: Moving to a Multimedia Educational Vehicle. J Am Coll Cardiol.
  4. (2006) Mindset: the new psychology of success. Choice Rev Online.
  5. Balasubramanian S, Saberi S, Yu S, Duvernoy CS, Day SM, Agarwal PP (2020) Women representation among cardiology journal editorial boards. Circulation.

Dr. Julia Grapsa serves as the Editor-in-Chief of JACC: Case Reports. Dr. Grapsa worked for Cleveland Clinic Abu Dhabi and then she moved to UK as a a consultant cardiologist for Barts Heart Center. In March 2020, Dr. Grapsa started working as consultant cardiologist at Guys and St Thomas NHS Trust. Within the UK’s leading structural valve disease group, Dr. Grapsa is responsible for the valvular heart disease network and echocardiography, a position previously held by Professor John Chambers. Dr. Grapsa has served as chair of the young community for multimodality imaging for the European Association of Cardiovascular Imaging and as a member of the European Society of Cardiology (ESC) education committee, leading the ESC clinical case gallery. She was responsible for ESC social media, since its birth and she has been a member of imaging and online education committees of Heart Failure Association. Prior to her role as JACC: Case Reports editor-in-chief, Dr. Grapsa served as an editorial consultant for JACC: Cardiovascular Imaging. She is a fellow of the ACC, the American Heart Association, the American Society of Echocardiography and the European Society of Cardiology.