58. Case Report: Constrictive Pericarditis – University of Tennessee

CardioNerds (Amit Goyal & Daniel Ambinder) join join University of Tennessee cardiology fellows (Rachel Goodwin, Emmanuel Isang, and William Black) for some chocolate cake and hikes in the Smoky Mountains! They discuss a fascinating case of constrictive pericarditis. Dr. Tjuan Overly 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 teachingReferencesProduction team

CardioNerds (Amit Goyal & Daniel Ambinder) join join University of Tennessee cardiology fellows (Rachel Goodwin, Emmanuel Isang, and William Black) for some chocolate cake and hikes in the Smoky Mountains! They discuss a fascinating case of constrictive pericarditis. Dr. Tjuan Overly 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.
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 man in his late 40s with a history of renal failure secondary to IgA nephropathy and now status post a kidney transplant 10-15 years ago was referred by hepatology for evaluation of recurrent ascites and LE edema. He appeared grossly volume overloaded on exam with JVP elevated past the mandible, RV heave, and 2+ pitting edema. TTE demonstrated LVEF of 55-60%, RVSP 40mmHg, abnormal septal motion with respiration, and respirophasic variation in mitral inflow across the mitral valve raising the suspicion for constrictive pericarditis. RHC pressures demonstrated a mean RA pressure of 20mmHg, RV 40/25mmHg, PA 38/30mmHg (mean 32 mmHg) and PCWP mean of 26 with V-waves at 28 mmHg. Simultaneous LV and RV pressure tracings showed ventricular discordance with respirophasic variation, consistent with constrictive physiology. Patient underwent pericardiectomy with markedly improved heart failure symptoms. Repeat TTE showed no evidence of constriction. 


Case Media

A. ECG
B. Pulsed-wave Doppler spectrum of tricuspid inflow velocities demonstrates a marked respiratory variation (In irregular rhythms, such as the atrial fibrillation seen here, respirophasic changes may still be seen but are confounded by the varying R-R interval)
C. Simultaneous LV and RV pressure tracings showing discordance with respirophasic variation

Apical 4-chamber view demonstrating abnormal septal motion due to interventricular dependence – dissociation of thoracic and cardiac chamber pressures leads to increased RV filling during inspiration
Short axis view of the LV demonstrating a D-shaped interventricular septum during inspiration.  Note the presence of a pericardial effusion as well.

Episode Schematics & Teaching


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

  1. The initial presentation clinically seemed to be right greater than left heart failure. What are the signs and common causes of right heart failure?   
  • The signs and symptoms of RHF are often similar to left-sided CHF, but may describe more severe dyspnea on exertion, significant abdominal distension, and early satiety due to ascites or gut edema. Symptoms of pulmonary edema from elevated left-sided filling pressures (orthopnea, paroxysmal nocturnal dyspnea) may be absent.
  • On examination, there will be elevated JVP with likely prominent v-waves, possibly Kussmaul’s sign (inspiratory rise in JVP rather than fall) depending on the pathology, abdominal ascites, pulsatile hepatomegaly, and lower extremity edema. An RV heave may be discernible along with a loud P2 component and murmur of TR.
  • Broadly, RV failure may be caused by pressure overload (ex: pulmonary hypertension, pulmonic stenosis), volume overload (ex: intracardiac shunt, tricuspid regurgitation), or myocardial disease (ex: cardiomyopathies, ischemia/infarct). The most common cause of chronic right heart failure is LV failure (causing post-capillary pulmonary hypertension). Other causes of RV failure include pre-capillary pulmonary hypertension, congenital heart disease (e.g., ASD, residual RVOT obstruction in Tetralogy of Fallot patients), ARVC, RV ischemia, myocarditis, right sided valvular disease, constrictive pericarditis, and restrictive cardiomyopathy.
  1. The patient in this case was diagnosed with constrictive pericarditis (CP). What are the causes of CP?  
  • Remember that the etiology of CP can vary considerably depending on the patient’s demographics. In developed countries, the majority of cases are idiopathic or viral, post-operative, or post-radiation therapy. In developing countries, infectious etiologies are more common, with tuberculosis the most common cause. 
  • Amongst the causes, remember that acute bacterial and tuberculosis pericarditis have the highest chances of progressing into constriction. With post-radiation constrictive pericarditis, remember there can be significant delay (even up to 20 years) between radiation therapy and development of constriction and often accompanies concomitant myocardial fibrosis with restrictive physiology as well. 
  • Other etiologies include immunologic disorders (e.g., rheumatoid arthritis, lupus, sarcoidosis), malignancy (e.g., breast and lung cancers, lymphoma, mesothelioma), and myocardial infarction.  

3.  What are the TTE findings suggestive of constrictive pericarditis?  

  • To understand the basic TTE findings, we need a basic understanding of the pathophysiology. Constriction leads to a noncompliant pericardium that encases the heart. Heart failure occurs because there is impaired diastolic ventricular filling.   
  • The ventricles fill almost entirely in early diastole, because once they can no longer expand because of the non-distensible pericardium, diastolic filling abruptly stops. This pathophysiology reflects one of the key findings in CP: equalization of the end-diastolic pressures. 
  • At the same time, the thickened/fibrotic/calcified pericardium prevents the normal transmission of intrathoracic pressures to the cardiac chambers. However, structures “outside” the pericardium – such as the pulmonary vasculature – still “see” the normal changes in intrathoracic pressure. Normally, when we take a breath in: the intrathoracic pressure falls and this is transmitted equally to the pulmonary capillaries (e.g., the wedge pressure) and the cardiac chambers. The gradient for mitral valve inflow reflects the difference in wedge pressure and intra-cardiac chamber (LV) pressure. 
  • In CP, the drop in intrathoracic pressure with inspiration is transmitted to the pulmonary capillaries but not the cardiac chambers. Thus, there is now a decreased gradient for mitral valve inflow during inspiration. This is called intrathoracic-intracardiac pressure disassociation. 
  • At the same time, with inspiration right heart preload increases and to accommodate this volume the RV expands. However, RV expansion is limited by the encasing noncompliant pericardium, and thus to accommodate the volume the interventricular septum shifts to the left. This, further decreases the gradient for mitral valve inflow and the physiology is termed enhanced ventricular interdependence. The opposite occurs on expiration.   
  • Thus, on echocardiogram we may see abnormal respirophasic septal shift, reflecting enhanced ventricular interdependence. The septum moves to the left in early diastole with inspiration and then back to the right on expiration. This is one of the most sensitive echocardiographic findings for CP. 
  • Reflecting compromised diastolic filling, markedly elevated filling pressures, and equalization of end-diastolic pressures, there will be a high E-wave velocity with a decreased A-wave velocity (E/A > 1) across the mitral valve. Due to pericardial restraint, this early rapid diastolic filling (high velocity with a tall E wave) stops abruptly and so the E wave has a short deceleration time. The latter is analogous to the pericardial knock heard on physical exam and the ventricular early diastolic “square root” sign (dip and plateau) on the RHC.  
  • Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, there will be increased respirophasic variation in mitral and tricuspid valve inflow. This typically is best demonstrated with the first few beats of inspiration and expiration. Specific cut-offs include a decrease in peak mitral E-wave velocity > 25% and increase in peak tricuspid E-wave velocity > 40% during inspiration (opposite during expiration). In other words, as you inspire there is increased filling of the RV with decreased filling of the LV.  
  • Expiratory hepatic vein diastolic flow reversal is one of the most specific findings of CP. Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, during expiration RV filling is compromised (as the LV is filling with septal shift to the right) and thus there is “back-flow” from the right heart and we see more prominent flow reversal in the hepatic veins during expiration. In contrast, hepatic vein diastolic flow reversal occurs predominantly during inspiration with restrictive physiology.  
  • Normally, the lateral e’ (tissue doppler) velocity > medial e’ velocity. In CP, we see annulus reversus, where the peak e’ at the medial annulus > lateral annulus because in constriction the lateral free wall may be tethered to the fibrotic/calcified pericardium and restricted in movement. In addition, when considering constriction vs restriction, normal or elevated annular e’ velocities are more consistent with constriction (normal myocardial relaxation) whereas reduced annular e’ velocities are more indicative of restriction (impaired myocardial relaxation).  

4. What are the characteristics of CP on invasive hemodynamics?  

  • All the findings on invasive hemodynamics are reflecting reliance on early diastolic filling and equalization of diastolic pressures. 
  • The end-diastolic pressures in the ventricles are usually within 5 mmHg of each other. 
  • We may see the square root sign on ventricular pressure tracings. The upward deflection in early diastole reflects rapid early diastolic filling and the subsequent plateau represents the abrupt halt in filling once the non-compliant pericardium can no longer expand. This is analogous to a pericardial knock on physical exam and a tall E wave with a short deceleration time on echocardiogram.  
  • The right atrial pressure waveform may have a “W-shape” reflecting rapid x and y descents. Conversely restrictive physiology may have rapid y descents but typically not with the x descent.  
  • Finally, simultaneous RV and LV pressures tracings will show discordance in pressures with respiration – with inspiration RV pressure increases and LV pressure decreases. This is analogous to respirophasic septal shift and changes in mitral and tricuspid inflow velocities seen on echocardiogram. This should not be present in patients with restriction.  
  • Note, if patients are hypovolemic, typical features of CP may not be seen, and thus a fluid bolus may be required to unmask the findings of CP.  

5. What’s the general approach to management of CP?  

  • If active inflammation is present on labs or imaging, trial a course of anti-inflammatory medications such as colchicine and NSAIDs is recommended before surgery. Similarly, patients with effusive-constrictive pericarditis a pericardiocentesis and a trial of medical therapy initially is recommended. Refractory cases may warrant anti-inflammatory escalation including steroids, steroid-sparing agents, and biologics including anti-IL1 agents. Prolonged courses may be required with therapy tailored to symptoms, inflammatory markers (ESR, CRP), and cardiac MRI. Enjoy Ep #33 – CMR with Dr. Kwon! 
  • If patient has persistent NYHA III or IV symptoms refractory to medical therapy without severe co-morbid illnesses, pericardiectomy may be indicated. Patients with idiopathic or viral pericarditis tend to have better outcomes with pericardiectomy than those with radiation therapy. 

References


CardioNerds Case Reports: Recruitment Edition Series Production Team

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

Jump to: Patient summaryCase figures & mediaCase teachingReferencesProduction team

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

53. Case Report: CTEPH & May Thurner Syndrome – Temple University

CardioNerds (Amit Goyal & Daniel Ambinder) join Temple Cardiology Fellows (Anika Vaidy and Anne- Sophie LaCharite-Roberge) in Philadelphia, PA! They discuss a fascinating case of pulmonary hypertension secondary to Chronic Thromboembolic Pulmonary Hypertension (CTEPH) associated with May Thurner syndrome and large uterine fibroids. Dr. Vaidya provides the E-CPR and message to applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. 

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

CardioNerds (Amit Goyal & Daniel Ambinder) join Temple Cardiology Fellows (Anika Vaidy and Anne- Sophie LaCharite-Roberge) in Philadelphia, PA! They discuss a fascinating case of pulmonary hypertension secondary to Chronic Thromboembolic Pulmonary Hypertension (CTEPH) associated with May Thurner syndrome and large uterine fibroids. Dr. Vaidya provides the E-CPR and message to applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, 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 woman in her late 40s with history of iron deficiency anemia, uterine fibroids, and recurrent DVTs/PEs for the past 6 years despite different anticoagulation regimens, presented with syncope and progressive dyspnea on exertion. Family history was negative for DVT/PE or hypercoagulable states. On exam, she was euvolemic. Labs were significant for anemia, a normal pro-BNP, and a negative extensive hypercoagulable workup. TTE showed interventricular systolic septal flattening, right ventricular outflow tract pulse wave doppler with mid-systolic notch, and shortened acceleration time consistent with elevated pulmonary artery pressure. A VQ scan showed bilateral right greater than left mis-matched perfusion defects. CT angiogram showed right greater than left chronic mural thrombus, correlating with pulmonary angiogram which showed severe proximal and mid-vessel disease on the right and distal disease on the left. RHC corroborated the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH) with mean pulmonary artery pressure of 41 and PVR of 5.2 Woods Units (WU).  

To determine the etiology of her recurrent clots, a lower extremity venogram was performed and showed 80% stenosis of her left common iliac vein by the overlying right common iliac artery confirming May-Thurner syndrome. Lower extremity venogram also showed severe proximal stenosis of right iliac vein thought to be due to large uterine fibroids. Given her severe proximal and mid-vessel clot burden, she underwent pulmonary thromboendarterectomy with a subsequent drop in pulmonary vascular resistance to 1 WU.  The etiology of DVTs and CTEPH was determined to be external compression related to both May-Thurner syndrome and uterine fibroids. To prevent future thromboembolic events, she underwent stenting of her left common iliac vein and hysterectomy. With these interventions, RV function returned to normal, and her symptoms completely resolved! 


Case Media

Figue Legend:
A. CXR
B. ECG
C. TTE: Interventricular systolic septal flattening, RVOT pulse wave Doppler with mid-systolic notch and shortened acceleration time, consistent with elevated PVR, RV:LV ratio 1.3, consistent with moderate RV enlargement, The RV is apex-sharing with an open apical angle
D. VQ Scan: Multiple b/l perfusion defects, R > L, V scan normal
E. CT Angiogram: 1) Enlarged R main PA2) large proximal chronic mural thrombus with minimal vessel count throughout R side, 3) Segmental LLL lining thrombus
F. Pulmonary angiogram significant for severe proximal and mid-vessel disease in the right segmental arteries. Patient also had severe distal disease in the left sub segmental disease (not shown).
G. Pulmonary Thromboendarterectomy (PTE)
H. LE Venogram: LEFT CIV  > 80% stenosis as a result of compression from an overlying right common iliac artery. This is consistent with May-Thurner syndrome. RIGHT EIV (not shown)– Significant proximal stenosis
I. Status Post left iliac vein stent
J. ECG: New typical atrial flutter


Episode Schematics & Teaching


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

  1. In patients with progressive dyspnea, exercise intolerance, and persistence of symptoms of PE despite adequate anticoagulation, there should be an evaluation for Chronic Thromboembolic Pulmonary Hypertension (CTEPH).  CTEPH is a form of pre-capillary pulmonary hypertension (PH) from incomplete resolution of pulmonary thromboemboli causing chronic, fibrotic, flow limiting changes to the pulmonary vascular bed. Risk factors include recurrent PE, hypercoagulable states, and medical conditions such as splenectomy, ventriculo-atrial shunts, infected intravenous catheters/devices, malignancy, and external venous compression. NOTE: many patients will not have a documented history of DVT/PE and so a high index of suspicion is important. 
  2. The following echocardiographic findings suggest pulmonary hypertension: interventricular systolic septal flattening indicating RV pressure overload, RV outflow tract (RVOT) pulse wave doppler with mid-systolic notch, decreased RVOT acceleration time, right atrial enlargement, right ventricular dilation and hypertrophy +/- functional tricuspid regurgitation, and an elevated estimated RV systolic pressure (RVSP). 
  3. CTEPH is rare and carries a high rate of morbidity and mortality; therefore, a high index of suspicion is necessary. There are two components to diagnosis:  
    • Diagnose CTEPH: Multiple imaging modalities are involved to confirm and assess severity. V/Q scan is highly sensitive and is the initial screening modality to detect perfusion abnormalities. Chest CT with IV contrast may identify parenchymal and mediastinal pathology not otherwise seen; although not sensitive, CT may show: PA dilation, eccentric filling defects with variable degrees of occlusion, vascular webs or bands, mosaic perfusion pattern of the lung parenchyma, and RV enlargement. RHC can confirm the diagnosis of pulmonary hypertension, differentiate pre-capillary from post-capillary PH, quantify vascular resistance and cardiac output, and can be a comparative marker post-intervention. Conventional PA angiography is useful for pre-operative planning. 
    • Diagnose the underlying predisposition/etiology: Think about Virchow’s Triad: Hypercoagulability, Stasis, and Endothelial injury. Apart from ruling out hypercoagulable states, evaluating for lower extremity vascular compression can be important in select patients with imaging such as venography. May-Thurner syndrome is a condition of extrinsic venous compression of the left common iliac vein by the common iliac artery. Evidence of any compression should be addressed to prevent future venous thrombi and subsequent emboli.  
  4. Treatment for CTEPH starts with lifelong anticoagulation. Pulmonary angiography aids in surgical planning as proximal disease is more likely to be operable than distal disease. Based on severity and other comorbidities, pulmonary endarterectomy (PEA) can be a favorable option. PEA improves symptoms, survival, hemodynamics parameters, and RV remodeling. Other treatment strategies include medical management, balloon pulmonary angioplasty, and lung transplant. Pulmonary artery denervation is being considered as an experimental modality.  
  5. Supraventricular tachycardia (SVT) is common in patients with pulmonary artery hypertension and CTEPH and often indicate progression of right-sided dysfunction. PH patients rely more on active than passive RV filling, and are highly sensitive to changes in RV afterload. Supraventricular tachycardias may further precipitate decompensation given (1) the loss of atrial kick which compromises diastolic filling, and (2) tachycardias which increase RV wall tension increasing RV afterload. Therefore, restoration of sinus rhythm is strongly encouraged. 

Educational Video

Produced by Dr. Karan Desai


References


CardioNerds Case Reports: Recruitment Edition Series Production Team

52. Women’s Heart Health & Women in Cardiology with Dr. Nanette Wenger

CardioNerds (Amit Goyal & Carine Hamo) discuss the past, present, and future of Women’s Heart Health & Women in Cardiology with Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger is a true leader in the field of women’s heart health and a strong proponent for women in cardiology and medicine. Her passion, dedication, and advocacy have inspired countless trainees to carry this torch and continue to build on her truly impactful work. Special introduction by Dr. Martha Gulati and birthday wishes to Dr. Wenger by the entire CardioNerds Team! Special thanks to Dr. Kimberly Manning for her invaluable mentorship.

CardioNerds (Amit Goyal & Carine Hamo) discuss the past, present, and future of Women's Heart Health & Women in Cardiology with Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger is a true leader in the field of women’s heart health and a strong proponent for women in cardiology and medicine. Her passion, dedication, and advocacy have inspired countless trainees to carry this torch and continue to build on her truly impactful work. Special introduction by Dr. Martha Gulati and birthday wishes to Dr. Wenger by the entire CardioNerds Team! Special thanks to Dr. Kimberly Manning for her invaluable mentorship.
Episode graphic by Dr. Carine Hamo

The Cardionerds CV prevention series  includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more!

CardioNerds Episode Page
CardioNerds Prevention Page
CardioNerds Women’s Cardiovascular Health Page
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Support our educational mission by becoming a Patron!

We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association.

Cardionerds Cardiovascular Prevention Series: by the Cardionerds Cardiology Podcast in Collaborate with the The American Society For Preventive Cardiology ASPC
Cardionerds Cardiovascular Prevention Series

References and Links

1. Wenger NK (2005) Women in cardiology: The US experience. Heart.

2. Douglas PS, Rzeszut AK, Noel Bairey Merz C, Duvernoy CS, Lewis SJ, Walsh MN, Gillam L (2018) Career preferences and perceptions of cardiology among us internal medicine trainees factors influencing cardiology career choice. JAMA Cardiol.

3. Wenger NK, Speroff L, Packard B (1993) Cardiovascular Health and Disease in Women. N Engl J Med.

4. Burgess S, Shaw E, Zaman S (2019) Women in Cardiology. Circulation.

Meet Dr. Wenger!

Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine.

Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America.

51. Case Report: Embolic Acute Coronary Syndrome from PFO & Pulmonary Hypertension – Lankenau Medical Center

CardioNerds (Amit Goyal & Dan Ambinder) join Lankenau Medical Center cardiology fellows (Gwen McNeill and Shaung Ooi) for some Philly cheesesteaks! They discuss a fascinating case of Embolic Acute Coronary Syndrome from PFO and Pulmonary Hypertension. Dr. John Clark provides the E-CPR and program director Dr. Jeanine Romanelli provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

CardioNerds (Amit Goyal & Dan Ambinder) join Lankenau Medical Center cardiology fellows (Gwen McNeill and Shaung Ooi) for some Philly cheesesteaks! They discuss a fascinating case of Embolic Acute Coronary Syndrome from PFO and Pulmonary Hypertension. Dr. John Clark provides the E-CPR and program director Dr. Jeanine Romanelli provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das 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 woman in her early 40s with history of tobacco and prior methamphetamine use presented with acute onset chest pain. She was found to have an elevated troponin, anterior T wave inversions, and apical akinesis on TTE. Coronary angiography showed a coronary embolism in the mid-distal LAD. Attempts to wire the lesion led to distal embolization of the clot, and IVUS showed no underlying arteriosclerosis.  

To investigate the etiology of the coronary embolus, a repeat TTE with agitated saline was done that suggested a PFO with right to left flow, as well as decreased RV function with an estimated RVSP of 70 mmHg. The clinical picture was that of a paradoxical coronary embolus, arising from the right (venous) side traveling to the left (arterial) side via a PFO. PFO closure was discussed but not performed given severe pulmonary hypertension with Right to Left shunt. In this circumstance, the PFO functions as a “pop-off valve” for the overloaded RV; closing it risks precipitating acute RV overload and failure. A RHC showed a PA pressure of 70/24 mmHg with mPAP of 40 mmHg, PCWP 5 mmHg, and PVR of 11 woods units. Given concern for idiopathic PH, a vasodilator challenge was done which did not show reactivity, and she was started on ambrisentan and sildenafil. Ultimately, the etiology of her pulmonary hypertension was felt to be due to PAH from prior methamphetamine use vs. idiopathic PAH. On follow-up, her PA pressures and RV function had greatly approved, allowing for safe and successful PFO closure in an attempt to prevent future emboli.  Final diagnosis: Embolic Acute Coronary Syndrome from PFO & Pulmonary Hypertension.


Case Media

1. Coronary angio of embolism
2. PFO on TEE with R to L shunt by Doppler
3. TTE bubble after PFO closure

Episode Schematics & Teaching


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

  1. Coronary emboli are an uncommon cause of myocardial infarction. We can think of the etiology of coronary emboli in three major categories: Direct, Paradoxical, or Iatrogenic. 
    1. Direct emboli originate from the left side of the heart: sources include clot (from atrial appendage, apical thrombus), valvular lesion (vegetation, thrombus, fibroelastoma), or left sided cardiac mass (atrial myxoma, rhabdomyosarcoma). 
    2. Paradoxical emboli originate from the right side or systemic venous circulation, and pass from right to left through an atrial septal defect, patent foramen ovale, or pulmonary arteriovenous malformation. 
    3. Iatrogenic emboli occur following procedures such as valve replacement or PCI. Note that iatrogenic is the most common etiology! 
  2. PFOs are present in up to 25% of adults, but are usually clinically insignificant. However, there is increasing evidence that PFO closure is moderately beneficial compared to antiplatelet therapy alone in patients less than 60 years old with cryptogenic, non-lacunar ischemic stroke. PFO closure may particularly benefit those with a large right-to-left shunt or an associated atrial septal aneurysm.
  3. Remember closing an ASD in the setting of significant pulmonary hypertension can lead to decompensation, as the interatrial connection may be serving as a “pop-off” valve to decompress the RV and maintain cardiac output in the setting of high PA pressures! Specifically, ASD closure is generally contraindicated if the PA systolic pressure is > 2/3 systolic blood pressure, pulmonary vascular resistance > 2/3 systemic vascular resistance, or if  a net right-to-left shunt is present. 
  4. Recall that the hemodynamic definitions of pulmonary hypertension changed in 2019. A mean pulmonary artery pressure of 20 or greater confirms a diagnosis of pulmonary hypertension. A PCWP ≤15 mmHg with pulmonary vascular resistance ≥3 woods units suggests pre-capillary pulmonary hypertension, while a PCWP >15 with pulmonary vascular resistance <3 woods units suggests isolated post-capillary PH.  
  5. During a right heart catheterization, a pulmonary vasodilator challenge can be done to identify vasoreactive patients who may respond to calcium channel blockers. This is typically recommended for idiopathic and hereditary PAH. A positive response is defined as a drop in mean PAP to <40 mmHg, with a decrease of at least > 10 mmHg, with unchanged or increased cardiac output. These patients can be started on amlodipine or nifedipine, but should be followed closely as they may not always remain vasoreactive and clinical deterioration is possible! 

Educational Video

Produced by Dr. Karan Desai

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.  

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

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

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.

35. Heart Failure with Preserved Ejection Fraction with Dr. Kavita Sharma

Heart Failure with Preserved Ejection Fraction with Dr. Kavita Sharma

We discuss Heart Failure with Preserved Ejection Fraction (HFpEF) with Dr. Kavita Sharma, director of the Heart Failure with Preserved Ejection Fraction Program and interim director of Advanced Heart Failure Transplant section at The Johns Hopkins Hospital. CardioNerds hosts Carine Hamo and Daniel Ambinder are joined by Dr. Beth Feldman (resident at The Johns Hopkins Hospital). Topics discussed include a definitions, diagnosis, phenotypic presentations, inpatient management of acute decompensated heart failure, role of dopamine, advanced therapies of HFpEF, and the Paraglide trial.

References mentioned in this episode can be found here

On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more.

Take me to the Heart Failure Topic Page
Take me to episode topics page

Acute Decompensated Heart Failure Primer – Youtube

Dr. Kavita Sharma graduated from the University of Virginia School of Medicine and completed her residency and served as the assistant chief of service, cardiology fellowship and advanced heart failure fellowship at the Johns Hopkins Hospital. She is the Director of the Johns Hopkins Heart Failure with Preserved Ejection Fraction Program and is currently the interim director of Advanced Heart Failure Transplant section at Hopkins. She has a specialized interest in heart failure with preserved ejection fraction (HFpEF), and directs one of the largest programs in the country dedicated to caring for patients with this condition. She is the principal investigator of numerous clinical and translational trials in HFpEF and leads a team of nurses, research coordinators, and fellows-in-training in this multifaceted program. She is an invited speaker at national meetings in topic areas covering advanced heart failure and HFpEF.

Dr. Beth Feldman graduated from Temple University School of Medicine and is currently on the Longcope Firm on the Osler Medical Service at Johns Hopkins University Hospital. Before pursuing a career in medicine, she worked in health care consulting focusing in health systems. She is passionate about health policy and health systems research. She is hoping to pursue a career in cardiology, with a particular interest in critical care.

34. Interventional Cardiology in Heart Failure with Dr. Jeffrey Moses

Cardionerds episode 34 with Dr. Jeffrey Moses discussing interventional cardiology in congestive heart failure.

Interventional cardiology and structural interventions in heart failure are discussed by Dr. Jeffrey Moses, Director of Interventional Therapeutics at Columbia University Medical Center Director of Advanced Cardiac Interventions at St Francis Hospital and Heart Center in Roslyn, NY. CardioNerds hosts Amit Goyal and Daniel Ambinder are joined by Dr. Jackie Latina (Cardiology fellow at The Johns Hopkins Hospital). Topics discussed include percutaneous intervention and complex and high-risk coronary intervention (CHIP), treatment of functional mitral and tricuspid regurgitation, aortic stenosis, and the utility of interatrial shunt devices for the treatment congestive heart failure.

On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more.

Take me to the Heart Failure Topic Page
Take me to episode topics page

Acute Decompensated Heart Failure Primer – Youtube

Dr. Jeffrey W. Moses completed medical school at the University of Pennsylvania School of Medicine and his internship, residency and fellowship in Cardiology at the Presbyterian University of Pennsylvania Medical Center. He currently serves as Director of Interventional Cardiovascular Therapeutics at Columbia University Medical Center and as Director of Advanced Cardiac Interventions at St Francis Hospital and Heart Center in Roslyn, NY. Dr. Moses is an Associate Director of the Transcatheter Cardiovascular Therapeutics (TCT) conference. He has served as lead investigator for numerous national and international clinical studies and he has made important contributions in the areas of clinical research and educational activities in interventional vascular therapy. He is also a pioneer in developing approaches involving minimally invasive surgery, angioplasty, gene therapy, novel imaging technologies and various support devices that allow for wider application of interventional cardiovascular procedures.

Dr. Jacqueline Latina was born and raised in the suburbs of Boston, MA, but fortunately escaped without a Boston accent. She is a graduate of Princeton University with an A.B. in chemistry. She earned her M.D. at Tufts University School of Medicine. Her internship and internal medicine residency were completed at Mount Sinai Hospital in New York City, where she stayed on for an American Heart Association postdoctoral research fellowship. She completed an M.S. in clinical research methods at the Columbia Mailman School of Public Health during that time. She is currently a cardiology fellow at Johns Hopkins Hospital, and plans to start interventional cardiology fellowship in June 2020.  She chuckles if you ask “Are you Latina?”