Cardionerds: A Cardiology Podcast

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74. Case Report: Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) – Summa Health Oct 22, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join Summa Health cardiology fellows (Jack Hornick, Phoo Pwint Nandar, and Sideris Facaros) for a hike on the Towpath Trail at Cuyahoga Valley National Park in Akron, Ohio! They discuss an informative case of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) complicated by ventricular tachycardia & cardiogenic shock. Dr. Kenneth Varian provides the E-CPR and program director, Dr. Marc Penn provides a message for 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 summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A female in her 40s with no past medical history presented 6 years prior with acute onset dizziness, palpitations and fatigue without chest pain. She had no family history of arrythmias, SCD, or prior syncope. Her heart rate was 170 bpm and EKG showed wide complex, regular tachycardia felt to be VT. She underwent synchronized cardioversion to sinus rhythm. Her baseline EKG showed sinus bradycardia with low voltage, incomplete RBBB, and ventricular ectopy. Labs were unrevealing, and social history was negative for toxic insults or illicit substance abuse. TTE showed preserved LVEF and normal valves, but RV was dilated with decreased systolic function. LHC was without obstructive coronary disease. She was diagnosed with ARVC and received an ICD for secondary prevention. She was discharged on sotalol for arrythmia management. Her genetic testing later returned positive for uncertain significance in the DSP gene and JUP gene, both commonly implicated in ARVC. She was followed in the outpatient setting for 5 years with no apparent shocks. Six years later, she presented with acute onset dizziness and palpitations similar to her initial presentation. EKG showed a wide complex tachycardia at 170 bpm treated with amiodarone and cardioversion. On ICD interrogation, she was found to have had several episodes of VT, but at a rates below the VT detection zone programmed in the ICD. Subsequent RHC showed significantly depressed cardiac index and RV dysfunction. She underwent successful inpatient VT ablation. She was then discharged home with plans for close follow up; however, 2 days later, she started feeling nauseous with fatigue and abdominal pain. She was sent straight to the nearest transplant-capable hospital where she was found to be in cardiogenic shock. She was admitted to ICU and started on inotropes. Due to refractory shock, she was cannulated for VA ECMO and successfully underwent cardiac transplantation two days later. Case Media 123Click to Enlarge A. Post cardioversion ECG: NSR, low voltage, incomplete RBBB, PVCB. TTE: RV enlargement C. TTE: Tissue Doppler velocity (S') low TEE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What is ARVC? Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) is a heritable cardiac muscle disorder that classically involves the RV (though LV involvement is increasingly being recognized) marked by loss of healthy myocardium and replacement with fibrofatty tissue predominantly due to genetic defects in both desmosomal and non-desmosomal proteins. Clinical manifestations include RV dysfunction, ventricular arrhythmias, and sudden cardiac death (SCD). This is a progressive disease that can affect the epicardium and/or mid-myocardium first and then move towards the sub-endocardium. It affects approximately 1 in 5000 individuals and is an important cause of (SCD) in young patients. 50% of patients have a positive family history and it is thought to be inherit in an autosomal dominant fashion, however prevalence is underestimated due to incomplete penetrance. Interestingly, males are more affected than females possibly due to interaction of sex hormones with pathophysiology or historically different levels of participation in competitive sports among men and women. The differential for ARVC should include Uhl's anomaly, myocarditis, sarcoidosis, and Brugada syndrome among other considerations. What genes are implicated and what is the pathophysiology? While 20-30% of ARVC is due to non-desmosomal gene variants (e.g., desmin, Titin) and non-genetic causes, 40-50% is due to autosomal dominant gene mutations that encode desmosomal proteins. These include plakophilin 2 PKP2 (in 10 to 45% of patients), followed by desmoplakin DSP (10 to 15%), desmoglein 2 DSG2 (7 to 10%), and desmocollin 2 DSC2 (2%). Rarely, there can be an autosomal recessive inheritance pattern, including Naxos disease (first recognized in the Cycladian Islands in the Aegean Sea) characterized by ARVC along with "wooly hair" and palmoplantar hyperkeratosis. Our understanding of the genetic underpinnings of ARVC continues to evolve. Desmosomes play a major role in intercellular adhesion and synchronized activation and signaling between myocytes. Defective desmosomes disrupt intercellular junctions which lead to myocyte detachment and myocyte death, and this process is especially exaggerated by mechanical stress like exercise. Athletes often have severe disease, possibly a result of high-intensity mechanical stress during exercise. Other resultant features of defective cardiac myocyte signaling is increased expression of adipogenic and fibrogeneic genes, resulting in the hallmark pathologic correlate of fibrofatty replacement of muscle tissue. The fibrofatty scar tissue that replaces the myocardium slows conduction and allows for formation of macro-entry circuits that lead to the propagation of arrythmias. Furthermore, dysregulation of otherwise synchronized excitability due to abnormal cellular connections increase propensity for fatal arrhythmias. What EKG findings may be seen in ARVC? EKG is an important tool in screening since 85-90% of patients will have at least one of the findings of ARVC. However, it is important to remember that the findings may evolve over time, including a normal ECG at presentation and thus serial re-assessment is crucial. ECG changes include inverted T-waves in the right precordial leads, which have been correlated with RV enlargement and risk for ventricular arrhythmias. T wave inversions (TWI) are present in up to 87% of adult patients with ARVC, but can be especially challenging to interpret in athletes who may have TWIs as normal variants in 5% of white athletes and 25% of black athletes. The preceding ST-segment may provide a clue as to whether the TWI is abnormal, as ARVC patients with precordial TWI often have an isoelectric ST-segment while athletes have preceding convex ST-segment elevation. Other findings include: (1) prolonged S-wave upstroke (≥55 milliseconds) in the absence of a RBBB (~90% of patients w/o a RBBB) (2) Epsilon wave (~ 5 to 30% of patients) which is a distinct positive deflection at the end of the QRS complex best seen in V1 and/or V2 reflecting delayed activation of some parts to of the RV. Fontaine bipolar precordial leads (repositioning of the limb leads) may help increase the sensitivity for detecting epsilon waves. Isoproterenol infusion can be used to induce ventricular arrhythmias in suspected patients How can we diagnose ARVC? In the "concealed phase," patients are often asymptomatic but are still at risk of sudden cardiac death, especially during exertion. Furthermore, in the early stages of disease, structural changes may be subtle (or even absent) and confined to a focal area of the RV. In the "electrical phase," patients can present with symptomatic ventricular arrhythmias and RV structural abnormalities that are detected by cardiac imaging. Sports and rigorous exercise increase risk of SCD and contribute to disease progression. Common first symptoms are palpitations and effort-induced syncope, though SCD can also be the first presentation. In the later stages, diffuse disease is possible with biventricular heart failure. In patients in whom there is a clinical suspicion for ARVC (e.g., positive family history, exercise-induced palpitations, unexplained right precordial TWI, patients who present with unexplained ventricular arrhythmias, and/or SCD), the diagnosis frequently requires multiple diagnostic tests. The 2010 revised Task Force Criteria is used to confirm the diagnosis of ARVC, though proposed changes continue to arise as our understanding of ARVC evolves. The criteria require a demonstration of structural, functional, and electrophysiological abnormalities that reflect underlying histological changes. Thus, the criteria include parameters defining (1) global and/or regional dysfunction and structural changes; (2) tissue characterization of the walls; (3) repolarization abnormalities on ECG; (4) depolarization/conduction abnormalities on ECG; (5) arrhythmias; and (6) family history. Criteria for diagnosis is based on meeting two major, one major and two minor, or four minor criteria. Cardiac MRI is the preferred imaging tool because it can quantitatively assess phenotypic structural and functional abnormalities such as global dilatation and/or systolic akinesia/dyskinesia. In suspected ARVC, late gadolinium enhancement can represent fibrofatty infiltration. It is important to note that endomyocardial biopsy is not indicated as routine testing, but may be considered to aid in securing a diagnosis amongst competing diagnoses. How is ARVC managed? In patients with suspected and/or confirmed ARVC, there are 5 pillars of management: Prevent sudden cardiac death....

73. Case Report: Wet Beriberi & Stiff Left Atrial Syndrome – Scripps Clinic Oct 20, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join Scripps cardiology fellows (Christine Shen and Andrew Cheng) for some Cardiology and California Burritos in San Diego! They discuss an informative case of Wet Beriberi and Stiff Left Atrial Syndrome. Dr. Thomas Heywood provides the E-CPR and program director Dr. Malhar Patel 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 summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-60s with history of rheumatic mitral stenosis s/p mechanical mitral valve replacement, HFpEF, and paroxysmal atrial fibrillation s/p ablation presents with subacute worsening dyspnea despite escalating diuretic doses. TTE shows an EF of 62%, normal gradients across the mitral valve without mitral regurgitation, and a dilated IVC. She is admitted with a presumed diagnosis of decompensated heart failure, and started given IV furosemide. Her symptoms slightly improve though do not resolve, and her creatinine increases from 1.4 to 2.1. In light of the unclear hemodynamic picture, a RHC is done, showing a RA pressure 9, RV pressure of 80/10, PAP 70/25 with mPAP 40, PCWP 30, SVR 872, CO 11 (by thermodilution), and CI 5.2. Notably, large V waves are noted on the RHC. Given concern for mitral regurgitation in the setting of large V waves, a TEE was pursued, which confirmed the lack of MR seen on TTE. Thus, her large V waves were felt to be due to stiff left atrial syndrome, and a cardiac CT showed a severely calcified "coconut left atrium". Labwork revealed a profoundly low thiamine level (21, with LLN of 70), raising concern for wet beri beri syndrome. The patient's unifying diagnosis was indolent left atrial syndrome that was exacerbated by high outout heart failure due to Wet Beri Beri syndrome. The patient received thiamine supplementation, and was diuresed to euvolemia with dramatic improvement in symptoms. A repeat RHC after thiamine replacement showed a CO of 5.7 and CI of 2.74 by thermodilution, demonstrating resolution of her high output heart failure. Case Media ABCDEFClick to Enlarge A. CXRB. ECGC. RHC: large V waves are noted on the RHCD. CO 11 and CI 5.2 by thermodilution pre-treatment E. Cardiac CT showed a severely calcified "coconut left atrium"F. Repeat CO of 5.7 and CI of 2.74 by thermodilution after thiamine replacement TTE 1 TTE 2 TEE 1 - Mitral Valve TEE 2 - Mitral Valve Cardiac CT Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This case featured a patient with Stiff Left Atrial Syndrome! Cardionerds, what the heck is that? Stiff Left Atrial Syndrome (SLAS) is fundamentally a disorder of atrial compliance, wherein a non-compliant left atrium (LA) leads to abnormal atrial diastole. During LV systole (atrial diastole), the LA receives blood from the low-resistance pulmonary veins. Under normal conditions, the LA pressures initially fall (x-descent). Then, as the atrium fills from both RV contraction and passive filling from the pulmonary veins, there is a steady and modest rise in LA pressure (v-wave). In patients with decreased LA compliance, the V-wave may be accentuated. In SLAS, left atrial compliance is significantly decreased, leading to very large v-waves that reflect the inability to accommodate LA filling and the steepened slope of the pressure-volume curve (see the below diagram from Urey et al). This leads to dramatically increased LA pressures during LV systole (especially in late LV systole), contributing to post-capillary pulmonary hypertension over time and symptoms of dyspnea on exertion. 2) Which patients are at risk of developing SLAS, how is it diagnosed, and how is it managed? Stiff Left Atrial Syndrome was first described in the late 1980s as a complication of mitral valve surgery, and has been increasingly recognized as a complication of left atrial ablation procedures leading to atrial fibrosis. While the condition is relatively rare (occurring in ~1.4% of patients following ablation), significant heart failure symptoms and pulmonary hypertension can develop. While no diagnostic criteria exist, SLAS should be considered in patients with HFpEF, a small or calcified LA on imaging, and risk factors including mitral valve surgery and/or prior left atrial ablations. Invasive hemodynamics will show large v-waves in the absence of mitral regurgitation (or disproportionate to the degree of MR) and an elevated PCWP out of proportion to the LVEDP. It is important to exclude pulmonary vein stenosis, another potential complication of ablation. Management consists primarily of diuretics and reducing ventricular afterload as tolerated, though an intra-atrial septostomy could be considered in refractory cases. Notably, SLAS may be asymptomatic in many patients due to the compliance of the pulmonary venous vascular system, which can store blood volume without significant increases in pressure. However, this compliance could become overwhelmed in certain stressed states or exercise. 3) Our patient experienced a stressor in the form of high output heart failure; what is the pathophysiology of high output heart failure, and what is your differential for high output heart failure? While a number of causes for high output heart failure exist, they share an underlying pathophysiology of excessively decreased systemic vascular resistance and increased metabolic demand. The persistently low SVR leads to decreased ventricular afterload, increased LV emptying and thus increased stroke volume and cardiac output. This subsequently leads to increased preload and symptoms of congestive heart failure. Furthermore, increased oxygen demands requires increased cardiac output. Additionally, the persistently low SVR causes low renal perfusion pressure (renal hypoperfusion) which leads to RAAS activation and volume expansion Diagnosis is based on echocardiographic evaluation, RHC hemodynamics, and an identified cause of a high output state. TTE may show normal or reduced ejection fraction; additional findings may include a dilated IVC, RV enlargement or dysfunction, elevated estimated pulmonary artery pressures, and/or LV enlargement. RHC typically shows a CO > 8 L/min or a CI > 4 L/min/m2, though these cutoffs are not absolute. The differential for high output heart failure includes etiologies secondary to predominantly low SVR (e.g., obesity, cirrhosis, AV fistula) versus those secondary to increased metabolic drive (e.g., hyperthyroidism, myeloproliferative disorders). See the CNCR episode from the Johns Hopkins Hospital for more details! 4) How does thiamine deficiency lead to high output heart failure? Thiamine is vital to aerobic metabolism in the Krebs cycle and the Pentose Phosphate Pathway. In states of thiamine deficiency, anaerobic metabolism is favored over aerobic metabolism, leading to increased levels of lactate and pyruvate. This leads to a decrease in adenosine triphosphate (ATP) and increase in adenosine monophosphate (AMP), which is released into skeletal muscle as adenosine. This release of adenosine leads to vasodilation and decreased systemic vascular resistance through shunt physiology. Arterial hypoperfusion of the kidneys leads to activation of the RAAS and expansion of plasma volume. Increased oxygen demand lead to an increased cardiac output. Importantly, CO by thermodilution and Fick may be discrepant in Beriberi! This is because mitochondria are unable to utilize O2 by performing aerobic metabolism. Thus, less oxygen is extracted from the blood, and venous oxygen saturations will be relatively elevated. This may leads to an erroneously elevated CO by Fick's method as compared to thermodilution! 5) Lets bring it all together! Cardionerds, what is your illness script for Beriberi? Pathophysiology: As detailed above, thiamine deficiency causes an increase in anaerobic metabolism, increased oxygen demand and systemic vasodilation through increased adenosine levels. Epidemiology: Patient populations at risk for severe thiamine deficiency include patients with severe malnutrition, chronic alcohol use, incarceration, social isolation, refugee populations, history of bariatric surgery, or chronic loop diuretic use. Notably, 90% of patients on diuretics can develop some level of thiamine deficiency. Signs/Symptoms: "Dry" beriberi involves symmetrical peripheral neuropathy, primarily in the distal extremities. "Wet" beriberi is characterized by high output heart fa

72. Case Report: Effusive Constrictive Pericarditis – University Hospitals Case Western Oct 19, 2020

Show notes

CardioNerds (Amit Goyal & Karan Desai) join University Hospitals Cleveland Medical Center cardiology fellows (Tarek Chami, Jamal Hajjari, and Haytham Mously) for some amazing pizza and coffee in Cleveland, Ohio! They discuss an important case of effusive constrictive pericarditis. Dr. Brian Hoit provides the E-CPR and assistant program director Dr. Claire Sullivan provides a message for applicants. We are grateful to chief fellow Scott Janus for his leadership in planning this episode! Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-70s presented to clinic with subacute onset shortness of breath. Her past medical history includes metastatic breast cancer s/p mastectomy, chemo/radiation, and hormonal therapy. Exam notable for tachycardia without hypoxia, muffled heart sounds, JVD with Kussmaul's sign, and 1+ LE edema. The patient was sent to the ED for evaluation of possible pericardial effusion. CTA chest in ED did not demonstrate a PE, but did show bilateral pleural effusions, and a moderate pericardial effusion with evidence of metastatic disease extending into the mediastinum. TTE obtained showing normal LVEF, moderate pericardial effusion with thickened pericardium, and significant respirophasic tricuspid and mitral inflow variations. Pulsus paradoxus was manually checked and found to be 16 mmHg. Due to concern for cardiac tamponade, she was taken to the cath lab for a RHC and pericardiocentesis. RHC prior to pericardiocentesis showed elevated left and ride sided filling pressures, blunted y decent in the RA, and equalization of diastolic pressures. Pericardiocentesis yielded 200 cc of bloody fluid with improvement, but continued elevation, in her L and R sided pressures. Blunted y decent did give way to a now rapid y descent concerning for constrictive pericarditis. She then underwent a cardiac MRI showing respirophasic septal motion suggestive of interventricular dependence and >1 cm thick pericardium with LGE c/w inflammation. Unfortunately, cytology of pericardial fluid was c/w a malignant effusion and despite treatment with a few months of anti-inflammatory therapy her symptoms did not improve. She then underwent a pericardial stripping with subsequent resolution of her symptoms. As her symptoms and hemodynamics were related to both the effusion and constriction, she was ultimately diagnosed with effusive constrictive pericarditis. Case Media ABCDEFGHIJKLMNOClick to Enlarge A. ECGB. CXRC-F. TTE (inflow velocities (mitral and tricuspid), IVC sniff test G-L: Right heart catheterization tracings M-N: Post pericardiocentesis TTE: Tissue Doppler O: Cardiac MRI CT Scan TEE - 1 TTE - 2 TTE - 3 TTE -4 CMR -1 CMR - 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is cardiac tamponade, what causes it, and how does it lead to hypotension? The pericardial cavity typically holds 50 cc of fluid, which acts as a lubricant for the beating heart. Accumulation of additional fluid in this space can increase intrapericardial pressure and cause compression of the cardiac chambers. Rapid accumulation of small amounts of fluid can lead to tamponade as the pericardium will not have time to expand. In instances of a slow accumulation, large volumes might accumulate before tamponade occurs as the pericardium will expand to accommodate the fluid. Many conditions can cause tamponade. The most common are malignancy (>50% of all cases), infection (viral most common, though TB is common in developing countries), trauma/post procedural (e.g. cardiac surgery, pacemaker placement), uremia, rheumatologic (e.g. SLE, RA), drug induced (e.g. hydralazine, procainamide), and radiation-induced. Note the epidemiology is different from causes of pericarditis without tamponade. Increasing pericardial pressure leads to a compensatory increase in diastolic pressure in all chambers until they become similar to the pericardial pressure. This happens more rapidly in the right side of the heart due to lower diastolic pressures in these chambers. The elevated intracardiac diastolic pressures reduces the driving pressure for filling (Flow = pressure gradient / resistance and so ↓∆P = ↓Flow ); this reduces diastolic filling (preload) and a causes a compensatory increase in contractility and heart rate to maintain stroke volume and cardiac output (CO = HR x SV so as SV decreases, the HR increases). As diastolic filling continues to decrease the transmural distending pressure of the RA and RV will also decrease and eventually lead to diastolic collapse. As reviewed in previous posts (Mayo and Tennessee), as ventricular interdependence worsens, left ventricular cardiac output can be further compromised and contribute to hypotension. Enjoy Episodes #58 and #59 discussing constrictive pericarditis. Tamponade can be a difficult clinical diagnosis. How is it diagnosed, what are some of the basic clinical markers of cardiac tamponade, and which are most useful in diagnosis? Though definitive diagnosis requires pericardiocentesis with hemodynamic and clinical improvement, there are many features that are useful for identifying tamponade. Unfortunately, no one clinical or echocardiographic feature is diagnostic of tamponade and a clinical diagnosis relies on the assimilation of multiple abnormalities. Beck's triad of hypotension, jugular venous distension, and muffled heart sounds Originally described in 1935 by Dr. Claude Beck, it focuses on these signs of tamponade, which were derived from surgical patients and are more characteristic of acute tamponade from trauma or cardiac/aortic rupture. Though ~90% of patients in trauma series have at least one of these findings, only about ~30% have all three. Muffled heart sounds and hypotension are both poorly sensitive findings, making the sensitivity of the overall triad poor. Tachycardia Though not specific, tachycardia is a very sensitive marker of cardiac tamponade as in some series it is present in 81-100% of patients with a pooled sensitivity of around 80%. Elevated JVP Elevated JVP is one of the key findings in tamponade and is present in almost all cases. Increased early diastolic pressure limits filling during this period, blunting the y descent. Studies show sensitivity ranges from 53-88% with a pooled average of 75%. Kussmaul's sign Kussmaul's sign is the failure of the JVP to fall during inspiration. This is rarely seen in cardiac tamponade; it is much more common in constrictive pericarditis, where it can be seen in up to 50% of cases. EKG findings of low voltage or electrical alternans As fluid builds around the heart it can insulate the heart's electrical activity from the EKG leads leading to low voltage on the EKG. Additionally, as the heart oscillates within the distended pericardial sack, the QRS amplitude can oscillate, which is called electrical alternans. As low voltage can be seen in a variety of conditions it is poorly specific, but sensitivity is around 70%. Electrical alternans on the other hand is rarely seen in tamponade, but if present it has a PPV > 95%. Enlarged cardiac silhouette on CXR The cardiac silhouette on a CXR does not appear enlarged until a pericardial effusion is around 200 mL. Given that many conditions also cause an enlarged silhouette it has both poor sensitivity and specificity. What is a pulsus paradoxus and what is the pathophysiology? How do you measure it and how clinically useful is it in the diagnosis of tamponade? What conditions might cause it to be absent in tamponade? In a normal heart, inspiration decreases intrathoracic pressure, thus increasing right-sided filling. As the RV stretches to accommodate the volume, the interventricular septum bulges towards the left causing reduced left-sided filling and therefore a drop in blood pressure (this is ventricular interdependence). During expiration the opposite happens and the blood pressure increases. This process is exaggerated in cardiac tamponade as both ventricles are completing for a limited amount of space, which leads to a larger than normal drop in blood pressure during inspiration. This exaggerated drop is called pulsus paradoxus (though pulsus exaggeratus may be a better name!). Pulsus paradoxus can be measured with a blood pressure cuff while a patient is breathing normally. First the cuff is inflated until no Korotkoff sounds can be heard and then slowly deflated until Korotkoff sounds can only be heard d

71. Case Report: Post-MI Ventricular Septal Rupture – University of Michigan Oct 14, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Michigan cardiology fellows (Apu Chakrabarti, Jessica Guidi, and Amrish Deshmukh) for some craft brews in Ann Arbor! They discuss a challenging case of Ventricular Septal Rupture after acute MI. Dr. Kim Eagle, editor of ACC.org & host of Eagle's Eye View Podcast, and Dr. Devraj Sukul provide the E-CPR and message for 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 summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his 60s with medical history of obesity and GERD presents with five days of progressive chest pressure radiating to bilateral arms and associated with dyspnea on exertion. Due to worsening chest pain with new lightheadedness, he decided to come to the ED. His presentation to the hospital was delayed due to fear of contracting COVID-19. In the ED, patient was afebrile, blood pressure 96/56, HR 137, RR 22, and oxygen saturation 94% on room air. On exam, he was ill appearing, acutely distressed, and altered. He had a 3/6 mid systolic murmur loudest at L sternal border, JVP to 10 cm H2O and had crackles up to mid-lung fields. His extremities were cool to touch. Labs notable for Cr 1.5, High-Sensitivity Troponin-T up to 5756, and lactate 3.9. EKG showed incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. Coronary Angiography showed mid-RCA occlusion with faint L to right collaterals. He underwent PCI with restoration of TIMI 3 flow. After PCI, he continued to be hypotensive requiring IABP and norepinephrine. PA catheter demonstrated (in mmHg): RA 26, RV 63/29 (31), 55/36 (44), PCWP 29, and CO 5 L/min, CI 2.2, and SVR 467. Shunt run of mixed venous O2 saturation showed: SVC 71%, RA 72%, RV 62%, PA 85% with oxygen step up in the R-sided circuit. Left ventriculogram then confirmed septal rupture with contrast extravasation from LV into RV. Due to worsening shock, he was stabilized on VA ECMO which was complicated by hemolysis and acute renal failure requiring CVVHD. On day 7 after presentation, he underwent surgery which revealed a large 6x6 cm ventricular septal defect on the posterior aspect of the septum and repaired with a large bovine pericardial path. He was eventually discharged after a prolonged stay and repeat TTE on follow up showed biventricular dysfunction and residual 1cm VSD. Case Media ABCDClick to Enlarge A. ECG: Incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. B. Coronary angiography: mid-RCA occlusion with faint L to right collaterals.C-D. A large (6x6cm) VSD was found at the posterobasal aspect of the septum. Infarcted tissues were removed and a large bovine pericardial patch was used to repair the defect (due to the size of the defect, there was very little viable septum remaining and the patch had to be sewn directly into the LV and RV walls). LV gram performed showing a left to right shunt. TEE -1 TEE - 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Classification and Management of Post-AMI VSR Why and in whom should we worry about VSR? Ventricular Septal Rupture or VSR is rare in the era of early reperfusion strategies. Historical incidence of VSR after AMI was thought to be 1-2% and has decreased to between 0.17% and 0.3%. It can be attributed to early identification and restoration of flow in the infarct related artery (IRA). Although the incidence has decreased, the mortality remains high (41-80%). Risk factors include older age, female sex, history of heart failure, and chronic kidney disease. If VSR does occur it tends to be in a patients presenting with their first MI with delayed, failed or no reperfusion therapy. The presence of collaterals is likely protective against developing VSR and reducing size of infarct. How do we recognize and diagnose VSR after AMI? Abrupt hemodynamic compromise after revascularization or refractory shock with AMI should prompt suspicion for mechanical complications, including VSR. Note: some patients may be stable early in their course. The classic presentation would be recurrent chest pain and hypotension several days after an MI, along with a new harsh holosystolic murmur usually best heard at the left lower sternal border sometimes accompanied by a thrill. Identifying this murmur requires a thorough baseline examination and frequent re-evaluation. Note, the absence of this murmur does not rule out VSR as the murmur may not be audible in a large VSR. In terms of making the diagnosis of VSR, TTE is the starting point. The location of the VSR will likely depend on the infarct related artery (see below), but the two most common locations are basal inferoseptal and anteroapical septal walls. To identify the VSR it is critical to use color doppler in the area of interest and to lower the Nyquist limit to readily identify lower velocity flow with better definition. TTE is also critical to define worsening pulmonary hypertension and/or left and right ventricular dysfunction as these are prognostic factors. When there are poor image quality and the defect cannot be readily identified, TEE may be necessary. If a RHC is available, we can identify a left to right shunt via an oxygen step-up. Normal oxygen saturation in the RV is typically 64 to 68%. When there is an increase in oxygen saturation from RA to RV (or PA) of greater than 5% that can be suggestive of a VSR. Further, we can calculate the shunt fraction to quantify the extent of the shunt. During a left heart catheterization, LV ventriculography can identify the VSR When does VSR occur post AMI and how does IRA relate to VSR location? It is historically thought to occur between 3-6 days after AMI, however newer studies show earlier development with one study showing median time of 16 hours after AMI. This may be related to more awareness, increased access to echo, or a change in the presentation of VSR due to earlier reperfusion strategies. The LAD and the RCA are the arteries most commonly implicated in the development of a VSD. Remember, anatomically, the LAD supplies the apical portion of the ventricular septum and the RCA gives posterior septal perforators that supply the basal inferoseptal wall. These areas are the most common locations for VSR after a transmural infarct as they are located at the border zone of a myocardial infarct. Remember the defect can be simple or complex. A complex VSR is associated with multiple areas and various dissection planes that track along the myocardium. What is the pathophysiology and classification for VSR We can classify VSR in 2 ways: the Becker and Mantgem system and simple vs. complex. The Becker and Mantgem system was originally made for cardiac free wall rupture, but is also used for pathological classification of VSR. There are 3 mechanisms and pathophysiologic findings that correlate with temporal presentation. Type 1 : Occurs acutely (24 hours) typically shows slow erosion of infarcted myocardium due to neutrophilic infiltration of ischemic/necrotic tissue Type 3: Occurs late following an MI and after aneurysm formation and then subsequent rupture In the simple vs. complex VSR classification, we classify VSR as simple if there is a direct connection between the LV and RV. Meanwhile, a complex VSR is a serpiginous connection (multiple planes) and more likely caused by hemorrhage. What are the goals of management and definitive therapy? Surgical repair is the ideal definitive treatment, though mortality is very high. Patients with worse outcomes after surgery are female, older, RV dysfunction and have higher level of cardiac circulatory compromise. Newly infarcted tissue is weak and friable, may not hold sutures well, and is prone to repeat defects. Successful repair requires complete debridement of necrotic tissue and sparing of healthy tissue which may be difficult to differentiate in the early stages after infarction. Surgical mortality appear to be higher with basal inferoseptal rupture associated with inferior MI, as these patients may need concomitant mitral valve repair as they often have ischemic MR as well Timing of surgery is a complex issue and there are no clear guidelines for timing of surgery and therefore it is an individualized decision....

70. Case Report: Post-MI Free Wall Rupture & Pseudoaneurysm – UCONN Oct 13, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour Almnajam, Justice Oranefo, Yasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture & pseudoaneurysm as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid 50s with no significant PMH presented with a 10-day history of chest pain that progressed to acute pleuritic pain and shortness of breath in the past 24 hours. On arrival, he was hypothermic, in rapid atrial fibrillation with HR in the 130-150s, and an initial BP was not able to be obtained. He was tachypneic with labored breathing, lethargic, and cyanotic. Exam revealed markedly elevated JVP, cool extremities, and diminished breath sounds with bibasilar rales. Labs demonstrated leukocytosis, significantly elevated liver enzymes, troponin-I at 10.91, elevated NT-proBNP, and lactate at 6. ECG demonstrated tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves concerning for a posterior infarct. He was immediately intubated, cardioverted into NSR, and started on vasopressors. Bedside echocardiogram demonstrated diffuse LV hypokinesis with akinesis of the inferolateral wall, LVEF 25-30%, and pericardial fluid with hyperechoic material adherent to the inferior wall as well as tamponade physiology. Chest CTA was negative for aortic dissection and confirmed hemopericardium. He was taken to the OR where he underwent a subxiphoid pericardial window. They found significant clot burden (both old and new), but no frank rupture. Adherent clot was not removed to prevent further hemodynamic compromise. Intraoperative TEE additionally demonstrated severe eccentric MR with partial posteromedial papillary muscle rupture. An IABP was placed and inotropic and vasoactive support was continued to temporize pending definitive therapy and the patient improved hemodynamically. Repeat TTE prior to surgery demonstrated a large apical and inferolateral pseudoaneurysm. Coronary angiogram revealed proximal occlusion of the LCx and diffuse three vessel coronary disease otherwise. He ultimately underwent CABG, mechanical mitral valve replacement, and pericardial patch repair of the ventricular pseudoaneurysm. Final diagnosis: Free Wall Rupture & Pseudoaneurysm. Thankfully, the patient ultimately made a complete recovery! Case Media ABCDEFClick to Enlarge A. ECG: tall, broad R-waves in V1-V4 with downsloping STD and upright T-wavesB. CXRC. CT angiogram thoracic aorta: Moderate sized hemopericardium with tamponade physiology. Transmural infarction of LV base to mid inferior wall. Circumflex occlusion just beyond the first obtuse marginal. Normal aorta without dissection or aneurysm.D-F. Coronary angiogram: LCx is occluded proximally, distal vessel fills via faint collaterals from the right, OM1: Fills via right to left collaterals. LAD: 70%, mid; 90%, apical, 1st diagonal: 50%, ostial; 60-70%, proximal; 90% of inferior subdivision, bifurcating vessel. RCA: (Dominant); 50%, mid: 40%, distal. PDA: 60%, proximal, small-caliber vessel. PLV: 60-70%, proximal TEE: Trans-gastric views TEE TEE: MV with color CORS: Occluded Lcx CORS: Obstructive CAD in LAD CORS: RCA TTE: PLA TTE: A4C TTE: A4C with contrast demonstrating an LV pseudoaneurysm Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case This patient presented with EKG showing a posterior myocardial infarction. Why was he not taken to the cath lab immediately for revascularization? Duration of ischemia, its relationship to infarct size, and the mortality benefit from reperfusion therapies are crucially related to time in the very early course of STEMI. However, this relationship breaks down in patients presenting late after a STEMI. In OAT (Occluded Artery Trial), hemodynamically stable patients who presented late (3-28 days) after a myocardial infarction with high risk features (e.g., proximal LAD occlusion with TIMI 0 to 1 flow) were randomized to PCI + optimal medical therapy (OMT) within 24 hours or OMT alone. There was no difference in the primary endpoint of all-cause mortality, nonfatal MI, or NYHA class III to IV heart failure. These findings are reflected in the ACC/AHA guidelines, where delayed PCI of a totally occluded infract artery >24 hours after STEMI in hemodynamically and electrically stable patients is given a Class III recommendation (no benefit). Although the patient presented with EKG findings concerning for a posterior STEMI, this was likely 10 days after his acute insult. In addition, his hemodynamic instability and bedside POCUS raised the concern for a mechanical complication of a STEMI. In a patient with suspected mechanical complication of acute MI, such as free wall rupture and acute MR, the priority of therapy is to rapidly identify the mechanical problem and perform emergency surgical therapy. Furthermore, the need for antiplatelet therapy following any PCI would complicate surgical planning. PCI may be helpful in patients with ischemia induced papillary muscle dysfunction ("ischemic MR"). However there is no role for immediate PCI when the mechanical integrity of the mitral valve has been compromised. This patient presented with hemodynamic instability and bedside POCUS revealed pericardial fluid with tamponade physiology. What are some causes of acute hemorrhagic pericardial effusion? When thinking about hemorrhagic pericardial effusions, expedited evaluation is critical. While there is overlap with traditional causes of pericardial effusion, some causes may need immediate intervention. Amongst these considerations are iatrogenic complication of cardiac surgery, cardiac catheterization, or electrophysiologic procedures. Other etiologies include complications of myocardial infarction including free wall rupture/pseudoaneurysm, complication of aortic dissection, and trauma. As with serous pericardial effusions, malignancy should remain on the differential, as well as tuberculosis in endemic areas. A CTA of the aorta ruled out dissection but showed a moderate sized hemopericardium raising concern for a mechanical complication of posterior MI, specifically a free wall rupture (FWR). What are the risk factors for a FWR after an MI? Ventricular free wall rupture is quite uncommon in the reperfusion era; however, if it does occur, mortality rates are high. FWR typically occurs acutely or sub-acutely, occurring within 2 weeks for 90% of patients. Risk factors include first myocardial infarction, poor collateralization of the infarcted territory, older age, female sex, persistent ST elevation and delayed presentation/unsuccessful revascularization. When patients present acutely, patients will typically develop tamponade, rapidly progress to pulseless electrical activity, and/or sudden cardiac death. When patients develop subacute FWR or contained rupture (i.e., pseudoaneurysm), they may present with signs and symptoms of pericarditis and subacute hypotension. When FWR occurs, it typically involves the anterior, posterior, or lateral left ventricular wall. The pathophysiology of ventricular free wall rupture is related to the timing of the rupture. Rupture will typically occur at the border of the necrotic and healthy (and often hyperkinetic) myocardium and in areas of the greatest shear stress. In the left ventricle, this tends to be near the anterior and posterior papillary muscles, regardless if they are compromised in the infarct. Note, pericardial effusions can be a common finding in the setting of an acute MI (~15-25% of patients in the acute setting); however, a rapidly expanding pericardial effusion associated with significant wall thinning along the infarcted region should raise the suspicion for LV free wall rupture. The patient was stabilized after surgical evacuation of pericardial fluid in the OR. When should you consider pericardiocentesis vs surgical management? In cases of cardiac tamponade with concern for circulatory collapse there are no absolute contraindications to pericardiocentesis. The goal is urgent drainage of pericardial fluid and how we drain the fluid will depend on the etiology, acuity, and available providers....

69. Case Report: Cardiac Allograft Vasculopathy (CAV) – UCSD Oct 13, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join University of California San Diego (UCSD) cardiology fellows (Harpreet Bhatia, Dan Mangels, and Quan Bui) for a relaxing beach bonfire in the beautiful city of San Diego! They discuss a challenging case of post-transplant cardiac allograft vasculopathy. Dr. Hao (Howie) Tran provides the E-CPR and program director Dr. Daniel Blanchard 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 summary - Case media - Case teaching - References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his late 20s with a past medical history of orthotopic heart transplant, presents with one-week of progressive lower extremity edema and dyspnea with NYHA class IV symptoms. 5 years prior, he underwent orthotopic heart transplant for arrhythmogenic right ventricular cardiomyopathy. Subsequently, he has had multiple episodes of rejection or recurrent graft dysfunction. On presentation, he was normotensive and borderline tachycardic. Exam revealed elevated JVP, decreased breath sounds, and pitting edema. Labs demonstrated leukocytosis, acute kidney injury, and elevated pro-BNP. TTE demonstrated LVEF 35%, apical akinesis, and grade III diastolic dysfunction (all similar to prior). He was initially diuresed and RHC/EMB was performed to evaluate for rejection. Early in his course, the patient unfortunately suffered a PEA arrest with ROSC was quickly achieved after 1 minute of CPR. He was intubated and cannulated for VA ECMO. EMB demonstrated ISHLT Grade 1R cellular rejection and he was ultimately listed for re-transplant. Shortly thereafter, the patient received an OHT. His pathology demonstrated intimal thickening of all his coronaries, consistent with coronary artery vasculopathy, felt to be the major contributor to his presentation. Case Media ECG Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is CAV? CAV stands for cardiac allograft vasculopathy. Within the transplanted heart, CAV is the proliferation of vascular smooth muscle and intimal thickening in the epicardial coronary arteries and microvasculature leading to diffuse narrowing. CAV is common, present in greater than 30% of patients at 5 years post-transplant. It is a significant contributor to post-transplant mortality after the first year. CAV, in contrast to typical atherosclerotic lesions, is diffuse and concentric while atherosclerosis tends to be focal with eccentric luminal narrowing and heterogenous plaque composition. Patients s/p OHT can still develop typical coronary artery disease, likely developed from pre-existing disease in the donor heart. CAV should be high on the differential for the cause of graft dysfunction, especially after the first year post-transplant. 2. How and Why Does CAV Occur? CAV has multiple contributing factors. There are immunologic and non-immunologic factors, but it appears the immunologic components play the larger role given that the pan-vasculopathy develops in the donor heart and not in the recipient's vasculature. In CAV, there is chronic immune-mediated injury creating a persistent inflammatory state in the donor coronary endothelium leading to a neointimal proliferative process in the coronaries. Amongst immunologic factors, it appears the number of episodes of cellular rejection correlates with the development of CAV. CAV occurs when foreign antigens are recognized by the host immune system as "non-self," a process termed allorecognition. T-cells are subsequently activated, and release a number of inflammatory cytokines that leads to additional T-cell stimulation, inflammatory cell proliferation, and endothelial cell propagation. Ultimately this inflammatory cascade leads to smooth muscle cell advancement and intimal growth into the arterial lumen. Other immunologic factors include HLA mismatch and antibody-mediated rejection. There are numerous non-immunologic factors, including older donor age, CMV infection, hyperlipidemia, insulin resistance, donor brain death secondary to intracranial hemorrhage, and prolonged ischemic time. 3. How Do Patients with CAV Present? Donor hearts are denervated at explantation, and so post-transplant patients typically will not develop classic anginal symptoms as seen with typical atherosclerotic coronary disease. Thus, routine surveillance is necessary (see below). If not diagnosed early, the clinical presentation may include LV dysfunction (with or without symptoms), acute myocardial infarction, heart block, arrhythmias, syncope, or sudden cardiac death. 4. How Do We Diagnose CAV? Routine surveillance is necessary because patients are generally asymptomatic and there is a high incidence of CAV posttransplant. The most common method for screening includes coronary angiography, but its sensitivity is reduced compared to traditional atherosclerotic disease as CAV is diffuse. Intravascular ultrasound (IVUS) significantly improves sensitivity and the early the detection of disease. The timing and method of screening will be center-specific. As the patient is farther removed from their transplant date, dobutamine stress echo may be a reasonable method to screen for CAV. Myocardial perfusion imaging, specifically with PET Rest/Stress with absolute myocardial blood flow quantification, and coronary CTA may also be effective methods to diagnose CAV. The ISHLT grading of CAV by angiography is as follows: CAV0 (Nonsignificant): No detectable angiographic lesion CAV1 (mild): Angiographic LM lesion

68. Case Report: WPW and HCM Phenotype – VCU Oct 09, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join Virginia Commonwealth University (VCU) cardiology fellows (Ajay Pillai, Amar Doshi, and Anna Tomdio) for a delicious skillet breakfast and amazing day in Richmond, VA! They discuss a fascinating case of a patient with Wolff-Parkinson-White (WPW) and hypertrophic cardiomyopathy (HCM). Dr. Keyur Shah provides the E-CPR and program director Dr. Gautham Kalahasty provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s presented to the ED after an episode of unwitnessed syncope while drinking. Patient had suddenly passed out from a seated position with no prodrome or post-ictal state. He had episodes like this in the past, which were thought to be seizures, but otherwise PMHx only notable for alcohol use disorder. He denied any FH of SCD or syncope. In the ED, exam was unremarkable. Labs notable for mild thrombocytopenia, mild hyponatremia with AKI, 2:1 AST/ALT ratio, elevated NT-proBNP, and a very high lactate that rapidly corrected with fluids. EKG was notable for sinus tachycardia, short PR interval, wide QRS, and delta waves consistent with Wolff-Parkinson-White (WPW) pattern. Echo showed preserved LVEF, thickened LV septum (1.6 cm) and posterior wall (1.3 cm) concerning for hypertrophic cardiomyopathy (HCM). No outflow tract gradient was noted at rest or with stress, and the strain pattern demonstrated apical sparing. Evaluation for cardiac amyloid, including plasma cell dyscrasia and PYP scan, was negative. Cardiac MRI confirmed severely thickened LV inferior and inferolateral walls at 1.7 cm with no LVOT obstruction. 25% of the myocardium demonstrated patchy LGE. Due to concern for WPW syndrome, the patient underwent an EP study. This revealed a malignant septal accessory pathway that was successfully ablated with resolution of the WPW EKG features. Given large LGE burden in setting of HCM, patient underwent placement of primary prevention ICD. Genetic testing for PRKAG2 mutation is pending given comorbid WPW and HCM. Case Media AECDBFClick to Enlarge A. CXR: Slightly increased interstitial markings in the lung bases, an elevated right hemidiaphragm. No acute airspace disease or pulmonary edemaB. ECG: Sinus tachycardia rate 120bpm, PR interval 80ms, QRS 130ms, WPW pattern. Arruda algorithm localizes to posterior septum.C. CMR: Myocardium nulls before blood pool.D. CMR: Delayed gadolinium enhancementE. Follow up ECG: NSR 78, repolarization abnormalities. T wave memory inferior leads.F. CXR status post dual chamber ICD implantation TTE: Apical 4 chamber TTE: Apical 2 chamber TTE: Apical 3 chamber TTE: Strain imaging CMR: 4 chamber cine CMR: 2 chamber cine CMR: 3 chamber cine CMR: Short axis cine at base level CMR: Short axis cine at mid-papillary level CMR: Short axis cine at apical level Episode Schematics & Teaching Hypertrophic Cardiomyopathy InfographicClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Our patient was found to have Wolff-Parkinson-White (WPW) pattern. What are the diagnostic criteria for WPW pattern and how does it differ from WPW syndrome? How can you localize the accessory pathway using the EKG? WPW pattern refers to the presence of the below criteria on a patient's surface EKG in the absence of symptomatic arrhythmias. If symptomatic arrhythmias related to the accessory pathway occur, then it is WPW syndrome. Symptoms may include palpitations, shortness of breath, presyncope, syncope, and sudden cardiac death (SCD). Not all patients with accessory pathways have EKG findings as only 60-75% of accessory pathways are "manifest" (meaning they conduct antegrade from atria to ventricles or are bidirectional). Conversely, a "concealed" accessory pathway only conducts retrograde (from ventricles to atria) and would not be apparent on resting sinus EKG; these patients can have WPW diagnosed after a ventricular premature beat, ventricular pacing, or an EP study that shows retrograde conduction through the accessory pathway. The WPW pattern is diagnosed by the following EKG criteria: Short PR interval 120 ms. The degree of pre-excitation on EKG depends on the position (how much of the ventricular myocardium is depolarized by the accessory pathway) and depolarization speed of the accessory pathway (more rapid conduction leading to earlier ventricular depolarization and wider delta wave). We can use EKG findings to localize accessory pathways using the Arruda Criteria, which has an overall sensitivity of 90% and specificity of 99%. Note, patients who have a left-lateral bypass tract as the antegrade limb may not have delta waves on surface EKG, as the atrial impulse can take longer to reach the bypass tract than the AV node. What are the major mechanisms for WPW and how do they lead to early activation of the ventricles? How can this precipitate arrhythmias? Accessory pathways are abnormal congenital connections between the atria and ventricles when there is incomplete atrio-ventricular isolation during fetal development. They can be associated with congenital cardiac malformations like Ebstein anomaly. Depolarization of the ventricles occurs via the AV node and the accessory pathway simultaneously, leading to early depolarization of a portion of the ventricles and the characteristic delta wave. Depolarization through the His Purkinje system reaches the apex first and travels back up the ventricle, meeting the slower cell to cell conduction from the accessory pathway and causing termination of the impulses. The resulting QRS complex is essentially a "fusion beat" between the two sources. Accessory pathways often have more rapid conduction, but longer refractory periods than the AV node. If a PAC occurs when the accessory pathway is refractory, there will be antegrade conduction solely through the AV node. As the impulse travels through the ventricles it can conduct retrograde through the accessory pathway from V to A. This creates a reentrant pathway that results in atrioventricular reentrant tachycardia (AVRT), which accounts for up to 80% of SVT in WPW. Orthodromic AVRT (antegrade through AV node, retrograde through accessory pathway) accounts for 90-95% of AVRT in WPW. Other tachycardias can occur where the accessory pathway is a bystander and not required for initiation and maintenance of the arrhythmia like in AVRT. This includes atrial arrhythmias (e.g., atrial fibrillation, atrial flutter), ventricular tachycardia, and ventricular fibrillation. Atrial fibrillation is relatively common (~20%) in WPW syndrome patients. Atrial fibrillation with an accessory pathway can produce rapid ventricular rates due to unencumbered conduction via the accessory pathway. In these situations, QRS width and morphology may vary due to variable conduction via the AV node vs accessory pathway. Depending on the rate of conduction, the patient can degenerate into VF. A shorter refractory period places patients at the highest risk for VF. How do we risk stratify patients with WPW pattern? When would an EP study (EPS) be beneficial? What features are high risk on EPS and would warrant treatment? Patients who are asymptomatic are typically at low risk of sudden cardiac death. Those who do have SCD typically have symptoms at some point prior to arrest. Patients with intermittent loss of the delta wave on a beat-to-beat basis are likely at lower risk, as it suggests the accessory pathway lacks the ability for rapid AV conduction. However, persistent delta wave in asymptomatic patients may still be at low risk. The risk for SCD is thought to be due to rapid conduction of Afib down the accessory pathway leading to VF. Accessory pathways with shorter refractory periods are able to conduct at higher rates (shorter R to R intervals). Delta waves disappear when R to R interval is less than the refractory period, at which point the atrial impulse only conducts through AV node. Thus, the lower the HR that delta waves become intermittent, the lower the risk of SCD. We can start risk stratification in most patients noninvasively with a resting EKG and exercise EKG stress test, unless we clearly demonstrate intermittent delta wave at rest. If preexcitation persists even with maximal sinus heart rates, then an EPS is recommended. High risk features on EPS include multiple accesso

67. Case Report: STEMI after EVALI Diagnosis – Baylor College of Medicine Oct 09, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join Baylor College of Medicine cardiology fellows (Khurrum Khan, John Suffredini, and Aliza Hussain) during restaurant week in Houston! They discuss an interesting case of STEMI in a patient with a recent diagnosis of e-cigarette or vaping product use-associated lung injury (EVALI). Dr. Vijay Nambi provides the E-CPR and APD Dr. Arunima Misra provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his mid 40s with a 30 pack year smoking history, EVALI (e-cigarette and vaping associated lung injury), and asthma presented with dyspnea and persistent chest pain. He had been vaping for the past year. One month prior , CT chest showed bilateral patchy infiltrates and he was diagnosed with EVALI and started on a steroid taper with resolution of his CT abnormalities. A nuclear stress test at that time was negative for ischemia. On arrival, he was in sinus tachycardia, normotensive, and not on oxygen supplementation. Physical exam was negative for volume overload or heart murmurs. EKG showed new Q waves with STE in V2-V4, with associated Q waves and TWI in the lateral leads and troponin returned moderately elevated. He was emergently taken to the cath lab which showed an abrupt cutoff of flow to the LAD. He received a single DES with resolution of coronary flow. A post-cath TTE showed an LVEF of 40-45% with apical anterior and anteroseptal WMA. He was monitored in the CCU the next day and he was treated with aspirin, ticagrelor, ACEi, metoprolol succinate and high intensity statin and subsequently discharged in stable condition with cardiac rehab follow-up. Case Media ABClick to Enlarge A. Presentation ECG (Anterior STEMI) B. Baseline ECG LAD occlusion Post PCI RCA TTE 1 TTE 2 TTE 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. The patient presented with a STEMI following a diagnosis of EVALI. What is known about the cardiovascular risks of vaping and e-cigarette use? The overall cardiovascular risks of e-cigarette use remains to be elucidated In preclinical studies, e-cigarettes use have been linked to increased sympathetic activity, oxidative stress, endothelial dysfunction, vascular injury, and altered platelet activity One observational study has suggested that daily e-cigarette users were 1.79 times more likely to experience MI than individuals who had never used e-cigarettes. Additional high-quality randomized controlled trials are needed to conclusively establish the safety and efficacy of e-cigarettes. 2. So the data is still emerging regarding the overall cardiovascular risks of e-cigarette use. Of note, the patient had a negative stress test a month prior. Should that not translate into low likelihood of cardiovascular events? Remember that stress testing for the diagnosis of obstructive coronary disease is most helpful in patients with an intermediate pretest probability for coronary artery disease. Further myocardial ischemia can occur not only secondary to obstructive epicardial disease (which may be new and acute from plaque rupture/erosion), but also from microvascular disease, vasospastic disease, and so forth. Stress testing with radionuclide myocardial perfusion imaging (e.g., SPECT, PET) is a well-established method for assessing coronary disease, but it is not an anatomic assessment. With nuclear stress tests, the causes of a false-negative result could include submaximal exercise (if doing exercise stress), collateral or overlapping epicardial circulation, suboptimal images (including artifact and poorly timed stress images), inaccurate interpretation, and balanced ischemia. Nonetheless, sensitivity for obstructive CAD in SPECT approaches 85-90% with specificity around 70-75%. As SPECT imaging is not an anatomic assessment, a recent negative nuclear stress test does not necessarily mean very low risk for future major adverse cardiovascular events. Even with a normal nuclear stress test, there is a 0.65% - 1.78% annual event rate of death or non-fatal MI. 3. Can non-obstructive and potentially "vulnerable" plaque be detected before an event? Remember ECG, echocardiographic and radionuclide stress testing are different modalities to assess for obstructive CAD after inducing ischemia via exercise or medications. These modalities typically assess for flow-limiting lesions (e.g., typically greater than 50%). However, acute coronary syndrome can occur subsequently from lesions that were not initially obstructive. In the PROSPECT study looking at patients who presented with ACS and underwent PCI to the culprit lesion and were followed afterward for ~ 3 years for adverse events, recurrent major adverse plaque rupture events were noted equally at the culprit lesion and at non-culprit lesions. Non-culprit lesions that were responsible for unanticipated events were angiographically mild on initial evaluation, had thin-cap fibroatheromas, or had large plaque burden as determined by gray-scale and radiofrequency intravascular ultrasound. This is where coronary CTA has an increasingly larger role. A study looking at coronary CTA determined that plaques with positive remodeling and low attenuation features were at higher risk of ACS developing over time. Those individuals with neither of those features had high NPV in ruling out future ACS events. Typically, as a lesion increases in size, it can compromise luminal blood flow when 50% or greater narrowing of the lumen is observed (remember this is slightly different than labeling a lesion as "obstructive" to the point of potentially necessitating intervention). However, when there is an absence of luminal loss regardless of lesion size in early lesions, this is called "positive coronary artery remodeling" and there is compensatory enlargement of the epicardial vessel. Post-mortem studies have found that vessels with positive remodeling have been associated with increased lipid content, as well as features associated with unstable plaque (e.g., thin-cap fibroatheroma). 4. The patient had an MI at age 45! Apart from e-cigarette use, what other evaluation is warranted in a young patient with ACS or STEMI? Traditional risk factors such as dyslipidemia, T2DM, HTN, and family history of premature CAD must be evaluated as plaque rupture events are still the most common cause of MI in young patients (age

66. Case Report: Severe Pre-eclampsia & Cardio-Obstetrics – UPMC Oct 06, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Pittsburgh Medical Center cardiology fellows (Agnes Koczo, Natalie Stokes, and Kayle Shapero) for a boat cruise down the Allegheny river as we tour all over beautiful Pittsburgh! They discuss an important case of severe pre-eclampsia, and explore some of the exciting dimensions of cardio-obstetrics. Dr. Malamo Eleni Countouris provides the E-CPR and program director Dr. Katie Berlacher 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 summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A G12P7 woman in her mid 30s in the third trimester of pregnancy presented with two months of progressive shortness of breath, orthopnea, and abdominal distension. She has a history of chronic HTN, untreated OSA, and obesity. Evaluation revealed a BP of 147/76 and spot urine protein:creatinine ratio elevated to 0.6, which in the context of her presentation was concerning for preeclampsia superimposed on chronic hypertension. TTE showed preserved ejection fraction, flattened interventricular septum during systole consistent with RV pressure overload, and moderate pulmonary HTN. She was diuresed with IV furosemide with improvement in symptoms and kept on ASA 81mg. The etiology of her elevated PA pressures was thought to be multifactorial, including untreated OSA for which she was started on CPAP. She was ultimately discharged on oral diuretics, and underwent an uncomplicated spontaneous vaginal delivery at 37 weeks. After delivery, follow-up in a clinic specializing in improving cardiovascular health in women with history of hypertensive disorders of pregnancy was arranged. Case Media ABCClick to Enlarge A. ECG: Sinus tachycardia otherwise unremarkableB. CXR: Within limitations of respiratory motion, no focal airspace consolidation; no pleural effusionsC. TTE: EF 55-60%, flattened IVS c/w RV pressure overload; normal RV size and function; mod TR; moderate pulmonary HTN (PASP 52mmHG); normal diastolic function Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. Cardionerds, we all should be familiar with #CardioObstetrics. What are the hypertensive disorders of pregnancy? There are four major categories for hypertensive disorders in pregnancy: (1) chronic hypertension (2) gestational hypertension; (3) preeclampsia (along with eclampsia and HELLP syndrome); (4) chronic hypertension with superimposed preeclampsia. Chronic Hypertension: Note, the definition of chronic hypertension was updated in the 2017 ACC/AHA guidelines as SBP ≥ 130 or DBP ≥ 90, but the diagnostic criteria for gestational hypertension, pre-eclampsia and chronic hypertension with super-imposed pre-eclampsia have not changed at this time. Gestational Hypertension (per ACOG guidelines): defined as SBP ≥ 140 mmHg or DBP ≥ 90 mmHg at least 4 hours apart diagnosed after 20 weeks of gestation without proteinuria or severe features of pre-eclampsia (e.g., renal insufficiency, elevated liver enzymes, thrombocytopenia, hemolysis, pulmonary edema, or CNS symptoms) Preeclampsia: diagnosis requires (1) SBP ≥ 140 mmHg or DBP ≥ 90 mmHg at least 4 hours apart after 20 weeks gestation or SBP ≥ 160 mmHg or DBP ≥ 110 mmHg once and (2) end organ damage. This includes proteinuria (≥ 300 mg/24hr urine collection, protein/creatinine ratio of ≥ 3 mg/dL, or dipstick reading of 2+ protein if other methods are not available), thrombocytopenia ( 1.1 mg/dL), elevated liver enzymes (at least 2x upper limit of normal), pulmonary edema, or neurological symptoms (e.g., new onset headache not responding to medications or visual disturbances not attributable to another diagnosis). Eclampsia: diagnosed when new-onset, grand mal seizure occurs in patients with pre-eclampsia. HELLP Syndrome: diagnosed when Hemolysis, Elevated Liver enzymes, and Low Platelets are the predominant features. HELLP is likely a subset of preeclampsia. Note, not all patients will have hypertension. Chronic hypertension with superimposed preeclampsia: (1) characterized by sudden increase in blood pressure that was previously controlled or recent up-titration of antihypertensives to manage blood pressure and/or (2) new onset proteinuria or increase in pre-existing proteinuria 2. This case featured a patient with super-imposed pre-eclampsia; what is pathophysiology behind this disorder? The pathophysiology of preeclampsia is complex and includes multi-organ manifestations. The initial insult is thought to be secondary to abnormal trophoblast (the outer cell layer of the blastocyst which eventually gives rise to the embryo) invasion of the endometrium. Normally, as trophoblasts implant in the endometrium, the small myometrial spiral arteries remodel with loss of smooth muscle and elastic lamina from the vessel wall. This allows increased blood flow to the placenta. In preeclampsia, there is incomplete spiral artery remodeling which can lead to placental ischemia. The incomplete arterial transformation is thought to be mediated by a number of factors, including soluble fms-like tyrosine kinase-1 (sFlt-1). sFlt-1, which circulates in the maternal bloodstream, has been implicated as an underlying culprit to the multi-system endothelial dysfunction we see in pre-eclampsia (e.g., CNS, renal dysfunction). There are other factors involved as well that ultimately lead to widespread oxidative stress, abnormal vascular reactivity, microemboli, and the clinical features of preeclampsia. There are additionally immunologic and genetic factors that lead to a preeclampsia phenotype by leading to a pro-inflammatory state and reduced trophoblast invasion. 3. Clearly, pre-eclampsia can have severe adverse effects on mother and child. Which patients are at increased risk of pre-eclampsia, and what can be done to lower their risk? High risk factors for developing preeclampsia include: diabetes, chronic hypertension, chronic kidney disease, multifetal gestation, autoimmune disorders (particularly systemic lupus erythematosus and antiphospholipid syndrome), and previous pregnancy with preeclampsia. Other risk factor include obesity, maternal age over 35 years, and nulliparity. There is no consensus guideline on what defines moderate to high risk. Following the USPSTF recommendations, any pregnant woman with a high risk factor or several moderate risk factors should be advised to start low-dose aspirin after 12 weeks of gestation to reduce the risk of preeclampsia. A recent Cochrane review that included trial data from nearly 37,000 women found aspirin prophylaxis reduced risk of preeclampsia by 18%. Calcium supplementation may be of benefit to prevent preeclampsia in women with low-baseline calcium intake. The proposed mechanism is that hypocalcemia may stimulate PTH or renin release, increasing intracellular calcium including in vascular smooth muscle. This may result in vasoconstriction and higher blood pressure and calcium supplementation may attenuate this process. There is an ongoing clinical trial to investigate the role of Pravastatin in the prevention of preeclampsia. 4. What if my patient has chronic HTN or gestational HTN? How do I approach the hypertensive pregnant patient? An ounce of prevention is worth a pound of cure! In hypertensive women who may become pregnant, nifedipine, labetalol, hydralazine, or methyldopa are preferred over teratogens like ACE inhibitors, ARBs, or direct renin inhibitors. Severe HTN (SBP ≥160, DBP ≥110) should always be treated to avoid pulmonary edema, stroke or placental abruption. A more conservative approach can be taken in mild to moderate HTN, as aggressive blood pressure lowering can compromise fetal circulation. However, the optimal blood pressure to initiate treatment below this threshold is less well defined and should be individualized to the patient including factors like underlying cardiovascular disease and baseline blood pressure. The timing of delivery is a critical aspect of managing a patient's hypertension. For a detailed discussion, review the ACOG practice bulletin. 5. How does a hypertensive disorder of pregnancy change a patient's cardiovascular risk? A history of a hypertensive disorder of pregnancy is an important risk factor for future cardiovascular disease. These patients are more likely to experience hypertension, ischemic heart disease, heart failure,...

65. Case Report: Spontaneous Coronary Artery Dissection (SCAD) Requiring Heart Transplantation – UCLA Oct 05, 2020

Show notes

CardioNerds (Amit Goyal & Daniel Ambinder) join join UCLA cardiology fellows (Jay Patel, Hillary Shapiro, and Ruth Hsiao) for some beach bonfire in Santa Monica! They discuss a challenging case of Spontaneous Coronary Artery Dissection (SCAD) requiring heart transplantation. Dr. Jonathan Tobis provides the E-CPR and program director Dr. Karol Watson provides 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 summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 40s presented with a one day history of intermittent chest pain. EKG showed anteroseptal and lateral STE with reciprocal ST depressions in the inferior leads. High-sensitivity troponin was elevated at 333 ng/mL. Emergent LHC showed a long and narrow left main with areas of additional contrast filling into a false lumen with no flow in the LAD. RCA and LCx were normal appearing (make sure you check out the angiogram videos below!). IVUS showed dissection and heavy thrombus burden in the left main artery. Shortly after the diagnostic angiogram, the patient went into V-fib arrest and received one shock with ROSC. Amiodarone was started and an Impella CP was placed for additional left ventricular support. ECMO and emergent CABG were not readily available at this time so the interventional team attempted revascularization with PCI to the left main given patient's hemodynamic instability from ongoing ischemia. However, even after PCI to left main, flow to LAD remained poor and the LCx now also appeared occluded. The decision was made to cease further attempts at revascularization. Unfortunately, post-procedure TTE showed a reduced EF of 22% with anterior and anterolateral hypokinesis. She was transferred to CCU on maximal Impella support. Patient eventually developed acute renal and liver failure secondary to cardiogenic shock and suffered an additional V-fib arrest with ROSC. Eventually, Ronald Reagan UCLA was contacted for transfer and the mobile ECMO team was dispatched. They placed the patient on VA-ECMO in the outside facility and transferred her to Ronald Reagan UCLA. At Ronald Reagan, revascularization was attempted given persistent cardiogenic shock and 3 stents were successfully deployed in the LAD. She was eventually weaned off of both Impella and ECMO after successful PCIs to LAD. However, TTE showed persistently low EF and patient eventually underwent successful heart-kidney transplantation. Case Media ABCDClick to Enlarge A. ECG: Anterior STE, STE in I/aVL but depressedions in V4-V6, inferior reciprocal ST depressionB. X-ray of explanted heart shows stents extending from LM -> dLADC. Cross-section of explanted heart from apex to base showing infarct in the anteroseptal areaD. Histological cross section of the explanted LAD. This film shows slit like LM with no LAD. High OM/RI and LCx look ok. BMW wire used to cross distal LM into high OM/RIArrested after diagnostic, got ROSC and then Impella CP inserted L femoral Attempting wiring the true lumen, stuck in mLAD after 1st septal comes off IVUS from RI to LM. Shows dissection plane and lots of thrombusLM IVUS details: 4.57 x 5.0mm proximally, 4.52mm distally Unable to pass a wire into mid LAD PCI of LM: Synergy 4.0 x 16mm DES deployed in LM and post-dilated with Emerge NC 4.5 x 8mm balloon Flow remained poor at mLAD even after PCI to LM LCx system closed after LM PCI, so no further attempts TTE: Apical 4 Chamber TTE: Apical 2 Chamber TTE: Apical 3 Chamber LCx occluded with large OM1/Ramus still patent Post PCI of the LAD Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is SCAD and what population is most at risk? SCAD stands for spontaneous coronary artery dissection. It is an acute coronary event and is defined as a spontaneous separation of the coronary artery wall that is not iatrogenic or related to trauma. It is an important cause of acute myocardial infarction. Women comprise 87%-95% of SCAD patients with a mean age of presentation between 44-53 years, just like the patient in this case. The "typical" SCAD patient is a middle-aged female with few traditional cardiovascular risk factors such as hypertension, hyperlipidemia, and tobacco use. However, our understanding of a "typical" SCAD patient is limited as the majority of patients in large series have been white and it is likely that patients of different ethnic and racial backgrounds have been under-represented in most current registries. In some studies, the prevalence of SCAD appears around 4% of all patients presenting with ACS and up to 35% in women 50 years or under presenting with ACS. Pregnancy associated SCAD is an important subset of patients. It can occur at any time during the pregnancy or post-partum, with the majority of cases occurring postpartum. SCAD associated with pregnancy tends to have a more severe clinical presentation, including left main involvement, multi-vessel dissection and cardiogenic shock. Both pregnancy and non-pregnancy associated SCAD tend to occur more frequently in multiparous women and those that report a higher prevalence of pre-eclampsia. What are the two hypotheses that have been proposed to explain the pathophysiology of SCAD? Before reviewing the pathophysiology, let's briefly review the coronary arterial wall structure. The intima is the inner layer in contact with the intraluminal space. In normal vasculature, the intima is only a few cell layers thick and is separated from the media by the internal elastic lamina. The media is the middle layer and is made up of layers of smooth muscle cells which help regulate vascular tone. The media is separated from the adventitia by the external elastic lamina. Finally, the adventitia surrounds the media and through fibrous connective tissue provides support for the epicardial vessel. In SCAD, a hematoma forms within the tunica media separating the intima or intima/media from the vessel and compressing the true lumen leading to ischemia. There are several proposed hypotheses for how this occurs: "Inside-out" hypothesis: an endothelial-intimal disruption or "flap" develops first and then blood enters the sub-intimal space from the true lumen via this "flap" "Outside-in" hypothesis: a hematoma forms within the media, possibly from disruption of traversing micro-vessels, and compresses and occludes the true lumen as the hematoma expands. In both hypotheses, the end result is separation of the layers of coronary artery wall, creating a false vs. true lumen. Currently, the evidence favors the "outside-in" theory because in most SCAD cases, there are no communication between the true and false lumens observed. What are the angiographic appearances of SCAD? Left anterior descending artery is the most commonly affected vessel in SCAD. There are three classifications of SCAD based on angiographic appearance (the Yip-Saw classification). Type 1: Contrast dye staining of the arterial wall demonstrates double or multiple radiolucent lumens separated by a radiolucent flap. There may be dye "hang-up" or slow contrast clearing. Type 2: This is the most common subtype. It is characterized by long, diffuse, and smooth narrowing that can vary from mild stenosis to complete occlusion, often with abrupt changes in lumen diameter. Type 2a SCAD demonstrates normal arterial segments proximal and distal to a dissection and does not extend into a distal vessel. Type 2b does extend into the distal tip of a vessel. Type 3: The angiographic appearance mimics a focal stenosis of atherosclerotic disease and typically requires intracoronary imaging to make a definitive diagnosis. There are other angiographic findings that may clue the cardiology team into a diagnosis of SCAD. SCAD tends to affect more distal segments than atherosclerotic disease. Furthermore, the left anterior descending (LAD) artery is the most commonly affected vessel in SCAD. Patients with SCAD tend to have more tortuous vessels and atherosclerotic lesions are usually absent from vessels not affected by the SCAD. Some reports have indicated the external luminal compression by the intramural hematoma (IMH) gives the appearance of a stick insect. What is the management of SCAD in the acute setting? As Dr. Hayes et al. note in their JACC review, the focus in the acute setting is to restore perfusion and maintain myocardial function as conservatively as possible rather than on how to restore normal coronary architectu

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