Cardionerds: A Cardiology Podcast

CardioNerds podcast explores a puzzling case of recurrent troponin elevation in a patient with a complex medical history involving alcohol use disorder and IV drug use. The speakers discuss challenges in interpreting troponin levels, diagnostic dilemmas, and the importance of thorough evaluation for accurate diagnosis and management. They also share insights into choosing cardiology as a specialty and training at the University of Washington's fellowship program.

This podcast features University of Mississippi Medical Center cardiology fellows discussing a case of severe functional mitral regurgitation treated with MitraClip. They explore the challenges in managing advanced heart failure, patient selection for transcatheter mitral valve interventions, and the impactful patient care provided in Mississippi. The episode highlights the complexities of diagnosing and treating mitral regurgitation, emphasizing the importance of collaborative efforts in cardiology specialties.

CardioNerds (Amit Goyal & Daniel Ambinder) join Boston University cardiology fellows (Yuliya Mints, Anshul Srivastava, and Michel Ibrahim) for some hotdogs at Fenway Park in Boston, MA. They discuss an educational case of carcinoid heart disease with severe tricuspid regurgitation. Program director, Dr. Omar Siddiqi provides the E-CPR and APD Dr. Katy Bockstall 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 woman in her mid 60s with history of neuroendocrine tumor (NET) presented to the cardio-oncology clinic with chronic progressive SOB and fatigue. She was diagnosed with NET after presenting with a small bowel obstruction (SBO) several years prior. At the time, she was found to have liver and pulmonary metastasis with MR enterography showing thickening of the terminal ileum. Ileocecetomy and biopsy of the liver lesions confirmed metastatic NET. Despite treatment with octreotide and everolimus, follow up CT showed progression of liver lesions and she was eventually started on telotristat and enrolled in a clinical trial. On presentation, she was not tachycardiac, hypotensive or requiring oxygen supplementation (KD: Correct?). On exam, she demonstrated elevated JVP with a positive hepato-jugular reflex and a 3/6 holosytolic murmur loudest at the LLSB that increased with inspiration. Lab work revealed urinary 5-HIAA was 212 (nl < 6mg/24 hours). TTE showed moderately dilated RV and severely dilated RA. Furthermore, there was a thickened, calcified and retracted TV with severe TR which was consistent with carcinoid heart disease. She was treated with diuretics and was continued on systemic therapies to help achieve control of her NET before surgical intervention for her valvular disease was considered.   Case Media A B Click to Enlarge A. ECGB. TTE: CW Doppler through tricuspid valve Carcinoid – TTE 1 Carcinoid – TTE 2 Carcinoid – TTE 3 Carcinoid – TTE 4 Carcinoid – TTE 5 Carcinoid – TTE 6 Carcinoid – TTE 7 Carcinoid – TTE 8 Carcinoid – TTE 9 Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case The patient had an NET history and presented with shortness of breath. Under what circumstances do patients with NETs present with cardiac symptoms?  Amongst patients with neuroendocrine tumors (NETs), carcinoid tumors refer classically to gastrointestinal NETs. Around 30 to 40% of these patients will presents with features of carcinoid syndrome, including vasomotor symptoms (e.g., flushing), diarrhea, and bronchospasm. The majority of patients with carcinoid syndrome have metastases to the liver and the vasoactive substances (e.g., 5-hydroxytryptamine [5-HT]) reach the systemic circulation via the hepatic vein bypassing degradation in the liver.   Similarly, cardiac involvement occurs after metastasis to the liver and exposure of the heart to vasoactive substances. Generally, symptoms are limited to the right heart as the lungs clear carcinoid-related substances. Left-sided involvement may occur, however, in a patient with carcinoid heart disease and an intracardiac right to left shunt is present.   In addition to the symptoms of carcinoid syndrome, patients with carcinoid heart disease including severe dyspnea, fatigue, and signs and symptoms of right heart failure (e.g., ascites, peripheral edema).    The patient was diagnosed with carcinoid heart disease. What are the typical echocardiographic findings of carcinoid heart disease?    The echocardiographic findings of carcinoid heart disease are heterogeneous from mild thickening of a single valve leaflet to advanced disease with significant thickening and retraction of multiple valves. The vasoactive substances of carcinoid can specifically cause valvular thickening (5-HT receptors being most prevalent on heart valves) and restricted leaflet motion that can result in a “club-like” appearance of the leaflets. This occurs on the right-sided heart valves (unless an intracardiac shunt exists), with TV involvement being most common.   Specifically, in mild cases, the normal concave curvature of the tricuspid leaflets is reduced and the leaflets straighten, This affects its motion during diastole leading to valve dysfunction. Eventually there is progressive thickening of the valve leaflets, chordae and papillary muscle leading to significant leaflet retraction and reduced leaflet motion. When carcinoid heart disease becomes severe, the leaflets can be fixed and fail to coapt leading to severe tricuspid regurgitation, tricuspid stenosis, and signs and symptoms of right heart failure.   As with the tricuspid valve, carcinoid heart disease can also affect the pulmonary valve leading to diffuse thickening and the formation of typical “carcinoid plaques.” This similarly can result in retraction of the valve cusps and mixed pulmonic regurgitation and pulmonic stenosis. Note pulmonic stenosis secondary to carcinoid has an extremely poor prognosis (with median survival typically less than 2 years) and is often not responsive to balloon vavuloplasty.   3 . What is the typical diagnostic evaluation of carcinoid heart disease in patients with NET?  In patients with NET and subsequently carcinoid syndrome, there should be monitoring for the development of heart failure, right-sided symptoms and new murmurs. Nonetheless, high index of suspicion is necessary as up to 57% of patients with moderate to severe TR can be asymptomatic or have mild symptoms and one-third of patients can lack a cardiac murmur.   NT-proBNP is a useful biomarker of carcinoid heart disease, and a cutoff level of 260 pg/ml (31 pmol/l) and has been used as a screening tool for carcinoid heart disease (sensitivity 60-92%, specificity 80-91%). Furthermore, plasma and urinary levels of 5-HIAA are significantly higher in patients with carcinoid heart disease compared with those without cardiac involvement. 5-HIAA levels >300 mmol/24 h conferred a 2- to 3-fold increased risk for developing or progression of carcinoid heart disease   TTE is the imaging modality of choice for patients with signs and/or symptoms of carcinoid heart disease, in patients with elevated NT-proBNP , and any patient undergoing surgical liver or abdominal intervention. The findings of carcinoid heart disease are on a spectrum, but there are some characteristic findings as outlined above. TEE can be an additional test to fully characterize valvular involvement and/or for surgical planning. Furthermore, cardiac CT and CMR may be valuable as adjuncts  4. How do you manage carcinoid heart disease?  The only definitive and effective therapy for carcinoid heart disease is valve intervention. Diuretics and aldosterone antagonists can be helpful to relieve symptoms, but typically only have temporary effectiveness. Telotristat ethyl, an oral tryptophan hydroxylase inhibitor used in combination with a somatostatin analog for management of diarrhea associated with carcinoid syndrome, has been used to try to prevent the development and progression of carcinoid heart disease.   Surgical valve intervention should be considered in patients with severe valvular disease and/or signs of right heart failure, with at least 12 months of anticipated post-operative survival fromt heir NET disease.   Symptomatic management primarily involves loops diuretics and aldosterone antagonists for relieving symptoms associated with RHF. Digoxin, vasodilators, and ACEi have no proven efficacy in this population. Bioprosthetic valves may be preferred over mechanical valves due to the inherent increased risk of bleeding in patients with advanced liver disease and hepatic dysfunction from carcinoid disease. However, bioprosthetic valves may be more prone to premature dysfunction and degeneration due to the underlying carcinoid process and thrombosis formation. A careful multi-disciplinary team and approach is needed to individualize valve choice for each patient.   Transcatheter valve replacement has been undertaken for pulmonic valve involvement, but transcatheter tricuspid valve replacement is not common.   5. What is the overall prognosis of patients with carcinoid heart disease with and without surgical management?   Carcinoid heart disease with NYHA III or IV symptoms have a poor prognosis and median survival is only 11 months. In carcinoid patients with cardiac symptoms and controlled systemic disease, cardiac valve replacement surgery alleviates otherwise intractable symptoms and appears to improve survival.  References JACC 2017 – Carcinoid Heart Disease  JACC 2017 – Carcinoid Heart Disease – ACC Review  https://www.uptodate.com/contents/carcinoid-heart-disease#H14  CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal & Daniel Ambinder) join Cleveland Clinic cardiology fellows (Ben Alencherry, Erika Hutt, Zach Il’Giovine, Kara Denby) for some delicious craft beer at Platform Brewery! They discuss a challenging case of Ehlers Danlos Syndrome with Papillary Muscle Rupture. Dr. Vidyasagar Kalahasti provides the E-CPR and program director Dr. Venu Menon 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.   This case has been published in JACC Case Reports: CardioNerds Corner! 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 pregnant woman at 29 weeks gestation presents with postpartum pulmonary edema, found to have papillary muscle rupture, is ultimately diagnosed with vascular Ehlers Danlos Syndrome. For a detailed course, enjoy the JACC case report. Case Media Visit the JACC Case Reports: CardioNerds Corner to review the case media! Episode Schematics & Teaching Coming soon! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is Ehlers-Danlos Syndrome?   Ehlers-Danlos Syndrome (EDS) is a clinically and genetically heterogenous group of heritable connective tissue disorders due to altered collagen metabolism. The inheritance pattern is variable, but is mostly autosomal dominant, with a range of mechanisms including deficiency of collagen-processing enzymes, mutant collagen chains, and haploinsufficiency.     Although the syndrome has varying and overlapping clinical manifestations based on subtype (per the 2017 International ED Consortium there are 17 subtypes) it is largely characterized by hyperextensibility of the skin, hypermobility of joints, atrophic scarring, and tissue fragility.  The cardiovascular system is involved in the vascular and cardio-valvular subtypes.  The incidence is estimated to be 1 in 2500 to 5000, however this is likely an underestimation since mild presentations may not be clinically diagnosed nor sent for genetic testing.    The differential diagnosis for suspected EDS includes osteogenesis imperfecta, Marfan syndrome, and Loeys-Dietz syndrome. Those with joint symptoms may be incorrectly diagnosed with fibromyalgia, chronic fatigue syndrome etc.    What is vascular EDS?   There are many subtypes of EDS. Type IV or vascular EDS (vEDS) is an autosomal dominant disorder that affects Type III procollagen protein synthesis. The incidence is rare – 1 in 50,000 to 250,000 people and is ~5% of all EDS cases.    It is commonly caused by a defect in the COL3A1 gene, most of which are single base substitutions, but more than 700 different mutations have been identified. Missense mutations at the C-terminal end of the molecule results in a more severe form of the disease.  Feared vascular manifestations include arterial dissection, rupture, and aneurysm formation. Death is most frequently secondary to complications from arterial dissection or hollow organ rupture. 70% of patients experience a first major event by age 20. Note, surgical repair of a ruptured aneurysm or dissection can be complicated by poor wound healing or hemorrhage because tissue in Ehlers-Danlos is friable.  In this subtype, the usual manifestations of joint hypermobility and skin hyperextensibility may not be as apparent.  The vascular type has the worst prognosis with median expectancy between 40-50 years of age.   How is vEDS diagnosed?   Vascular EDS should be considered in anyone with unexplained arterial or hollow viscus rupture, commonly the sigmoid colon, especially at a young age.  Diagnosis is confirmed by either finding of structurally abnormal type III procollagen in a culture of dermal fibroblasts or COL3A1 gene mutation. Clinical criteria can aid in the decision to pursue testing.    Molecular testing is recommended when meeting one or more major clinical criteria or several minor criteria. Major criteria include family history of vEDS, unexplained arterial rupture at young age, spontaneous intestinal  perforation (in absence of risk factors), uterine rupture during pregnancy and labor, or carotid-cavernous sinus fistula formation.    Some minor criteria include bruising without trauma (especially in unusual locations), spontaneous pneumothorax, tendon/muscle rupture, gingival recession, early onset varicose veins, and characteristic facial appearance amongst other criteria. Characteristic facial features include presence of prominent eyes due to lack of adipose tissue around the orbit, thin punched nose, small lips, hollow cheeks, and lobeless ears.   How should patients with vEDS be managed?   Management of patients with vEDS requires a multidisciplinary team including a clinical geneticist. Baseline arterial imaging is needed but recommendations for follow-up imaging are not well defined. TTE should be performed at least every 3 years, to screen for cardiac complications.    Contact sports should be avoided, as should anti-platelet and anti-coagulation therapy to minimize bleeding risks. Arterial and intramuscular punctures, arteriography, and routine colonoscopy should also be avoided. Surgical or endovascular management of complications can be challenging due to tissue friability.   Ascorbic acid is a co-factor for collagen fibrils and may reduce bruising. Desmopressin, vasopressin, and recombinant factor 8a have also been shown to reduce bleeding complications.   Patients with vEDS have decreased intima media thickness which imposes additional mechanical stress onto already fragile tissue. Celiprolol is a cardio-selective beta blocker and beta-2 partial agonist which has been showing to prevent arterial complications. However, this drug lacks FDA approval and is not available in the USA.   Importantly, cascade genetic testing should be offered to all first-degree relatives.   How can pregnancy–related complications be avoided?   Pregnancy in women with vEDS is considered high risk with maternal death rates over 10%. Pregnancy increases risks in two major ways: (1) increased risk of complications related to the gravid uterus and hypermobility (e.g., premature rupture of membranes, ligament laxity and rupture) or uterine/vascular rupture; (2) worsening of pre-existing pathology such as mitral valve prolapse of aortic dilation due to physiologic changes during pregnancy.    Pre-pregnancy risk stratification and counseling is recommended for those with known vEDS. Some recommend termination of pregnancy in patients with known vEDS, but one study suggests that pregnancy does not influence life-expectancy. Current guidelines recommend a risk-benefit discussion with the patient and their family.    In a patient with vEDS who becomes pregnant, care should involve a multidisciplinary team at a specialized center with vascular surgery, general surgery, and high-risk obstetrics. It is uncertain which mode of delivery improves the risk-benefit ratio for the patient and fetus. Furthermore, spinal or epidural anesthesia can have increased risk of complications in patients with vEDS.  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. References Hutt, Erika, Celeste Santos-Martins, Jose Aguilera, Per Wierup, Vidyasagar Kalahasti, and Carmela Tan. “A 27-Year-Old Woman With Postpartum Papillary Muscle Rupture.” JACC: Case Reports, October 2020, S2666084920311748.   M.J. Eagleton. Arterial complications of vascular Ehlers-Danlos syndrome. J Vasc Surg, 64 (2016), pp. 1869-1880  Miklovic, Tyler, and Vanessa C. Sieg. “Ehlers Danlos Syndrome.” In StatPearls. Treasure Island (FL): StatPearls Publishing, 2020.  CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Dr. Binh An Phan provides E-CPR and Dr. Atif Qasim shares a message for applicants. They discuss a case of STEMI due to coronary vasospasm, delving into the diagnostic process and treatment options. The episode highlights the physiology of vasospasm, risk factors, and management complexities. UCSF fellows share insights on clinical training experiences and complex cardiac cases, emphasizing the importance of comprehensive care in challenging scenarios.

In this episode, cardiology fellows Jack Hornick, Phoo Pwint Nandar, and Sideris Facaros from Summa Health dive into a complex case of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). They explore a patient's unexpected palpitations and dizziness, unraveling diagnostics like EKG analysis and the nuances of ventricular tachycardia. Dr. Kenneth Varian adds expert insight on management strategies, including the necessity of multi-disciplinary approaches and the role of genetic testing in ARVC. Join them as they merge intriguing medical discussions with the beauty of nature!

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 A B C D E F Click 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 failure and can lead to shock in severe cases.   Diagnosis: Thiamine deficiency is difficult to diagnose. Blood thiamine levels can be low in acute illness and do not reflect total body stores. Erythrocyte transketolase activity and thiamine pyrophosphate effect tests can be used, though these tests have poor specificity and sensitivity. The gold standard is high performance liquid chromatography, though access to this test is expensive and not commonly available.   As a historical note, in 1945, Marion Blankenford developed diagnostic criteria for wet beriberi, which includes evidence of an enlarged heart with normal rhythm, dependent edema, elevated venous pressure, peripheral neuritis or pellagra, nonspecific alternans on ECG, no evidence of other cardiac disease, at least 3 months of thiamine deficiency, and improvement in symptoms and reduction in heart size following thiamine replacement.   Treatment: The cornerstone of wet beriberi management is supportive treatment of heart failure while replacing thiamine stores. A rapid and dramatic improvement following thiamine replacement is diagnostic of wet beriberi.   References Bisbal, F., Baranchuk, A., Braunwald, E., et al. (2020). Atrial Failure as a Clinical Entity: JACC Review Topic of the Week. Journal of the American College of Cardiology, 75(2), 222–232.   Gibson, D. N., Di Biase, L., Mohanty, P., Patel, J. D., Bai, R., Sanchez, J., Burkhardt, J. D., Heywood, J. T., Johnson, A. D., Rubenson, D. S., Horton, R., et al. (2011). Stiff left atrial syndrome after catheter ablation for atrial fibrillation: clinical characterization, prevalence, and predictors. Heart rhythm, 8(9), 1364–1371.   Maeder, M. T., Nägele, R., Rohner, P., & Weilenmann, D. (2018). Pulmonary hypertension in stiff left atrial syndrome: pathogenesis and treatment in one. ESC heart failure, 5(1), 189–192.   Urey, M. A., Darden, D., Stoller, D., et al. (2017). Stiff Left Atrial Syndrome After Multiple Percutaneous Catheter Ablations: Role for Invasive Hemodynamic Exercise Testing. Circulation. Heart failure, 10(5), e003885.   Durstenfeld, M. S., & Hsue, P. Y. (2020). An Unusual, Reversible Cause of Acute High-Output Heart Failure Complicated by Refractory Shock. Circulation, 142(9), 901–905.   Reddy, Y., Melenovsky, V., Redfield, M. M., Nishimura, R. A., et al. (2016). High-Output Heart Failure: A 15-Year Experience. Journal of the American College of Cardiology, 68(5), 473–482.   CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

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 A B C D E F G H I J K L M N O Click 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 during expiration (say 120 mmHg). The cuff is further deflated until sounds can be heard throughout the respiratory cycle (say 100 mmHg). If the difference in these two numbers (here 20 mmHg) is ≥ 10 mmHg it is deemed a clinically significant pulsus paradoxus.  Pulsus paradoxus is an important finding in cardiac tamponade as a pulsus > 10 mmHg occurs in almost all patients with tamponade. A cutoff of 12 mmHg improves specificity and is 98% sensitive and 83% specific in patients with a known pericardial effusion.  There are a few situations where a patient might be in tamponade, but might not have pulsus paradoxus. They include extreme hypotension, low pressure tamponade (e.g., dehydration), atrial septal defects, severe AI, loculated/local effusions, and a very poorly compliant LV or RV.  Pulsus can also be present in patients without pericardial disease, including (but not limited to) patients with COPD or asthma, obstructive sleep apnea, and significant obesity.   What are the signs of cardiac tamponade on echo and RHC?  Echocardiography is the primary imaging modality to evaluate for signs of tamponade. Consistent with the previously described pathophysiology, signs of tamponade on TTE include early diastolic collapse of the RV free wall, diastolic collapse of the RA, swinging of the heart in the pericardial sac, dilated IVC without collapse, a >60% increase in TV flow and >30% decrease in MV flow during inspiration (more specific for tamponade than the cut-offs of 40% and 25% seen in constriction), and septal deviation into the LV with inspiration. Remember to differentiate the size and composition of the effusion. Of these findings early diastolic collapse of the RV free wall is most specific and dilation of the IVC, and late diastolic collapse of the RA are most sensitive.   Though RHC is not routinely performed for the diagnosis of tamponade, there are a few key findings that are relevant. As discussed above, equalization of diastolic pressures, pulsus paradoxus, and pulsus alternans can all be seen on the pressure tracings and measurements in a RHC. Additionally, the RA waveform can show a blunted y descent as discussed above.  What is effusive constrictive pericarditis (ECP) and how does one differentiate it from tamponade or constrictive pericarditis? How is it treated?  Effusive constrictive pericarditis is a clinical entity comprised of both decreased pericardial compliance and a hemodynamically significant pericardial effusion. This is often found when patients undergo pericardiocentesis for suspected tamponade only to reveal continued elevation in RA pressures and constrictive physiology. Some use a cut-off of a failure to fall by 50% or to less than 10 mmHg in the RA.   Though ECP can initially present with some signs of constriction (elevated medial e’ velocities) true constrictive pericarditis should not have signs of a hemodynamically significant effusion (RA/RV diastolic collapse, blunted y descent) and is much less likely to have pulsus paradoxus.  Though there is no uniform consensus on how to treat ECP, it is generally agreed that anti-inflammatory medications are first line. The decision to use NSAIDs or steroids ± colchicine is provider dependent. Prolonged anti-inflammatory therapy may be necessary and escalation versus de-escalation should be guided by symptoms, inflammatory markers, and possibly cardiac MRI. For patients with symptoms refractory to anti-inflammatory medications, pericardiectomy is recommended. Note in effusive-constrictive pericarditis, there tends to be extensive involvement of the visceral pericardium, which requires epicardiectomy, and may need a specialized center.   References Adler, Y., Charron, P., Imazio, M., Badano, L., Barón-Esquivias, G., Bogaert, J., Brucato, A., Gueret, P., Klingel, K., Lionis, C., Maisch, B., Mayosi, B., Pavie, A., Ristić, A. D., Sabaté Tenas, M., Seferovic, P., Swedberg, K., Tomkowski, W., Group, E. S. D., … Nesukay, E. (2015). 2015 ESC Guidelines for the diagnosis and management of pericardial diseasesThe Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal, 36(42), 2921–2964.  Ang, K. P., Nordin, R. B., Lee, S. C. Y., Lee, C. Y., & Lu, H. T. (2019). Diagnostic value of electrocardiogram in cardiac tamponade. The Medical Journal of Malaysia, 74(1), 51–56.  Ariyarajah, V., & Spodick, D. H. (2007). Cardiac Tamponade Revisited. Texas Heart Institute Journal, 34(3), 347–351.  Ayan, M., Siraj, A., & Bhatti, S. (2018). Effusive Constrictive Pericarditis. Journal of the American College of Cardiology, 71(11 Supplement), A2383.  BECK, C. S. (1935). TWO CARDIAC COMPRESSION TRIADS. Journal of the American Medical Association, 104(9), 714–716.  Chiabrando, J. G., Bonaventura, A., Vecchié, A., Wohlford, G. F., Mauro, A. G., Jordan, J. H., Grizzard, J. D., Montecucco, F., Berrocal, D. H., Brucato, A., Imazio, M., & Abbate, A. (2020). Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 75(1), 76–92.  Effusive-Constrictive Pericarditis: Maybe Not as Rare and as Bad as We Thought. (n.d.). American College of Cardiology. Retrieved October 13, 2020, from https://www.acc.org/latest-in-cardiology/articles/2019/04/08/10/42/effusive-constrictive-pericarditis Fowler, N. O. (1993). Cardiac tamponade. A clinical or an echocardiographic diagnosis? Circulation, 87(5), 1738–1741.  Guntheroth, W. G. (2007). Sensitivity and specificity of echocardiographic evidence of tamponade: Implications for ventricular interdependence and pulsus paradoxus. Pediatric Cardiology, 28(5), 358–362.  Jesper K., Poulsen, Steen Hvitfeldt, & Mølgaard, Henning. (n.d.). Cardiac tamponade: A clinical challenge. Retrieved October 13, 2020, from https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Cardiac-tamponade-a-clinical-challenge Kearns, M. J., & Walley, K. R. (2018). Tamponade: Hemodynamic and Echocardiographic Diagnosis. Chest, 153(5), 1266–1275.  Klein, A. L., Abbara, S., Agler, D. A., Appleton, C. P., Asher, C. R., Hoit, B., Hung, J., Garcia, M. J., Kronzon, I., Oh, J. K., Rodriguez, E. R., Schaff, H. V., Schoenhagen, P., Tan, C. D., & White, R. D. (2013). American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: Endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. Journal of the American Society of Echocardiography: Official Publication of the American Society of Echocardiography, 26(9), 965-1012.e15. https://doi.org/10.1016/j.echo.2013.06.023  Little William C., & Freeman Gregory L. (2006). Pericardial Disease. Circulation, 113(12), 1622–1632.  McGee, S. R. (2018). Evidence-based physical diagnosis (4th edition). Elsevier.  Pérez-Casares, A., Cesar, S., Brunet-Garcia, L., & Sanchez-de-Toledo, J. (2017). Echocardiographic Evaluation of Pericardial Effusion and Cardiac Tamponade. Frontiers in Pediatrics, 5.  Roy, C. L., Minor, M. A., Brookhart, M. A., & Choudhry, N. K. (2007). Does this patient with a pericardial effusion have cardiac tamponade? JAMA, 297(16), 1810–1818.  Spodick, D. H. (2003). Acute cardiac tamponade. The New England Journal of Medicine, 349(7), 684–690.  Stashko, E., & Meer, J. M. (2020). Cardiac Tamponade. In StatPearls. StatPearls Publishing.  Swami, A., & Spodick, D. H. (2003). Pulsus paradoxus in cardiac tamponade: A pathophysiologic continuum. Clinical Cardiology, 26(5), 215–217.  CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Dr. Kim Eagle and Dr. Devraj Sukul discuss a challenging case of Ventricular Septal Rupture after acute MI. Topics include managing complications post-myocardial infarction, the impact of delayed medical care seeking during the pandemic, and the vital role of teamwork in cardiology.

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 A B C D E F Click 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. Emergent surgical management should generally be considered first line in patients with traumatic hemopericardium, aortic dissection related hemopericardium, or free wall rupture. In the setting of aortic dissection, controlled drainage of very small amounts of hemopericardium can be considered as a temporizing measure to maintain SBP > 90 mmHg. With purulent or loculated effusions, surgical drainage over pericardiocentesis may be the preference as well.   Supportive measures include ensuring adequate preload, avoiding diuretics and/or vasodilator therapy, and inotropic and vasopressor therapy as needed.   The patient was found to have a pseudoaneurysm rather than a frank free wall rupture. What is a pseudoaneurysm and how is it different than a true ventricular aneurysm?  Ventricular pseudoaneurysm is caused by a contained rupture of the LV free wall where the rupture is contained by adherent pericardium, thrombus, or hematoma with no myocardial tissue in the outpouching. In a true ventricular aneurysm, the outer walls are formed by the infarcted myocardium and scar tissue. Pseudoaneurysms have a high propensity to rupture and thus surgical management is recommended.   A small, narrow neck typically connects the ventricular cavity with the contained pericardial space. On echocardiogram, pseudoaneurysm can demonstrated the following differentiating features: (1) neck diameter to maximal aneurysmal diameter < 0.5; (2) color and spectral doppler demonstrating bidirectional flow through the narrowed neck; (3) thrombus and/or spontaneous echo contrast in the pericardial space.   References Alkhalil Mohammad, Choudhury Robin P. Reperfusion Treatment in Late Presentation Acute Myocardial Infarction. Circ Cardiovasc Interv. 2018;11(9):e007287. doi:10.1161/CIRCINTERVENTIONS.118.007287  Hochman JS, Lamas GA, Buller CE, et al. Coronary Intervention for Persistent Occlusion after Myocardial Infarction. N Engl J Med. 2006;355(23):2395-2407. doi:10.1056/NEJMoa066139  Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseasesThe Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318  Hutchins KD, Skurnick J, Lavenhar M, Natarajan GA. Cardiac rupture in acute myocardial infarction: a reassessment. Am J Forensic Med Pathol. 2002 Mar;23(1):78-82. doi: 10.1097/00000433-200203000-00017. PMID: 11953501.  Griffin, Brian P. 2019. Manual of cardiovascular medicine.  CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD