Transthoracic Echocardiogram Research Articles

Abstract 4137689: Artificial Intelligence Assessment of Diastolic Dysfunction by Electrocardiogram: Outcomes in Cardiac Intensive Care Unit Patients

Background: Left ventricular diastolic dysfunction (LVDD) predicts mortality in cardiac intensive care unit (CICU) patients. A novel artificial intelligence enhanced electrocardiogram (AIECG) algorithm can predict LVDD and mortality in general populations but has not been examined in the cardiac intensive care unit (CICU). We aim to assess if LVDD by AI-ECG is associated with in-hospital and one-year mortality in CICU patients. Methods: In this retrospective cohort study, we included consecutive unique adults admitted to the Mayo Clinic CICU from 2007 to 2018 with an admission AIECG, which AI assigned LVDD grade (0 to 3). Medial mitral E/e’ ratio >15 on transthoracic echocardiogram (TTE) defined elevated filling pressures. AIECG and TTE assessment of LVDD were used to assign patients to four groups based on TTE as gold standard: true and false negative, and true and false positive. In-hospital mortality was evaluated using multivariable logistic regression. One-year survival was evaluated using Kaplan-Meier curves and multivariable Cox proportional-hazards. Results: We included 11,868 patients (median age 69.5 years, 37.7% females); 48% had heart failure and 44% had acute coronary syndromes. AIECG LVDD grades were: grade 0 (normal), 33%; grade 1, 7%; grade 2, 39%; grade 3, 21%. In-hospital (adjusted OR) and one-year (adjusted HR) mortality increased in each higher AIECG LVDD grade (Figure A/B), before and after adjustment including TTE measurements. Patients with grade 2-3 LVDD by AIECG and medial mitral E/e’ ratio >15 by TTE (true positive) had the highest in-hospital (adjusted OR 2.5 [1.7-3.9]) and one-year (adjusted HR 1.9 [1.5-2.5]) mortality (Figure C/D), and mortality was elevated similarly in patients with either grade 2-3 LVDD by AIECG (false positive) or medial mitral E/e’ ratio >15 by TTE (false negative). Conclusions: The AIECG LVDD grade was strongly associated with in-hospital and one-year mortality in CICU patients, even after adjusting for clinical variables and TTE measurements. Patients with concordant AIECG and TTE for elevated filling pressures (true positive) were at highest risk.

Abstract 4114220: Majority of Patients with New Ventricular Dysfunction After Acute COVID-19 Infection Did Not Have Cardiac Recovery

Background: It is still not well understood whether cardiac injury observed during acute COVID-19 infection extends after recovery from the initial viral infection. The purpose of this study was to determine the incidence of left and right ventricular dysfunction in patients hospitalized with acute COVID-19 and evaluate for cardiac recovery. Methods: A multicenter, retrospective cohort study was conducted. Adult patients were identified by hospitalizations using ICD-10 code U07.1 from March 2020 to October 2021. Patients were included if they had: 1) acute COVID-19 infection confirmed by RT-PCR and 2) a transthoracic echocardiogram (TTE) performed during their hospitalization. Clinical and echocardiographic data were collected and analyzed. Longitudinal TTE parameters were obtained from follow-up studies performed after discharge. Results: A total of 750 patients (mean age 64.3 ± 15.3 years, 60.0% male) were included. The average time to follow-up TTE was 8.7± 7.4 months. 133 patients (17.7%) had new LV dysfunction seen on TTE ( Figure 1 ). LV recovery (defined as normalization of LVEF or improvement of LVEF by > 10% from baseline) was observed in 28 of 74 (37.8%) survivors. 9 of 26 patients (34.6%) who had a follow-up TTE <6 months post-discharge recovered their LV function, while 19 of 48 patients (39.6%) who had a follow-up TTE ≥6 months had LV recovery. 94 of 725 patients (13.0%) with reported RV parameters had new RV dysfunction seen on TTE. RV recovery (defined as normalization of RV function) was observed in 11 of 38 (28.9%) survivors. 6 of 18 patients (33.3%) who had a follow-up TTE <6 months post-discharge recovered their RV function, while 5 of 20 patients (25%) who had a follow-up TTE ≥6 months had RV recovery. Conclusions: Most surviving patients who developed new LV or RV dysfunction did not recover their ventricular function at follow-up, but recovery extended beyond 6 months follow-up.

Abstract 4136565: Atrial Fibrillation Linked to Right Ventricular Dysfunction in Patients with Acute Pulmonary Embolism

Background: Atrial fibrillation (AF), both new-onset and preexisting, is linked to increased mortality in acute pulmonary embolism (APE). The causal pathway for this association, whether through increased right ventricular dysfunction (RVD) is less well understood. Hypothesis: AF independently predicts RVD in APE patients, affecting mortality and clinical outcomes. Goals: Examine the relationship between AF and RVD to understand its impact on APE survival. Guide further research into optimal APE therapeutic strategies, focusing on early rhythm control. Methods: We conducted a retrospective, multi-center cohort study using data from our Pulmonary Embolism Response Team (PERT) registry. Inclusion criteria included PERT activation and adults over 18. Exclusions were for missing transthoracic echocardiogram (TTE) within 3 days or incomplete TTE data. Patients were categorized by AF status, with RVD assessed by TTE markers. Analysis involved logistic regression and Cox proportional hazards models. Results: Among 535 APE patients, 15% had AF. These patients showed higher unadjusted RVD rates (56% vs. 39%, p=0.006) and significant differences in TTE parameters: TAPSE (1.72 vs. 1.89 cm, p=0.007), S` (11.5 vs. 13.4 cm/s, p=0.0002), and RVOT VTI (13 vs. 14 cm, p=0.019). Adjusted analyses confirmed AF's significant association with RVD (OR 2.32, CI 1.3-4.1), inpatient mortality (OR 4.9, CI 1.5-17, p=0.0106), acute renal failure (OR 2.2, CI 1.2-4.1, p=0.0102), and one-year mortality (HR 1.9, CI 1.06-3.44, p=0.03). Conclusions: AF significantly influences mortality in APE, partly through increased RVD. These findings underline the need for further studies to confirm these relationships and enhance treatment strategies.

Abstract 4136480: A Rare Cause of a Classic Presentation of NSTEMI: Case of 39-Year-Old Female with Hypothyroidism Induced Myocarditis

Background: Myocarditis is a cause of non-ischemic cardiomyopathy (NICM) and troponin elevation. There are many causes including uncontrolled thyroid disorder (TD). A thorough history, cardiac MRI (cMRI) followed by an endomyocardial biopsy (EMB) is necessary for diagnosis. This case illustrates a classic presentation of NSTEMI with a rare cause of myocarditis due to uncontrolled hypothyroidism. Description of Case: A 39-year-old female with history of congenital hypothyroidism and tobacco use disorder presented to the Emergency Department with sudden onset of unprovoked sub-sternal chest pain. She stated she had stopped taking her levothyroxine years ago due to side effects such as abdominal discomfort. On admission, work up included high sensitivity troponin (Hs-cTn), EKG, urine drug screen (UDS), and thyroid panel. There was no evidence of ischemic changes on EKG, Hs-cTn was 3600 (normal: 3-54) which up-trended to 43,742, and UDS was negative. She was placed on appropriate medical therapy for NSTEMI and taken for urgent coronary angiography wbich showed normal epicardial arteries. A transthoracic echocardiogram (TTE) was unremarkable with a normal ejection fraction (EF). However, she continued to complain of chest discomfort and palpitations. Her vital signs remained stable but her thyroid panel revealed a TSH of 127 (normal: 0.27-4.2), T4 of 0.18 (normal: 0.92 – 1.6) and T3 of 1.0 (normal: 2.3-4.2). Inflammatory markers were also elevated. A cMRI was obtained revealing gadolinium enhancement in the anterior septal wall with extension into the subepicardium of the inferior wall suggestive of possible myocarditis. An EMB was performed to elucidate etiology. Pathology results were only remarkable for edema but newly reduced EF of 30-35% was noted on TTE at time of biopsy. Endocrinology was consulted for untreated hypothyroidism and patient was initiated on levothyroxine leading to improvement of her symptoms. Discussion: Our patient's history and work up were consistent with myocarditis induced by severe hypothyroidism. TD is a rare cause of reversible NICM and symptoms improve once TD is controlled. While there are several cases reported on hyperthyroidism associated myocarditis, there are only a few cases of myocarditis associated with uncontrolled hypothyroidism. Clinicians should maintain a broad differential to ensure a thorough work up in a patient presenting with NSTEMI, and a thyroid panel should be included especially if myocarditis is suspected.

Abstract 4125252: Pre-Hematopoietic Stem Cell Transplantation Echocardiographic Indices and Post-Transplant Cardiovascular Outcomes

Introduction: Hematopoietic stem cell transplantation (HSCT) is associated with adverse cardiovascular (CV) events including the development of heart failure (HF) and arrythmias. While transthoracic echocardiogram (TTE) is routinely obtained prior to HSCT, its role in predicting the incidence of HSCT related CV events is poorly understood. Methods: We used data from the Cardiovascular Registry in Bone Marrow Transplantation (CARE-BMT) study, a multicenter observational study of adult patients (aged ≥18 years) who underwent autologous/allogeneic HSCT for malignant or nonmalignant bone marrow disorders at the University of Michigan Health System (UMHS) and Rush University Medical Center from 2008-2019. In this analysis, we included patients from UMHS with a baseline TTE. Data on pre-HSCT TTE parameters and post-HSCT CV outcomes were collected through manual chart review. Left ventricular (LV) function and dimensions were categorized into normal, mildly abnormal, and moderately/severely abnormal based on American Society of Echocardiography guidelines. The primary outcomes were new-onset HF and atrial fibrillation/flutter post-HSCT. Analyses were conducted using a Fine-Gray model adjusted for the pre-HSCT CARE-BMT CV risk score. Results: Of the 2071 patients (mean age at HSCT 55.5 + 12.9 years; 59.5% male) with a pre-HSCT TTE (median 25 days pre-HSCT), 116 (5.6%) and 128 (6.2%) patients experienced HF and atrial fibrillation/flutter, respectively, over a median period of 2.2 years. Greater abnormalities in left ventricular internal diameter at end-diastole (LVIDd) and end-systole (LVIDs) were linearly associated with a higher risk of HF (P-trend 0.018 and 0.004, respectively) (Table). Similarly, moderately/severely abnormal LVIDd was associated with a 2.41-fold (95% CI: 1.07, 5.43) increase in risk of atrial fibrillation/flutter (Table). Pre-HSCT ejection fraction (EF) was not associated with either endpoint. Conclusion: LV dilation, even when mild, was notably associated with increased risk of developing new HF or atrial arrythmias post-HSCT, regardless of EF. Whether evidence of LV dilation should prompt the initiation of guideline directed medical therapy to minimize the risk of incident HF warrants further study.

Abstract 4118882: Decompensated Heart Failure Secondary to a Non-Coronary Sinus of Valsalva to Right Atrium Fistula: A Case Report

Introduction: Sinus of Valsalva aneurysm (SVA) accounts for 3.5% of all congenital cardiac anomalies. Rupture occurs in 35% of cases and can lead to life-threatening fistulas, predominantly involving the right ventricle or right atrium. Description of Case: 62-year-old female with hypertension and hypothyroidism presented to the ER with progressively worsening dyspnea over the past week. She also reported worsening lower extremity edema, orthopnea, and paroxysmal nocturnal dyspnea. Chest X-ray showed large pleural effusions. Her ejection fraction was 66% ejection fraction with a fistula between the right sinus of Valsalva and the right atrium on transthoracic echocardiogram (TTE) which was also seen on transesophageal echocardiogram (TEE). Her heart failure was due to the fistula as she had no coronary artery disease on coronary angiogram. She had cardiothoracic surgery for fistula repair. Postoperatively, she developed complete heart block requiring a permanent pacemaker. She had no further complications and was discharged home in good condition. Discussion: SVA affects the right sinus (94%), with the non-coronary (5%) and left sinus (1%) being less commonly involved. Aneurysm rupture typically forms a fistula into the right ventricle (60%), right atrium (29%), left atrium (6%), or left ventricle (4%), and rarely into the pericardial cavity (1%). Symptoms vary by rupture size and location. TTE is the initial diagnostic tool but has limited sensitivity (50%) for detecting fistulas, whereas TEE has a 90% sensitivity. Cardiac MRI and CT can further refine diagnoses, and cardiac catheterization assesses coronary arteries preoperatively. Surgical closure with a patch is the primary treatment for ruptured SVA, significantly improving survival rates compared to non-surgical management.

Abstract 4135212: An Overlap Between Takotsubo Cardiomyopathy and Hypertrophic Obstructive Cardiomyopathy Causing Dynamic Left Ventricular Outflow Tract Obstruction: A Unique Case Report

Background: Takotsubo cardiomyopathy (TC) can cause dynamic left ventricular outflow tract (LVOT) obstruction leading to cardiogenic shock. Due to differential wall-motion abnormalities, flow acceleration in the LVOT can lead to systolic anterior motion (SAM) of the mitral valve which worsens LVOT obstruction and leads to hemodynamic compromise. We present a case of overlap between TC and hypertrophic obstructive cardiomyopathy (HOCM) with worsening LVOT obstruction leading to cardiogenic shock. Case: A 76-year-old female presented with typical chest pain, nausea, and worsening shortness of breath. On examination, she was hypotensive and cold to touch. EKG showed T-wave inversions in lateral leads with elevated cardiac troponins. Coronary angiogram showed non-obstructive coronary artery disease, and right heart catheterization revealed elevated filling pressures. Transthoracic echocardiogram (TTE) showed septal hypertrophy and SAM of the mitral valve causing dynamic LVOT obstruction (Figure 1) and ejection fraction (EF) of 20%. TTE with contrast showed apical ballooning consistent with TC (Figure 2). Decision Making: Initially with diuresis, she became hypotensive so it was stopped and she received controlled intravenous fluids along with phenylephrine to reduce LVOT obstruction. Her blood pressure improved and she was started on low-dose metoprolol succinate along with ivabradine to reduce heart rate. She tolerated this therapy and hemodynamics stabilized. Conclusion: Cardiogenic shock can be a severe complication of TC. Early detection of LVOT obstruction in cardiogenic shock is important as traditional management strategies of increased inotropy and reduction of afterload can be fatal in these cases. The treatment strategy focuses on reducing the LVOT gradient and includes fluid administration to increase preload, beta-blockers to increase diastolic filling time, and vasopressors to raise afterload.

Abstract 4134560: Sex Differences in Repolarization Abnormalities Associated with Ventricular Arrhythmia in Mitral Valve Prolapse

Background: Compared to men, women with mitral valve prolapse (MVP) are more likely to present with sudden death, and most women who die suddenly are premenopausal. Repolarization abnormalities are common in patients with MVP-attributed sudden death. However, differences in repolarization between men and women with MVP are not known. Hypothesis: Repolarization abnormalities are associated with ventricular arrhythmia and are more common in women than men with MVP. Aims: To investigate associations of ECG repolarization abnormalities with sex and ventricular arrhythmia in MVP. Methods: We reviewed 12-lead ECGs from 272 adults with MVP for T-wave inversion, ST segment elevation, ST depression, QTc and QT dispersion. Patients were excluded if they had prior MI, coronary artery disease, mitral valve surgery, moderate or severe LVH, heart failure, reduced left ventricular ejection fraction, atrial fibrillation or QRS duration >120ms. Transthoracic echocardiograms were reviewed for mitral regurgitation, mitral annular disjunction, bi-leaflet or myxomatous MVP. Ambulatory ECGs (n=94) were assessed for NSVT or PVCs (> 1% burden) and ECGs for >1 PVC on any 10 second tracing. Associations were evaluated using Fisher’s exact test, Wilcoxon rank-sum test or multiple linear regression. Results: Among 272 patients, median (IQR) age was 58 (47-67) years, 162 (59.6%) were women, 46 (16.9%) were African American, and 34 (12.5%) had frequent ventricular ectopy. Women and men had similar rates of NSVT (15/66 [22.7%] vs 4/28 [14.3%], p=0.41) and frequent ventricular ectopy (25/162 [15.4%] vs 9/110 [8.1%], p=0.093). The QTc was longer in women (433 [417, 446] vs 423 [406, 442] ms, p=0.023) and in those with NSVT (437 [421, 444] vs 421 [405, 436] ms, p=0.028), but not in those with ventricular ectopy (437 [420, 445] vs 428 [410, 444] ms, p=0.15). There was a trend towards increased QTc in patients with mitral annular disjunction (433 [418, 454] vs 429 [408, 444] ms, p=0.054) and myxomatous MVP (434 [414, 450] vs 427 [408, 444] ms, p=0.076). Female sex was the only independent predictor of QTc (R 2 =0.14, p=0.0032). Conclusion: Among patients with mitral valve prolapse, women have longer QT interval than men, and longer QT interval is associated with nonsustained ventricular tachycardia. Subtle or dynamic delay in repolarization may promote malignant ventricular arrhythmias in women. Understanding these relationships may help identify patients at risk for sudden death.

Abstract 4138449: High Output Heart Failure from an Aortocaval Fistula

Introduction: High output heart failure (HOHF) due to a post-traumatic aortocaval fistula is a rare entity. This case seeks to explore the presentation as well as complexities of management of these patients. Case Presentation: A 50-year-old male with a prior right abdominal stab wound requiring exploratory laparotomy 20 years ago presented with worsening dyspnea on exertion and palpitations. Physical examination was remarkable for jugular venous distention, lower extremity edema, and a pulsatile mass in the right abdomen with an audible bruit. A 12-lead ECG showed rapid atrial flutter. A transthoracic echocardiogram (TTE) showed a reduced left ventricular ejection fraction (LVEF) of 30-35%, severely dilated atria and inferior vena cava (IVC) with high velocity flow. Abdominal computed tomography venogram showed dilation of the IVC up to 8cm and an aortocaval fistula at the level of the right renal vessels, resulting in an atrophic right kidney. Cardiac catheterization was notable for a cardiac output (CO) of 12L/min, cardiac index (CI) of 7L/min/m2 and reduced systemic vascular resistance (SVR). He was managed with beta blockers and diuretics, followed by TEE-guided cardioversion for atrial flutter to restore sinus rhythm. Vascular surgery performed a successful, first of its kind endovascular repair of the abdominal aorta with stenting of the right common iliac artery and placement of a 20mm Amplatzer Septal Occluder device in the right renal artery. He tolerated the procedure well, and post-operative TTE showed a recovered LVEF of 55-60% and CO of 6L/min. Discussion: HOHF is defined by a CO more than 8L/min or CI more than 4L/min/m2 along with clinical symptoms. Decreased SVR leads to sympathetic activation and stimulation of the renin-angiotensin-aldosterone system, leading to fluid retention, cardiac remodeling, and exacerbation of symptoms. Challenges present in the management of HOHF and the use of vasodilatory agents should be avoided, as they can exacerbate the problem. In our case, limitations were also faced in the use of many traditional HF therapies due to renal dysfunction as a result of the fistula. Therefore, repair was the only viable long-term solution. Conclusion: This case displays an uncommon etiology of HOHF, emphasizing the need for meticulous evaluation to ensure proper management. Early detection of aortocaval fistulas is crucial to prevent worsening cardiac dysfunction, with symptoms resolving rapidly post-repair.

Abstract 4135360: Eosinophilic Myocarditis: An Atypical Presentation with a Labile Course: A Case Report

Case presentation: A 64-year-old man presented with one day of chest pain. Initial evaluation showed elevated cardiac enzymes (CE) and normal eosinophil count. Electrocardiogram (EKG) was unremarkable. Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 40% and a moderate-large pericardial effusion with signs of tamponade. Pericardiocentesis was deferred due to the lack of a safe window. Left and right heart catheterization showed no occlusive disease or chamber pressure equalization. The patient developed worsening shock, raising suspicion for myocarditis and prompting an endomyocardial biopsy (EMB). He was placed on extracorporeal membrane oxygenation (ECMO) on day 3. The EMB resulted as eosinophilic myocarditis (EM), and high dose Methylprednisolone was started. He was decannulated from ECMO on day 10. Intra-operative transesophageal echocardiogram (TEE) post-decannulation showed a normal EF without segmental abnormalities. Three hours later, a rise in CEs was noted, and EKG showed ST elevations inferiorly. TTE showed a reduced EF with multiple segmental abnormalities concerning for myocardial infarction. A repeat coronary angiogram was unremarkable. Due to the residual pericardial effusion, the patient underwent a pericardial window draining 200 cc of serosanguinous fluid. Intra-operative TEE showed an EF of 20% with no improvement after drainage. He had a cardiac arrest during the procedure and was placed back on ECMO. High-dose steroids were resumed along with intravenous immunoglobulin. Despite interventions, the patient continued to deteriorate and he ultimately expired. Discussion: EM has high mortality and a variable course, often requiring EMB for diagnosis. As in our case, about 25% of cases present without peripheral eosinophilia. Pericardial effusion occurs in 34% of cases and tamponade in 6%. A distinct feature of this case is the decompensation associated with ST elevation and segmental abnormalities, thought initially to be myocardial infarction (MI), after an initial response to steroids. While the etiology of such decompensation is unclear, relapsing EM in the setting of tapering steroids is one explanation, as myocarditis and MI can share similar clinical features. Another explanation is cardiac tamponade, which has also been reported to mimic MI and myocarditis. Air embolism from ECMO decannulation is another possibility, though air embolisms may include cerebrovascular pathology, which was not observed.

Heart ultrasound and biomechanical evaluation of radiation‐induced heart toxicity using transthoracic echocardiogram (TTE) and dynamic mechanical analysis (DMA)

AbstractRadiation‐induced heart disease (RIHD) is a serious complication but difficult to assess in patients undergoing thoracic radiotherapy (RT). We aim to analyze RIHD using heart ultrasound and elastic modulus, exploring relationships between functional, anatomical or biomechanical changes of the heart and radiation dose.Twenty BALB/c mice were divided into four groups (control, 10 Gy, 20 Gy and 25 Gy) with a single fraction of image‐guided volumetric modulated arc radiotherapy (VMAT) to murine heart on a linear accelerator. Transthoracic echocardiography (TTE) was performed on a small‐animal ultrasound imaging system with a handheld microscan transducer. E‐wave/A‐wave ratio (E/A) and myocardial performance index (MPI) for diastolic performance were noninvasively evaluated weekly, as well as ejection fraction (EF%), fractional shortening (FS%), left ventricle (LV) mass and heart wall thickening for systolic performance. At the end of the fifth week, all mice were sacrificed for elastic modulus measurement on a dynamic mechanical analyzer (DMA) and for histopathological staining. All experiments were conducted in accordance with the local institution's animal research committee guideline.Significant difference was observed in E/A ratio between the control and 25 Gy irradiated groups (1.8±0.5 and 0.7±0.9, respectively; p<0.05), indicating reduced diastolic performance and increased stiffness in left ventricle after high‐dose heart radiation. Diastolic dysfunction in irradiated groups was also observed with significantly increased MPI. In contrast, posterior wall thickness, aortic peak velocity, heart rate, EF and FS were not significantly different after RT. Heart elasticity was reduced substantially with the increased radiation dose. HE and Masson Trichrome staining confirmed more fibrosis deposition in irradiated hearts.RIHD evaluation with ultrasound imaging noninvasively and biomechanical modulus measurement invasively in the image guided, precision dose‐escalated murine heart irradiation is feasible. Increased myocardial stiffness, abnormal diastolic relaxation, more collagen deposition, and reduced tissue elasticity are observed in irradiated heart tissue. This study may facilitate our understanding of RIHD and facilitate improving patients’ quality of life in the future.

Abstract 4119619: Congruency of Stated Aortic Stenosis Severity and Reported Doppler Exam Values in a Large Health Care System Based on ACC/ASE Guidelines

Background: Peak aortic valve Doppler velocity, mean aortic valve gradient, and Doppler estimated aortic valve area are key measures recommended for assessing aortic stenosis severity. Discordance often occurs among these measures, posing diagnostic challenges. Failure to accurately diagnose severe aortic stenosis is critical. This study focuses on the discordance between reported aortic valve area (AVA) and stenosis severity, comparing guidelines from the ASE and ACC seen in Table 1. Goals: Assess the incidence of discordance between reported AVA and severity of aortic stenosis and compare how the differing guideline recommendations of the ASE versus ACC for defining severe AS by AVA would affect reporting severity in a large clinical practice. Methods: A query of all transthoracic echocardiograms obtained in patients 18 years of age and above was performed in a large multi-hospital healthcare system between Jan 1 and Jun 30 of 2023. This group was then filtered to include only exams in which the reported aortic valve area was 1 cm2 or less, excluding all cases with prosthetic aortic valves. This group was then further filtered to contain only those patients in whom the physician did NOT report severe aortic stenosis. Results: Between Jan and June 2023, 16,675 subjects ages 18-95 (avg 74) underwent transthoracic echocardiograms in our healthcare system, with 190 (1.1%) reported as having an AVA ≤ 1 cm2. Of those exams, 63 (33% of those with AVA ≤ 1) were not reported as having severe aortic stenosis. Of those 63 exams, 35 (56%) had a reported SVI < 35 ml/m2 compatible with a low flow state. However, only 1 of those 35 cases mentioned flow-status in labeling the stenosis severity in the report. Based on the ASE Doppler AVA definition of severe AS (< 1.0 cm2 (≤ 0.94 )) vs ACC (≤ 1 cm2 (≤1.04), the AV Doppler and SVI data contained in the reports should have led to the grading of the aortic valve as being ”Severe” or “Moderate” aortic stenosis as described in Table 2. Conclusion: Discordance in labeling severe aortic stenosis relates to differing AVA criteria. Cases are often termed "moderate to severe" under ACC criteria. The majority (56%) of cases failing to describe severe AS despite meeting AVA criteria were in low flow states, suggesting this phenomenon is not well understood in clinical practice. Various factors contribute to these findings, warranting further investigation.

Abstract 4131838: Heart’s Deception: A Venous Villain Hiding in the Heart

A 66-year-old male presented with 5 months of worsening left flank and lower back pain. Three weeks prior to this presentation, he was seen at an outside facility where he was found to have a left renal mass that was not further worked up. CT Abdomen and Pelvis showed an enhancing heterogenous lesion at the left superior renal pole, left adrenal gland lesion, and a pulmonary artery filling defect. This defect, along with concern for metastasis, led to a CT chest angiogram that reported small left upper and lower lobe pulmonary emboli. A transthoracic echocardiogram (TTE) was ordered and showed a linear highly mobile mass in the right atrium that was intermittently protruding into the right ventricle and into the main pulmonary artery through the pulmonic valve. There was no visible evidence of tumor extension of the renal mass into the inferior vena cava. Based on this, the highest differential was a clot-in-transit. After collaboration with the pulmonary embolism response team and echo team, the patient underwent aspiration thrombectomy via AngioVac system with transesophageal echocardiography (TEE) guidance. Most of the mass was removed, but there was a residual small portion adherent to the superior vena cava that was not amenable to aspiration. Grossly, the removed mass did not have the classic appearance of thrombus. The specimen was sent to pathology and returned as poorly differentiated carcinoma with spindle cell pattern positive for PAX8, CK7, CD10, pancytokeratin, and vimentin concerning for renal cell carcinoma. Post procedural transthoracic echo found to have new basal septal globular mass with vascularity seen on echo contrast imaging concerning for vascular involvement consistent with myocardial metastatic invasion. Cardiac magnetic resonance imaging could have aided in more precise tissue characterization to differentiate between clot or tumor prior to aspiration thrombectomy. This case demonstrates the significance of a detailed history and physical exam, use of multimodality imaging, and multidisciplinary collaboration to manage a rare cardiac condition.

Abstract 4135303: Acute Pericarditis Secondary to Secukinumab Therapy

Background: Pericarditis is the most common pericardial disease worldwide and has a high recurrence rate of 15-30%. It is primarily idiopathic but can arise from infectious and non-infectious causes; drug related cases are rare. Secukinumab, a fully human anti-interleukin-17A monoclonal antibody used for treating psoriasis, has been identified through the FDA Adverse Event Reporting System as potentially inducing pericarditis, though literature is scant. We report a case of acute pericarditis related to secukinumab use. Case presentation: A 28-year-old male with history of psoriasis on secukinumab therapy presented with sharp, central chest pain, and progressive shortness of breath for 3 weeks. He was evaluated for similar chest pain 3 weeks prior; CT chest showed small pericardial effusion and he was managed with analgesics without improvement. This admission, he had tachycardia, and ECG showed sinus rhythm with diffuse ST elevation and PR depression (Figure 1A). Troponin I levels were normal and inflammatory markers were elevated. Transthoracic echocardiogram (TTE) revealed a large pericardial effusion without tamponade physiology (Figure 1B). CT chest confirmed large pericardial effusion, increased in size compared to CT done 3 weeks prior (Figure 2). He was diagnosed with pericarditis and started on ibuprofen and colchicine which improved his symptoms. Search for viral etiology including testing for COVID, influenza A and B, RSV, hepatitis and HIV were negative. Immunological workup for ANA and rheumatoid factor was negative. Thus, secukinumab was thought to be the likely culprit. Follow-up TTE in 3 months showed resolution of pericardial effusion. Conclusion: This case underscores the importance of considering medication-induced pericarditis in patients presenting with typical symptoms, especially when on treatment with drugs like secukinumab. Given the growing evidence from pharmacovigilance databases and the severe potential outcomes of untreated pericarditis, clinicians should maintain vigilance for such adverse effects. Further research is warranted to clarify the mechanisms by which secukinumab may contribute to pericardial inflammation in order to optimize management strategies in affected patients.

Abstract 4112944: A diagnostic challenge overcome with persistent clinical suspicion in a case of cardiac AL amyloidosis

Case: A 62-year old male with a history of chronic kidney disease and paroxysmal atrial fibrillation presented with several months of fatigue, a progressive decline in functional status (NYHA IIIb-IV), weight loss, and intermittent lower extremity swelling. Blood pressure was 92/72 mmHg on presentation, and heart rate was 90 bpm. Physical examination revealed a jugular venous pressure of 12-14 cm H2O and 2+ bilateral lower extremity edema with mild wheezing. Methods/workup: Laboratories are shown in Table 1 and were notable for a serum free light chain ratio of 0.14. Transthoracic echocardiogram (figure 1) revealed a left ventricular (LV) ejection fraction of 33% with increased LV wall thickness and severe bi-atrial enlargement. Bone marrow biopsy revealed 2% lambda restricted plasma cells without evidence of amyloid deposits; metastatic bone survey was negative. A fat pad biopsy and endomyocardial biopsy stained negative for amyloid with Congo red. Cardiac MRI showed diffuse, circumferential subendocardial late gadolinium enhancement, most compatible with cardiac amyloidosis (figure 2). The patient also had a chest CT scan that demonstrated a few patchy nodular pulmonary infiltrates. Given his extensive negative workup, he was referred to pulmonary and endobronchial biopsy was positive for amyloid on Congo red staining (figure 3). Biopsy tissue typing revealed Lambda subtype AL amyloidosis. Management: The patient was started on Daratumumab, Cyclophosphamide, Bortezomib, and Dexamethasone by Hematology. Unfortunately, about a month after his diagnosis, he developed worsening heart failure despite treatment. He was admitted to an outside hospital with refractory cardiogenic shock and passed away during that admission. Discussion: The diagnosis of AL amyloidosis requires a high index of suspicion for prompt diagnosis and treatment. We present a case in which cardiac amyloidosis was suspected based on the patient’s clinical picture and cardiac imaging; however, multiple initial biopsies were negative. An expedited, multimodal and interdisciplinary diagnostic assessment is imperative as prognosis with chemotherapy is highly dependent on extent of AL disease, patient functional status, and presence of cardiac compromise. Elevated natriuretic peptides, troponins, autonomic dysfunction, and hypotension are negative prognostic features.

Abstract 4144514: Human Immunodeficiency Virus Associated Cardiomyopathy- A Rare Cause of Heart Failure With Reduced Ejection Fraction in Era of Highly Active Antiretroviral Therapy

Introduction: Human Immunodeficiency Virus Associated Cardiomyopathy (HIVAC) is characterized by left ventricular (LV) systolic or diastolic dysfunction with or without LV dilatation and heart failure symptoms. The introduction of antiretroviral therapy (ART) has changed the fulminant systolic heart failure presentation of HIV myocarditis to diastolic heart failure. We present a unique case of dilated cardiomyopathy in a young patient without advanced HIV illness which has rarely been documented in the literature. This is a rare presentation of HIVAC in the post-ART era. Case Report: A 32-year-old male with a past medical history (PMH) of the human immunodeficiency virus (HIV) presented with complaints of new onset worsening shortness of breath and lower extremity edema for four weeks. He was diagnosed with HIV seven years ago and was not compliant with ART. Laboratory testing showed a cluster of differentiation 4 (CD4) 823 and HIV load 2550. Myocarditis was ruled out by normal troponin levels and no new changes on the electrocardiogram (ECG). Transthoracic echocardiogram (TTE) showed dilated left ventricle (LV), LV global hypokinesis, LV ejection fraction (LVEF) 10-15%, dilated right ventricle, biatrial dilation, moderate to severe mitral regurgitation, severe tricuspid regurgitation, pulmonary artery (PA) systolic pressure 73 mmHg and no pericardial effusion. Coronary angiography was negative for coronary artery disease (CAD). The patient was started on carvedilol and outpatient evaluation for a left ventricular assistance device. Discussion: Systolic dysfunction in patients with HIVAC carried a poor prognosis in the pre-ART era and was common in patients with elevated c-reactive protein (CRP), tobacco use, and previous myocardial infarction (MI). After the advent of ART, systolic dysfunction is rare and replaced by diastolic cardiomyopathy in the setting of ART use. Diagnosis is usually by excluding other etiologies and biopsy is not necessarily required. Management is usually guideline-directed medical therapy (i.e. beta blocker, renin-angiotensin-aldosterone antagonists, sodium-glucose cotransporter-2) and device-based therapy but there is still data lacking to assess its benefit.

Abstract 4136452: Acute Cardiac Function Change After Catheter Ablation of Ventricular Arrhythmias in Patients with Arrhythmogenic Right Ventricular Cardiomyopathy

Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder characterized by fibrofatty replacement of myocardial tissue, creating areas of electrical heterogeneity and increasing the risk of ventricular arrhythmias (VAs) and sudden cardiac death (SCD). Catheter ablation is commonly performed in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) for management of ventricular arrhythmias (VAs). Whether catheter ablation affects cardiac function post-procedurally is uncertain. Research Question: Does catheter ablation for ARVC result in acute change in cardiac function? Goals/Aims: To assess the impact of catheter ablation for VAs on cardiac function in the acute post-procedure setting. Methods: This retrospective study included patients with ARVC who underwent catheter ablation for VAs at Mayo Clinic. Cardiac function was assessed on pre- and post-procedure transthoracic echocardiograms (TTEs). Post-procedure TTEs were obtained within 4 weeks after the ablation procedure. Right ventricular (RV) enlargement and systolic dysfunction were evaluated as continuous variables (0=none, 1=mild, 2=mild-moderate, 3=moderate, 4=moderate-severe, 5=severe). Results: The study included 32 patients who underwent a total of 44 ablations. Mean age at the time of ablation was 49±16 years, and 24 (75%) were male. After a mean follow-up duration of 2.6±5.5 days, there was a significant worsening in mean RV dysfunction (1.6±1.5 to 2.0±1.4, P = 0.001). There were no significant changes in mean left ventricular ejection fraction (LVEF), left ventricular (LV) dimensions, and RV size. 6 (14%) patients had a >5% decline in LVEF, and 14 (32%) patients had worsening RV function. Transient inotropic support was required in 4 (9%) patients. Conclusion(s): This study is the first to assess the acute impact of catheter ablation for VAs on cardiac function in ARVC patients. These results underscore the importance of careful post-procedure monitoring and planning of the ablation target in these patients to avoid excessive ablation and therefore impairment in cardiac function.

Abstract 4143264: A Case of Spike-on-T Phenomenon and Polymorphic Ventricular Tachycardia

Background: R-on-T phenomenon occurs when an electrical stimulus is delivered at a critical point during ventricular repolarization. This can initiate ventricular arrhythmias like polymorphic ventricular tachycardia (PMVT). We describe a case of ventricular pacemaker spikes delivered on the T wave causing PMVT. Case: A 53-year-old female with CAD s/p stent, postpartum cardiomyopathy s/p Bi-V CRT-D (Boston Scientific G124), and paroxysmal atrial fibrillation presented for elective endoscopy and colonoscopy to evaluate her dysphagia and abdominal pain. Her CRT-D was reprogrammed from DDD pacing with lower rate limit (LRL) 50 bpm to an asynchronous Bi-V DOO mode at 50 bpm (‘electrocautery mode’) for the procedure (tachy therapy disabled). Her LV-RV offset was 40 msec. Prior to receiving sedation or medications, she was found unresponsive. Telemetry showed Spike-on-T phenomenon which initiated PMVT. She was externally defibrillated with 200J and received magnesium and an IV amiodarone bolus. She returned to sinus rhythm, but one minute later had another Spike-on-T event initiating PMVT. She was successfully defibrillated with 360J. Post-shock EKG showed an asynchronous Bi-V paced rhythm at 50 bpm. Decision Making: The patient was admitted to the CCU for post-resuscitation care. Her electrolytes and cardiac enzymes were unremarkable. Her CRT-D was reprogrammed to DDD 80-140 bpm. Transthoracic echocardiogram showed normal biventricular systolic function. Cardiac catheterization did not show obstructive CAD. After reprogramming of her device, she had no further events. After initial treatment with IV amiodarone load, she was discharged home on oral magnesium gluconate. Discussion: The only intervention prior to her procedure was device reprogramming (DDD 50 bpm to DOO 50 bpm). Telemetry showed pacer spikes initiating PMVT. Given the LV-RV offset of 40 msec, she would have received these two tightly coupled pacemaker spikes in an asynchronous mode, in this unfortunate instance during her T wave. While her bowel preparation may have led to electrolytes abnormalities, post-resuscitation electrolytes were normal. Fortunately, she received prompt therapy and was reprogrammed with increased LRL. Conclusion: We described a case of Spike-on-T PMVT prior to colonoscopy without obvious provocation other than asynchronous pacemaker spikes. Reprogramming devices in DOO mode with increased LRL may prevent PVCs and asynchronous pacemaker spikes from triggering PMVT.

Abstract 4124120: Rare but Deadly - Eosinophilic Myocarditis in a Patient with Eosinophilic Granulomatosis Polyangiitis

Eosinophilic myocarditis (EM) is a rare inflammatory myocarditis characterized by eosinophilic infiltration of myocardial tissue. Despite the high mortality rate, EM is frequently underdiagnosed and is often first identified in postmortem studies. We share a case of EM as an early manifestation of newly diagnosed eosinophilic granulomatosis polyangiitis (EGPA). The patient is a 46-year-old female with a past medical history of ulcerative colitis and adult-onset asthma who presented to the emergency department with a 2–3-week history of worsening positional chest pain radiating to the left upper extremity. Associated symptoms include 3 months of fatigue, headaches, right foot neuropathy, urticaria, and B-symptoms. Prior to admission, the patient was started on empiric prednisone for presumed EGPA. Initial lab work on admission was notable for elevated troponin (602 ng/L), hyper-eosinophilia (19.5%), thrombocytosis (680K/uL), and elevated ESR (42 mm/h) that have improved since initiation of prednisone. Transthoracic echocardiogram revealed a newly reduced LVEF of 40% with basal and mid-septal wall motion abnormalities. Cardiac catheterization showed normal coronaries confirming the diagnosis of non-ischemic cardiomyopathy. Late gadolinium enhancement in cardiac MRI was seen in basal to mid segments with patchy pericardial enhancement, meeting the Lake Louise criteria for myocarditis. An endomyocardial biopsy showed substantial myocardial infiltration with lymphocytes, histiocytes and eosinophils, confirming the diagnosis of EM. After multidisciplinary team discussion with cardiology and rheumatology, the patient was started on guideline-directed medical therapy for her HFrEF and pulse dose steroids with a prolonged taper and cyclophosphamide. She is tolerating her treatment well. This case highlights the importance of early recognition, comprehensive assessment and targeted treatment for EM depending on its underlying etiology. In the case of autoimmune dysfunction, it involves a combination of immunosuppressive and symptomatic therapy. Ongoing research is crucial to enhance our understanding and improve clinical outcomes, like arrhythmias and cardiogenic shock, for this complex condition.

Abstract 4145899: The Danger of Moderator Band Ectopy: A Case of Premature Ventricular Contraction induced Recurrent Ventricular Fibrillation

Introduction: Premature Ventricular Contractions (PVCs) are often a benign arrhythmia. However, those originating from the Purkinje system can result in fatal arrhythmias. One example is PVCs originating from the moderator band (MB) within the right ventricle (RV) of the heart. We present a case of PVCs originating from the MB triggering idiopathic ventricular fibrillation (VF) and electrical storm. Case: A previously healthy 49-year-old woman was admitted following a witnessed VF cardiac arrest. She had recurrent episodes of VF, initially treated with Amiodarone and Procainamide which failed to suppress the recurrent VF. She received 54 external defibrillations before a transvenous pacer (TVP) was placed to override the PVCs at a pacing rate of 110 bpm. Post-resuscitation ECGs revealed frequent PVCs originating from the RV free wall, potentially from the lateral part of MB (Figure 1). Quinidine was added to suppress the PVCs ultimately allowing removal of the TVP. Transthoracic Echocardiogram revealed normal cardiac function and a prominent MB. A cardiac MRI was performed showing no infiltrative disease or any other abnormalities. The patient underwent sympathectomy and defibrillator placement. Despite recurrent cardiac arrest, she had excellent neurologic recovery and was subsequently discharged on Quinidine. Discussion: MB extends from the septal wall to the base of the anterior papillary muscle in the RV, carrying Purkinje fibers(PF) from the right bundle branch as it exits the septum. Purkinje fibers have been shown to initiate arrhythmias by several mechanisms including enhanced automaticity, triggered activity and re-entry. In the genesis of PVCs, triggered activity is the likely mechanism. This can degenerate into VF in a structurally normal heart, hence the term “idiopathic VF”. Familiarity with this entity and ECG features of MB ectopy leads to timely management and may potentially prevent lethal arrhythmias in symptomatic patients with such PVCs. Further studies are required to fully understand the arrhythmogenic mechanisms and the optimal management approach for MB ectopy.