Hybrid management of postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia in the era of modern electrophysiology, cardioneuromodulation, and telemedicine: A case report.

Morbity and mortality in Texel sheep following feed-based monensin overdose in Brazil.

Electrocardiographic and echocardiographic abnormalities in systemic lupus erythematosus : Initial data from Cameroonian patients

Background/Objectives: Electrocardiographic (ECG) findings such as sinus tachycardia and right bundle branch block are commonly associated with acute pulmonary embolism (PE). This study aimed to investigate the prevalence of advanced interatrial block (IAB) in patients with acute PE and its association with atrial fibrillation (AF) and hemodynamic changes. Methods: This retrospective, single-center study included patients diagnosed with acute PE (42% female, 58% male) between January 2014 and September 2024 at University Hospital Münster. A control group of individuals without manifest heart disease (45% female, 55% male) served as a control group. All patients underwent clinical, laboratory, ECG, and echocardiographic evaluations. Results: A total of 351 patients with acute PE and 120 control patients were included. The PE group had a mean age of 62.5 years. Advanced IAB was detected in 35% of PE patients, significantly higher than in controls (2%). In contrast, typical ECG signs of PE such as sinus tachycardia (23%), right bundle branch block (8%), and S1Q3 pattern (20%) were less frequent. A subgroup analysis demonstrated that patients with IAB were older, had a higher CHA2DS2-VA score, and were more likely to have pre-existing and new-onset AF. IAB was not associated with right heart dysfunction on echocardiography. Conclusion: For the first time, this study revealed that advanced IAB was present in many patients with acute PE. IAB was associated with a higher risk of AF and greater thromboembolic risk but not with hemodynamic changes typical of PE. Detecting an advanced IAB at the initial presentation in the emergency department could provide an important indication of PE.

Dyspnea in adolescents is often underestimated as a simple respiratory infection, yet it may represent the fairst sign of complex autoimmune multiorgan disease. This report highlights the autoimmune mechanisms underlying dyspnea to promote early recognition of autoimmune disease in adolescents. An 18-year-old female presented with acute worsening of chronic dyspnea. She was tachypneic hypertensive, hypoxemic, and severe anemia. Examination revealed pallor, edema, basal fine crackles, and gallop. Laboratory findings showed renal impairment with proteinuria and hematuria. The albumin was normal and blood gas indicated respiratory alkalosis with compensatory metabolic acidosis. Infectious work-up revealed yeast-like fungi and mixed gram-positive cocci/gram-negative bacilli, while GeneXpert MTB was negative. Chest radiograph demonstrated pulmonary edema with pneumonia. Electrocardiography showed sinus tachycardia 119 bpm with right axis deviation and right ventricular hypertrophy. Echocardiography revealed right atria and ventricle enlargement, moderate tricuspid regurgitation, mild pericardial effusion, intermediate pulmonary hypertension, and preserved EF 64%. ANA test was positive, but performed only at discharge before referral for definitive immunological workup. The patient's life-threatening multiorgan dyspnea could be concluded as four major mechanisms, such as : 1) Renal & Volume Overload; 2) Cardiopulmonary Vasculopathy; 3) Autoimmune and Infectious Pulmonary Damage; 4) Severe Anemia. The profound multiorgan involvement and severe systemic inflammation provided a strong clinical rationale for highly active systemic autoimmune disease (SAID), most probable being Systemic Lupus Erythematosus. This case illustrates how adolescents' dyspnea with complicated systemic symptoms deserves an early diagnosis of autoimmune disease without waiting for infectious exclusion, to prevent the devastating consequences associated with diagnostic latency and delayed targeted intervention. As life-threatening dyspnea in an adolescent may be the catastrophic initial presentation of Probable Systemic Lupus Erythematosus.

Cardioneuroablation (CNA) is increasingly used worldwide in the treatment of functional bradyarrhythmia mediated by excessive vagal tone. However, a potential early or long-term complication is the development of postprocedural inappropriate sinus tachycardia (IST), which remains difficult to manage. Recent data suggest that sinus node (SN)-sparing hybrid ablation may offer promising long-term outcomes in patients with IST and postural orthostatic tachycardia syndrome (POTS). We present what is, to our knowledge, the first documented case of such a procedure performed for IST/POTS following an uncomplicated CNA for symptomatic vagally mediated sinus bradycardia (SB). The comprehensive treatment strategy included on-site cardiac rehabilitation, a home-based telerehabilitation program, and evaluation using cardiovascular autonomic functional testing (CAFT) and the Malmö POTS scoring system. We present a 33-year-old woman with a 6-month history of dizziness, palpitations, exercise and orthostatic intolerance, dyspnea, presyncope, and one syncope episode. Symptoms of IST (130-170bpm) appeared within 1 week after CNA for symptomatic SB. Despite the diagnosis of IST, CAFT have confirmed POTS. Other causes of sinus tachycardia (ST) were excluded according to guidelines. Nonpharmacological and pharmacological treatment proved ineffective. Following shared decision-making, the patient was referred for SN-sparing hybrid ablation with right-sided video-assisted thoracoscopic surgery (VATS). The patient subsequently participated in hybrid cardiac rehabilitation. At the 3-month follow-up, she was drug free and maintained a normal sinus rhythm. No evidence of bradycardia, IST/POTS, or vasovagal syncope (VVS), including CAFT, was documented during the follow-up. The serial MALMO POTS scoring system before and 3, 6, 9, 12 and 18 months after SN-sparing hybrid ablation demonstrated consistent and significant improvement, with scores decreasing from 46 to 13, 10, 6 and 12 points, respectively, values comparable to those observed in the healthy population. This is the first reported case of SN-sparing hybrid ablation for IST/POTS that developed after primary, uncomplicated CNA. Although not yet included in guidelines, the implementation of both procedures for cardiovascular autonomic dysfunction (CVAD) requires comprehensive and multidisciplinary heart team management. The MALMO POTS scoring system might be a useful tool for assessing CVAD before and after cardioneuromodulation procedures and further comprehensive evaluation.

Description of Case: A 76-year-old female with a past medical history including HTN, DM, HLD, bilateral breast cancer (status post bilateral mastectomy and radiation), and prior thymoma presented with acute-onset dyspnea and chest pain. Initial evaluation revealed elevated troponin levels up to 9 ng/mL and sinus tachycardia with RBBB on ECG. CT chest demonstrated a large left anterior mediastinal mass infiltrating the pericardium, with suspected invasion into the left inferior pulmonary vein.Transthoracic echocardiography revealed a heterogeneous mediastinal mass invading the aortic root, causing extrinsic compression of the left main coronary artery, as well as involvement of the left superior pulmonary vein, left atrial lateral wall, and basal lateral left ventricular wall. A 2.1 x 2.1 cm echogenic mass was noted in the left atrial cavity. Initial coronary angiography revealed 75% narrowing of the left main coronary artery, but no intervention was performed. Surgical consultation with both cardiothoracic and thoracic surgery deemed the patient not a suitable candidate for resection or bypass due to extensive local invasion and overall frailty. A repeat angiogram one week later revealed progression to 90% left main stenosis, prompting an urgent high-risk PCI with successful stent placement. Discussion: Given rapid progression of left main coronary stenosis secondary to extrinsic tumor compression, and the patient’s inoperable status, a heart team approach led to the decision for high-risk PCI. The procedure was performed successfully, restoring perfusion and relieving symptoms.This case is an example of uncommon etiology of left main coronary artery compression from an invasive mediastinal tumor. When surgery was not feasible, PCI offered a successful alternative and served as a palliative measure when other options were not viable.

Background: Clinical 12-lead ECGs are used to diagnose a range of conditions, but the diagnostic utility of wearable and portable devices is limited to a limited number of rhythm disorders. These devices capture lead I ECG, which are displayed as a PDF. We present a vision-text transformer – WAVE-AI - capable of generating accurate and comprehensive interpretations from images (e.g., PDFs) of single-lead ECGs recorded on wearable and portable devices. Methods: We fine-tuned an ECG image-text foundation model, ECG-GPT, using 389,482 ECGs and accompanying corresponding diagnosis statements from a large tertiary health system to develop a model that could infer a full ECG report from a printed lead I image. For this, we plotted lead I in multiple image formats to enable the model to generate reports from PDF outputs from various consumer devices ( Figure 1 ). We evaluated model performance in a held-out test set across structured clinical assessment, semantic similarity, and conventional natural language generation metrics. Results: In 43,108 ECGs distinct from development, the model performed well across 20 rhythm and conduction abnormalities extracted from diagnosis statements, with high AUROCs, sensitivities, and specificities (Table 1). The AUROCs for detecting atrial fibrillation, right bundle branch block, and sinus tachycardia were 0.92, 0.94, and 0.95, respectively. The model identified the full context of diagnosis statements, including all associated modifiers and conditions, with a median pairwise similarity of 0.87 (IQR 0.80-0.94), significantly greater than the similarity of 0.74 (IQR 0.69-0.80, p < 0.001) between two randomly selected statements ( Table 2 ). The model also performed well across conventional metrics, with ROUGE-L and BLEU-1 scores of 0.576 and 0.472, respectively. Conclusions: WAVE-AI is a vision encoder-decoder model capable of generating ECG reports from single-lead ECG images. This approach represents an automated and accessible strategy for generating expert-level complete ECG reporting on lead I ECGs that can be acquired from wearable and portable devices.

A 27-year-old woman on 4th postpartum day presented to ED with fatigue, dysphagia, and chest tightness. Appeared anxious and had sinus tachycardia. Labs revealed leukocytosis, elevated hsTrop, and pro-BNP. TTE demonstrated LV systolic dysfunction (EF 35%), with basal hypokinesis and preserved apical function, raising suspicion for reverse Takotsubo cardiomyopathy. Workup for dysphagia included brain MRI, which revealed a CLIPPERS-like brainstem lesion. She was treated with high-dose IV steroids, DAPT for 21 days, and GDMT. Readmitted within days with new-onset expressive aphasia and right lower extremity weakness. MRI showed an acute infarct in the left anterior cerebral artery (ACA) territory. Cerebral angiography confirmed moderate to severe vasculitis and vasospasm of the bilateral ACA and left MCA. Steroids were escalated, and rituximab was initiated for presumed steroid-refractory postpartum vasculitis. Immunosuppressive therapy included prednisone and mycophenolate mofetil. Further testing confirmed VZV CNS vasculitis (positive VZV IgM, oligoclonal bands, and angiographic vasculitis); valacyclovir was later added. Repeat echocardiogram two weeks later showed EF normalization to 55–60% with no regional wall motion abnormalities, confirming transient rTTC. This case illustrates an unusual neurocardial interaction: VZV-induced CNS vasculitis triggered reverse Takotsubo cardiomyopathy in a postpartum woman. The catecholaminergic surge and neuroinflammatory milieu a/w CNS involvement likely contributed to myocardial stunning. The postpartum period may further predispose to immune dysregulation, explaining the fulminant course of vasculitis. rTTC is classically associated with neurological insults like subarachnoid hemorrhage or seizures, but to our knowledge, this is the first reported case linking VZV vasculitis to rTTC . This emphasizes the need to consider stress cardiomyopathy variants in postpartum patients presenting with cardiac and neurological symptoms and supports early echocardiography and CNS imaging in such scenarios. We report a rare and complex case of reverse Takotsubo cardiomyopathy secondary to VZV-induced CNS vasculitis in the postpartum period. This case highlights the critical interplay between the central nervous system and cardiac function, the importance of early multidisciplinary involvement, and the potential reversibility of both cardiac and neurological complications with timely immunosuppressive and antiviral therapy.

Intermittent high-grade atrioventricular (AV) block is a rare bradyarrhythmia in the young. In the absence of structural conduction system disease, it may result from heightened vagal tone. We present a unique case of a young adult with coexisting incessant atrial tachycardia (AT) and high-grade AV block, both of which resolved following catheter ablation targeting the AT arising in the left atrial appendage (LAA). Description of Case: A 25-year-old obese male with a 10-year history of exertional fatigue, palpitations, and presumed sinus tachycardia was referred for evaluation. Baseline ECG showed AT at 103 bpm with negative P waves in I and aVL. Ambulatory monitoring for 13 days revealed frequent tachycardia to a max of 181, average 99 bpm, but also 277 episodes of high-grade AV block up to 3 nonconducted P waves, including daytime pauses up to 2.5 seconds. An electrophysiology study for symptomatic “near incessant” AT demonstrated a focal AT arising from the base of the LAA with epinephrine infusion. Radiofrequency ablation at this site (6 lesions) rendered the AT non-inducible. AV nodal function and His-Purkinje conduction were normal. Follow-up ECGs and 2 week monitors immediately and at 6 months post-ablation revealed inappropriate sinus tachycardia (IST), and no AT nor AV block. Discussion: This case illustrates a rare co-occurrence of focal LAA AT, intermittent high-grade AV block, and IST, for which LAA ablation targeting AT also eliminated AV block. Whether all the findings are linked due to an autonomic mechanism or whether the AT was serendipitously located near ganglionated plexi that were responsible for the AV block is uncertain. These findings support the emerging role of autonomic modulation with ablation in the management of high-grade AV block in the young.

Background: Pulmonary Embolism is a potentially life-threatening condition that may present with a spectrum of ECG abnormalities. Among these, the S1Q3T3 pattern: a prominent S in lead I, Q in lead III, and inverted T in lead III, is classically associated with PE. However, it is neither sensitive nor specific, occurring in approximately 12-20% of cases. The Daniel score assigns points (0–21) to predict an increased pressure in pulmonary artery and right ventrivule dysfunction. A score > 8 is associated with worsened clinical outcomes, experts agree that evidence of RV failure warrants escalation of therapy beyond anticoagulation, including fibrinolytics and thrombectomy. Case: A 77-year-old female with medical history of Breast Cancer on anastrozole, Hypertension and recent left total knee arthroplasty (postoperative day 17) on Aspirin twice daily for prophylaxis. She presented with acute dyspnea and diaphoresis, on arrival to the ED, she was tachypneic, tachycardic, and hypotensive. An ECG demonstrated sinus tachycardia with S1Q3T3 pattern, incomplete right bundle branch block (RBBB), inverted T wave in V1 and V3. Her Daniel Score was calculated at 9, indicating a high risk for hemodynamic instability. Troponin was 0.10 and BNP 8030. PE was suspected and a CTA confirmed a large saddle PE involving both main pulmonary arteries, with signs of RV strain, including RV dilation and contrast reflux into the IVC. Despite initiation of IV heparin, the patient developed worsening hypotension and was started on norepinephrine and systemic thrombolysis with tPA. Plans were made for urgent catheter-directed thrombectomy, unfortunately, the patient suffered multiple episodes of pulseless electrical activity and ultimately succumbed to cardiac arrest. Discussion: This case underscores the prognostic value of ECG in the early evaluation of a PE. The Daniel Score offers a structured approach to quantify ECG abnormalities and predicts the likelihood of adverse outcomes. Risk stratification tools, including ECG scoring systems, cardiac biomarkers (troponin), Echocardiography and CT, should guide timely management strategies in high-risk PE. ECG findings, especially when interpreted using scoring systems like the Daniel Score, can provide valuable insight into disease severity and prognosis. Clinicians should maintain a high index of suspicion and prioritize early diagnostic imaging and intervention when characteristic ECG changes are present in the appropriate clinical setting.

Background: Immune checkpoint inhibitors (ICIs), such as pembrolizumab, have revolutionized cancer therapy but can trigger immune-related adverse events (irAEs), including myocarditis and myositis. Double M syndrome, myositis with concurrent myocarditis, is a rare, high-risk phenotype typically presenting acutely, though smoldering presentations are often underrecognized and constitute a diagnostic challenge. Clinical case: A 67-year-old woman with stage IIb triple-negative breast cancer, treated with pembrolizumab-carboplatin/paclitaxel followed by doxorubicin/cyclophosphamide per KEYNOTE-522 protocol, presented four months after completing ICI therapy with worsening myalgias, weakness, low-grade fever, and transaminitis. Labs revealed elevated CK (7,760 U/L), transaminases (AST 369 U/L, ALT 626 U/L). ECG showed sinus tachycardia and diffuse ST depressions, with troponin-I (>15,000 ng/L), and CK-MB (185 ng/mL). TTE demonstrated preserved LVEF without wall motion abnormalities. Differential diagnoses included non-ST elevation myocardial infarction, ICI-related myocarditis, and viral myocarditis. Decision-Making: Initial ACS management was initiated but discontinued after coronary angiography showed non-obstructive disease. Endomyocardial biopsy (EMB) revealed lymphocyte-predominant myocarditis with CD8+ cytotoxic T-cell infiltrates and PD-L1 overexpression in myocytes, confirming ICI-associated myocarditis (Figure 1). She was treated with pulse-dose methylprednisolone (1 g/day x 5 days), followed by oral prednisone taper. Follow-up cardiac PET/CT at two months showed complete resolution of myocardial inflammation (Figure 2). Conclusion: This unique case illustrates a rare, delayed-onset presentation of pembrolizumab-induced Double M syndrome with smoldering myocarditis (Figure 3) and myositis, highlighting the importance of considering ICI-related myocarditis even in asymptomatic or subacute settings post-immunotherapy to avoid fatal cardiac complications. EMB played a critical role in diagnosis and tailored corticosteroid therapy. Timely recognition and coordinated multidisciplinary management are crucial for improving outcomes in ICI-related cardiotoxicity and other irAEs.

Case Description: A 71-year-old male presented to the hospital for dyspnea and chest discomfort for the past 2 weeks. He has a history of AAA status post stent and current tobacco use with emphysema. On admission, he was found to be tachycardic with rates reaching as high as 180 with systolic blood pressure of 89/61 and hypoxic with SpO2 of 80%. EKG revealed AFib with RVR with no acute ischemic changes. Troponins were negative and proBNP was 307. Infectious workup was negative. CTA chest showed no evidence of PE or dissection, however, moderate pericardial and bilateral pleural effusion was shown with mediastinal lymphadenopathy. After starting an esmolol and amiodarone drip, he converted to sinus tachycardia. TTE showed an EF 55%, echo dense debris measuring 2 cm with 1 cm effusion within the pericardial space resulting in significant compression of RA and RV. Findings were concerning for tamponade evidenced by invagination of RA and RV during systole and diastole respectively and greater than 50% variation and tricuspid inflow velocities with respiration. He was taken emergently to the OR for a pericardial window, thoracentesis, and chest tube. 300 mL and 400 mL of cloudy straw-colored fluid were removed from the pericardial and pleural space respectively. Fluid studies were negative for malignant cells and cultures remained negative. Repeat TTE showed an EF 55%, with epicardial fat pad and small posterior pericardial effusion. ANA testing was positive; however, other autoimmune studies are negative. His symptoms improved and he was discharged home. Discussion: Cardiac tamponade is commonly caused by large pericardial effusions. Mild pericardial effusion less than 1 cm on TTE does not typically cause symptoms. However, the presence of significant pericardial debris can be problematic with minimal pericardial effusion. In this case, the patient developed cardiac tamponade complicated by AFib with RVR. Fortunately, hemodynamics and symptoms improved post pericardial window draining 300 mL of bloody fluid, but the diagnosis remains unknown given negative fluid studies. It's postulated that the debris is inflammatory in nature, but the absence of a diagnosis puts the patient at high risk for shock if the pericardial window fails. Patients with pericardial debris up to 2 cm on TTE with risk of developing pericardial effusion should be monitored with follow up TTE. Further studies are necessary to unveil the underlying etiology of large pericardial debris.

Introduction: Right atrial perforation resulting in cardiac tamponade is a rare but life-threatening complication of hemodialysis catheter placement. While this is recognized with superior central venous access, perforation originating from a femoral hemodialysis catheter is exceedingly uncommon. We present a case of acute cardiac tamponade secondary to right atrial perforation following femoral hemodialysis catheter exchange. Case: A 61-year-old woman with heart failure with reduced ejection fraction (EF 25%), end-stage renal disease on hemodialysis, and a history of breast cancer presented with a malfunctioning hemodialysis catheter. After unsuccessful local alteplase, interventional radiology performed a left femoral hemodialysis catheter exchange. Within one hour post-procedure, the patient developed syncope, hypotension (60/40 mmHg), tachycardia (120 bpm), and reported chest discomfort, weakness, and lightheadedness. Bedside electrocardiogram showed sinus tachycardia with electrical alternans. Emergent echocardiography revealed a moderate circumferential pericardial effusion with right atrial systolic and right ventricular diastolic collapse, distended inferior vena cava, and marked respirophasic variation of atrioventricular inflow velocities, consistent with cardiac tamponade. Chest radiography suggested the catheter tip abutting the right atrial free wall. The delayed perforation was likely due to catheter migration and erosion. Despite aggressive fluid resuscitation and norepinephrine infusion (up to 35 mcg/hr), the patient remained unstable. Bedside pericardiocentesis drained approximately 700 mL of blood, resulting in rapid hemodynamic improvement and discontinuation of vasopressors within one hour. Computed tomography confirmed the catheter tip’s proximity to the right atrial wall. Cardiothoracic surgery determined that surgical intervention was unnecessary as the perforation had sealed spontaneously. Conclusion: This case highlights the need for vigilance for mechanical complications, even with femoral central venous access. Immediate bedside echocardiography was critical for rapid diagnosis and intervention. The patient made a complete recovery following pericardiocentesis and was discharged asymptomatic on hospital day four.

Background: Ventricular arrhythmias during pregnancy present complex management challenges requiring careful balance between maternal safety and fetal well-being. While outflow tract ventricular tachycardia (OTVT) is generally considered benign in non-pregnant patients, pregnancy-related hemodynamic changes can increase arrhythmic burden. Limited data exist regarding optimal management strategies for sustained ventricular tachycardia in pregnancy, particularly when patients prefer outpatient management. Case Presentation: We report a 39-year-old G4P3 female at 29 weeks gestation with chronic palpitations who underwent ambulatory cardiac rhythm monitoring with a Zio patch due to worsening symptoms. Following detection of sustained ventricular tachycardia, the patient was evaluated in the emergency department with continuous telemetry monitoring, echocardiography, and multidisciplinary consultation. Ambulatory monitoring revealed sustained monomorphic ventricular tachycardia episodes lasting up to 12 minutes with heart rates up to 200 bpm, consistent with right ventricular outflow tract origin. The patient experienced lightheadedness but denied syncope or hemodynamic compromise. During hospitalization, telemetry showed sinus tachycardia (90-120 bpm) with frequent premature ventricular contractions but no sustained VT episodes. Beta-blocker therapy was initiated with good tolerance. Given documented sustained VT episodes, symptoms, and patient preference against prolonged hospitalization, a WCD was prescribed for continuous protection until delivery. The patient was successfully discharged home with close outpatient follow-up. Discussion: Wearable cardioverter defibrillator therapy represents a viable management strategy for sustained ventricular tachycardia in pregnancy when patients decline inpatient monitoring. This approach provides continuous arrhythmia protection while respecting patient autonomy and avoiding prolonged hospitalization. The WCD served as an effective bridge to delivery, allowing safe outpatient management with planned post-partum evaluation. This case supports WCD therapy consideration in selected pregnant patients with sustained ventricular arrhythmias appropriate for outpatient management.

Background: Cardiac complications are common in the Multisystem Inflammatory Syndrome in Children (MIS-C); however, data on arrhythmias and other electrocardiogram (ECG) abnormalities are limited. Objective: To characterize the frequency of and risk factors for ECG abnormalities and arrhythmias in patients with MIS-C, and their associated outcomes. Methods: Secondary analysis of ECG and ambulatory monitor data from a 32-center cohort study of patients with MIS-C hospitalized between 03/2020 to 11/2021 with a follow-up period of 2 years. ECG and ambulatory monitor interpretation was performed at each participating site. Greater illness severity was defined as one or more of the following: vasoactive medications, cardiac dysfunction or elevated troponin, intubation or mechanical support. Results: From 1,204 patients in the MUSIC cohort, ECG data were available for 1,104 patients (92%). Overall, ECG was abnormal in 864 (78%) of patients (Figure), most frequently sinus tachycardia (37%), ST-T waves anomalies (30%), prolonged QTc interval (23%), sinus bradycardia (16%), and left ventricular hypertrophy (14%). Arrhythmias were reported in 71/952 (7%) patients with myocarditis and included atrioventricular block (AVB, n=22; 1 st degree in 14, Mobitz 1 in 1, Mobitz 2 or higher in 7), ventricular tachycardia (n=8), supraventricular tachycardia (n=5), junctional tachycardia (n=5) and isolated ectopy (n=5 atrial, n=6 ventricular). Risk factors for ECG abnormalities included older age, White or Hispanic/Latino ethnicity, elevated troponin, myocarditis or cardiac dysfunction, and pericarditis or pericardial effusion (Table). Risk factors for arrhythmias included older age, obesity, elevated troponin and myocarditis or cardiac dysfunction (Table). Patients with arrhythmias and other ECG abnormalities were more likely to have greater illness severity and prolonged length of stay. Ambulatory rhythm monitoring was performed in 156 patients (13%) at median 64 [IQR 22, 164] days after hospital discharge, with normal results in 140 (88%) patients. The most frequent abnormalities were AVB (n=8, 5%) and isolated ectopy (>100 beats/24 hours; n=6, 4%) , with no high-grade AVB or tachyarrhythmias identified. Conclusion: ECG anomalies are frequent in MIS-C and associated with myocarditis, greater illness severity and prolonged hospital length of stay. Arrhythmias and other ECG abnormalities mostly occurred during acute hospitalization, and were very uncommon during outpatient follow-up.

Background: Pericarditis is a rare obstetric complication. Severe pericardial disease may lead to tamponade physiology, jeopardizing both the mother and fetus. We report a case of a 29-year-old woman, G1P0 at 21 weeks gestation, presenting with recurrent pericarditis complicated by early signs of cardiac tamponade. Methods: A 29-year-old (G1P0) female with a history of Graves' disease on methimazole, drug-induced lupus, and recent pericarditis presented to the hospital at 21-weeks gestation due to recurrent chest pain. She was recently admitted for pericarditis and placed on aspirin and colchicine. Transthoracic echocardiogram (TTE) revealed a small pericardial effusion with diastolic inversion. Thyroid function tests were elevated, and methimazole was increased to 20 mg daily. The patient remained home for two weeks until developing recurrent positional chest pain. On admission, the patient was hemodynamically stable. EKG revealed sinus tachycardia. Repeat TTE confirmed recurrence of acute pericarditis, now with pericardial thickening, fibrinous material adjacent to the visceral pericardium, and a large 2-centimeter pericardial effusion (Figure 1). Evidence of RV inversion and a plethoric IVC were present, concerning for early tamponade physiology. Results: Differential diagnosis at the time was broad, including pericarditis of viral etiology or secondary to drug-induced lupus or Graves disease. Given early tamponade physiology and hemodynamic stability, a multidisciplinary team chose medical management over pericardial window due to ongoing pregnancy, suboptimal window for drainage, and procedure-related risks. Aspirin was started at 650 mg twice a day along with 20 mg methylprednisolone and 0.6 mg colchicine. Intravenous fluid resuscitation was provided to maintain preload. Serial TTE was utilized to monitor the progression of the effusion. Methimazole was maintained at 20 mg daily. Viral and autoimmune pericarditis workup was unremarkable. After two weeks of serial echocardiograms, the patient was gradually tapered to aspirin 81 mg daily, prednisone 15 mg daily, and colchicine 0.6 mg daily and discharged. The rest of her pregnancy was uncomplicated, and she delivered a healthy baby at 38 weeks gestation. Conclusion: This case highlights the complexities of managing pericarditis in pregnant patients with autoimmune conditions. Medical management and serial TTE were useful in managing early tamponade while minimizing risks to both the mother and fetus.

Introduction: Human granulocytic anaplasmosis (HGA), caused by Anaplasma phagocytophilum, is a tick-borne illness ranging in manifestation from mild febrile syndromes to life-threatening complications. Cardiac manifestations are rare and often attributed to co-infection with Lyme or – even more rarely – myocarditis. 1 We present a case of isolated HGA associated with prolonged QTc and polymorphic ventricular tachycardia (PMVT) cardiac arrest in an immunocompetent adult. Case Presentation: A 61-year-old man with hypertension and hyperlipidemia presented to a New England ED in late May with four days of fevers, malaise, and headaches, culminating in syncope. He was febrile (101.2°F) and tachycardic (121 bpm) but otherwise hemodynamically stable. Labs showed thrombocytopenia (135,000/µL), hyponatremia (Na 133 mEq/L), hypokalemia (K 3.4 mEq/L), elevated transaminases (AST 81 IU/L, ALT 121 IU/L), and high-sensitivity troponin (294 ng/L). ECG showed sinus tachycardia with normal QTc; telemetry revealed multiple salvos of non-sustained polymorphic VT (Figure 1). Initial infectious workup—including cultures, urinalysis, viral panels, Lyme serology, and lumbar puncture—was unrevealing. Empiric doxycycline was started for suspected tick-borne illness. On hospital day 1, he had two episodes of PMVT cardiac arrest, two hours apart, requiring CPR and defibrillation. Post-arrest ECG showed QTc >550 ms. He received magnesium and was started on amiodarone and lidocaine. On hospital day 3, Anaplasma testing returned positive. Cardiac workup (TTE, coronary angiography, cardiac MRI) showed no structural disease, obstructive CAD, or myocardial edema/scar, with normal systolic function. With doxycycline and supportive care, QTc normalized and anti-arrhythmics were weaned with no further PMVT. As no reversible cause was identified, he underwent ICD placement for secondary prevention. Discussion: A few case reports describe HGA-associated atrial arrhythmias and myopericarditis, but there are no reports of HGA-associated ventricular arrhythmias or associated cardiac arrest. 2–4 The initial hypothesis was that HGA-associated myocarditis led to QTc prolongation and PMVT. However, normal cardiac MRI and no other identifiable causes of QT prolongation raise the possibility of QTc prolongation via a yet-undiscovered direct mechanism or inflammatory cascade secondary to anaplasmosis. Further research is warranted to define the arrhythmogenic potential of anaplasmosis.

Introduction: Tricuspid regurgitation (TR) contributes to severe cardiovascular complications by causing atrial and ventricular dilation, retrograde blood flow, and abnormal cardiac remodeling, leading to electrical disturbances and disease progression. The lack of reliable preclinical models limits our understanding of TR pathophysiology and hinders early biomarkers for timely intervention of disease. Research Questions: Our study aims to establish a new reproducible, minimally-invasive, and valve-harmless porcine model to mimic TR, enabling the investigation of disease progression and the identification of novel molecular signatures underlying this condition. Methods: TR was induced by catheter-based placement of an inferior vena cava filter to prevent tricuspid leaflet coaptation between right chambers. Hemodynamic, echocardiographic and electrophysiological assessments, jet flow, heart rate, and chamber dimensions, were weekly assessed over 30- and 60-days post implantation. Results: Following device implantation, TR led to significant increases in heart rate, right chamber dilation, and arrhythmogenic events. Early manifestations included sinus tachycardia and multifocal atrial tachycardia, progressing to brief episodes of paroxysmal atrial fibrillation. Histological analysis also revealed cellular hypertrophy and fibrosis in both the right atrium (RA) and sinoatrial node (SAN), accompanied by upregulation of the TGF-β/Smad2/3, and -4 signaling axis, along with increased MMP2, and MMP9, suggesting its involvement in disease progression. To investigate in further detail, progressive downregulation and spatial redistribution of the pacemaker HCN4 channel were observed over time (Figure 1), accompanied by increased phosphorylation of Gap junction Connexins -43, and -45, along with elevated CaMKII and PKA levels, while SERCA2A and PLN levels remained unchanged. These findings addresses for the first time, how TR signaling disrupts cardiac conduction velocity and pacemaker function through dual pathways: (1) impairing SAN electrophysiology via HCN4 dysregulation, and (2) creating electrical uncoupling through connexin remodeling mediated by CaMKII/PKA-dependent phosphorylation. Conclusions: We successfully established a percutaneous porcine model of TR that recapitulates human disease pathophysiology. This experimental breakthrough bridges the gap between mechanistic and phenotyping manifestations, accelerating therapeutic discovery for TR-related cardiac complications.

Case Description: An 18-year-old female presented to the emergency department with acute-onset dyspnea, chest pain, nausea, vomiting, and syncope after four months of oral contraceptive use and active vaping. Physical examination revealed tachycardia (135 bpm) and tachypnea, with ECG showing sinus tachycardia. Laboratory studies demonstrated dramatically elevated D-dimer (12,756), elevated proBNP (660), and troponin (299 225). Echocardiography revealed the D-sign [Image 1] classic McConnell sign - severely dilated right ventricle with hyperkinetic apex and hypokinetic basal-to-mid free wall [Image 2], confirming massive PE with acute cor pulmonale. CT angiography revealed extensive bilateral pulmonary emboli with signs of right heart strain [Image 3]. Immediate anticoagulation with heparin was initiated, followed by ICU admission where alteplase was administered for massive PE. Remarkably, the patient demonstrated complete heparin resistance with no APTT response despite escalating doses over 24 hours and the decision was made to switch to rivaroxaban 15mg twice daily. Patient symptoms significantly improved on day 3 and was eventually discharged with follow up appointment to hematology. Discussion: Thrombophilia workup revealed a multi-hit scenario: antithrombin III deficiency (68%, normal 85-135%) directly caused heparin resistance, as AT-III serves as heparin's primary cofactor. Heterozygous Factor V Leiden mutation creates activated protein C resistance, increasing VTE risk 4-8 fold. In addition to that, she was found to have PAI-1 4G/5G genotype which impairs fibrinolysis, amplifying thrombotic risk. Combined with OCPs (which increase clotting factors while decreasing natural anticoagulants) and vaping (causing endothelial dysfunction), these factors created exponential hypercoagulability in this young patient. Conclusion: This case demonstrates how multiple thrombotic risk factors can synergistically create catastrophic pulmonary embolism in young patients. Early recognition and aggressive intervention with thrombolysis can be life-saving. The identification of heparin resistance as a clinical clue to underlying thrombophilia opens new diagnostic pathways for personalized anticoagulation strategies, potentially revolutionizing PE management in the era of precision medicine.