Risultati per: La gestione del paziente depresso da parte del medico di medicina generale: case reports

Circulation, Volume 150, Issue Suppl_1, Page A4115543-A4115543, November 12, 2024. Background:Leadless cardiac pacemakers (LCP) have evolved as an excellent alternative to transvenous pacemaker (TVPM) for bradycardia therapy with excellent safety and efficacy outcomes. MicraTMwas the first commercially available LCP. The device attaches to the right ventricular myocardium with four Nitinol FlexFix™tines. Its inherent design poses problems with retrievability. This leads to many devices being turned off and left behind in the right ventricle at the end of its life. The Aveir retrieval catheter was recently launched as part of the Aveir family of LCP and has a tri-loop snare re-docking mechanism, steerability, and protective sleeve.Goals:We aim to show the safety and efficacy of using this novel retrieval catheter for extraction of the Micra™ LCP in lieu of abandoning the LCP in the right ventricle.Results:We present a case series of 8 successful retrievals of Micra™ LCP using the Aveir™ retrieval catheter. Four patients had the LCP removed during upgrade to cardiac resynchronization therapy and the other four had the LCP removed at the time of replacement of the LCP at device end-of-life. The mean age of the cohort was 72.6±9.4 years (62.5% female). The average age of the retrieved LCP was 4 years and 4 months with the oldest device being in place for 7 years and 7 months. Median retrieval time, defined as time from retrieval catheter in to retrieval catheter out, was 4.8±2.4 minutes. In 100% of the cases the LCP was successfully retrieved in its entirety via femoral venous access. There were no intra- or post-procedural complications, including vascular complications, pericardial effusions, right ventricular dysfunction or worsening tricuspid regurgitation. At six months follow up, patients continued to remain free of the above complications.Conclusion:This case series demonstrates the safety and feasibility of using the Aveir™ retrieval catheter for extraction of the Micra™ LCP device in lieu of abandonment. Additional studies should be considered to assess the risk and benefits of abandoning the device in the right ventricle extraction of the LCP with this novel technique. The authors acknowledge the steep learning curve associated with this procedure. Further multicenter analysis of this technique is necessary to determine its generalizability.

Circulation, Volume 150, Issue Suppl_1, Page A4146198-A4146198, November 12, 2024. Introduction:Lung cancer is divided broadly into two main types: Small cell lung cancer (SCLC) and non-small cell lung cancer-NSCLC. Approximately 70% of SCLC cases have metastasized to other parts of the body including lymph nodes, bone, liver, adrenal glands, and brain [1]. SCLS metastasis to cardiac tissue is rare. Primary cardiac tumors are as rare with a reported prevalence of 0.028% [2]. Here we present a 59-year-old female (59F) with recurrent SCLC metastasis with evidence of a newly diagnosed primary cardiac tumor.Case Presentation:59F with a past medical history of SCLC status-post chemotherapy and radiation presented for evaluation of worsening left upper extremity pain, paresthesia, motor weakness, and neck pain. During the hospital admission, an echocardiogram demonstrated extensive thrombus from the Superior Vena Cava (SVC) into the right atrium (RA) and an irregular echogenic 37 mm x 26 mm mass partially attached to the posterior leaflet of the tricuspid valve. The RA mass was successfully removed by mechanical thrombectomy. Pathological results of the RA mass revealed significant malignant epithelioid and spindled neoplasm with myxoid stroma– concerning for myoepithelial disease.Discussion:Cardiac tumors, although uncommon, should be included in the list of possible diagnoses when observing any abnormal mass detected through cardiovascular or thoracic imaging techniques. Cardiac tumors are likely due to metastatic origins as metastatic cardiac tumors occur 20 times more frequently than primary cardiac tumors[3].When metastatic cardiac tumors are suspected, malignant melanoma and leukemia are the most frequent origins[4]. Rarely does SCLC metastasize to cardiac tissue. Primary cardiac tumors are typically benign (90%), with primary malignant tumors being very rare[5]. Patients may be asymptomatic, or present with nonspecific symptoms such as exertional dyspnea, fevers, arthralgias, or life-threatening cardiac tamponade[6]. For right atrial tumors, treatment strategies are usually dependent on symptomatology, in which removal via aspiration or surgical resection has demonstrated a favorable prognosis[7].Conclusion:Given the rarity of primary cardiac tumors in the setting of metastatic SCLC, there exist no evidence-based guidelines for optimal management of right atrial tumors. In our patient, mechanical aspiration was performed without complications and prevented potential adverse cardiopulmonary events from occurring.

Circulation, Volume 150, Issue Suppl_1, Page A4147178-A4147178, November 12, 2024. Background:Loeffler endocarditis is a rare and clinically challenging presentation of hypereosinophilic syndrome (HES). Early detection and treatment are critical for this disease that otherwise carries a high risk of morbidity and mortality. We present a complex case of a patient with HES and sequelae.Case:A 41-year-old male with history of asthma presented with cough, dyspnea on exertion, orthopnea, and right arm pain. He noted a 15-pound weight loss in the past few months. In addition to right upper superficial vein thrombus, he was initially diagnosed with pneumonia, but labs were concerning for significant leukocytosis (WBC 54.23 103/uL) and hypereosinophilia (45%), as well as anemia and thrombocytopenia. Cardiology was consulted for evidence of cardiac involvement with high sensitivity troponin 480 ng/L and BNP 399 pg/mL. Transthoracic echocardiography and cardiac MRI showed mild apical biventricular dilatation with moderate apical hypokinesis. There was nonenhancing T2 hypointense eccentric signal in both apices, suggestive of organized thrombus. Circumferential mid-cavity subendocardial delayed enhancement in the left ventricle and right ventricular apex was noted. Systolic function was preserved, but there were signs of pulmonary arterial hypertension. These findings were consistent with Loeffler endocarditis. He underwent bone marrow biopsy, which confirmed diagnosis of FIP1L1-PDGFRA+ HES.The presence of the FIP1L1-PDGFRA mutation is correlated with an increased risk of cardiac involvement in patients with HES and is also associated with worse prognosis. Following an interdisciplinary discussion between the hematology, rheumatology, and cardiology teams, he was started on imatinib, methylprednisolone followed by prednisone taper, and apixaban. His symptoms and blood counts have since drastically improved, and he is being monitored closely for resolution of the thrombi and for any signs of heart failure.Conclusion:HES complicated by Loeffler endocarditis is a unique presentation of infiltrative disease causing inflammatory, thrombotic, and fibrotic cardiac sequelae. It can portend deadly complications, including valvular involvement, thromboembolic events, and heart failure. A high clinical suspicion is required due to the multitude of possible symptom presentations. Multimodality imaging and interdisciplinary management with early accurate diagnosis and treatment are necessary to slow disease progression and reduce morbidity risk.

Circulation, Volume 150, Issue Suppl_1, Page A4136480-A4136480, November 12, 2024. 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.

Circulation, Volume 150, Issue Suppl_1, Page A4119267-A4119267, November 12, 2024. Background:Sarcoidosis, a systemic granulomatous inflammatory disorder can involve various organs, including the heart but isolated bi-atrial cardiac involvement is rare. Advanced cardiac imaging especially in atypical presentations, can aid in early diagnosis.Case:A 59 year-old man with history of biopsy-proven pulmonary sarcoidosis presented with non exertional chest pain for 2 months. EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable. Stress echocardiogram ruled out myocardial ischemia. CT scan noted mediastinal lymphadenopathy consistent with known sarcidosis. In absence of other explainable etiolgies for chest pain, Cardiac MRI was done and showed preserved biventricular function, subepicardial enhancement in the basal inferior, inferolateral, and anterolateral walls. The enhancement raised suspicion for CS. However, symptoms resolved spontaneously, cardiac workup paused and he was monitored conservatively with serial Echocardiogram(TTE) until onset of dyspnea 3 years later. Repeat TTE and EKG then noted newly enlarged left atrium and atrial tachycardia. Further testing with Cardiac positron emission tomographic imaging with F-18 fluorodeoxyglucose (FDG-PET CT) showed abnormal myocardial uptake in both atrial posterior walls but no ventricular involvement, indicative of isolated bi-atrial inflammation in CS. He was treated with prednisone and methotrexate. Successful symptom and inflammation resolution on FDG-PET CT occurred in 3 monthsDiscussion:CS is rare and seen clinically in about 5% and diagnosed postmortem in 25% of sarcoidosis cases. Symptoms vary widely, with potential for severe heart complications. Left ventricle and interventricular septum are commonly involved, but isolated bi-atrial involvement is rare. Early diagnosis aided by Cardiac MRI and FDG-PET CT is crucial. Prednisone is mainstay of treatment, often combined with methotrexate. Cases of concurrent atrial CS involvement and bi-atrial fibrosis with Left ventricular hyperenhancement are documented, but this is the first known report of isolated bi-atrial hyperenhancement on FDG-PET CT for CS. This case highlights the need for symptom correlation with clinical and imaging follow-up, especially in atypical presentations.

Circulation, Volume 150, Issue Suppl_1, Page A4129440-A4129440, November 12, 2024. Background:Ventricular stunning refers to a transient mechanical dysfunction of the myocardium, typically manifesting in response to ischemic insults, reperfusion injury, inflammatory states, or neurohormonal overload. Here, we present an unusual case of ventricular stunning precipitated by direct current electrical cardioversion (DEC).Case Report:A 73-year-old man with a history of heart failure with reduced ejection fraction, paroxysmal atrial fibrillation (AF), coronary artery disease, and chronic kidney disease was admitted to a Veterans Affairs hospital for heart failure exacerbation. His hospitalization was complicated by recurrent episodes of symptomatic AF with ventricular rates in the 120-150’s. This was initially managed with intravenous amiodarone and eventually DEC. He continued to experience symptomatic episodes of AF. Later in the hospitalization a repeat DEC with a single 200 joule shock was performed with restoration of sinus rhythm. Several hours afterwards he was found to be unresponsive and hypotensive. Cool extremities and rising serum lactate raised suspicion for cardiogenic shock resulting in transfer to the intensive care unit where vasopressor and inotropic support were initiated. Echocardiogram revealed a precipitous decrease in left ventricular ejection fraction from 25% to 5%. Serum troponin concentrations were unchanged from prior and ECGs demonstrated rate-controlled AF.Clinical Decision Making:This case highlights an episode of unexpected decrease in cardiac output following an otherwise routine repeat DEC for recurrent AF requiring escalation to mechanical circulatory support. His decompensation worsened, necessitating transfer to the local university center for placement of catheter-based miniaturized ventricular assist device (Impella 5’5). Over the subsequent days, with supportive care, his left ventricular ejection fraction recovered to baseline, and mechanical and inotropic support were withdrawn.Conclusion:Ventricular stunning, leading to cardiogenic shock, is a rare and incompletely understood complication of DEC. It warrants consideration when monitoring patients after cardioversion. Implementing vigilant observation protocols post-DEC to detect ventricular stunning and predisposing risk factors could significantly enhance clinical management strategies.

Circulation, Volume 150, Issue Suppl_1, Page A4134619-A4134619, November 12, 2024. Background:Ebstein anomaly (EA) is a rare congenital heart defect occurring in 1.2 to 5 in 100,000 live births, characterized by a downward displacement of the tricuspid valve, thin-walled right ventricle, and tricuspid valve regurgitation. It can present variably from asymptomatic cases to severe symptoms like arrhythmias and right-sided heart failure. EA is often associated with other anomalies such as interatrial communication and mitral valve prolapse. The condition can lead to accessory atrioventricular pathways, frequently resulting in Wolff-Parkinson-White syndrome (WPW), which involves abnormal heart electrical activity and increases the risk of sudden cardiac death. While the genetic basis of EA is not fully understood, it appears to involve multiple genes like FLNA and NKX2-5, MYH6, MYH7 suggesting a complex polygenic inheritance pattern. TNNT2 is known to be associated with Cardiomyopathy but has not been previously associated with EA and WPW.Case:In this report, we present findings from a lebanese family with EA, comprising 2 affected individuals. Whole exome sequencing in the affected individuals identified a pathogenic variant in the TNNT2 gene at coding strain position 260 (a missense mutation: C to T), resulting in the substitution of Proline with Leucine at position 87 in affected individuals (Figure 1). No variants were detected in any other candidate gene examined. Individuals I:1 and II:2 were found to be normal, with no EA findings on echocardiography.Methods:Whole exome sequencing in the patients involved collecting blood samples after obtaining consent. These samples were sent to Centogene lab, where genomic DNA is enzymatically fragmented. The regions of interest are then enriched using DNA capture probes, facilitating detailed genetic analysis.Results:The whole exome sequencing identified a heterozygous missense mutation in both the father and his daughter. This nonsynonymous variant is located on chromosome 1 (GRCh37) in the TNNT2 gene region. The specific variant, NM_001276345.1:c.260C >T p.(Pro87Leu), was found in both individuals.Conclusion:In conclusion, the genetic basis of EA is rather complex and remains poorly understood. It is established that mutations in the TNNT2 gene are linked to several cardiomyopathies, none of them overlap with the described phenotype of our patients. In this report, we therefore confirm the potential role of TNNT2 gene mutation in the genetic basis of familial EA with WPW.

Circulation, Volume 150, Issue Suppl_1, Page A4138514-A4138514, November 12, 2024. Introduction:Brugada syndrome is an inherited cardiac disorder characterized by specific ECG patterns, notably the coved-type ST-segment elevation in the right precordial leads (V1-V3), leading to an increased risk of sudden cardiac death. This condition often stems from mutations in the SCN5A gene, which impair cardiac sodium channel function. The manifestation of Brugada Pattern, showing typical ECG findings without clinical criteria like sudden cardiac arrest or syncope, is significant. We highlight a case where atomoxetine, a selective norepinephrine reuptake inhibitor used for ADHD, unveiled a type 1 Brugada pattern.Case Presentation:A 26-year-old male with a history of ADHD on atomoxetine only presented to the emergency department with sudden substernal chest pain radiating to his left arm. His initial ECG showed right bundle branch block and type 1 Brugada pattern (Figure.1). Despite normal troponin levels and a negative coronary CT angiography, the patient’s ECG abnormalities raised concerns. With no personal or familial history of arrhythmia or SCD and no other medications, atomoxetine was suspected as the trigger. Upon discontinuation, the patient’s ECG type 1 Brugada pattern resolved (Figure. 2), and he remained asymptomatic with a normal Holter monitor at a 1-month follow-up.Discussion:Brugada syndrome is marked by dynamic ECG abnormalities, which can surface due to triggers like fever, certain medications, and electrolyte imbalances. Atomoxetine, an ADHD treatment and selective norepinephrine reuptake inhibitor, affects the human cardiac sodium channel (hNav1.5), encoded by the SCN5A gene. This interaction can disrupt heart action potentials, leading to conditions like long QT syndrome and Brugada pattern, by slowing cardiomyocyte depolarization and conduction. Its effect on hNav1.5 resembles that of antidepressants like Fluoxetine, increasing the risk of Brugada pattern. In our case, a patient’s type 1 Brugada pattern, with no underlying heart disease or family history, pointed to atomoxetine as the cause. Discontinuing the drug resolved the ECG abnormalities.Conclusion:This case emphasizes the importance of assessing cardiovascular risk before prescribing atomoxetine, especially in individuals at risk for cardiac sodium channel dysfunctions. Immediate intervention and monitoring are critical to prevent severe arrhythmias.

Circulation, Volume 150, Issue Suppl_1, Page A4146986-A4146986, November 12, 2024. Case Description and Procedural Technique:86 year old female with a prior history of coronary artery bypass grafting presented with non-ST elevation MI underwent subtotal occlusion of vein graft supplying the large obtuse marginal artery.The left coronary bypass catheter was used to cannulate the vein graft, supplying the obtuse marginal artery. Balanced middleweight universal wire (BMW) was used to cross the lesion. Given the critical nature of the lesion, it was pre-dilated using a 2 mm balloon. Bare wire and emboshield NAV6 (2.5-4.8mm) embolic protection was then used for distal protection. Due to hemodynamically intolerance, direct stenting was opted for, and a 3.5 x 16 mm synergy stent was deployed over the BMW wire with accidental entrapment of the bare wire and embossed filter protection system behind the stent frame.We have then placed an un-inflated 2.5 mm balloon inside the stent frame over the BMW wire. A 1 mm sapphire balloon was advanced over the bare wire, and its distal tip was placed behind the proximal edge of the stent. It was then inflated at 8 atmospheres. Serial inflations behind the stent frame were done with slow advancement of the balloon, covering the entire length of the stent. The balloon was then upsized to 2 mm, and serial inflations were performed behind the stent frame. After creating enough lumen, the filter was pulled back and re-captured. The 2.5 mm balloon was then inflated inside the stent frame. The balloon was upsized to 3.5 mm for the good apposition of the stent frame. TIMI III flow was obtained without any complications.Discussion:Distal embolic protection with intravascular filters is often used during percutaneous intervention of saphenous venous grafts. Accidental entrapment of emboshield filter systems can occur behind the stent in emergent situations when buddy wire technique is used in the vein graft. Our technique describes removal of the entrapped filter in a safe manner keeping the stent frame in place without surgical intervention. A few similar cases have been reported in the literature with surgical removal of wire.

Circulation, Volume 150, Issue Suppl_1, Page A4138487-A4138487, November 12, 2024. Introduction:A 79-year-old male patient with a history of surgical AVR presented with severe bioprosthetic aortic stenosis requiring valve-in-valve TAVR. The plan was to place an Evolut CoreValve after intentionally fracturing the basal ring of his surgical valve. Through an 18F sheath, a 25mm x 4.5cm True balloon was advanced to the surgical valve over a Lunderquist wire. However, the balloon ruptured immediately after fracturing the valve ring.Decision making:Efforts were made to remove the ruptured True balloon while maintaining the position of the wire, but attempts to withdraw it through the 18F sheath were unsuccessful due to resistance at the distal tip of the sheath. Subsequently, the proximal portion of the balloon catheter was partially detached and removed.An exchange was made to a 22F Gore DrySeal sheath, but again, efforts to withdraw the ruptured balloon were unsuccessful (Figure 1). Various snares were employed, but all attempts to manipulate the balloon into the sheath were ineffective. The ruptured balloon remained in the abdominal aorta and eventually detached from the hypotube.The 22F sheath was then exchanged for a 20F Inari Protrieve sheath. Two Supracore wires were then inserted through the sheath, with one designated for snare delivery and the other for maintaining vessel access. A Tulip snare was guided over one Supracore wire to the descending thoracic aorta, where the snare was opened and the Lunderquist wire was captured at the junction between the stiff and soft parts of the wire (Figure 2). The snared wire and ruptured balloon were retracted into the exposed Nitinol cone of the Inari sheath, successfully engulfing the balloon and compressing it (Figure 3). The sheath, wire, balloon, and snare were then removed as a unit while the wire access was maintained.A new 22F Gore DrySeal sheath was inserted. Inspection confirmed the complete removal of all components of the ruptured True balloon and the catheter. The procedure concluded with the successful deployment of a 29mm Evolut pro CoreValve. The patient made an uneventful recovery and was discharged home the following day.Conclusion:The Inari Protrieve sheath proved valuable in this case of complicated intravascular equipment entrapment. The soft, funnel-shaped nitinol cone aided in capturing and compressing the bulky ruptured balloon, obviating the need for a surgical cutdown.

Circulation, Volume 150, Issue Suppl_1, Page A4135212-A4135212, November 12, 2024. 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.

Circulation, Volume 150, Issue Suppl_1, Page A4140574-A4140574, November 12, 2024. Introduction:Atrial myxomas are cardiac tumors that can cause arterio-occlusive diseases due to embolization of myxomatous fragments. Treatment is through prompt surgical resection, with recurrence rates relatively rare. Herein, we present a case of recurrent left atrial myxoma with hemorrhagic, cerebral embolization.Case Report:A 34-year-old male presented with acute onset numbness and tingling of the left arm. He was vitally stable with unremarkable physical examination or bloodwork. CT Head showed multifocal brain metastases in the bilateral parietal and left frontal lobes. Brain MRI demonstrated multiple hemorrhagic masses throughout the cerebral hemispheres with vasogenic edema. The patient’s past medical history was pertinent for bilateral occlusion of the femoral and popliteal arteries, with workup revealing a left atrial myxoma that was surgically resected in 2005. The patient presented again in 2021 with right facial paresthesia and arm weakness. Brain MRI showed bilateral cortical and subcortical MCA ischemic strokes. TEE confirmed the recurrence of a left atrial myxoma, requiring a repeat sternotomy and resection.Since then, the patient was frequently hospitalized with seizures and strokes. Surveillance brain MRIs consistently demonstrated hemorrhagic masses of varying sizes and vasogenic edema, localized to the watershed territories of the cerebral arteries. The patient underwent left frontal craniotomy and resection of a left frontal lobe lesion in 2023, with pathology specimens representing organizing cerebral hemorrhage of unclear etiology. Repeat echocardiograms did not show recurrence of a myxoma. The overwhelming clinical opinion states that these are myxomatous metastasis from before the patient’s last cardiac surgery. Given the tumor burden and progressive nature of the disease, the patient was deemed inappropriate for neurosurgery or chemotherapy.Discussion:Recurrence after surgical resection of atrial myxomas is rare, with 0.5 cases reported per 1000-person years, and is mainly attributed to inadequate surgical resection. Limited research exists regarding malignant atrial myxomas. The prevailing hypothesis points to the neoplastic transformation of myxomatous emboli into malignant lesions. Our patient is a unique case of a recurrent atrial myxoma with symptomatic cerebral metastasis. This case highlights the importance of adequate resection of cardiac myxomas to prevent the malignant transformation of an otherwise benign tumor.

Circulation, Volume 150, Issue Suppl_1, Page A4144217-A4144217, November 12, 2024. Background:The ISCHEMIA trial questioned revascularization in chronic coronary syndrome (CCS) patients, but excluding subjects with left main (LM) coronary artery disease (CAD). A widely available diagnostic method excluding LMCAD would expand the implementation of an initial noninvasive strategy.Objective:Assessing the ability of excluding LMCAD through clinical and ECG stress testing (EST) variables in patients undergoing coronary angiography (CAG) for CCS.Methods:In a multicenter retrospective case-control study we evaluated CCS subjects undergoing CAG after a maximal EST.Caseswere patients with angiographic ≥50% LM stenosis or ≥70% stenoses of both proximal left anterior descending and proximal circumflex arteries; we matched them with similar patients without LMCAD (Controls)in a 1:3 ratio. Models were internally validated through logistic regressions.Results:219Caseswere matched with 554Controls. The c-statistic was 0.80 (optimism-adjusted: 0.73). Assuming LMCAD prevalence of 5% and a misclassification cost ratio of 1:100 (ratio of the cost of performing CAG in a subject without LMCAD to the cost of not performing CAG in a patient with LMCAD), the negative predictive value was 98.6%, correctly classifying 84.5% ofCases. CAG could be spared in 57.0% of subjects, missing one LMCAD diagnosis every 70 CAGs spared in patients without LMCAD (Figure).Conclusions:Among patients with CCS, LMCAD can be predicted withacceptablediagnostic accuracy anda very highnegative predictive value through a model based on clinical and EST parameters, allowing an initial noninvasive management of most patients able to perform an EST, reducing the costs of routine coronary imaging. Such results should enlarge the applicability of the ISCHEMIA results when coronary computed tomography angiography, used in ISCHEMIA, is not available, limiting the referral to invasive CAG.

Circulation, Volume 150, Issue Suppl_1, Page A4125893-A4125893, November 12, 2024. Introduction:Drug combinations offer increased therapeutic efficacy and reduced toxicity and plays a vital role in treating chronic complex diseases. Understanding a drug combination’s mechanism of action (MoA) can provide important insights into its therapeutic efficacy. The MoA of many FDA-approved drugs, however, often remains unclear.Methods:In this study, we investigated the combination of a statin [atorvastatin (ATO) or simvastatin (SIM) plus ezetimibe (EZE)] and utilized drug-treated RNA-seq transcriptome data from SOAT2-only-HepG2 cells (treated with ATO 5 umol/L, EZE, 25 umol/L, their combination or vehicle) and from liver biopsies of patients with uncomplicated cholesterol gallstone disease in the Stockholm Study (a single-blind, randomized trial with SIM 80 mg daily, EZE 10 mg daily, their combination, or placebo) to decipher the underlying molecular mechanisms of the drug combination. We proposed a Boolean logical modeling framework to simulate the MoA of a drug combination. Specifically, fourteen two-variable Boolean models were used to describe the combinatory relationships of ATO/SIM and EZE. Thereafter, a pattern matching approach was applied to associate drug-induced differentially expressed genes with the idealized differential expression templates derived from Boolean models.Results:We found 1,560 and 594 genes differentially expressed in at least one treatment condition in SOAT2-only-HepG2 cells and liver biopsies, respectively. Our analysis revealed both expected and novel combinatorial modes of ATO/SIM and EZE. For example, ATO independently activates downstream genes (i.e. B4(ATO,EZE)=ATO), and ATO and EZE synergistically inhibits downstream genes (i.e. B15(ATO,EZE)=NOT (ATO AND EZE)) , as the two most prevalent MoAs in SOAT2-only-HepG2 cells (Figure 1). Similarly, the combination of SIM and EZE synergistically inhibiting downstream genes was also the most prevalent MoA in the liver biopsies. We mapped the downstream genes of each combinatorial mode to the human interactome and obtained underlying subnetworks, which are important for understanding the therapeutic effects of the drug combination. Functional enrichment and disease-association analyses of the downstream suggest the additional therapeutic indications of the drugs.Conclusion:Drug-induced transcriptomes are informative in deciphering the MoA of drug combinations using Boolean logical modeling. This framework can be easily extended to the combinations of three drugs.

Circulation, Volume 150, Issue Suppl_1, Page A4139677-A4139677, November 12, 2024. Background:Epicardial patch defibrillators (EPDs) were commonly implanted in the 1990s for secondary prevention of sudden cardiac death. Despite being largely obsolete, some EPDs remain in patients and can cause late complications. This case highlights such a scenario.Case:A 75-year-old female with a history of cardiac arrest 30 years ago presented with shortness of breath and left leg swelling. She had idiopathic ventricular fibrillation in 1992, treated with an EPD (Picture 1A), later replaced by a transvenous ICD.She was diagnosed with left femoral deep venous thrombosis and bilateral pulmonary embolism and started on therapeutic anticoagulation. She experienced massive hemoptysis, leading to respiratory and cardiac arrest, but was resuscitated. A CT angiogram showed no active bleeding but noted the EPD was close to the lower lobe of the left lung. Upper gastrointestinal endoscopy showed no active bleeding. Bronchoscopy revealed clots in the left lower lobe. Despite empiric bronchial artery embolization, hemoptysis persisted. A repeat bronchoscopy showed reaccumulation of clots. A repeat CT angiogram indicated contrast extension into the ventricular myocardium near the EPD but no lung spillage suggestive of pseudoaneurysm (Picture 1B).She was transferred to our institution for further evaluation. A coronary angiogram revealed normal arteries, while a left ventriculogram revealed contrast extravasation through the lateral wall (Picture 1C). An urgent surgery revealed two EPDs: anterior and lateral. The lateral EPD had eroded into the ventricle, creating a ventriculo bronchial fistula (Picture 1D). The lateral EPD was removed (Picture 1E); the anterior EPD was left in place (Picture 1F). The ventricular defect was debrided and repaired. Postoperative recovery was successful, with no further hemoptysis, and the patient was discharged to a rehabilitation facility.Discussion:EPDs are no longer used due to high failure rates and complications like scar formation and constrictive pericarditis. However, patients with EPDs from the 1990s may present with delayed complications. Accurate diagnosis using multimodality imaging and early management is crucial to reduce morbidity and mortality.

Circulation, Volume 150, Issue Suppl_1, Page A4139810-A4139810, November 12, 2024. Background:Bilateral breast swelling is a rare and often overlooked presentation of congestive heart failure (CHF) exacerbation. It can mimic other conditions like cellulitis or malignancy, posing a diagnostic challenge. Recognizing this unusual manifestation is crucial for timely diagnosis and appropriate management.Case Presentation:A 77-year-old female presented with acute onset bilateral breast enlargement, tenderness, and erythema, along with symptoms of CHF exacerbation including dyspnea, orthopnea, and lower extremity edema. Physical examination revealed markedly enlarged, tender breasts. Imaging studies including mammography (Figure 1: Right and left craniocaudal views; Figure 2: Right and left mediolateral oblique views) and breast ultrasound showed diffuse skin and subcutaneous edema without evidence of infection or malignancy. Echocardiography confirmed reduced ejection fraction and diastolic dysfunction. Skin biopsy findings were consistent with CHF-related changes. The patient’s symptoms improved with diuresis and optimization of guideline-directed medical therapy for heart failure.Conclusion:This case highlights breast edema as a rare manifestation of CHF exacerbation that clinicians should be aware of. It can mimic inflammatory breast disorders or malignancy, leading to delayed diagnosis. A high index of suspicion in patients with cardiovascular disease and close collaboration between specialties are key for accurate diagnosis. Treatment involves managing the underlying CHF with diuretics, medical therapy, and supportive measures. Prompt recognition can help alleviate symptoms, prevent complications, and improve patient outcomes.