Left ventricular (LV) thrombus is a severe complication of acute myocardial infarction (AMI) and chronic heart failure. While current guidelines support the use of direct oral anticoagulants (DOAC) as alternatives to vitamin K antagonists (VKA), their benefit across different aetiologies remains uncertain. This study aimed to compare the efficacy and safety of DOAC versus VKA across different aetiologies of LV dysfunction. We conducted a multi-centre observational study including 901 patients with confirmed LV thrombus treated with either a VKA or DOAC. The primary outcome was thrombus resolution, secondary outcomes included stroke and systemic embolisation (SSE), major bleeding and mortality with analyses performed by aetiology. The principal aetiologies were AMI (38.3%), ischaemic cardiomyopathy (ICM) (38.0%) and non-ischaemic cardiomyopathy (NICM) (23.7%). Overall, thrombus resolution was significantly higher in DOAC treated patients, but this was driven by the AMI sub-group (p=0.018). DOAC use independently predicted thrombus resolution (OR 2.0, 95% Cl 1.29-3.24, p=0.010). Major bleeding events (BARC ≥3) were more common with VKA use (p=0.008). NICM had the highest SSE rate (15.3%, p=0.002), which were significantly raised in those treated with DOAC (p<0.001). The underlying aetiology of LV dysfunction significantly influences both treatment response and outcomes in patients with LV thrombus. DOAC were associated with superior efficacy and safety in AMI-related LV thrombus, but were linked to increased rates of SSE in NICM. These findings highlight the importance of aetiology on LV thrombus management and the potential need for tailored approaches.

Isolated Callosal Infarction Associated With Left Ventricular Thrombus in the Absence of Documented Atrial Fibrillation: A Case Report

Executive summary of the SISET position paper on the management of antithrombotic therapy in left ventricular thrombus

Background: Tubercular myocarditis is an exceedingly rare manifestation of Mycobacterium tuberculosis, with pediatric cases being exceptionally uncommon. Children typically present with pulmonary or lymph node tuberculosis (TB), while myocardial involvement is reported only in isolated cases. This report highlights a rifampicin-resistant pediatric TB case complicated by myocarditis and left ventricular thrombus. Case Presentation: A 11-year-old girl presented with chronic fever, cough, dyspnea, and generalized edema. Examination showed anasarca, tachycardia with gallop rhythm, systolic murmur, and bilateral crackles. Chest radiograph revealed infiltrates. Echocardiography showed left ventricular dysfunction (Ejection fraction - 30%) and an apical thrombus. Sputum was positive for acid-fast bacilli and CB-NAAT detected rifampicin-resistant TB. She received MDR-TB therapy, anticoagulation, and heart failure treatment. Serial echocardiograms showed thrombus regression and full recovery in four months. Conclusion: Pediatric tubercular myocarditis is extremely rare. Myocardial involvement should be suspected in TB children presenting with heart failure. CB-NAAT is essential for rapid diagnosis. Anticoagulation helps thrombus resolution and improves outcomes.

Methamphetamine (MA) abuse has emerged as a multisystem insult driving cardiovascular and neurovascular consequences. Methamphetamine-associated cardiomyopathy (MACM) remains an underrecognized cause of cardioembolic stroke through left ventricular thrombus (LVT) formation. MA-induced gut dysbiosis and enteric neural disruption exacerbate systemic inflammation and autonomic imbalance, resulting in broader dysregulation of the brain-heart-gut axis. This study aimed to synthesize contemporary evidence on chronic MA exposure and its role in LVT formation, stroke pathogenesis, diagnostic approaches, and anticoagulation management. We conducted a focused narrative review of PubMed- and Scopus-indexed literature (1990-2025) addressing cardiovascular, neurovascular, and gut-mediated consequences of chronic MA exposure. Observational cohorts and case reports were integrated to characterize pathophysiology, imaging approaches, and therapeutic considerations, supplemented by a representative clinical case. Chronic MA exposure mediates persistent catecholamine excess, myocardial fibrosis, ventricular dysfunction, and a prothrombotic milieu. Gut dysbiosis-related inflammation and autonomic dysregulation further promote intracardiac stasis. Affected individuals are typically young men with severe systolic dysfunction (left ventricular ejection fraction 20-30%), with a substantial proportion demonstrating apical or mural LVT on systematic imaging. Case-level evidence highlights a broader systemic embolic burden, involving the limbs, kidneys, and aorta. Echocardiography remains the first-line screening method, while cardiac CT and MRI offer greater sensitivity for thrombus detection. Anticoagulation is challenged by bleeding risk, inconsistent adherence, and the absence of standardized protocols. MACM represents a critical and underrecognized etiology of cardioembolic stroke in young adults. Early recognition of brain-heart-gut axis disruption, systematic cardiac imaging, and individualized anticoagulation are crucial for preventing emboli. Prospective registries and standardized imaging-guided treatment strategies are needed to improve outcomes in this high-risk population.

BackgroundInfective endocarditis (IE) is a serious infection of the heart lining and valves, associated with high morbidity and mortality.1 Diagnosis is guided by the Modified Duke’s Criteria, which integrate microbiological, imaging and clinical features, and were most recently updated in 2023.2 Culture-negative IE (CNIE) occurs in up to 20% of cases, often after prior antibiotic exposure or infection with fastidious organisms, making diagnosis particularly difficult.3 Antimicrobial stewardship (AMS), defined as optimizing antimicrobial use to improve outcomes while minimizing toxicity and resistance, is vital to addressing antimicrobial resistance (AMR).4ObjectivesThis abstract presents a complex CNIE case with complete heart block (CHB) and embolic stroke, illustrating the role of Duke’s Criteria, multidisciplinary decision-making and AMS.MethodsA retrospective case review was conducted on a patient admitted in June 2025 with suspected infective endocarditis at an NHS Foundation Trust. Data included clinical presentation, microbiology, imaging, echocardiography, management and multidisciplinary team (MDT) discussions. The case was assessed using the Modified Duke’s Criteria to establish diagnostic certainty and guide clinical decision-making.ResultsAn 85-year-old patient presented with progressive shortness of breath and tiredness. On admission, electrocardiography (ECG) demonstrated CHB with a ventricular rate of 38 bpm. Verapamil was withheld, and the patient was commenced on isoprenaline; a temporary pacing wire was not tolerated. During admission, he developed a right middle cerebral artery (MCA) infarct secondary to an M2 thrombus, resulting in expressive aphasia. No atrial fibrillation or left ventricular thrombus was identified, raising suspicion of septic embolism. Despite persistently negative blood cultures, echocardiography revealed a mobile structure within the aortic root near the non-coronary cusp with trivial regurgitation, and a mobile mass on the posterior mitral leaflet, though difficult to define due to calcification. According to the Modified Duke’s Criteria, the case met one major criterion (positive echocardiographic findings) and three minor criteria (predisposing heart disease, vascular event, clinical features), consistent with likely infective endocarditis. The patient was treated empirically with IV amoxicillin, flucloxacillin and gentamicin. From AMS perspective, broad-spectrum therapy was regularly reviewed by the multidisciplinary team, with toxicity monitoring and consideration of diagnostic refinement to enable targeted treatment.ConclusionsThis case demonstrates the diagnostic complexity of CNIE. Although blood cultures were persistently negative, Duke’s Criteria and multimodal imaging supported the diagnosis. From an AMS perspective, key recommendations include:Optimizing microbiological sampling and using molecular diagnostics before initiating broad-spectrum therapy.Applying guideline-directed empirical regimens with early stewardship review and de-escalation where possible.Close collaboration between microbiology, cardiology, neurology and infectious diseases to tailor therapy to optimize antibiotic use and decrease AMR.Careful monitoring of nephrotoxic combinations (e.g. aminoglycosides) and considering oral or less toxic alternatives in frail patients.

BackgroundLeft ventricular (LV) thrombus is a complication of myocardial infarction and dilated cardiomyopathy and is associated with a high thromboembolic risk. Although warfarin has traditionally been used, direct oral anticoagulants (DOACs) offer a more convenient alternative. With the addition of the RIVAWAR trial, we conducted an updated systematic review and meta-analysis to assess the efficacy and safety of DOACs compared with warfarin in patients with LV thrombus.MethodsA systematic search of electronic databases (PubMed, EMBASE, Cochrane and clinicaltrials.gov) from inception to April 2025 identified randomised clinical trials (RCTs) comparing DOACs with warfarin for the treatment of LV thrombus. The main outcome of interest was thrombus resolution at 3 months. Risk ratios (RRs) with 95% CIs were calculated using random-effects models.ResultsSeven RCTs comprising 554 patients were included. Non-contrast transthoracic echocardiography was used for LV thrombus assessment in all RCTs. There was no difference between DOACs and warfarin in thrombus resolution at 3 months (RR 1.02; 95% CI 0.95 to 1.09), major adverse cardiovascular events (RR 0.50; 95% CI 0.16 to 1.54), all-cause mortality (RR 0.92; 95% CI 0.36 to 2.31), stroke/systemic embolism (RR 0.76; 95% CI 0.12 to 4.68), rehospitalisation (RR 1.36; 95% CI 0.47 to 3.94) or major bleeding (RR 0.54; 95% CI 0.20 to 1.48). Subgroup and sensitivity analyses confirmed the robustness of these results.ConclusionsDOACs demonstrated similar efficacy and safety to warfarin for LV thrombus management in this meta-analysis, supporting their use for the treatment of LV thrombus. However, large-scale RCTs with longer follow-up periods and using diagnostic modalities with higher sensitivity and specificity for detecting LV thrombus resolution are warranted to confirm these findings and clarify long-term outcomes.PROSPERO registration numberCRD420251023513.

Assessment of left ventricular thrombi using cardiac CT: A comparative evaluation of non-contrast, CT-angiography, delayed-enhanced images, and extracellular volume maps.

Description of Case: Left ventricular (LV) thrombus is generally a contraindication to transcatheter aortic valve replacement (TAVR) due to thromboembolic risk. However, non-surgical patients with valvular cardiogenic shock (CS) require urgent valve correction for meaningful recovery. Prior valve prostheses and/or the presence of LV thrombus complicates management, often barring intervention. We present the novel use of tissue plasminogen activator (tPA) as bridge to valve-in-valve (ViV) TAVR in a 58-year-old woman with critical bioprosthetic stenosis and valvular CS complicated by large LV thrombus. A 58 year old female with a history of surgical bioprosthetic aortic valve replacement presented emergently with rapidly progressive dyspnea. Echocardiogram revealed critical low-flow, high gradient aortic stenosis (peak velocity 4.5m/s, mean gradient 51 mmHg) secondary to bioprosthesis degeneration, a newly reduced ejection fraction (15-20%), and a 2.8x2.6cm mobile LV thrombus. She subsequently developed valvular CS requiring dual ionotropic support. Surgical risk was prohibitive as she was not an advanced heart failure therapy candidate based on multi-disciplinary discussion. Medical debulking of the thrombus was planned following a novel protocol from an ongoing clinical trial. Pulsed 6-hour infusions of 25 mg tPA were administered with serial echocardiography demonstrating step-wise reduction in thrombus dimensions. Valve selection was assisted by DASI ® computational modeling. Dual SENTINEL ® devices were placed and the patient underwent ViV-TAVR (23mm Evolut FX+ ®) with ICE guidance of the LV wire to minimize instrumentation of the thrombus. Hemodynamic and echocardiographic results were excellent. The patient was rapidly liberated from ionotropes and has no neurological sequelae to date. Discussion: To date there are no guidelines or large studies to inform the use of systemic fibrinolysis as a bridge to structural cardiology intervention in patients with LV thrombi. There are case reports of ICE guidance during ViV-TAVR with LV thrombus and use of systemic fibrinolysis for treatment of aortic valve thrombosis, however outcomes are mixed. To our knowledge, there is no report of tPA bridge to successful ViV-TAVR in acute valvular CS complicated by LV thrombus. More data are needed.

Background: The incidence, management, and outcomes of left ventricular (LV) thrombus in nonischemic cardiomyopathy (NICM) remain poorly defined. Research question: Do outcomes differ between DOACs and warfarin in treating LV thrombus in patients with HFrEF or HFpEF secondary to NICM? Methods: This retrospective cohort study utilized data from the TriNetX database. Patients diagnosed with HFrEF or HFpEF not secondary to ischemic disease with subsequent left ventricular thrombus, between December 1, 2004 and December 1, 2024, were included. Propensity score matching (PSM) was performed on all data to account for differences in potential confounding variables (Table 1). Subgroup analyses compared outcomes for patients anticoagulated with a DOAC versus warfarin after diagnosis of LV thrombus. Primary outcomes of stroke, major bleeding, systemic embolism, and all-cause mortality were assessed at 3 months, 6 months, 1 year, and 2 years after initiation of anticoagulation using risk and Kaplan–Meier survival analysis. Results: The study included 1,916 HFrEF patients and 562 HFpEF patients. Among HFrEF patients, DOAC treatment compared to warfarin was associated with a lower incidence of systemic embolism at all time points: 3 months (relative risk [RR] 0.04; 95% confidence interval [CI] (0.36-0.98, p = 0.04)), 6 months (RR 0.62 (CI 0.41-0.95, p = 0.03)), 1 year (RR 0.65 (CI 0.44-0.95, p = 0.02)), and 2 years (RR 0.67 (CI 0.48-0.95, p = 0.02)) and lower risk of bleeding at 3 months (RR 0.49 (CI 0.30-0.79, p &lt; 0.01)), 6 months (RR 0.52 (CI, 0.34-0.79, p &lt; 0.01)), 1 year (RR 0.55 (CI 0.38-0.79, p &lt; 0.01)), and 2 years (RR 0.53 (CI 0.38-0.74, p &lt; 0.01)). There were no significant differences in the risk of stroke or all-cause mortality at any time point. Among HFpEF patients, DOAC treatment compared to warfarin was associated with a lower incidence of systemic embolism at 6 months (RR 0.40 (CI 0.20-0.79, p &lt; 0.01)), 1 year (RR 0.37 (CI 0.20-0.69, p &lt; 0.01)), and 2 years (RR 0.41 (CI, 0.23-0.72, p &lt; 0.01)). There were no significant differences in the risk of stroke, bleeding, or all-cause mortality at any time point (Table 2). Conclusions: In NICM patients with HFrEF or HFpEF and LV thrombus, DOACs were associated with reduced risk of systemic embolism and bleeding, compared to warfarin. These findings support the consideration of DOACs as a preferred anticoagulation strategy in this population.

Introduction: Legionnaires’ disease, caused by Legionella pneumophila, primarily manifests as severe pneumonia but can lead to rare cardiac complications. Left ventricular (LV) thrombus formation is uncommon and typically occurs in the presence of severe LV dysfunction, systemic inflammation, and hypercoagulability. We present a case of LV mural thrombus in a 62 year old patient with Legionnaires’ disease, emphasizing the importance of recognizing cardiovascular involvement in severe infections. Description of the Case: A 62-year-old male was admitted with altered mental status, fever, hypotension, and respiratory distress. Initial workup revealed sepsis with severe hyponatremia (Na 114 mEq/L), acute kidney injury (Cr 1.54 mg/dL), elevated lactate (4.0 mmol/L), and rising troponin levels (195→483 ng/L). He developed transient atrial flutter that resolved spontaneously. Chest imaging showed right lower lobe infiltrates, and urine antigen testing confirmed Legionella pneumophila. Echocardiography revealed severe global hypokinesis with an ejection fraction (EF) of 20–25% and an apical LV mural thrombus (2.8 × 1.2 cm). The cardiomyopathy was attributed to a combination of sepsis-related myocardial dysfunction and possible tachycardia-induced cardiomyopathy. He was managed with intravenous fluids, vasopressors, azithromycin, and anticoagulation (enoxaparin transitioning to apixaban). Despite initial stabilization, the patient developed respiratory failure requiring intubation and intensive care support. With appropriate antimicrobial therapy and guideline-directed heart failure treatment (carvedilol, losartan), his cardiac function improved, and he was discharged to a rehabilitation facility on apixaban with close follow-up. Discussion: Legionella pneumophila can lead to rare but serious cardiac complications, including myocarditis, endocarditis, and LV thrombus, due to bacterial invasion, inflammation, and sepsis-related dysfunction. In this case, reduced ejection fraction and severe hypokinesis resulted in a 2.8 × 1.2 cm LV thrombus, worsened by atrial flutter and tachycardia-induced cardiomyopathy. Effective management required coordinated anticoagulation and infection control. Legionnaires’ disease, often linked to contaminated water systems, is notifiable due to its outbreak risk. Early cardiac evaluation and prompt treatment are critical for improving outcomes in cases with cardiac involvement.

Introduction: Testosterone replacement therapy (TRT) is linked to venous thromboembolism (VTE) and cardiovascular risks, but intracardiac thrombus formation has not been reported. This case highlights rapid left ventricular (LV) thrombus development and thromboembolic events in a patient on TRT, with no traditional hypercoagulable risk factors. Case Presentation: A 48-year-old male with tobacco use and daily alcohol intake presented with progressive dyspnea. Transthoracic echocardiography (TTE) revealed reduced ejection fraction (24%) and left ventricular dilatation (LVIDD 6 cm). There was no thrombus visualized in the left ventricle. Coronary angiography showed no obstructive disease. Guideline-directed medical therapy (GDMT) was initiated. He returned within 24 hours of discharge with dizziness and aphasia. Computed tomography angiography (CTA) identified a partially occluding embolus in the left middle cerebral artery (MCA), confirmed by MRI as an acute left frontoparietal infarct. Repeat TTE (5 days from prior TTE) demonstrated a large, mobile apical septal LV thrombus. CT imaging also revealed pulmonary embolism and splenic infarction. Hypercoagulable workup (prothrombin mutation, Factor V Leiden, cardiolipin antibodies) was negative. The patient disclosed scheduled testosterone injections for hypogonadism, with a total testosterone level of 1,081 ng/dL (reference: 300–1,000 ng/dL). Discussion: This case illustrates rapid LV thrombus formation and thromboembolism temporally linked to TRT. Despite guideline-based heart failure management, thrombus developed within 5 days of prior TTE. Prior studies associate TRT with VTE and stroke, but this is the first report of acute LV thrombus and multi-organ emboli in the absence of traditional hypercoagulable states. Proposed mechanisms include TRT-induced erythrocytosis, platelet activation, and endothelial dysfunction [1–4]. Conclusion: TRT may precipitate intracardiac thrombosis and thromboembolic events even without classical risk factors. Clinicians should consider TRT cessation and anticoagulation in similar cases, emphasizing cautious patient selection and monitoring. Further research is needed to clarify TRT’s role in hypercoagulability and cardiac remodeling.

Background: Left ventricular thrombus (LVT) is a significant complication following acute myocardial infarction (AMI), posing substantial risks of stroke and systemic embolism. Warfarin remains the traditional standard for anticoagulation, but direct oral anticoagulants (DOACs) have emerged as practical alternatives despite limited comparative evidence. Methods: We systematically searched PubMed, Embase, and Cochrane databases for RCTs comparing DOACs and warfarin in patients with LVT. Outcomes of interest included thrombus resolution rates at 1- and 3-month follow-up and safety outcomes, including major bleeding, stroke/systemic embolism, and all-cause mortality. Results: This meta-analysis included 7 RCTs comprising 554 patients, of whom 319 (58%) received DOACs. No significant differences were found between DOACs and warfarin regarding LVT resolution at 1 month (OR: 1.69; 95% CI: 0.62–4.60; p=0.31) or 3 months (OR: 1.39; 95% CI: 0.83–2.34; p=0.22). At 1 month, LVT resolution was achieved in 31.1% of those receiving DOACs and 26.9% of those receiving warfarin. At 3 months, the resolution rates were 88.2% and 81.1%, respectively. Secondary outcomes, including major bleeding (OR: 0.51; 95% CI: 0.18–1.48), stroke/systemic embolism (OR: 0.69; 95% CI: 0.10–4.64), and all-cause mortality (OR: 0.88; 95% CI: 0.34–2.29), were not statistically different between groups. Conclusion: In patients with LVT, DOACs demonstrated comparable efficacy and safety to warfarin, offering practical advantages such as simplified management. Our findings support DOACs as a reasonable alternative to warfarin for treating LVT. However, further large-scale trials using advanced imaging and standardized anticoagulation protocols are warranted.

Background: Left ventricular thrombus (LVT) is a known and serious complication of myocardial infarction (MI) and cardiomyopathy, associated with systemic embolism including stroke. The standard management includes anticoagulation (AC) to prevent thromboembolic complications. However, when a patient simultaneously presents with an acute ischemic stroke, initiating AC poses a significant clinical dilemma due to the potential for hemorrhagic conversion (HC). Case: A 56-year-old male with type 2 diabetes, presented with altered mental status, speech difficulty, and slurred speech. Vital signs were stable on admission. Labs showed hyperglycemia and elevated high-sensitivity troponin (peak: 3359 ng/L). EKG revealed sinus tachycardia at 109 bpm, T wave inversions in Leads 3, avF and inferior Q waves. Imaging consistent with an acute infarction in the posterior left MCA territory without hemorrhage. Transthoracic echocardiography demonstrated severely reduced ejection fraction (25–30%) with regional wall motion abnormalities and a well-defined apical thrombus. Cardiology diagnosed non-ST elevation MI with decompensated heart failure and LVT. Heparin infusion was started and was closely monitored due to very high risk of HC. Neurological status remained stable on heparin and then transitioned to apixaban prior to discharge. The patient remained neurologically stable and discharged with plans for outpatient coronary angiography and follow-up with neurology and cardiology. Methods: Case report highlighting complexities of balancing ischemic prevention and bleeding risk in concurrent LVT and middle cerebral artery infarct. Results: This case required balancing the high embolic risk of untreated LVT against the risk of HC of a large-vessel stroke. The team employed a multidisciplinary approach involving cardiology, neurology, and critical care to guide timing and selection of AC. Heparin used initially for its short half-life and reversibility, then transitioned to apixaban for long-term management. Conclusion: In patients with concurrent LVT and acute ischemic stroke, AC timing must be cautiously individualized. This case supports a multidisciplinary, stepwise approach—delaying initiation during the highest risk period, using short-acting agents first, and considering direct oral AC's when clinically appropriate. As evidence for DOAC use in LVT continues to evolve, this case adds to the growing support for their safety and efficacy in select high-risk patients.

Background: Whether oral anticoagulation (OAC) can be discontinued after the resolution of left ventricular thrombus (LVT) remains controversial, particularly in patients without risk factors such as left ventricular aneurysms. This study aimed to identify patients who may safely discontinue OAC. Methods: We conducted a retrospective cohort study of patients with LVT resolution who completed their anticoagulation course and excluded patients with left ventricular (LV) aneurysm. Clinical and echocardiographic factors were compared between patients who experienced LVT recurrence (n = 22) and those without recurrence during follow-up (n = 94). Results: The cohort had a mean age of 64.5 ± 15.0 years, and half (50%) were male. Most had an ischemic cardiomyopathy (64.6%). LVT recurred in 19% (22/116) of patients following initial resolution. Patients with recurrence were older (mean age 71.3 ± 11.9 vs. 63.4 ± 15.7 years, p = 0.03) and were more likely to have prior ischemic stroke and arterial thromboembolism (18.2% vs. 4.3%, p = 0.02 for both). At the time of thrombus resolution, LVEF was significantly lower among patients who had recurrence (33.4 ± 13.6% vs. 42.5 ± 15.5%, p = 0.012). Stroke, systemic embolism, and mortality rates were similar regardless of recurrence status. Recurrence risk by presence or absence of stroke and LEVF &gt;50% on the LVT resolution echocardiogram is shown in Figure 1. Notably, no recurrences were observed among patients with both LVEF &gt; 50% and no history of stroke (0/32), which was statistically significant compared to each other category. Conclusion: Among patients without left ventricular aneurysm who discontinued oral anticoagulation after LVT resolution, those with preserved LVEF (&gt;50%) and no prior history of stroke had a very low risk of recurrence, with no events observed in this subgroup. These findings suggest that some patients may safely discontinue anticoagulation after LVT resolution.

Background: Left ventricular thrombus (LVT) is often associated with anterior myocardial infarction (MI) and reduced ejection fraction (EF). However, it could be present in patients with no prior history of MI or heart failure. The JAK2 V617F mutation presents with myeloproliferative neoplasms and contributes to arterial and venous thrombosis. We are presenting a case of LVT with totally occluded left anterior descending (LAD) coronary artery in a patient with JAK2 V617F mutation. Case Presentation: A 60-year-old male with no prior medical history presented with lightheadedness and stable exertional chest pain. Vital signs and physical examination were unremarkable. Electrocardiogram showed normal sinus rhythm with an old inferior and anteroseptal infarction. Echocardiography revealed normal EF with no clear wall motion abnormalities. A myocardial perfusion stress test showed moderate fixed reduced radiotracer uptake with mild reversibility at the LAD territory (Figure 1). Coronary computed tomography angiography revealed a calcified and non-calcified plaque in the proximal to mid LAD with apical LVT (Figure 2[A-B]). Left heart catheterization showed a total mid LAD occlusion with collateral circulation from the acute marginal branch of the right coronary artery to distal LAD (Figure 3[A-B]). Further work-up revealed a JAK2 V617F mutation. The patient was treated with apixaban, atorvastatin, and metoprolol. Conclusion: We are presenting a rare case of LVT with occluded LAD coronary artery in a patient with JAK2 V617F mutation. The presence of the JAK2 V617F mutation indicates an underlying prothrombotic condition, which may have increased the risk of hypercoagulation. Screening for JAK2 V617F mutation in patients with incidental LVT and totally occluded coronary arteries may deserve further investigation.

Introduction: Left ventricular thrombus (LVT) remains a significant complication after anterior MI and among patients with reduced systolic function. VKAs have traditionally been the treatment of choice for LVT although have the disadvantages of having a less predictable pharmacokinetic profile, need for INR monitoring, and slower onset of action as compared to DOACs. Clinically, DOAC have been used for LVT but they remain an off-label use as per the FDA. The purpose of this pooled analysis is to quantify the safety and efficacy of DOACs versus VKAs for LVT resolution. Methods: A systematic review according to PRISMA guidelines was conducted of MEDLINE to search for randomized controlled trials comparing a DOAC to VKA for any LVT. Search terms included “Rivaroxaban, Apixaban, Edoxaban, Dabigatran” and “LV thrombus OR left ventricular thrombus”. Studies were only included if they were prospective and randomized with a control group using VKA. Clinical characteristics and dichotomous outcomes of LVT resolution at 3 months were aggregated using a random effects model to calculate odds ratios with 95% confidence intervals using the Mantel-Haenszel method. Revman 5.4 was used to aggregate statistics and generate the forest plot. Results: A total of 546 patients from seven randomized controlled trials were included. The average age ranged from 50-60 years. Females were presented about 5-20% in the trials. Most patients represented were within 2 weeks from an anterior STEMI with an average EF of 30%. Four trials utilized rivaroxaban while 3 trials used Apixaban. LVT resolved in 257 of the 317 patients in the DOAC arm versus 183 in the VKA arm representing an odds ratio of 1.15 [0.71, 1.87] P=0.57. Study heterogeneity was not significant (p=0.41). Conclusions: In this pooled analysis of seven randomized studies, DOAC’s were non-inferior to VKAs for LVT resolution at 3 months. Further long-term data from an adequately powered RCT are needed to quantify safety outcomes including the risk of systemic embolism and stroke.

Background: Left main (LM) coronary artery thrombus is a rare but life-threatening condition, typically associated with acute coronary syndromes requiring urgent intervention. Certain conditions such as myopericarditis contribute to a prothrombotic state through systemic inflammation. In rare cases, this may predispose to coronary thrombosis, particularly in patients with additional risk factors. We describe a case in which myopericarditis likely contributed to the formation of a non-obstructive left main coronary artery thrombus in the setting of overlapping systemic inflammation and underlying prothrombotic risk, managed conservatively without percutaneous intervention. Case Presentation: A 36-year-old male with a history of well-controlled HIV on ART, presented with fever, hypotension, and a morbilliform rash shortly after initiation of trimethoprim-sulfamethoxazole for a skin and soft tissue infection. He was found to have elevated troponins (peak 661 ng/L) and diffuse ST elevations on EKG, consistent with myopericarditis. He was vitally stable and did not complain of chest pain or shortness of breath throughout his hospital course. Initial investigation with coronary CTA revealed a possible LM thrombus, which was confirmed on left heart catheterization (LHC) as a non-obstructive thrombus (30% stenosis) in the mid-LM. The patient was managed with a tirofiban bolus and infusion, a heparin drip, and dual antiplatelet therapy with aspirin and clopidogrel. Repeat LHC five days later demonstrated complete resolution of the thrombus. TEE was performed to exclude possible sources of embolization including valvular vegetation or left ventricular thrombus. This was notable for a small mobile echodensity on the tricuspid valve which appeared to be consistent with redundant tissue, but no left-sided source of embolism, and he did not have evidence of a patent foramen ovale. The patient was discharged on apixaban and clopidogrel for 6 and 12 months respectively, with plans for outpatient cardiology follow-up and cardiac MRI. Conclusion: In patients with non-obstructive coronary thrombus trigerred by a prothrombotic state, conservative management with anticoagulation and antiplatelet therapy may be appropriate in those who are hemodynamically stable. Clinicians should maintain a high index of suspicion for thrombotic complications in patients with systemic inflammation, especially those with HIV or other prothrombotic risk factors.

Background: MELAS is a rare mitochondrial disorder characterized by multisystem involvement, including stroke-like episodes, seizures, and cardiomyopathy. Cardiac involvement in MELAS may include left ventricular dysfunction, arrhythmias, and structural abnormalities, yet the occurrence of cardioembolic stroke as a direct consequence of these manifestations is exceedingly rare. To date, no literature has clearly described this association. Case Presentation: A male in his twenties with known MELAS syndrome, epilepsy, and heart failure with reduced ejection fraction (EF 25%) presented with acute right hemiparesis and aphasia. Investigations: CT angiography and CT perfusion revealed reduced opacification in the left MCA bifurcation and a left M2 thrombus (Figure 1A). The contrast echocardiogram showed a normal-sized left ventricle with severely reduced ejection fraction (25%, down from 30% six months prior), diffuse hypokinesis, grade III diastolic dysfunction, and a left ventricular thrombus, with no patent foramen ovale. Treatment: Given the high suspicion for cardioembolic stroke, the patient received intravenous tenecteplase within the 3-hour window. Mechanical thrombectomy was planned but aborted due to spontaneous recanalization. Post-thrombolytic angiography confirmed reperfusion of the left MCA with residual distal M3 thrombus (Figure 1B).MRI confirmed infarcts in the left MCA distribution and right precentral gyrus, with no evidence of hemorrhagic transformation. Anticoagulation was initiated for secondary prevention. Statins were withheld due to concerns about mitochondrial toxicity. Follow-up: On a 3-month follow-up, the patient remained neurologically stable and continued oral anticoagulation without recurrent events. Discussion: The clinical scenario posed a diagnostic challenge—stroke-like episodes in MELAS are metabolic and typically non-territorial. However, an LV thrombus, territorial infarction, and perfusion mismatch pointed to an ischemic etiology. Timely thrombolysis led to significant neurological recovery. This case highlights the importance of distinguishing cardioembolic stroke from mitochondrial stroke-like events, especially in patients with known cardiac involvement. Conclusion: In MELAS patients with cardiac dysfunction, cardioembolic stroke must be considered when clinical and imaging findings suggest a vascular event. Early recognition and intervention, including thrombolysis, can lead to favorable outcomes.

Background: Chagas cardiomyopathy is a common cause of nonischemic cardiomyopathy in Latin America and often presents with ventricular arrhythmias. With increasing global migration, the prevalence of Chagas cardiomyopathy in non-endemic regions is rising, including the United States. As such, evaluating the etiology of ventricular arrhythmias requires a broad differential. We present the diagnostic work up of a patient presenting with monomorphic ventricular tachycardia (VT), ultimately found to have Chagas cardiomyopathy. Case: A 54-year-old Spanish-speaking male with no past medical history presented after being found unconscious and diaphoretic. Electrocardiogram demonstrated sustained monomorphic VT. After stabilization, transthoracic echocardiography revealed a left ventricular (LV) ejection fraction 30-35% with global hypokinesis and severely dilated LV cavity. Coronary angiography revealed patent coronaries. Further workup with cardiac magnetic resonance imaging demonstrated transmural late gadolinium enhancement in the basal to mid-lateral wall corresponding with hypokinetic myocardium, with a LV thrombus adjacent to the mitral valve and developing apicolateral aneurysm. An 18-fludeoxyglucose positron emission tomography scan was done which showed increased glucose uptake in the dysfunctional mid-lateral to apicolateral and anterolateral myocardium, without extracardiac evidence of sarcoid. Serologic testing was notable for an initially positive Lyme IgM, but confirmatory testing was negative. Further, serologies for Trypanosoma cruzi returned positive. Discussion: Although imaging was initially concerning for cardiac sarcoidosis, it did not meet clinical diagnostic criteria given absence of extracardiac involvement and presence of positive Trypanosoma cruzi titers. Empiric treatment was initiated for suspected Lyme carditis as he endorsed a history of rash resembling erythema migrans prior to presentation but was discontinued once confirmatory testing was negative. He was ultimately diagnosed with Chagas cardiomyopathy, but given his high-risk Rassi score, antiparasitic therapy was deferred and confirmatory testing was not pursued. He was started on guideline-directed medical therapy for cardiomyopathy and anticoagulation for LV thrombus. Amiodarone was initiated for VT, and an automatic implantable cardioverter defibrillator was placed for secondary prevention.