Left Ventricular Thrombus in Oncology Patients and Beyond: Imaging, Treatment Choices, and Duration.

Introduction
Left ventricular thrombus (LVT) is well known as a significant complication of various cardiac disease include myocardial infarction, left ventricular dysfunction, and various forms of cardiomyopathy. The development of LVT is associated with significant increases in the risk of systemic embolization, ischemic stroke, and mortality.1–3 LVT has been demonstrated to be closely linked to anterior ST-segment elevation myocardial infarction (STEMI), but its occurrence has expanded and is now observed in a broader spectrum of conditions, including non-ischemic cardiomyopathies. Additionally, LVT incidence is interestingly rising more and more among oncology patients, especially those who have cardiac injuries or dysfunction from using cancer therapies.4–6
Cancer-associated hypercoagulability, chemotherapy induced cardiotoxic effects, and persistent systemic inflammation, all these factors collectively establish an environment vulnerable to intracardiac thrombus formation.7–9 Cancer patients have a higher risk of thromboembolic events compared to the general population.
10
The development of LVT in such setting complicates the case and adds a clinical challenge, and usually associated with development of some serious complications include embolic stroke and peripheral arterial occlusion. The mechanisms that underlie thrombosis in cancer patients are multifactorial, such mechanisms include tumor-driven expression of procoagulant proteins such as tissue factor and cancer procoagulant, increased levels of circulating microparticles, platelet activation, and the release of inflammatory cytokines like interleukin-6 and tumor necrosis factor-α. All these factors collectively increase thrombin generation in oncology patients.11,12
Anthracyclines, trastuzumab, and newer agents like tyrosine kinase inhibitors are cardiotoxic cancer therapies, and can significantly impair left ventricular systolic function and lead to structural remodeling.13,14 Among these, Bruton tyrosine kinase inhibitors (BTKi), particularly first-generation agents such as ibrutinib, have been increasingly associated with cardiovascular toxicity, including atrial fibrillation, ventricular arrhythmias, and left ventricular dysfunction. Recent clinical data demonstrated how patients who used ibrutinib had higher incidence of atrial fibrillation and higher risk of arrythmia according to the Age-Creatinine-Ejection Fraction (ACEF) score.
15
Mediastinal radiation induces microvascular damage, fibrosis, and endothelial dysfunction which are factors that contribute to both thrombosis and reduced cardiac contractility.
16

Figure 1 presents the Cancer-specific pathways leading to LVT.
Despite the significant clinical relevance of LVT, currently known guidelines actually derived from research conducted on post-myocardial infarction patients or those without cancer.
17
There's a significant gap in data regarding incidence, which imaging techniques work best, and treatment outcomes specifically for oncology patients. Addressing this gap has become increasingly more important. This review aims to explore LVT pathophysiology in both cancer and non-cancer populations, with a particular focus on underlying mechanisms, imaging strategies, treatment decisions, and duration of anticoagulation therapy.

Pathophysiology of Left Ventricular Thrombus Formation

Virchow's Triad and General Mechanisms
The pathophysiology of LVT formation is explained by Virchow's triad (Figure 2), the main components of this triad are stasis of blood flow, endothelial injury, and hypercoagulability.
18
All these factors collectively provide a vulnerable environment for thrombus development in conditions such as LV dysfunction or injury.
Blood stasis usually develops in areas where the heart wall isn’t moving properly, examples include regions of akinesis or dyskinesis after myocardial infarction. Also, in cases of dilated cardiomyopathy, and left ventricular aneurysms. Patients who experience large anterior infarctions or have a left ventricular ejection fraction less than 30% are at increased risk for thrombus formation.19,20 According to recent studies, emerging imaging techniques demonstrate that even minor abnormalities in the motion of left ventricular wall can create localized regions of low shear stress that promote thrombus development.
21

Endothelial injury results from different causes, most commonly due to ischemic necrosis, reperfusion injury, or direct mechanical stress. This type of injury will result in exposure of subendothelial collagen and tissue factor, which promote platelet adhesion and fibrin formation.
22
In addition, activation of the endothelium leads to increased expression of adhesion molecules like P-selectin and ICAM-1, which facilitate leukocyte recruitment and local inflammation, and both further contribute to thrombus growth.
23

Hypercoagulability represents the tendency of the body toward increased clot formation. Prothrombotic factors include fibrinogen and plasminogen activator inhibitor-1 increase in response to Inflammatory mediators and neurohormonal responses. Comorbidities such as diabetes, chronic kidney disease, and ongoing systemic inflammation are associated with an increased risk.23,24 Although in the absence of acute injury, a prothrombotic environment can develop from persistent left ventricular remodeling following myocardial infarction or chemotherapy-induced cardiomyopathy.25,26
Recent modalities in cardiac magnetic resonance imaging (CMR) have identified additional independent predictors of LVT. Predictors including overall infarct size, degree of transmural involvement, and apical extension.
27
The use of late gadolinium enhancement (LGE) provide a chance to differentiate between thrombus and fibrosis, offering valuable insight into the dynamics of post-injury ventricular remodeling.
28

Cancer-Specific Mechanisms
Cancer has distinct prothrombotic mechanisms that amplify the effect of the traditional pathways of LVT formation. Tumor cells are known to have the ability to release procoagulants such as tissue factor and cancer procoagulant, these factors directly activate the extrinsic coagulation cascade.
29
Active tissue factor and phosphatidylserine carried on a microparticles originating from both tumor and host cells can accelerate thrombin generation and fibrin deposition.
30
Increased secretion of cytokines such as IL-6, IL-1β, and TNF-α levels is associated with disruption of endothelial function and in turn, increase platelet activation and promote a persistent prothrombotic environment.
31

Figure 3 illustrates the cancer-associated hypercoagulability at the tumor–vessel interface.
Side effects like Oxidative stress, mitochondrial dysfunction, and cardiomyocyte apoptosis are linked to the chemotherapeutic agents such as anthracyclines and taxanes. Radiation therapy is also associated with effects such as myocardial fibrosis, capillary loss, and microvascular thrombosis.32–34 Trastuzumab and immune checkpoint inhibitors are agents that contribute to left ventricular dysfunction through immune-mediated myocarditis or myocardial stunning.35,36
Systemic factors can exacerbate thrombotic risk, factors like dehydration, anemia, reduced mobility can exacerbate thrombotic risk.
37
Recent literature has mentioned LVT as a rare but significant complication in cancer patients, especially those receiving cardiotoxic therapies.37–39 Factors like left ventricular dysfunction, endothelial injury, and hypercoagulability produce a high-risk phenotype that can challenge conventional anticoagulationtherapies.

Epidemiology and Clinical Context

Incidence and Distribution
LVT is a known complication in patients demonstrating significant left ventricular (LV) dysfunction. In the general cardiology population, especially after extensive anterior myocardial infarctions, the reported prevalence of LVT ranges from approximately 4% to 15%. This variation arises from disparities in patient populations and current treatment methods. For instance, prompt reperfusion in acute myocardial infarction has reduced the occurrence of LVT to the lower limit of that spectrum.
40
Data concerning LVT in cancer patients is inadequate due to the absence of significant studies focused on this demographic.
41
Nevertheless, certain oncological circumstances are increasingly dangerous. Patients with cancer therapy-induced cardiomyopathy, such as left ventricular dysfunction resulting from anthracyclines or trastuzumab, appear to have a greater risk for thromboembolic events. In a cohort of 121 patients with chemotherapy-induced severe left ventricular dysfunction (mean ejection fraction ∼26%), approximately 7.4% were found to have a LVT.41,42 LV dysfunction resulting from cancer treatment represents an uncommon and significant risk factor for LVT, necessitating careful cardio-oncology follow-up.
Cancer creates a hypercoagulable condition that likely promotes intracardiac thrombosis in susceptible individuals. Hematologic malignancies and certain solid tumors, especially lung, pancreatic, and brain cancers, are known to be linked with increased thrombotic risks, particularly in metastatic cases. Patients often experience venous thromboembolism, which may also increase their vulnerability to arterial and intracardiac thrombi. Although comprehensive epidemiological data are lacking, multiple case reports highlight the potential life-saving benefits of screening for cardiac thrombus in high-risk cancer patients.
41
The incidence of LVT in oncology patients is generally considered low; however, it is elevated in individuals with advanced cancer and concurrent LV dysfunction. This distribution illustrates the relationships between conventional cardiac risk factors, such as low ejection fraction, and cancer-specific factors, including hypercoagulability and cardiotoxic treatments.

Prognostic Implications
An LV thrombus significantly adversely impacts prognosis. LVT significantly increases the risk of systemic embolization. Patients with LVT are at risk for ischemic stroke, limb ischemia, renal or mesenteric infarctions, and various embolic complications. Historical data indicate that an untreated LVT can increase the risk of stroke or systemic embolism by 10%–15% annually. LVT remains an independent predictor of thromboembolic events in current clinical practice, significantly elevating the risk of embolism compared to patients without LVT.
40
Prompt identification and management of LVT is crucial to prevent potentially serious complications.
Oncology patients face greater health risks, and their management presents significant challenges. Patients diagnosed with cancer and LVT must evaluate the risk of thromboembolic events in relation to the potential for bleeding and their general state of weakness. Anticoagulation is the standard treatment for LVT; however, patients with active cancer exhibit an increased risk of bleeding due to tumor-related coagulopathies, chemotherapy-induced thrombocytopenia, and invasive procedures.
43
One study indicated that approximately 12% of cancer patients receiving anticoagulation experienced major bleeding after 12 months, a rate significantly higher than that observed in the general population.
44
Comorbidities and treatment limitations, including the necessity to stop anticoagulation for surgical interventions or reduced platelet counts, often impede optimal therapy. Consequently, oncology patients with LVT exhibit a higher incidence of both embolic events and bleeding complications, resulting in an increased mortality risk for this population. The presence of advanced malignancy worsens prognosis; thus, an LVT in a cancer patient is a critical finding that underscores the need for careful, individualized management. Multidisciplinary cardio-oncology teams are increasingly essential for addressing these issues and improving outcomes for this at-risk population.
44

Diagnostic Imaging Modalities
Early LVT detection and anticoagulation reduce the risk of stroke and other embolic complications. Many imaging modalities can detect LVT, each with pros and cons. Transthoracic echocardiography (TTE) is the first-line test, followed by contrast enhancement or advanced imaging in cases of uncertainty, according to current guidelines. TTE, contrast-enhanced echocardiography, CMR, computed tomography (CT), and positron emission tomography are the main LVT imaging modalities. We will focus on their functions, efficacy, and optimal uses for cancer patients. Table 1 and Figure 4 compare these methods.

Transthoracic Echocardiography (TTE)
TTE is the primary imaging modality employed for evaluating a suspected LVT. It is readily accessible, painless, and can be performed at the bedside, which makes it ideal for real-time assessment of cardiac structure and function.
41
Echocardiography allows clinicians to detect regional wall-motion abnormalities, ventricular aneurysms, and distinct masses within the left ventricular cavity. Due to its portability and rapid performance, TTE is typically the initial diagnostic modality employed to assess LVT in individuals exhibiting LV dysfunction or systemic embolic manifestations. New echocardiographic techniques, such as harmonic imaging and various perspectives, have enhanced visualization of the left ventricular apex, the typical site for thrombus formation. Nonetheless, conventional TTE possesses considerable limitations in the detection of LVT. It may lack sensitivity for small mural thrombi that adhere closely to the endocardium or for patients with suboptimal acoustic windows. Echocardiography is fundamentally reliant on the operator, and image quality can be adversely affected by body composition, pulmonary interference, or inadequate acoustic windows, especially in critically ill or post-operative patients. Studies comparing TTE to more advanced imaging techniques have shown that TTE can miss a substantial number of thrombi. In a comprehensive review, non-contrast TTE demonstrated a sensitivity of approximately 24% to 33% for detecting LV thrombus, while achieving a high specificity of about 94% to 95%.
45
This suggests that small thrombi often evade conventional echocardiographic identification. Contrast-enhanced echocardiography serves as an effective solution to this issue. Utilizing ultrasound contrast agents to render the left ventricular cavity opaque allows for the visualization of even minor apical or mural thrombi. The application of contrast significantly enhances TTE's sensitivity for LVT, reportedly increasing it to between 50% and 60% or higher, while its specificity remains exceptionally high.
41
When LVT is suspected and preliminary echocardiographic images are unreliable, a contrast-enhanced transthoracic echocardiogram is recommended to improve diagnostic accuracy. Overall, TTE (particularly with contrast) remains the most accessible first-line modality for LVT due to its accessibility. A negative echo does not entirely exclude thrombus in a high-risk patient.

Cardiac Magnetic Resonance Imaging (CMR)
CMR imaging with LGE sequences is the gold standard for LVT diagnosis.
41
CMR has higher spatial resolution and tissue characterization than other imaging methods. After LGE, thrombi appear dark (non-enhancing) defects that contrast with bright-enhancing myocardium or blood pools, making them easy to identify. Thrombi are accurately detected and distinguished from other heart masses and tissue changes using this method. Organizing thrombi do not absorb gadolinium, but ventricular tumors show varying contrast enhancement or perfusion on first-pass imaging.
46
CMR can distinguish an apical thrombus from endocardial fibrosis or scar tissue, which gadolinium better visualizes.
41
In a focused study, CMR distinguished cardiac thrombi from tumors with 95% accuracy, demonstrating its value in ambiguous situations.
46
CMR provides detailed information about ventricular function and wall motion, including akinetic apical aneurysm dimensions that may increase thrombus formation. CMR is the most accurate cancer diagnosis method, but it presents several practical challenges in cancer patients. Patients with significant renal impairment (due to the risk of nephrogenic systemic fibrosis) or multiple scans are advised to avoid gadolinium-based contrast in many CMR protocols.
47
Chemotherapy and tumor effects may impair renal function in advanced cancer patients, limiting gadolinium use. Severely ill patients may have trouble getting a good CMR study. Advanced cancer patients may not be able to lie supine or hold their breath during the scan, resulting in motion artifacts and poor images. Some patients have magnetic resonance imaging (MRI) incompatible implantable devices or metal hardware. Since echocardiography is more widely available, CMR may be harder to access and more expensive.
41
Thus, physicians use CMR only when echocardiographic findings are ambiguous or when a definitive diagnosis is needed, such as confirming thrombus before treatment or distinguishing it from a heart tumor. After completion, CMR with LGE provides physicians with extensive patient management information and is highly accurate for LVT diagnosis.

CT and Positron Emission Tomography–Computed Tomography (PET-CT)
CT is not a standard primary diagnostic method for left ventricular (LV) thrombus, but it can have a complementary role, especially in oncology patients who frequently receive CT scans for staging. Gated CT angiography, or contrast-enhanced cardiac CT, shows the heart's anatomy, including the left ventricular apex and filling defects. LVT has been found on CT as a low-attenuation filling defect with akinetic myocardium in case series. Thorough cardiac image review during thoracic or whole-body CT for cancer evaluation may reveal an unexpected thrombus. CT can assess thrombus morphology and dimensions under certain conditions, but formal studies supporting routine LVT screening are limited to case reports.
30
It is useful for determining anatomy, such as thrombus layering or protruding, and for planning interventions. CT uses radiation and contrast dye, so it is usually done when other scans are needed rather than to test for LVT. Due to advances in CT technology and cardiac gating, routine oncology CT imaging now includes cardiac evaluation, reflecting the trend toward proactive cardio-oncology monitoring.
41
While not specifically used to detect left ventricular thrombi, FDG PET-CT can provide valuable insights in the presence of an intracardiac mass.45,48 For cancer patients, FDG-PET is essential for distinguishing heart thrombosis from tumors. On PET scans, metabolically active tumor tissue absorbs FDG, appearing “hot”, a bland thrombus is metabolically inactive and seldom absorbs FDG. If a cancer patient's staging PET-CT shows an unexpected cardiac uptake, one may suspect a cardiac metastasis or tumor thrombus rather than a clot. An avascular thrombus may appear on a PET-CT as a ventricle filling defect without PET activity, confirming its benign thrombotic properties. Research shows that FDG PET-CT can distinguish tumor and benign thrombi. This helps doctors avoid prescribing anticoagulants for heart cancer.
48
PET-CT is a practice tool. Usually used when a cardiac mass is found in a cancer patient, raising the question of “tumor versus thrombus.” Multimodal imaging assessments are increasing as oncology and cardiology merge.

Treatment Strategies
LVT causes severe complications like systemic embolization. The cornerstone of its management and thereby reducing the risk of complications is effective anticoagulation while minimizing the risk of hemorrhage. Patient's clinical context, etiology of Left ventricular dysfunction and risk factors especially in complex oncology patients individualize the therapeutic approach.
30

General Principles of Anticoagulation
Prompt initiation of systemic anticoagulants and early treatment, particularly in the first 1–2 weeks after thrombus formation which is the highest risk period, reduces the risk of systemic embolization and stroke significantly. Any delay in therapy can lead to irreversible morbidity and mortality.30,49 The type, dose and duration of anticoagulation should be balanced in the competing risk between thrombosis and bleeding. This balance is delicate in oncology patients amplifying the therapeutic dilemma due to coexistent hypercoagulability, chemotherapy-induced cytopenia, mucosal involvement and drug-drug interactions increasing baseline bleeding risk.5,50 Therefore, it is essential to follow a patient-centered, risk-adapted approach guided by multidisciplinary cardio-oncology consultation as a critical first step in formulating a treatment plan.5,50 Before therapy initiation, baseline evaluation of renal and hepatic function, platelet count, and potential pharmacologic interactions should be taken.5,30 Patients who are already on antiplatelet therapy (post-myocardial infarction) have increased bleeding risk when adding anticoagulants. Thus, whenever feasible in most clinical scenarios, minimizing to dual therapy (typically one anticoagulant with a single antiplatelet) is preferred to mitigate bleeding complications associated with triple regimens.51–53

Choice of Anticoagulants
Choosing an anticoagulant agent has evolved significantly. Vitamin K antagonist (VKAs) (Warfarin) has traditionally been the mainstay of LVT management. The target INR 2.0–3.0 is effective in thrombus resolution and reducing embolic events.
30
However, the narrow therapeutic window, wide dietary and pharmacologic interactions and the need for frequent monitoring have limited the usage of it particularly in patients who receive complex chemotherapy regimens that profoundly affect VKAs metabolism thus further complicating its prescription.
49
Nowadays, adoption of Direct Oral Anticoagulants (DOACs) including factor Xa inhibitors (apixaban, rivaroxaban, and edoxaban) and direct thrombin inhibitors (dabigatran) as a viable alternative to VKAs for LVT has increased as they have shown to be non-inferior to VKAs in thrombus resolution and embolic prevention on top of having comparable or even less bleeding rates.54–57 Fixed dosing, predictable pharmacokinetics, and fewer drug interactions are additional advantages of DOACs over VKAs. Current guidelines encourage using DOACs in this setting although large-scale randomized controlled trials are still lacking.
30
In specific clinical scenarios, low molecular weight heparin (LMWH) can be a critical tool especially in patients with active malignancy, gastrointestinal or genitourinary tumors, and high bleeding risk.58–60 It is often used in hospitalized patients as bridging therapy when initiating VKAs.
30
It is also preferred for patients who have active gastrointestinal malignancies where DOACs have been associated with higher risk of luminal bleeding in these patients.58,59 Patients with high bleeding risk or severe thrombocytopenia may also be better suited to receive LMWH as its shorter half-life allows for rapid reversal if needed. It is also preferred when enteral absorption is unreliable or when drug–drug interactions limit oral agents.58,59 Assessing renal function is critical before initiation of DOACs or LMWH as impaired clearance can lead to accumulation and bleeding (Table 2).
58

Cancer-Specific Considerations
Managing LVT in active cancer patients is challenging as it has complex prothrombotic tendency via tumor-derived tissue factors, systemic inflammation, and endothelial injury yet increased bleeding risk with treatment thus requiring a specialized approach.5,50 A common complication of myelosuppressive chemotherapy is chemotherapy-induced thrombocytopenia which significantly increases bleeding risk and thus may require adjusting anticoagulation dose if platelets drop between 25,000–50,000/µL or even temporarily interrupt it if fall below 25,000/µL unless thrombotic risk is critical.37,61,62 Another key consideration is drug-drug interactions between anticoagulants (both VKAs and DOACs) and anticancer agents (including chemotherapy, targeted therapies, and immunotherapies). Many of these agents share metabolic pathways, such as the cytochrome P450 system causing unpredictable effects on both bleeding and thrombotic risk due to altered anticoagulant levels.5,50 Gastrointestinal or genitourinary malignancies patients are particularly prone to mucosal bleeding with DOACs making LMWH the preferred option.58,59 Thus, regular medication revision and coordination with clinical pharmacists are advised. Also, complex multidisciplinary collaboration between cardiology, oncology, hematology and clinical pharmacology is critical to ensure efficacy and safety of this vulnerable patient population.5,50
Figure 5 illustrates the anticoagulant classes and mechanisms used for LVT.

Duration of Therapy and Follow-Up
Deciding the optimal duration of anticoagulation for LVT is a dynamic process by doing serial imaging and assessing the prothrombotic state. It is inappropriate to give specific timing that fits all patients. The standard duration in general is 3–6 months. Therapy needs to be continued until complete thrombus resolution is confirmed by imaging and left ventricular systolic function has recovered. The duration may need to be extended in many cases of persistent unresolved thrombus, persistent left ventricular dysfunction (eg, Left Ventricular Ejection Fraction LVEF <35-40%), apical aneurysm or in patients with persistent risk factors especially in oncology patients with ongoing cancer-related hypercoagulability. After the initiation of therapy, follow-up imaging is recommended at approximately 3 months to assess for thrombus resolution.
30
The most used imaging modality is TTE with contrast, though CMR offers better tissue characterization and sensitivity for detecting small, residual, or laminated thrombi thus it should be used when TTE is inconclusive or when it is necessary to distinguish tumor from thrombus.63–65 If thrombus persists or is recurrent, therapy extension and serial imaging every 2–3 months until resolution is warranted. The decision to discontinue therapy must not be guided based on time alone but should be guided by both imaging and functional recovery. Removal of the inciting prothrombotic stimulus should be coupled with complete thrombus resolution on imaging and significant improvement in LV function (eg, LVEF >40-45%) to consider cessation of anticoagulation. Recurrence, ongoing LV remodeling or persistence of the underlying substrate for thrombus formation may justify prolonged or indefinite therapy while managing the risk of bleeding.
30

Surgical and Interventional Approaches
In selected subsets of patients who have high-risk features (patients with large, pedunculated, mobile thrombi causing very high risk of embolization or recurrent embolization despite adequate anticoagulation, patients undergoing concurrent LV aneurysm repair after myocardial infarction) or refractory cases where medical therapies have failed, advanced therapeutic options may be warranted. These approaches are not first-line treatment as they have procedural risks. Thrombectomy, either as a standalone procedure or in conjunction with LV aneurysm resection (more common) can be performed during cardiac surgery. This approach aims to definitively eliminate the source of emboli and prevent future thrombus formation by removing the thrombus and akinetic or dyskinetic myocardial tissue. Surgical thrombectomy is rarely required (<5% of LVT cases).30,45 In patients with metastatic or advanced malignancy, operative risk must be balanced against the embolic potential and the overall prognosis. Emerging percutaneous catheter-based approaches using aspiration thrombectomy or mechanical retrieval under imaging guidance are under investigation as less invasive alternatives.66–69 These are currently considered experimental but promising for the future management of refractory or high-risk LVT as they offer a safer option for poor surgical candidates . Early reports suggest that they are feasible, but limited experience and procedural embolic risk is still a concern.70–73 Future studies may clarify the role of these minimally invasive options in selected oncology and non-oncology populations. Given the lack of data, these procedures should be reserved for specialized centers with multidisciplinary expertise.30,66

Outcomes and Prognosis
Cancer and its treatment are associated with hypercoagulability, endothelial injury, and venous stasis, all of which directly influence the development of LVT. Prognosis depends on thrombus morphology, degree of ventricular dysfunction, and the success of anticoagulation therapy in achieving complete thrombus resolution.2,74
Lattuca et al's cohort reported that major adverse cardiovascular events occurred in 37.1% of patients, with mortality reaching 18.9%.
2
This is in the general population, and significant morbidity and mortality are expected to be present in the oncology populations, but there are few cohort studies on this. Lemaître et al's heart failure (HF) and LVT patients demonstrated 20% mortality rate as well.
74
Persistent LVT was associated with higher bleeding rates, and recent studies have focused on predictors of thrombus resolution and recurrence.
2
Kim et al identified that a larger thrombus size, lower ejection fraction, and left ventricular aneurysms are independent predictors of LVT.
75
In cancer, cardiac complications might result from different cancer therapies, resulting in cardiomyopathy or left ventricular systolic dysfunction.
70
This ties cancer to LVT and raises concerns regarding the prognosis of cancer patients with LVT.
Zhou et al found that 24.3% of patients experienced LVT recurrence after resolution, and with individuals who continued anticoagulation had a reduced recurrence risk.
71
The study demonstrated that the lack of anticoagulation use was one of the strongest predictors of recurrence, thus emphasizing the importance of continuing anticoagulation in LVT patients. Yang et al created a model which predicted LVT persistence and recurrence using prospective and retrospective data. Their results demonstrated that mural thrombus morphology and thickness, and aneurysm presence were highly associated with poor outcomes.
72
Individuals with cancer and these high-risk features are more likely to have recurrent or persistent LVT despite the use of anticoagulation. Leow et al also demonstrated that despite the use of anticoagulants, long-term outcomes are not the best, as major bleeding occurred in 13% according to their study.
73
This demonstrates how controlling thrombosis without resulting in hemorrhage is a thin line that requires careful monitoring.
In cancer patients, outcomes are further complicated by the occurrence of thrombocytopenia and the need to stop anticoagulation because of cancer treatment. In Carney et al's multicenter cohort study, changing the dose of anticoagulation in cancer patients with thrombocytopenia decreased major bleeding from 12.8% to 6.6% without increasing thromboembolic events.76,77 This emphasizes the need for specific guidelines with modified dosages for cancer patients facing thromboembolic challenges and LVT. The prognosis and outcomes of patients with LVT are determined by a multitude of factors, and many risk factors are prevalent in cancer patients. Cancer patients are at risk for complications because of the hypercoagulability, endothelial damage, and interruptions in anticoagulation therapy they face. Individualized management strategies and follow-ups are critical to improve outcomes in this high-risk group.

Guidelines and Controversies
Current guidelines and statements on the management of LVT, issued by both the American Heart Association (AHA) and the European Society of Cardiology (ESC), are not specific to cancer patients. Instead, these guidelines primarily address post MI and non-cancer populations.30,78
According to Levine et al's statement with the AHA, oral anticoagulation with a vitamin K antagonist for a minimum of 3–6 months is recommended, ensuring serial images are taken to confirm thrombus resolution. Their statement acknowledges that DOACs may represent a reasonable alternative, but that this practice is based on limited data and expert consensus rather than prospective randomized trials. When making treatment decisions, the AHA also urges that bleeding risk, comorbidities including cancer, and other therapies given should be taken into consideration.
30
The ESC's HF Guidelines recommend anticoagulants for LVT in patients with reduced ejection fraction, but notes that evidence is primarily derived from observational studies. Their guideline recommends taking into consideration degree of left ventricular dysfunction, the presence of mural versus mobile thrombus, and the anticipated duration of anticoagulation.
78

The lack of standardization in treatment or quality indicators demonstrates an evidence gap, as current recommendations aren’t representative of the cancer population, thus it doesn’t take into consideration the associated thrombotic and bleeding risks.79,80 Certain associations such as The European Hematology Association (EHA) have guidelines on dealing with cancer-associated thrombosis, but not specifically LVT. The EHA recommends utilizing LMWH as initial therapy for thrombocytopenic cancer patients, transitioning to a DOAC or VKA once platelet counts normalize, and only withholding anticoagulation if counts fall below 25 × 10^9/L.
81
A review of guidelines by Streiff et al also demonstrated that the ASCO, ISTH, ITAC, and NCCN panels agree with LMWH being the first-line therapy for most patients with active malignancy, while DOACs may be considered in those without significant gastrointestinal involvement or severe thrombocytopenia.
82
Martin et al's cohort compared DOACs and warfarin in low-weight patients, which is a problem cancer patients also face due to cachexia, and reported limited evidence of DOAC efficacy in those patients.
83
Issues regarding DOAC efficacy have been raised in this cohort, but also official associations such as the AHA and ESC have raised similar concerns.
Another problem with lack of guidelines has been demonstrated in Hui et al's cohort. They reported that anticoagulation did not reduce recurrent thrombosis in patients with tumor thrombosis, and was rather associated with higher bleeding rates, demonstrating where issues rise in cancer patients when it comes to making decisions regarding anticoagulation.
84
To solve this, more research and clinical trials are required in order to create specific guidelines regarding type of anticoagulation, dosage, and the duration of therapy. Additionally, individualized treatment plans which are able to balance both thrombosis prevention and hemorrhagic risk are needed. A multidisciplinary team involving hematologists, oncologists, and cardiologists is needed.
81

Research Gaps and Future Directions
Major knowledge gaps and lack of studies persist regarding LVT in the cancer population, thus causing problems in creating guidelines to help doctors treat individuals. Any evidence available is usually tied with heart-failure of post-MI population, and LVT itself is not represented often. There is a lack of prospective studies following cancer patients with LVT, and most data is available as case reports which are not representative. Large cohort and multi-center studies are required, in order to better understand the recurrence and embolic risk of LVT in cancer patients.
Additional limitations, which are caused by the lack of studies, is the lack of standardized anticoagulation guidelines for oncological populations, and the guidelines which exist fail to provide information regarding LVT. Guidelines which address issues such as thrombocytopenia, the drug-drug interactions that might occur between chemotherapy and anticoagulants, and cancer staging are all required. In Carney et al's study, modifying the dosage of anticoagulants from guidelines resulted in decreased percentage of major bleeding, emphasizing the need for specific frameworks for the cancer population.
76
There is a lack of information on the recommended duration and type of anticoagulation to be used for LVT, and prospective trials comparing LMWH, DOACs, and VKAs in the cancer population are required.
Risk prediction models for LVT occurrence or recurrence should be created, as they could help in deciding if anti-coagulants should be continued and weighing the thrombosis and hemorrhagic risks associated. Yang et al's prediction model for LVT recurrence and persistence was able to identify predictors, and creating a model based on prospective and retrospective studies for the cancer population would allow physicians to identify patients who require prolonged anticoagulant use.
72
Additional research should also be done on the role of advanced imaging and radiomic analysis in differentiating thrombus from tumor tissue. In Lee et al's CT-radiomic model, an AUC of 0.983 was achieved, demonstrating the promise for improving the accuracy in diagnosis and treatment.
85
Using artificial intelligence in radiomic tools, or for risk prediction and biomarker identification is a promising direction. The need for a more multidisciplinary approach when treating LVT in cancer is required, especially in individuals still undergoing chemotherapy. Future research should focus on collecting enough data in order to address the other limitations such as lack of guidelines, and create a strong base of evidence in order to start working on AI models and risk-prediction and radiomic tools. With this, improved outcomes and reduced complications and mortality can be achieved in cancer patients with LVT.

Conclusion
LVT in oncology patients is increasingly recognized and represents a significant clinical issue, the hypercoagulable state occurs in malignancy, in addition to modern chemotherapeutics that impair cardiac function, magnifies the risk of thromboembolic complications in the oncology population.
Current approaches to imaging and treatment are derived from the post-myocardial infarction populations. but oncology patients present specific challenges because they have higher bleeding tendency, frequent thrombocytopenia, and numerous potential drug–drug interactions complicate standard protocols. Because of this reason, suboptimal response result from application of standard strategies. The lack of cancer-specific guidelines remains a critical gap in clinical care, and prompts an urgent need for prospective research and standardized treatment pathways.