ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده: 2

Left ventricular thrombus

Left ventricular thrombus
Authors:
Wilson S Colucci, MD
Gregory YH Lip, MD, FRCPE, FESC, FACC
Section Editor:
Stephen S Gottlieb, MD
Deputy Editor:
Todd F Dardas, MD, MS
Literature review current through: May 2025. | This topic last updated: May 27, 2025.

INTRODUCTION — 

Thrombus in the heart chambers can lead to embolic stroke, systemic embolic events, or pulmonary embolism. This topic will discuss risk factors, testing, and treatment of left ventricular (LV) thrombus with a focus on patients with reduced systolic function or acute myocardial infarction (MI).

Antithrombotic therapy in clinical settings associated with HF is discussed separately:

●(See "Atrial fibrillation in adults: Use of oral anticoagulants".)

●(See "Cardiac amyloidosis: Treatment and prognosis", section on 'Atrial fibrillation'.)

●(See "Isolated left ventricular noncompaction in adults: Management and prognosis", section on 'Management of complications'.)

●(See "Chronic Chagas cardiomyopathy: Management and prognosis".)

●(See "Hypertrophic cardiomyopathy in adults: Supraventricular tachycardias including atrial fibrillation".)

●(See "Acute coronary syndrome: Oral anticoagulation in medically treated patients" and "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".)

Left ventricular aneurysm is discussed in detail separately. (See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction".)

RISK FACTORS

Systolic dysfunction — In patients with LV systolic dysfunction, the risk of thrombi is increased. This includes patients with systolic dysfunction that is chronic or acute in nature. Manifestations of systolic dysfunction and their association with ventricular thrombus include:

●Ejection fraction – An association between LV systolic dysfunction and stroke or thromboembolism has been found in some studies [1,2] but is less clear in others [3-5]. The LV ejection fraction (LVEF) is an important risk factor for thrombus formation, as is the presence of dyskinetic or akinetic segments even with an overall normal ejection fraction. Severe mitral regurgitation may have a protective effect by decreasing stasis [6].

●Left ventricular aneurysm – The presence of an LV aneurysm further increases the risk of LV thrombus. LV thrombus is most often seen in patients with large areas of systolic dysfunction or aneurysm. As such, LV thrombus is more common in patients with infarction in the left anterior descending artery distribution, though LV thrombus can occur in other distributions [7]. Apical systolic dysfunction is a greater risk factor than basal systolic dysfunction [7].

●Spontaneous echocontrast – In patients with systolic dysfunction, echocardiography may reveal spontaneous echocontrast, which is a sign of low flow and a risk factor for LV thrombus. However, in addition to low flow, the appearance of spontaneous contrast may depend on the gain and other settings used to acquire the echocardiographic images. Nonetheless, the risk of embolic events is increased in patients with spontaneous echocontrast. One report suggested that the risk of stroke increased in patients with spontaneous echocontrast who were not anticoagulated or in atrial fibrillation (AF; adjusted hazard ratio 2.6, 95% CI 1.7-3.9) [8].

Acute myocardial infarction — Acute MI may also increase the risk of thrombus formation due to exposure of blood to damaged endothelium. Delayed or no reperfusion further increases the risk of LV thrombus. In two series of patients with ST-elevation MI (STEMI) treated with primary percutaneous coronary intervention, the incidence of LV thrombus was between 4 to 8 percent, with higher incidence when the gold-standard of cardiovascular magnetic resonance (CMR) imaging was used [7,9,10]. The incidence of LV thrombi after STEMI without reperfusion may be as high as 40 percent in patients with anterior infarction [11,12]. Most thrombi developed within the first two weeks (median five to six days) after MI [11-15].

Atrial fibrillation — AF is a risk factor for stroke or thromboembolism among patients with heart failure (HF) and is discussed separately. (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

Heart failure with preserved ejection fraction — Data in patients with HF with preserved ejection fraction suggest that the risk of stroke or thromboembolism is similar to that in patients with HF with reduced ejection fraction, though it remains unclear whether these events are attributable to LV thrombus [4,16].

TESTING AND DIAGNOSIS

Suspected embolism — In patients with evidence of suspected embolism to the brain (ie, stroke) or periphery (eg, kidney infarction, limb ischemia), echocardiography to identify the source of embolism is typically performed unless another source of embolism is established. The approach to assessment for the source of embolus in these clinical settings is discussed separately. (See "Overview of the evaluation of stroke", section on 'Echocardiography' and "Clinical features and diagnosis of acute arterial occlusion of the lower extremities", section on 'Embolism'.)

Choice of imaging study — In patients in whom LV thrombus is suspected or in whom follow-up imaging is required, transthoracic echocardiography (TTE) is typically the initial test of choice (image 1 and movie 1). If standard echocardiographic imaging or echocardiographic contrast imaging suggests the presence of LV thrombus but cannot conclusively confirm or exclude LV thrombus, CMR imaging with a long inversion time is the next step in testing. Transesophageal echocardiography (TEE) is a reasonable choice if CMR is not available but is not preferred due to limitations in imaging the LV apex. Contrast-enhanced cardiac computed tomography is another option for the detection of LV thrombus, but it is not widely available.

CMR is considered the gold standard for the noninvasive diagnosis of LV thrombus. Long inversion time late gadolinium enhancement (LGE)-CMR has a greater sensitivity than TTE and a similarly high specificity for the detection of LV thrombus in an ischemic cardiomyopathy population [17-19]:

●In a retrospective study of 160 patients with a remote prior MI who had surgical and/or pathologic confirmation of the presence (48 patients [30 percent]) or absence of LV thrombus, all patients underwent nonsimultaneous preoperative LGE-CMR, TTE, and intraoperative TEE [17]. CMR was significantly more sensitive (88 versus 23 and 40 percent with TTE and TEE, respectively). All imaging modalities had specificities of 96 percent or greater.

●In another study, 201 patients were evaluated with noncontrast and contrast TTE, cine-CMR, and LGE-CMR 7 to 30 days after STEMI [7]. Using LGE-CMR as the gold standard for determining the presence of absence of LV thrombus, the sensitivity of noncontrast and contrast TTE was only 35 and 64 percent, respectively. The specificity of noncontrast and contrast TTE was 98 and 99 percent, respectively. Only 12 percent of patients with thrombus had a LVEF ≤30 percent, and LV aneurysm was present in only 24 percent. On both noncontrast and contrast TTE, apical dysfunction was strongly correlated with the presence of LV thrombus.

Findings diagnostic of thrombus — The presence of a protrusion into the LV, typically arising from the apex, suggests the presence of a thrombus. Independent mobility relative to the myocardium can be used to help differentiate a thrombus from other myocardial structures. Though difficult to distinguish with confidence, thrombi may be acute or older:

●Acute thrombus – TTE characteristics of LV thrombus include a mural or pedunculated echodensity, often of similar acoustic properties to myocardium. Acute thrombi are typically independently mobile or irregular compared with the surrounding myocardium.

●Signs of older thrombus – Though determining the age of a thrombus is characterized by uncertainty, some features that suggest the presence of an older thrombus include the presence of echodensities or a layered or lamellar appearance due to endothelialization. An older thrombus may not be independently mobile compared with the surrounding myocardium.

Differential diagnosis — Other entities that resemble LV thrombus on imaging include:

●Ventricular trabeculations

●Papillary muscle anatomy

●Near-field artifacts

●Rarely, cardiac tumors

PREVENTION

Systolic dysfunction — In patients with LV systolic dysfunction and no other indication for anticoagulation (eg, AF, mechanical heart valve), we suggest not anticoagulating.

Professional guidelines suggest that prophylactic anticoagulation for low LVEF alone is not indicated [20,21].

Evidence from randomized trials and meta-analyses suggests that anticoagulation with warfarin or a direct-acting oral anticoagulant (DOAC) may reduce the risk of stroke by a small amount in patients with systolic dysfunction, albeit with an increased risk of major bleeding [5,22-25]. There is no direct evidence that the reduction in stroke was attributable to a decreased risk of LV thrombus, though patients with AF were excluded from these trials. Notably, most trials did not enroll large numbers of patients with extremely low LVEF. Examples include:

●In the COMMANDER HF trial, 5022 patients with chronic HF, LVEF ≤40 percent, coronary artery disease, elevated plasma natriuretic peptide level, and no AF were randomly assigned to receive rivaroxaban 2.5 mg twice daily or placebo [22]. During the median follow-up of 21 months, the composite outcome of death from any cause, MI, or stroke occurred at a similar rate in the rivaroxaban and placebo groups (25 versus 26.2 percent). There was a small but statistically significant reduction in the risk of stroke (2 versus 3 percent; hazard ratio [HR] 0.66, 95% CI 0.47-0.96) that was potentially offset by a higher risk of major bleeding in the rivaroxaban group (3.3 versus 2.0 percent; HR 1.68; 95% CI, 1.18 to 2.39).

●In a meta-analysis of four randomized trials that included 3663 patients with reduced systolic function and a low prevalence of AF, warfarin therapy reduced the rates of stroke (2.1 versus 4.0 percent; relative risk [RR] 0.56, 95% CI 0.38-0.82) and ischemic stroke (1.9 versus 4.0 percent; RR 0.45, 95% CI 0.24-0.86) compared with aspirin, and increased the risk of major bleeding (5.6 versus 2.8 percent; RR 1.95, 95% CI 1.37-2.76) [26]. There was no difference in all-cause mortality. Other analyses of the same data arrived at the same conclusion [27,28].

Acute myocardial infarction — In patients with acute MI with or without LV systolic dysfunction, the use of prophylactic anticoagulation varies among our experts. Some contributors to this topic do not provide prophylactic anticoagulation for LV thrombus regardless of the severity of LV dysfunction or the presence of high-risk morphologic features (eg, LV aneurysm), while others anticoagulate if there is severe LV dysfunction, apical akinesis, or aneurysm formation. Among those who provide empiric anticoagulation, the duration of therapy is typically three months. After three months, echocardiography or other imaging can be repeated to guide the approach to continued therapy.

Professional guidelines do not recommend empiric anticoagulation after STEMI [29,30]. There are no high-quality studies that directly address prophylactic anticoagulation after STEMI, and older studies that suggest a benefit of anticoagulation took place before routine dual antiplatelet therapy became a standard practice [12,31-33]. Trials that addressed the choice of agent (eg, DOAC or warfarin) were small and inconclusive [34].

Other scenarios — For other diseases that cause systolic dysfunction or that increase the risk of thrombus independent of factors mentioned in this topic, specific guidance on the approach to anticoagulation is discussed separately. Such conditions include:

●Left ventricular noncompaction – The approach to anticoagulation in patients with LV noncompaction is discussed separately. (See "Isolated left ventricular noncompaction in adults: Clinical manifestations and diagnosis".)

●Chagas disease – Anticoagulation in patients with Chagas disease is discussed separately. (See "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Thromboembolism treatment' and "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Thromboembolism prophylaxis'.)

●Mechanical circulatory support – Issues related to intracardiac thrombus associated with mechanical assist devices are discussed separately. (See "Management of long-term mechanical circulatory support devices", section on 'Antithrombotic therapy'.)

●Congenital heart disease – Management of patients with congenital heart disease is discussed separately. (See "Medical management of cyanotic congenital heart disease in adults", section on 'Thromboembolism'.)

TREATMENT — 

In patients with a newly identified LV thrombus, we recommend anticoagulation. Anticoagulation therapy should begin immediately with intravenous heparin, subcutaneous low molecular weight heparin, or a direct-acting oral anticoagulant (DOAC). Intravenous therapy can be replaced with oral anticoagulation with either a DOAC or warfarin.

Anticoagulation should continue for at least three months. Upon reassessment with imaging after three months, management of common scenarios includes:

●No change in thrombus size or characteristics – In patients with no change in the size or characteristics of the thrombus, we continue anticoagulation and continue to reassess.

●Decrease in size of thrombus or development of characteristics of older thrombus – In patients whose thrombus decreases in size or who have features of a thrombus less likely to embolize, the decision to continue or discontinue anticoagulation is based on the persistence of risk factors for embolization and thrombus formation. Due to the uncertainty of accurately determining the age or embolic risk of a thrombus, we typically continue anticoagulation in such patients and reassess with imaging. (See 'Risk factors' above and 'Findings diagnostic of thrombus' above and 'Risk of embolism' below.)

●Resolution of thrombus and persistence of risk factors for new thrombus – In patients with resolution of thrombus on repeat imaging, the decision to anticoagulate is based on the persistence of risk factors for thrombus (eg, LVEF, spontaneous echocontrast, aneurysm formation, other disorders of coagulation) and the risk of bleeding with ongoing anticoagulation. (See 'Risk factors' above.)

●Resolution of both thrombus and risk factors – In patients in whom there is no evidence of residual thrombus, in whom systolic function has improved or returned to normal, and who do not have an LV aneurysm or other indication (eg, AF, mechanical valve) for anticoagulation, it is reasonable to stop anticoagulation and reassess for redevelopment of thrombus or risk factors.

This approach is consistent with professional guidelines [29,30,35].

This approach is based on our experience, the high morbidity and mortality of embolic events (eg, stroke), the observation that thrombus can resolve with anticoagulation, and lower-quality data (eg, older studies, mixed etiologies of HF, inclusion of patients with AF) that suggest a potentially large benefit of anticoagulation in acute MI [36]. In patients with other diseases and in settings in which the thrombus may be chronic, the data are less certain. As examples:

●In a meta-analysis of studies of patients with anterior MI, the presence of an LV mural thrombus identified by noncontrast TTE increased the incidence of an embolic event (odds ratio [OR] 5.5, 95% CI 3.0-9.8) [31]. In patients with a known thrombus, anticoagulation was associated with a lower rate of embolic events (OR 0.32, 95% CI 0.2-0.52).

●Among 126 patients with nonischemic cardiomyopathy in whom AF was not detected, seven patients had LV thrombus at echocardiography and were anticoagulated [37]. In patients who were anticoagulated, there were no embolic events.

In patients who will undergo anticoagulation for LV thrombus, there are few data to guide the choice of agent or duration of therapy. In one meta-analysis of small trials, DOACs and warfarin had similar efficacy and safety [38]. Observational studies came to similar conclusions [39-41].

PROGNOSIS

Risk of embolism — The natural history of LV thrombus and risk factors for embolization include:

●Natural history – The risk of embolization in patients with a documented LV thrombus who are not treated with anticoagulant therapy has been reported to be 10 to 15 percent [31,37]. Most emboli occur within weeks of detection. As examples:

•In a series of 85 patients with LV thrombus (most of whom had a recent MI) followed for almost two years, an embolic event occurred in 13 percent of those with a thrombus compared with only 2 percent of matched controls without a thrombus [42].

•Among a group of 406 patients with chronic systolic HF, systemic thromboembolism occurred in 1 of 10 patients with a known LV thrombus [43]. The association between LV thrombus, AF, anticoagulation, and embolic events was not reported.

•In a study of 25 patients with nonischemic cardiomyopathy with confirmed LV thrombus, thromboembolism occurred in 20 percent of patients [44].

•Retrospective data suggest that most embolic events occur within the first three to four months after detection of an LV thrombus [31-33,42,45-47], though some occurred later [42].

●Risk factors for embolization – Two major echocardiographic risk factors for embolization have been identified: thrombus mobility and thrombus protrusion [42,45,47,48].

•Mobility – In one report, embolization occurred in 22 percent of 119 patients with an LV thrombus after acute MI [45]. Free mobility of the thrombus was present in 58 percent of patients with embolization compared with 3 percent without embolization. Among the 18 patients with free thrombus mobility, embolization occurred in 83 percent compared with 11 percent without mobility.

•Protrusion – In one study, protrusion of the thrombus into the LV cavity was present in 88 percent of those patients with clinical thromboembolism compared with 18 percent without [45]. Among the 40 patients with thrombus protrusion, embolization occurred in 58 percent compared with 4 percent in those without protrusion.

Resolution — Patients with LV thrombi may have complete resolution, partial resolution, or endothelialization. An observational study of 159 patients with a confirmed LV thrombus, most of whom were anticoagulated, reported the following at a median follow-up of 103 days [49]:

●A reduction of the thrombus area from baseline was observed in 76 percent, with total regression in 62 percent.

●During a median follow-up of 632 days, death occurred in 18 percent, stroke in 13 percent, and major bleeding in 13 percent.

●LVEF ≥35 percent and anticoagulation therapy >3 months were independently associated with lower rates of major adverse cardiovascular outcomes.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

●Risk factors – Risk factors for the development of left ventricular (LV) thrombus include LV systolic dysfunction and acute myocardial infarction (MI). (See 'Risk factors' above.)

●Testing and diagnosis

•Suspected embolism – In patients with evidence of suspected embolism to the brain (ie, stroke) or periphery (eg, kidney infarction, limb ischemia), echocardiography to identify the source of embolism is typically performed unless another source of embolism is established. (See "Overview of the evaluation of stroke", section on 'Echocardiography' and "Clinical features and diagnosis of acute arterial occlusion of the lower extremities", section on 'Embolism'.)

•Choice of imaging study – In patients in whom LV thrombus is suspected or in whom follow-up imaging is required, transthoracic echocardiography (TTE) is typically the test of choice (image 1 and movie 1). If standard echocardiographic imaging or echocardiographic contrast imaging suggests the presence of LV thrombus but cannot conclusively confirm or exclude LV thrombus, cardiovascular magnetic resonance (CMR) imaging with a long inversion time is the next step in testing.

Transesophageal echocardiography (TEE) is a reasonable choice if CMR is not available but is not preferred due to limitations in imaging the LV apex. Contrast-enhanced cardiac computed tomography is another option for detection of LV thrombus but is not widely available. (See 'Choice of imaging study' above.)

•Findings diagnostic of thrombus – The presence of a protrusion into the LV, typically arising from the apex, suggests the presence of a thrombus. Independent mobility relative to the myocardium can be used to help differentiate a thrombus from other myocardial structures. Though difficult to distinguish with confidence, thrombi may be acute or older (see 'Findings diagnostic of thrombus' above):

-Acute thrombus – TTE characteristics of LV thrombus include a mural or pedunculated echodensity often of similar acoustic properties to myocardium. Acute thrombi are typically independently mobile compared with the surrounding myocardium.

-Signs of older thrombus – Though determining the age of a thrombus is characterized by uncertainty, some features that suggest the presence of an older thrombus include the presence of echodensities or a layered or lamellar appearance. An older thrombus may not be independently mobile compared with the surrounding myocardium.

•Differential diagnosis – Other entities that resemble LV thrombus on imaging include (see 'Differential diagnosis' above):

-Ventricular trabeculations

-Papillary muscle anatomy

-Near-field artifacts

-Rarely, cardiac tumors

●Prevention

•Systolic dysfunction – In patients with LV systolic dysfunction and no other indication (eg, atrial fibrillation [AF], mechanical heart valve) for anticoagulation, we suggest not anticoagulating. (Grade 2C). (See 'Systolic dysfunction' above.)

•Acute MI – In patients with acute MI with or without LV systolic dysfunction, the use of prophylactic anticoagulation varies among our experts. Some contributors to this topic do not provide prophylactic anticoagulation for LV thrombus regardless of the severity of LV dysfunction or the presence of high-risk morphologic features (eg, LV aneurysm), while others anticoagulate if there is severe LV dysfunction, apical akinesis, or aneurysm formation. (See 'Acute myocardial infarction' above.)

•Other scenarios – Some diseases that cause systolic dysfunction or are particularly prone to the formation of ventricular thrombus have recommendations for anticoagulation distinct from those described in this topic. (See 'Other scenarios' above.)

●Treatment – In patients with a newly identified LV thrombus, we recommend anticoagulation (Grade 1C). Anticoagulation should continue for at least three months. Upon reassessment with imaging after three months, management of common scenarios includes:

•No change in thrombus size or characteristics – In patients with no change in the size or characteristics of the thrombus, we continue anticoagulation and continue to reassess.

•Decrease in size of thrombus or development of characteristics of organized thrombus – In patients whose thrombus decreases in size or who have features of a thrombus less likely to embolize, the decision to continue or discontinue anticoagulation is based on the confidence that the thrombus is at low risk of embolization and the persistence of risk factors for embolization and thrombus formation. Due to the uncertainty of accurately determining the age or embolic risk of a thrombus, we typically continue anticoagulation in such patients and reassess with imaging. (See 'Findings diagnostic of thrombus' above and 'Risk of embolism' above.)

•Resolution of thrombus and persistence of risk factors for new thrombus – In patients with resolution of thrombus on repeat imaging, the decision to anticoagulate is based on the persistence of risk factors for thrombus (eg, LV ejection fraction [LVEF], spontaneous echocontrast, aneurysm formation, other disorders of coagulation) and the risk of bleeding with ongoing anticoagulation.

•Resolution of both thrombus and risk factors – In patients in whom there is no evidence of residual thrombus, in whom systolic function has improved or returned to normal, and who do not have an LV aneurysm or other indication (eg, AF, mechanical valve) for anticoagulation, it is reasonable to stop anticoagulation and reassess for redevelopment of thrombus or risk factors.

●Prognosis

•Risk of embolism – The risk of embolization in patients with a documented LV thrombus who are not treated with anticoagulant therapy is approximately 10 to 15 percent. Risk factors for embolism include mobility and protrusion in to the LV. (See 'Risk of embolism' above.)

•Resolution – Patients with LV thrombi may have complete resolution, partial resolution, or endothelialization. (See 'Resolution' above.)

  1. Loh E, Sutton MS, Wun CC, et al. Ventricular dysfunction and the risk of stroke after myocardial infarction. N Engl J Med 1997; 336:251.
  2. Freudenberger RS, Hellkamp AS, Halperin JL, et al. Risk of thromboembolism in heart failure: an analysis from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). Circulation 2007; 115:2637.
  3. Abdul-Rahim AH, Perez AC, Fulton RL, et al. Risk of Stroke in Chronic Heart Failure Patients Without Atrial Fibrillation: Analysis of the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORONA) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca-Heart Failure (GISSI-HF) Trials. Circulation 2015; 131:1486.
  4. Solomon SD, Anavekar N, Skali H, et al. Influence of ejection fraction on cardiovascular outcomes in a broad spectrum of heart failure patients. Circulation 2005; 112:3738.
  5. Cokkinos DV, Haralabopoulos GC, Kostis JB, et al. Efficacy of antithrombotic therapy in chronic heart failure: the HELAS study. Eur J Heart Fail 2006; 8:428.
  6. Kalaria VG, Passannante MR, Shah T, et al. Effect of mitral regurgitation on left ventricular thrombus formation in dilated cardiomyopathy. Am Heart J 1998; 135:215.
  7. Weinsaft JW, Kim J, Medicherla CB, et al. Echocardiographic Algorithm for Post-Myocardial Infarction LV Thrombus: A Gatekeeper for Thrombus Evaluation by Delayed Enhancement CMR. JACC Cardiovasc Imaging 2016; 9:505.
  8. Zhou X, Shi R, Wu G, et al. The prevalence, predictors, and outcomes of spontaneous echocardiographic contrast or left ventricular thrombus in patients with HFrEF. ESC Heart Fail 2021; 8:1284.
  9. Rehan A, Kanwar M, Rosman H, et al. Incidence of post myocardial infarction left ventricular thrombus formation in the era of primary percutaneous intervention and glycoprotein IIb/IIIa inhibitors. A prospective observational study. Cardiovasc Ultrasound 2006; 4:20.
  10. Gianstefani S, Douiri A, Delithanasis I, et al. Incidence and predictors of early left ventricular thrombus after ST-elevation myocardial infarction in the contemporary era of primary percutaneous coronary intervention. Am J Cardiol 2014; 113:1111.
  11. Nihoyannopoulos P, Smith GC, Maseri A, Foale RA. The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity. J Am Coll Cardiol 1989; 14:903.
  12. Weinreich DJ, Burke JF, Pauletto FJ. Left ventricular mural thrombi complicating acute myocardial infarction. Long-term follow-up with serial echocardiography. Ann Intern Med 1984; 100:789.
  13. Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography. N Engl J Med 1981; 305:297.
  14. Greaves SC, Zhi G, Lee RT, et al. Incidence and natural history of left ventricular thrombus following anterior wall acute myocardial infarction. Am J Cardiol 1997; 80:442.
  15. Nayak D, Aronow WS, Sukhija R, et al. Comparison of frequency of left ventricular thrombi in patients with anterior wall versus non-anterior wall acute myocardial infarction treated with antithrombotic and antiplatelet therapy with or without coronary revascularization. Am J Cardiol 2004; 93:1529.
  16. Sandhu RK, Hohnloser SH, Pfeffer MA, et al. Relationship between degree of left ventricular dysfunction, symptom status, and risk of embolic events in patients with atrial fibrillation and heart failure. Stroke 2015; 46:667.
  17. Srichai MB, Junor C, Rodriguez LL, et al. Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation. Am Heart J 2006; 152:75.
  18. Mollet NR, Dymarkowski S, Volders W, et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 2002; 106:2873.
  19. Barkhausen J, Hunold P, Eggebrecht H, et al. Detection and characterization of intracardiac thrombi on MR imaging. AJR Am J Roentgenol 2002; 179:1539.
  20. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2022; 145:e895.
  21. McDonagh TA, Metra M, Adamo M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021; 42:3599.
  22. Zannad F, Anker SD, Byra WM, et al. Rivaroxaban in Patients with Heart Failure, Sinus Rhythm, and Coronary Disease. N Engl J Med 2018; 379:1332.
  23. Cleland JG, Findlay I, Jafri S, et al. The Warfarin/Aspirin Study in Heart failure (WASH): a randomized trial comparing antithrombotic strategies for patients with heart failure. Am Heart J 2004; 148:157.
  24. Massie BM, Collins JF, Ammon SE, et al. Randomized trial of warfarin, aspirin, and clopidogrel in patients with chronic heart failure: the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial. Circulation 2009; 119:1616.
  25. Homma S, Thompson JL, Pullicino PM, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med 2012; 366:1859.
  26. Lee M, Saver JL, Hong KS, et al. Risk-benefit profile of warfarin versus aspirin in patients with heart failure and sinus rhythm: a meta-analysis. Circ Heart Fail 2013; 6:287.
  27. Hopper I, Skiba M, Krum H. Updated meta-analysis on antithrombotic therapy in patients with heart failure and sinus rhythm. Eur J Heart Fail 2013; 15:69.
  28. Shantsila E, Lip GY. Antiplatelet versus anticoagulation treatment for patients with heart failure in sinus rhythm. Cochrane Database Syst Rev 2016; 9:CD003333.
  29. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2025; 151:e771.
  30. Levine GN, McEvoy JW, Fang JC, et al. Management of Patients at Risk for and With Left Ventricular Thrombus: A Scientific Statement From the American Heart Association. Circulation 2022; 146:e205.
  31. Vaitkus PT, Barnathan ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol 1993; 22:1004.
  32. Keating EC, Gross SA, Schlamowitz RA, et al. Mural thrombi in myocardial infarctions. Prospective evaluation by two-dimensional echocardiography. Am J Med 1983; 74:989.
  33. Cregler LL. Antithrombotic therapy in left ventricular thrombosis and systemic embolism. Am Heart J 1992; 123:1110.
  34. Mansouri P, Jazi ZA, Mansouri MH, et al. Evaluation of the efficacy and safety of rivaroxaban compared to warfarin in patients with left ventricular apical thrombus: a randomized clinical trial. Thromb J 2024; 22:66.
  35. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:e362.
  36. Garg RK, Gheorghiade M, Jafri SM. Antiplatelet and anticoagulant therapy in the prevention of thromboemboli in chronic heart failure. Prog Cardiovasc Dis 1998; 41:225.
  37. Ciaccheri M, Castelli G, Cecchi F, et al. Lack of correlation between intracavitary thrombosis detected by cross sectional echocardiography and systemic emboli in patients with dilated cardiomyopathy. Br Heart J 1989; 62:26.
  38. Sahlén AO, Jiang H, Lau YH, et al. Direct Oral Anticoagulation Versus Warfarin in Left Ventricular Thrombus: Pooled Analysis of Randomized Controlled Trials. J Clin Pharmacol 2023; 63:1101.
  39. Kwok CS, Bennett S, Borovac JA, et al. An evidence-based evaluation of left ventricular thrombus treatment, outcomes, and resolution: a systematic review, pooled analysis and meta-analysis. Coron Artery Dis 2023; 34:260.
  40. Michael F, Natt N, Shurrab M. Direct Oral Anticoagulants vs Vitamin K Antagonists in Left Ventricular Thrombi: A Systematic Review and Meta-analysis. CJC Open 2021; 3:1169.
  41. Robinson AA, Trankle CR, Eubanks G, et al. Off-label Use of Direct Oral Anticoagulants Compared With Warfarin for Left Ventricular Thrombi. JAMA Cardiol 2020; 5:685.
  42. Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation 1987; 75:1004.
  43. Cioffi G, Pozzoli M, Forni G, et al. Systemic thromboembolism in chronic heart failure. A prospective study in 406 patients. Eur Heart J 1996; 17:1381.
  44. Falk RH, Foster E, Coats MH. Ventricular thrombi and thromboembolism in dilated cardiomyopathy: a prospective follow-up study. Am Heart J 1992; 123:136.
  45. Visser CA, Kan G, Meltzer RS, et al. Embolic potential of left ventricular thrombus after myocardial infarction: a two-dimensional echocardiographic study of 119 patients. J Am Coll Cardiol 1985; 5:1276.
  46. Küpper AJ, Verheugt FW, Peels CH, et al. Left ventricular thrombus incidence and behavior studied by serial two-dimensional echocardiography in acute anterior myocardial infarction: left ventricular wall motion, systemic embolism and oral anticoagulation. J Am Coll Cardiol 1989; 13:1514.
  47. Keren A, Goldberg S, Gottlieb S, et al. Natural history of left ventricular thrombi: their appearance and resolution in the posthospitalization period of acute myocardial infarction. J Am Coll Cardiol 1990; 15:790.
  48. Meltzer RS, Visser CA, Fuster V. Intracardiac thrombi and systemic embolization. Ann Intern Med 1986; 104:689.
  49. Lattuca B, Bouziri N, Kerneis M, et al. Antithrombotic Therapy for Patients With Left Ventricular Mural Thrombus. J Am Coll Cardiol 2020; 75:1676.
Topic 3502 Version 38.0

References

1 : Ventricular dysfunction and the risk of stroke after myocardial infarction.

2 : Risk of thromboembolism in heart failure: an analysis from the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT).

3 : Risk of Stroke in Chronic Heart Failure Patients Without Atrial Fibrillation: Analysis of the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORONA) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca-Heart Failure (GISSI-HF) Trials.

4 : Influence of ejection fraction on cardiovascular outcomes in a broad spectrum of heart failure patients.

5 : Efficacy of antithrombotic therapy in chronic heart failure: the HELAS study.

6 : Effect of mitral regurgitation on left ventricular thrombus formation in dilated cardiomyopathy.

7 : Echocardiographic Algorithm for Post-Myocardial Infarction LV Thrombus: A Gatekeeper for Thrombus Evaluation by Delayed Enhancement CMR.

8 : The prevalence, predictors, and outcomes of spontaneous echocardiographic contrast or left ventricular thrombus in patients with HFrEF.

9 : Incidence of post myocardial infarction left ventricular thrombus formation in the era of primary percutaneous intervention and glycoprotein IIb/IIIa inhibitors. A prospective observational study.

10 : Incidence and predictors of early left ventricular thrombus after ST-elevation myocardial infarction in the contemporary era of primary percutaneous coronary intervention.

11 : The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity.

12 : Left ventricular mural thrombi complicating acute myocardial infarction. Long-term follow-up with serial echocardiography.

13 : Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography.

14 : Incidence and natural history of left ventricular thrombus following anterior wall acute myocardial infarction.

15 : Comparison of frequency of left ventricular thrombi in patients with anterior wall versus non-anterior wall acute myocardial infarction treated with antithrombotic and antiplatelet therapy with or without coronary revascularization.

16 : Relationship between degree of left ventricular dysfunction, symptom status, and risk of embolic events in patients with atrial fibrillation and heart failure.

17 : Clinical, imaging, and pathological characteristics of left ventricular thrombus: a comparison of contrast-enhanced magnetic resonance imaging, transthoracic echocardiography, and transesophageal echocardiography with surgical or pathological validation.

18 : Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease.

19 : Detection and characterization of intracardiac thrombi on MR imaging.

20 : 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

21 : 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.

22 : Rivaroxaban in Patients with Heart Failure, Sinus Rhythm, and Coronary Disease.

23 : The Warfarin/Aspirin Study in Heart failure (WASH): a randomized trial comparing antithrombotic strategies for patients with heart failure.

24 : Randomized trial of warfarin, aspirin, and clopidogrel in patients with chronic heart failure: the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial.

25 : Warfarin and aspirin in patients with heart failure and sinus rhythm.

26 : Risk-benefit profile of warfarin versus aspirin in patients with heart failure and sinus rhythm: a meta-analysis.

27 : Updated meta-analysis on antithrombotic therapy in patients with heart failure and sinus rhythm.

28 : Antiplatelet versus anticoagulation treatment for patients with heart failure in sinus rhythm.

29 : 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

30 : Management of Patients at Risk for and With Left Ventricular Thrombus: A Scientific Statement From the American Heart Association.

31 : Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis.

32 : Mural thrombi in myocardial infarctions. Prospective evaluation by two-dimensional echocardiography.

33 : Antithrombotic therapy in left ventricular thrombosis and systemic embolism.

34 : Evaluation of the efficacy and safety of rivaroxaban compared to warfarin in patients with left ventricular apical thrombus: a randomized clinical trial.

35 : 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.

36 : Antiplatelet and anticoagulant therapy in the prevention of thromboemboli in chronic heart failure.

37 : Lack of correlation between intracavitary thrombosis detected by cross sectional echocardiography and systemic emboli in patients with dilated cardiomyopathy.

38 : Direct Oral Anticoagulation Versus Warfarin in Left Ventricular Thrombus: Pooled Analysis of Randomized Controlled Trials.

39 : An evidence-based evaluation of left ventricular thrombus treatment, outcomes, and resolution: a systematic review, pooled analysis and meta-analysis.

40 : Direct Oral Anticoagulants vs Vitamin K Antagonists in Left Ventricular Thrombi: A Systematic Review and Meta-analysis.

41 : Off-label Use of Direct Oral Anticoagulants Compared With Warfarin for Left Ventricular Thrombi.

42 : Increased embolic risk in patients with left ventricular thrombi.

43 : Systemic thromboembolism in chronic heart failure. A prospective study in 406 patients.

44 : Ventricular thrombi and thromboembolism in dilated cardiomyopathy: a prospective follow-up study.

45 : Embolic potential of left ventricular thrombus after myocardial infarction: a two-dimensional echocardiographic study of 119 patients.

46 : Left ventricular thrombus incidence and behavior studied by serial two-dimensional echocardiography in acute anterior myocardial infarction: left ventricular wall motion, systemic embolism and oral anticoagulation.

47 : Natural history of left ventricular thrombi: their appearance and resolution in the posthospitalization period of acute myocardial infarction.

48 : Intracardiac thrombi and systemic embolization.

49 : Antithrombotic Therapy for Patients With Left Ventricular Mural Thrombus.

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