Anti-Coagulation for Left Ventricular Thrombus

Publication: 01/10/2019  --
Last review: 01/01/1900  
Next review: 01/10/2022  
Clinical Guideline
CURRENT 
ID: 6143 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2019  

 

This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Anti-Coagulation for Left Ventricular Thrombus

Summary of Guideline

  • Left ventricular thrombus complicates 4-8% of cases of acute myocardial infarction.
  • Incidence is highest (19%) in anterior ST segment elevation myocardial infarction with left ventricular ejection fraction <50%
  • Diagnosis is usually based on detection of left ventricular thrombus on echocardiography or magnetic resonance imaging carried out to assess left ventricular function after myocardial infarction.
  • Anti-coagulation is recommended to reduce the risk of stroke and thromboembolism.
  • Direct oral anti-coagulant or warfarin therapy should be initiated by the cardiology team and continued in primary care for minimum of 3 months.
  • Repeat imaging and cardiology clinic follow up will be arranged at 3 months to decide whether anti-coagulation can be discontinued.
  • If anticoagulation needs to be continued this will be reviewed again at 6 months

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Background

Left ventricular (LV) thrombus is detectable by echocardiography in 4%-8% of patients with myocardial infarction receiving reperfusion therapy [1,2]. Cardiac magnetic resonance imaging (MRI) or contrast echocardiography are more sensitive at detecting left ventricular thrombus than conventional echocardiography [3]. Incidence is highest in large anterior wall infarcts and in patients who do not receive prompt reperfusion [4,5]. In a recent meta-analysis, 96% of cases of LV thrombus occurred in patients with anterior MI, with incidence reaching 19.2% in patients with anterior myocardial infarction (MI) and left ventricular ejection fraction (LVEF) <50% [6]. The presence of left ventricular thrombus leads to five-fold increased risk of thromboembolism, which occurs in 10-15% of patients without anti-coagulation [7,8]. Most thromboembolic complications occur within the first four months [8]. Echocardiographic evidence of thrombus mobility and protrusion into the left ventricular cavity are major predictors of thromboembolism [7,9-11]. Observational studies indicate that the risk of embolism can be substantially reduced by anti-coagulation with warfarin [8]. Optimum duration of anti-coagulation is unknown, although therapy is usually continued for a minimum of three months. Repeat imaging may be helpful to determine whether thrombus has resolved or become organised, although evidence is limited [4,10,12]. LV thrombus resolves within 3-6 months in the majority (88%) of cases [6]. Anticoagulation reduces the risk of embolization during thrombus resolution but does not necessarily accelerate resolution [5]. Screening of high-risk cases with acute myocardial infarction (anterior infarction + apical wall akinesis) with contrast echo or MRI has been advocated [6]. However, whether reduction in thromboembolism outweighs bleeding risk in patients with small thrombi detected on contrast echocardiography or MRI is unknown and requires further research.

As most patients with left ventricular thrombus will have received a coronary stent, combined therapy with an anticoagulant and anti-platelet agent is usually required.

Experience of direct oral anti-coagulants in patients with left ventricular thrombus is limited. However, direct oral anticoagulants (DOACs) are routinely used in combination with anti-platelet agents to reduce the risk of cardiac thromboembolism in patients with atrial fibrillation undergoing coronary stenting [13-15]. The risk of bleeding is lower when DOACs are used in combination with dual antiplatelet therapy in this setting compared to warfarin in combination with dual antiplatelet therapy [16]. There are also data to support safe and effective use of DOACs to prevent thromboembolism in patients with established thrombus in the left atrium [17,18]. It appears reasonable, therefore, to extrapolate these data to support the use of DOACs to prevent thromboembolism in patients with left ventricular thrombus. In the context of left ventricular thrombus, use of DOACs has been reported in small case series [19] and a small randomized clinical trial comparing apixaban with warfarin is ongoing [NCT02982590].

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Diagnosis

Left ventricular thrombus is usually detected incidentally on echocardiography or MRI carried out to assess left ventricular function following myocardial infarction. On rare occasions, left ventricular thrombus may be identified in patients presenting with an acute atherothrombotic event (e.g. stroke).

Late-presentation anterior infarction, suboptimal reperfusion and severe left ventricular dysfunction indicate a higher risk of left ventricular thrombus.

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Investigation

Echocardiography should be carried out in all patients following myocardial infarction before discharge from hospital to assess left ventricular ejection fraction. Most cases of left ventricular thrombus are detected incidentally on the post-myocardial infarction echocardiogram.

Screening for LV thrombus in high-risk individuals
Patients with the following clinical criteria without detectable thrombus on transthoracic echocardiography should undergo pre-discharge contrast echocardiography or cardiac MRI to exclude left ventricular thrombus [6]:

  • anterior myocardial infarction +
  • infarct related artery wraps around the left ventricular apex on angiography +
  • apical wall akinesia on echocardiography

Detection of LV thrombus on research imaging studies
When LV thrombus is identified in patients within three months of myocardial infarction attending for a research scan, the on-call cardiology registrar or ischaemic heart disease consultant should be informed. The cardiology registrar or consultant is responsible for initiating anti-coagulation, informing primary care and arranging follow-up imaging and clinical review.

Follow-up imaging
Repeat imaging and clinical follow up should be carried out at ~3 months using the same imaging modality by which left ventricular thrombus was diagnosed (echo or MRI) – see below.

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Treatment / Management

Initiation of anti-coagulation (in-patient)
Selection of anti-coagulation therapy should be made by a cardiologist following discussion with the patient and considering renal function, body weight and requirement for concurrent anti-platelet therapy. In most cases, the cardiologist responsible for in-patients with ischaemic heart disease will be responsible for initiation of anticoagulation. All in-patients in whom LV thrombus is detected, who are not under the care of cardiology, should be discussed with the on call cardiology registrar. No oral anticoagulant has a marketing authorisation for thromboembolism prophylaxis in the setting of left ventricular thrombus. This represents an unlicenced use of a licenced medication and should be discussed with the patient and recorded in the clinical notes and discharge advice notification or correspondence.

The following options are recommended:

A: Direct oral anticoagulant (DOAC) (rivaroxaban, dabigatran, apixaban). Treatment with a DOAC should be initiated as soon as left ventricular thrombus is detected. Use the dose licensed for stroke prevention in atrial fibrillation. Edoxaban is not currently recommended due to lack of evidence.

or

B: Warfarin loading and maintenance therapy – target international normalised ratio (INR) 2.5 (range 2.0 – 3.0). Parenteral anticoagulation with low molecular weight heparin should be initiated as soon as left ventricular thrombus is detected and continued until INR ≥2.0 has been achieved. See note below regarding INR monitoring during warfarin initiation.

The information sheet ‘Anti-coagulation for left ventricular thrombus - Information for patients’ should be provided.

Points for consideration when initiating anticoagulation

Timing of diagnosis of left ventricular thrombus. This guidance relates to left ventricular thrombus detected in the early post-myocardial infarction period. If left ventricular thrombus is identified beyond the first three months after myocardial infarction, anti-coagulation in not routinely indicated unless there are features suggesting increased risk of embolisation e.g. persisting disorganized thrombus, severe left ventricular dysfunction, left ventricular aneurysm.

Baseline monitoring. Renal function, liver function, full blood count and clotting screen should be evaluated at baseline. Consider concomitant drug therapy which may interact with warfarin or DOACs in selecting therapy. Consider discussion with pharmacist.

Patients with creatinine clearance <30mL/min. Experience of DOAC use in patients with severe renal impairment is limited. Warfarin is recommended in this group.

Patients with body mass >120kg. Experience of DOAC use in this group is limited and therapeutic levels of anti-coagulation may not be achieved. Warfarin is recommended in this group. If a DOAC is used, referral to the Leeds anti-coagulation service for monitoring of levels is recommended.

INR monitoring during initiation of warfarin in patients receiving anti-platelet therapy. Care is required when initiating warfarin in this group of patients. For in-patient initiation, daily INR measurements are required. Low molecular weight heparin should be discontinued when INR ≥2.0 has been achieved. Similar arrangements should be made in conjunction with the anti-coagulation service for out-patient initiation.

Concomitant anti-platelet therapy in patients with coronary stent. Consider using DOAC rather than warfarin in patients requiring a period of dual anti-platelet therapy following coronary stenting, as the risk of bleeding is lower. Refer to ‘Leeds Teaching Hospitals guidance on anti-platelet therapy in patients receiving oral anti-coagulants for non-valvular atrial fibrillation (NVAF) undergoing Percutaneous Coronary intervention (PCI)’ on Leeds Health Pathways. In general, a DOAC should be used in combination with clopidogrel 75mg daily. Ticagrelor and prasugrel are not currently recommended at LTHT for use in combination with an anti-coagulant. If switching from ticagrelor or prasugrel in the acute setting, a 600mg loading dose of clopidogrel is recommended. Requirement for aspirin therapy should be decided on a case-by-case basis taking into account bleeding risk and atherothrombotic risk (usually maximum 4 weeks; aspirin may be omitted at cardiologist’s discretion).

Dose of DOAC
In the absence of specific dose recommendations for this indication, it is reasonable to use the dose of DOAC licensed for stroke prevention in atrial fibrillation. Refer to product summary of product characteristics (SPC) for information on contra-indications, interactions and dose adjustment in relation to patient age, renal function and body weight.

When used in conjunction with a P2Y12 inhibitor (e.g. clopidogrel) after coronary stent implantation, assess bleeding risk and consider a DOAC regime investigated in clinical trials for patients with atrial fibrillation (13-15) e.g. rivaroxaban 15mg once daily (10mg once a day if CrCl 30 - 50 ml/min), dabigatran 150mg twice daily (110mg twice daily if 80 years old or older) or apixaban 5mg twice daily (2.5mg twice daily if two of: 80 years old or above, creatinine >133 umol/L, weight < 60kg).

 

Duration of anti-coagulation and monitoring

Follow up imaging and out-patient review should be arranged with the ischaemic heart disease team.

Repeat imaging and clinical follow up should be carried out at ~3 months using the same imaging modality by which left ventricular thrombus was diagnosed (echo or MRI).

If left ventricular thrombus has resolved or appears organised at three months, anti-coagulation should be withdrawn. Dual anti-platelet therapy should be resumed in patients who have received a coronary stent to complete the recommended treatment duration (usually 12 months). The decision to stop anti-coagulation and the type and duration of subsequent anti-platelet therapy will be made by the cardiologist and clearly communicated to primary care.

If left ventricular thrombus persists at three months with adverse features (failure to organize, pedunculated appearance) anti-coagulation should be continued with further imaging and clinical review arranged at 6 months.

In some patients with adverse features (e.g. persisting disorganized thrombus, severe left ventricular dysfunction, left ventricular aneurysm) a decision for indefinite anti-coagulation may be made by the cardiologist.

In all cases, the decision to continue or stop anti-coagulation at the three-month or six-month review should be clearly communicated to the patient’s GP.

If during therapy the patient develops a condition which may increase the risk of anti-coagulation, e.g. anaemia, thrombocytopenia, significant bleeding, significant deterioration of renal function, their management should be discussed with the cardiologist.

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Provenance

Record: 6143
Objective:

Aims
To improve the diagnosis and management of left ventricular thrombus in adult patients following myocardial infarction.

Objectives
To provide guidance to cardiologists and primary care physicians on anti-coagulation to prevent thromboembolism in adult patients with left ventricular thrombus within the first three months following acute myocardial infarction.

Clinical condition:

Myocardial infarction

Target patient group: Patients diagnosed with left ventricular thrombus following myocardial infarction
Target professional group(s): Pharmacists
Secondary Care Doctors
Secondary Care Nurses
Primary Care Doctors
Adapted from:

Evidence base

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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
  6. Bulluck H, Chan MHH, Paradies V et al. Incidence and predictors of left ventricular thrombus by cardiovascular magnetic resonance in acute ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: a meta-analysis. J Cardiovasc Magnetic Resonance. 2018; 20:72
  7. Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation 1987; 75:1004.
  8. 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.
  9. 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.
  10. 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.
  11. Meltzer RS, Visser CA, Fuster V. Intracardiac thrombi and systemic embolization. Ann Intern Med 1986;104:689.
  12. Nesković AN, Marinković J, Bojić M, Popović AD. Predictors of left ventricular thrombus formation and disappearance after anterior wall myocardial infarction. Eur Heart J 1998; 19:908.
  13. Gibson CM, Mehran R, Bode C et al. Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing PCI.N Engl J Med. 2016;375:2423-2434.
  14. Cannon CP, Bhatt DL, Oldgren J et al. Dual Antithrombotic Therapy with Dabigatran after PCI in Atrial Fibrillation. N Engl J Med. 2017;377:1513-1524.
  15. Lopes RD, Heizer G, Aronson R, Vora AN, Massaro T, Mehran R, Goodman SG, Windecker S, Darius H, Li J, Averkov O, Bahit MC, Berwanger O, Budaj A, Hijazi Z, Parkhomenko A, Sinnaeve P, Storey RF, Thiele H, Vinereanu D, Granger CB, Alexander JH; AUGUSTUS Investigators. Antithrombotic Therapy after Acute Coronary Syndrome or PCI in Atrial Fibrillation. N Engl J Med. 2019 Mar 17. doi: 10.1056/NEJMoa1817083. [Epub ahead of print]
  16. Sindet-Pedersen C, Lamberts M, Staerk L, et al. Combining oral anticoagulants with platelet inhibitors in patients with atrial fibrillation and coronary disease. J Am Coll Cardiol. 2018;72:1790-1800.
  17. Lip GY, Hammerstingl C, Marin F, Cappato R, Meng IL, Kirsch B, van Eickels M, Cohen A; X-TRA study and CLOT-AF registry investigators. Left atrial thrombus resolution in atrial fibrillation or flutter: Results of a prospective study with rivaroxaban (X-TRA) and a retrospective observational registry providing baseline data (CLOT-AF). Am Heart J. 2016 Aug;178:126-34.
  18. Fleddermann A, Eckert R, Muskala P, et a. Efficacy of direct acting oral anticoagulant drugs in treatment of left atrial appendage thrombus in patients with atrial fibrillation. Am J Cardiol. 2018;Epub ahead of print.
  19. Robinson A, Ruth B, Dent J. Direct oral anticoagualnts compared to warfarin for left ventricular thrombi: a single centre experience. J Am Coll Cardiol. 2018; 17: Suppl. DOI: 10.1016/S0735-1097(18)31522-5

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Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.0

Related information

Conflicts of Interests

Dr Wheatcroft has received speaker fees and funding for conference attendance from companies who manufacture anti-platelet agents and/or DOACs (Bayer, Astra Zeneca, Sanofi-Aventis).

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