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Abstract

Left ventricular thrombus (LVT) complicates both ischemic and non-ischemic cardiomyopathies and is a potential cause of thromboembolic complications such as stroke. Management of LVT in the 21st century is primarily based on studies before the widespread use of potent pharmacological and interventional therapies such as primary percutaneous coronary intervention, especially in the setting of acute myocardial infarction. Though advances in diagnostic technology have improved detection of LVT, clinicians face several uncertainties in the management of LVT in daily practice. The aim of this paper is to examine several controversies in the diagnosis and management of LVT. Prospective studies are needed to advance therapy of LVT.

Keywords

left ventricular thrombus anterior myocardial infarction thrombus

Introduction

With improvement in interventional and pharmacological therapies, patients with cardiovascular disease are enjoying longer lives despite extensive myocardial disease. Left ventricular thrombus (LVT) can complicate left ventricular (LV) systolic dysfunction both in ischemic and non-ischemic cardiomyopathies and can lead to thromboembolic complications such as stroke. Thrombus formation reflects the presence of factors that represent the Virchow’s triad in the ventricle – reduced wall motion, local myocardial injury and hypercoagulability/stasis of blood flow.¹

The prototypical substrate for LVT is a recent anterior myocardial infarction (MI) with an akinetic apex that provides the perfect milieu for thrombus formation. Advances in imaging techniques (contrast echocardiography and MRI) have also increased the sensitivity of diagnosing LVT. Once diagnosed, the initial treatment is anticoagulation.

There are, however, several uncertainties in the management of LVT. Most studies on treatment of LVT occurred before the era of rapid percutaneous coronary intervention (PCI) and without concomitant use of potent dual anti-platelet and ventricular reverse remodeling therapies. The aim of this paper is to examine several controversies in the diagnosis and management of LVT.

Is the incidence of LVT lower in the PCI era?

The overall prevalence of LVT in the general population is low. In a retrospective review of more than 80,000 medical records, the incidence of LVT was 7 per 10,000 patients.² Eighty percent of these cases were related to ischemia, while the rest were due to dilated cardiomyopathy (DCM) and stress-induced cardiomyopathy (8.15% and 4.8% respectively).²

Multiple observational studies have noted LVT in 4–39% of anterior MIs.^1,3–16 The degree of myocardial damage influences thrombus formation. For example, in a recent study 28 out of 65 (43%) patients with anterior ST-elevation MI (STEMI) had LVT compared to only 1 out of 20 (5%) patients with anterior non-STEMI.¹⁷ In addition, there was a significant difference in incidence between patients who presented earlier versus later than 12 h of onset of chest pain (15.4% versus 63.6%).¹⁷ LVT is less frequent in non-anterior MI compared to anterior MI, reflecting the degree of myocardial damage as well as the unique properties of a hypocontractile apex that predispose to LVT (2.5% versus 11.5%).¹⁸ The incidence of LVT in DCM is 11–44%,^17,19,20 but there are insufficient data to study temporal trends. In addition, LVT complicates Chagas disease, where it can be seen in approximately 15% of patients with Chagic cardiomyopathy.^21,22

Figure 1a depicts the temporal trends in incidence of LVT in patients presenting with MI. Incidence was much higher in the pre-PCI era (before 1995) and is generally lower in the current era, with a few exceptions. Assessment of temporal trends is affected by variables such as imaging modality used (echo versus MRI) and delay between the time of MI and imaging (early versus late). Since imaging technology has improved over the years, these trends would suggest that the incidence of LVT has indeed been reduced by timely and effective reperfusion (Figure 1b). However, the two studies with an incidence rate higher than 20% in the current era bear scrutiny. One study included mostly late-presenting patients and those less likely to be treated with PCI,¹¹ while the other was a prospective study in which all patients after an MI underwent echo and MRI at a median of 12 days after MI.³ These studies indicate that despite advances in therapy, LVT may remain underdiagnosed unless a careful and meticulous search (especially a few days to weeks after MI) is undertaken.

Figure 1.

(a) Temporal trends in incidence of LV thrombus (LVT) in patients presenting with anterior myocardial infarction. (b) Cumulative incidence of LVT in studies reported in the pre-PCI era compared to PCI era (before and after 1995).

What are the risk factors for developing LVT?

A Virchow’s triad of factors – reduced ventricular motion, local myocardial injury and hypercoagulability/stasis of flow contribute to formation of LV thrombus.

Reduced ventricular contractility – Blood stagnation in the weak non-contractile segment of the ventricle plays a major role in formation of thrombi. Studies have shown that patients with reduced ejection fraction at admission are more prone to developing LVT.^23–25 Additionally, patients with reduced ejection fraction by the time of discharge are also at a higher risk than those who leave the hospital with a normal ejection fraction.^24,25 Patients with LVT have worse wall motion abnormalities than patients without thrombi.²⁰ Increased LV internal diastolic dimension (odds ratio 1.10) is another risk factor which suggests the importance of overall reduction in ventricular contractility.²¹ Similarly, right ventricular (RV) thrombus may occur in patients with co-existing RV dysfunction.

Local myocardial injury – Patients presenting with STEMI were more likely to have LVT in comparison to patients with non-STEMI (43.1% versus 5%).¹⁷ Severity and depth of cardiac injury correlates with the increase in risk of developing a thrombus. Acar and colleagues noted peak levels for both troponin and CKMB values were significantly higher in patients who were diagnosed with LVT in comparison with the non-thrombus group.¹¹ Mean peak values for troponin were 32.63 versus 18.7 ng/ml and mean peak values for CKMB were 245.47 versus 167.37 IU/L.¹¹ Late presentation after MI (more than 12 h of chest pain onset) is another significant risk factor reflecting more myocardial damage.¹⁷ In addition, delayed percutaneous intervention was an independent predictor in two other studies,^23,24 suggesting the role of ischemia-reperfusion injury in addition to more extensive infarction. Faint antegrade flow (TIMI 1) or no antegrade flow (TIMI 0) before angioplasty is another independent predictor.²⁴ Finally, the apex appears to be uniquely susceptible to LVT formation. In a retrospective study, all patients with LVT were noted to have apical akinesis irrespective of the principle MI location.²³

Hypercoagulability – Patients with MI who develop LVT display hematological abnormalities that suggest a hypercoagulable and pro-inflammatory state. Mean platelet volume (9.03 fl versus 8.06 fl, p-value 0.0001) and white blood count (14,010 versus 11,300 cells per microliter, p-value 0.0001) are more common in patients with MI who develop LVT.¹¹ Mean platelet volume was found to be an independent risk factor of LVT formation with the use of logistic regression analysis. Shacham and colleagues have studied the role of serum inflammatory markers as a predictor for risk of thrombus formation. They reported that patients with LVT had significantly higher C-reactive protein (CRP) values than the non-thrombus group (48 versus 8.4 mg/L). They also concluded that admission CRP and fibrinogen levels are independent predictors of early LVT formation complicating a first anterior wall STEMI.²⁶

What is the best diagnostic modality for diagnosis of LVT?

In the current era, the majority of LVT are diagnosed incidentally by echocardiography after an MI, while some are diagnosed in the search for an embolic pathology in the setting of a stroke or other thromboembolic complication. Echocardiography is readily available, safe and relatively cheap, but is operator-dependent. Improved ultrasound technology and use of harmonic imaging have improved detection of apical LVT. The sensitivity of echocardiography can be further improved by the use of ultrasound contrast agents.²⁷

Cardiac magnetic resonance imaging (CMR) can be considered the gold standard of diagnosis of LVT with cine-CMR and contrast-enhanced CMR (CE-CMR) being the most useful modalities. In most studies comparing CMR and transthoracic echo (TTE), CMR is superior for detection of LVT. Intra- and inter-observer variation for detection of LVT were lower for CMR in comparison to TTE.¹ Sensitivity of routine TTE has been reported in the range 21–94.7%,^1,3,4,9,27 while specificity was 94–98.3%.^1,3,4,27 Thrombi missed by TTE were smaller in size and located at the apex.²⁸ The use of ultrasound contrast agents greatly improves sensitivity of TTE. In one study, the sensitivity of TTE increased from 33% to 61%, specificity from 95% to 99% and accuracy from 82% to 92% by using ultrasound contrast when compared to CMR.²⁷ This is especially true in patients with a layered thrombus (thrombus with no protruding element and which conforms to area of the ventricular wall). Three-dimensional echocardiography may also improve diagnostic accuracy, though it has not been systematically studied (Figure 2). A protruding and mobile thrombus indicates a higher embolic risk compared with a flat, immobile thrombus.

Figure 2.

Illustrative example of the use of echocardiography in the diagnosis of LVT. In this case, while the standard apical four-chamber view (a) was inconclusive, off-axis imaging provided a better appreciation of the size of thrombus (b). Appearance of the same thrombus using ultrasound contrast and live three-dimensional echocardiography (c and d). The protruding nature of the thrombus is better evident with these modalities.

Among CMR modalities, CE-CMR leads to better LVT detection rates than cine-CMR.^9,27,29 In a recent systematic analysis, late gadolinium enhancement by CE-CMR imaging was the most accurate modality for the detection of LVT (sensitivity 88%, specificity 99%), followed by cine-CMR imaging (sensitivity 58–79%, specificity 99%, accuracy 95%, positive predictive value 93–95%, negative predictive value 95–96%), contrast TTE (sensitivity 23–61%, specificity 96–99%, accuracy 92%, positive predictive value 93%, negative predictive value 91%), and, finally, non-contrast TTE (sensitivity 24–33%, specificity 94–95%, accuracy 82%, positive predictive value 57%, negative predictive value 85%). Figure 3 offers an illustrative example.

Figure 3.

Illustrative example of the importance of late gadolinium enhancement (LGE) imaging in detection of left ventricular thrombus. The presence of apical thrombus (arrow) is clearly evident in LGE cardiac magnetic resonance (b) compared to cine-cardiac magnetic resonance (a).

Recent evidence highlights that delay of imaging for more than 5 days after acute MI was associated with significantly higher detection rates of LVT compared to imaging within 5 days. Subgroup analysis showed that CMR performed 9–12 days post-MI gives the highest detection rate.⁸ This delay is often not practical in current medical practice (in the United States and most developed countries) where patients with MI are often discharged in 48–72 h.

In this context, it is important to understand the limitations of contrast ventriculography that is often performed at the time of percutaneous intervention. Contrast ventriculography provides good specificity (85–90%) but poor sensitivity (30%). It is performed soon after an MI, is not practical for repeat evaluation of thrombus and carries a small risk of systemic embolization during catheter manipulation.³⁰

Despite its diagnostic superiority, CMR is costly, time consuming and not available in all centers. It is thus impractical to perform CMR in all cases of MI. A practical approach to improve diagnostic sensitivity is the following: transthoracic echocardiography should be performed in all patients with MI (even in those with contrast ventriculography). Ultrasound contrast should be used in all patients with poor ultrasound windows and in patients with apical wall motion abnormality. CMR should be performed where contrast-enhanced echo is non-diagnostic. An alternative approach is to perform contrast CMR in all patients with reduced apical wall motion on non-contrast echo. This is 100% sensitive for detection of LVT after MI and prevents unnecessary CMR.⁹

What is the impact of pharmacological therapy on incidence of LVT?

The role of medical therapy in the reduction of the incidence of LVT is less understood. Current recommendations for treatment of acute MI include the use of beta blockers and ACE inhibitors, which decrease the extent of myocardial injury and reduce the mortality rate. No systematic study has investigated the effect of these therapies in reduction of LVT formation.

In GISSI-3 trial patients, no significant difference was found between the rates of LVT in patients who received oral beta blockers compared to those who did not.¹⁸ LVT formation was also similar in patients treated with or without aspirin, nitrates and lisinopril. The effect of routine dual anti-platelet therapy in reducing LVT is also less understood. Currently, dual anti-platelet therapy with aspirin and a P2Y₁₂ inhibitor is used in patients with MI who were managed either medically or with PCI. It would be intuitive to assume this would help reduce thrombus formation. However, these agents have little inhibitory effect on thrombin and fibrin formation. Similarly, no comparative data for use of GpIIb–IIIa inhibitors exist. A prospective study demonstrated that the incidence of LVT while patients received PCI and Gp IIb–IIIa inhibitors was 10.8% for anterior MI and was less compared to the pre-PCI era (no active control group).³¹

Overall, current evidence suggests that the most important means of reducing LVT formation is prompt revascularization and preservation of LV myocardial function.

Once diagnosed, how long should anticoagulant therapy be used in treatment of LVT?

Anticoagulant therapy is used to reduce embolic complications from LVT while improved cardiac function and innate fibrinolytic mechanisms help resolve the thrombus. Vitamin K antagonists such as warfarin have been used and their efficacy and safety have been evaluated in non-randomized studies. Table 1 summarizes the recommendations of three major scientific societies in the treatment of LVT. While the ACCF/AHA guidelines do not prescribe a defined duration,³² the ACCP guidelines suggest 3 months of anticoagulation.³³ The ESC guidelines define 6 months of anticoagulation while acknowledging that the duration has never been tested in the era of dual anti-platelet therapy.³⁴ Table 1 summarizes the various major society guidelines in the management of LVT.

Table 1.

Summary of recommendations of the American College of Cardiology (ACCF/AHA), American College of Chest Physicians (ACCP) and European College of Cardiology (ESC) for treatment of left ventricular thrombus (LVT).

ACCFAHA 2013	Anticoagulation with warfarin is reasonable for patients with ST-elevation myocardial infarction (STEMI) and asymptomatic LV mural thrombi (class IIa, LOE C). Duration can be limited to 3 months in patients with or at risk for LVT*, whereas continuation of dual anti-platelet therapy (DAPT) as per ACS recommendations.
ACCP 2012	Patients with anterior myocardial infarction (MI) and LVT, or at high risk for LVT*: No stenting : warfarin plus low-dose aspirin 75–100 mg daily for the first 3 months over single anti-platelet therapy or DAPT (Grade 1B). Thereafter, recommend discontinuation of warfarin and continuation of anti-platelet therapy per the ACS recommendations. Bare-metal stent (BMS) placement : Triple therapy^# for 1 month over DAPT; warfarin and single anti-platelet therapy for the second and third month; discontinuation of warfarin thereafter and resumption of DAPT for up to 12 months (Grade 2C). Drug-eluting stent (DES) placement : Triple therapy^# for 3–6 months (Grade 2C); discontinue warfarin thereafter and continuation of DAPT for up to 12 months.
ESC 2012	Anticoagulation should be considered in patients with large anterior wall motion abnormalities, if they are at low risk of bleeding, to prevent the development of thrombi. Definite thrombus : Oral anticoagulant therapy with warfarin for up to 6 months. However, optimal duration of triple antithrombotic therapy is unknown and should take into account the relative risks of bleeding and stent thrombosis. Repeated imaging of the left ventricle after 3 months – consider discontinuation of anticoagulation earlier than 6 months, if no evidence of thrombus, particularly if there is recovery of apical wall motion.

(*)

High risk for LVT is defined as patients with ejection fraction less than 40%, anteroapical wall motion abnormality.

(#)

Triple therapy includes warfarin (INR target 2–3), low-dose aspirin (75–100 mg) and clopidogrel 75 mg.

Target INR for warfarin therapy is 2.5, maintaining a range between 2–3.³⁵ In general, duration of therapy <3 months leads to a higher rate of recurrence. In one study, 2 months of treatment was enough to resolve 12 thrombi, but 5 recurred after stopping warfarin.³⁶ Though low molecular weight heparin has been studied, the use of long-term subcutaneous injections and cost make it a less favored treatment option.

What is the risk of thromboembolism in patients with LVT?

While older studies reported a higher incidence of thromboembolism despite anticoagulation, the risk appears to be lower in the current era. Figure 4a depicts the decreasing incidence of thromboembolism in studies over the years, while Figure 4b provides a cumulative incidence of thromboembolism in the pre- versus post-PCI era (before and after 1995). This is likely a testament to the use of better ventricular remodeling therapies, dual anti-platelet therapy (DAPT) as well as better time in therapeutic range with warfarin. Most embolic events occur in the first 3–4 months after MI.³⁷ In addition, risk of thromboembolism appears to be higher with non-ischemic cardiomyopathies. In one study, significant independent predictors of post-treatment thromboembolism were dilated cardiomyopathy (HR 61.3), previous cerebrovascular accident (CVA) (HR 7.06), female gender (HR 7.11) and larger LV end diastolic diameter (HR 1.15).² Thrombus usually effects the later stages of dilated cardiomyopathy (compared to acute phases of myocardial infarction) where the LV has remodeled despite effective medical therapy.

Figure 4.

(a) Incidence of thromboembolism in left ventricular thrombus (LVT). (b) Cumulative incidence of thromboembolism with LVT in studies reported before and after 1995.

What is the optimal treatment for persistent or recurrent LVT?

If LVT recurs after resolution, longer-term anticoagulation may be indicated. The recurrence rate after 6 months of anticoagulation is about 18.5%.³⁸ The treatment of persistent LVT despite anticoagulation is, however, uncertain. Some LVT become organized and may never resolve. Echocardiographically they appear flat, immobile and may even be calcified. However, it is often challenging to distinguish between an organized old thrombus and a new thrombus. Many experts suggest that if the thrombus is old and has organized, anticoagulation can be stopped since endothelialization of the thrombus reduces its embolic potential.^39,40

CMR characteristics enable distinction between acute versus older thrombus. Acute thrombus shows high signal intensity on T1- and T2-weighted images while older thrombus has low signal intensity in both T1 and T2 sequences and occasionally shows evidence of calcification.⁴¹ Presence of an immobile thrombus with no protruding elements also suggests low embolic potential.

It is important to understand that thromboembolism is uncommon in the presence of a persistent thrombus after an MI. In a landmark study of longitudinal follow-up of patients with LVT after anterior MI who did not receive anticoagulation, thrombus was persistent in 8 (38%) and 5 (24%) of the 21 patients at 1 and 2 years respectively.¹³ No episodes of thromboembolism occurred in these patients. In clinical practice, however, there is considerable anxiety (both among patients and clinicians) with cessation of anticoagulation in the presence of a persistent thrombus. It is important to discuss the risks and benefits of chronic anticoagulation and lack of scientific evidence behind either decision. In Figure 5 we describe a decision-making flowchart that highlights areas of therapeutic equipoise in the management of anticoagulation in patients with LVT. A prospective, randomized controlled trial is needed to compare the merits of cessation versus maintenance of anticoagulation in these cases.

Figure 5.

Flowchart for guiding left ventricular thrombus management after myocardial infarction in the authors’ practice. The cells in orange are management decisions faced by clinicians for which no evidence exists.

Role of non-vitamin K antagonist oral anticoagulants

Data on the use of non-vitamin K antagonist oral anticoagulants (NOACs) to treat LVT is limited to case reports and series.^42–48 Despite the practical advantages of NOACs (predictable dosing, lack of need for regular monitoring), their use instead of warfarin cannot be recommended due to the lack of evidence that they prevent systemic embolism.

When an NOAC is considered, a major issue for clinicians to consider is the dose of NOAC – should one use the dose required to prevent thrombus in atrial fibrillation or the dose approved for treatment of venous thromboembolism (VTE)? Depending on the NOAC used, these doses may be different (for example, while dabigatran 150 mg BID is approved for both indications in the United States, rivaroxaban is approved at 20 mg daily for atrial fibrillation (AF) indication while the dose is 15 mg twice daily for 21 days followed by 20 mg daily in the treatment of VTE). While it would be intuitive to use the VTE treatment dose since a thrombus is already present, the effect on bleeding rates especially in the context of DAPT is unknown.

Though a randomized controlled trial may be optimal, prospective registries may be useful and more practical in helping understand the efficacy and safety of NOACs in the setting of LVT. Warfarin is the preferred drug till such evidence is available.

Is there a role for prophylactic anticoagulation to prevent LVT?

The role of prophylactic anticoagulation in patients with a large anterior MI to reduce LVT formation is unknown. There are no prospective studies to address this question in the modern era of rapid reperfusion, effective neurohumoral blockade and DAPT. Despite this, both the ACCP and the ESC guidelines suggest that anticoagulation may be considered in those patients with a large anterior wall MI.^33,34 If anticoagulation is chosen for this indication, it should be limited to 3 months (ACCP guidelines).³³

Additional clinical dilemmas

In addition to the above clinical scenarios, there are several other instances in which clinical judgment is required. For example, what is the optimal duration of anticoagulation in patients who suffered systemic embolism during anticoagulation? Are they at a higher risk of recurrent events and should long-term anticoagulation be considered? Should anticoagulation be recommended in patients with ischemic or dilated cardiomyopathy who have suspected embolic stroke but for whom no LVT is detected by imaging? In the absence of evidence, discussions between patient and physician with careful consideration of risks and benefits should guide decision-making in these cases.

Summary

We have summarized the current knowledge of the diagnosis and management of LVT. Most evidence that forms the basis of current guidelines is from an earlier era with markedly different management practices. Clinicians will continue to face uncertainty in decision-making till prospective studies are conducted in the modern era.

Footnotes

Funding

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Conflict of interest statement

The authors declare that there is no conflict of interest.

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Challenges in management of left ventricular thrombus

Abstract

Keywords

Introduction

Is the incidence of LVT lower in the PCI era?

What are the risk factors for developing LVT?

What is the best diagnostic modality for diagnosis of LVT?

What is the impact of pharmacological therapy on incidence of LVT?

Once diagnosed, how long should anticoagulant therapy be used in treatment of LVT?

What is the risk of thromboembolism in patients with LVT?

What is the optimal treatment for persistent or recurrent LVT?

Role of non-vitamin K antagonist oral anticoagulants

Is there a role for prophylactic anticoagulation to prevent LVT?

Additional clinical dilemmas

Summary

Footnotes

Funding

Conflict of interest statement

References