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Circulation. 2022;146:00–00. DOI: 10.1161/CIR.0000000000001092 TBD TBD, 2022
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? 2022 American Heart Association, Inc.
AHA SCIENTIFIC STATEMENT
Management of Patients at Risk for and With
Left Ventricular Thrombus: A Scientific Statement
From the American Heart Association
Glenn N. Levine, MD, FAHA, Chair; John W. McEvoy, MB, BCh, BAO, MEHP, MHS, PhD, Vice Chair; James C. Fang, MD;
Chinwe Ibeh, MD; Cian P. McCarthy, MB, BCh, BAO; Arunima Misra, MD; Zubair I. Shah, MD; Chetan Shenoy, MBBS, MS;
Sarah A. Spinler, PharmD, FAHA; Srikanth Vallurupalli, MD; Gregory Y.H. Lip, MD; on behalf of the American Heart Association
Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; and Stroke Council
ABSTRACT: Despite the many advances in cardiovascular medicine, decisions concerning the diagnosis, prevention, and
treatment of left ventricular (LV) thrombus often remain challenging. There are only limited organizational guideline
recommendations with regard to LV thrombus. Furthermore, management issues in current practice are increasingly
complex, including concerns about adding oral anticoagulant therapy to dual antiplatelet therapy, the availability of direct
oral anticoagulants as a potential alternative option to traditional vitamin K antagonists, and the use of diagnostic modalities
such as cardiac magnetic resonance imaging, which has greater sensitivity for LV thrombus detection than echocardiography.
Therefore, this American Heart Association scientific statement was commissioned with the goals of addressing 8 key clinical
management questions related to LV thrombus, including the prevention and treatment after myocardial infarction, prevention
and treatment in dilated cardiomyopathy, management of mural (laminated) thrombus, imaging of LV thrombus, direct oral
anticoagulants as an alternative to warfarin, treatments other than oral anticoagulants for LV thrombus (eg, dual antiplatelet
therapy, fibrinolysis, surgical excision), and the approach to persistent LV thrombus despite anticoagulation therapy. Practical
management suggestions in the form of text, tables, and flow diagrams based on careful and critical review of actual study
data as formulated by this multidisciplinary writing committee are given.
Key Words: AHA Scientific Statements ? anticoagulants ? thrombosis
D
espite the many advances in cardiovascular medi-
cine, decisions concerning the diagnosis, preven-
tion, and treatment of left ventricular (LV) thrombus
often remain challenging. There are only limited Ameri-
can Heart Association (AHA), American Stroke Associa-
tion (ASA), and American College of Cardiology (ACC)
guideline recommendations with regard to LV throm-
bus
1,2
and limited recommendations in other organiza-
tional guidelines and expert consensus documents.
3–8
Management issues in current practice are increasingly
complex, including concerns about adding oral anticoag-
ulant (OAC) therapy to dual antiplatelet therapy (DAPT),
the availability of direct OACs (DOACs) as a potential
alternative option to traditional vitamin K antagonists
(VKA; predominantly warfarin), and the use of diagnostic
modalities such as cardiac magnetic resonance (CMR)
imaging, which has greater sensitivity for LV thrombus
detection than echocardiography.
There are on the order of 1 million myocardial infarc-
tions (MIs) each year in the United States alone.
9
The
incidence of LV thrombus after anterior ST-segment ele-
vation MI (STEMI) varies widely in different reports, from
4% to 39%, likely reflecting the patient population stud-
ied, timing and frequency of screening, and era of obser-
vation,
10,11
and would probably be higher than reported
in most series if CMR had been used routinely.
12–15
Although the temporal incidence of LV thrombus after
MI may be decreasing,
10,11,16
likely related to improved
reperfusion interventions, the risk of LV thrombus in
such patients remains significant.
16,17
Furthermore, it
is estimated that there are many millions of patients
in the United States alone with dilated (nonischemic)
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cardiomyopathy (DCM),
18,19
and to our knowledge there
are no study data showing that the risk of LV thrombus
in those with DCM has decreased substantially over the
past decades. The incidence of LV thrombus in DCM
may be anywhere between 2% and 36%.
17,20–22
Thus, a
large number of patients are potentially at risk for devel-
oping or do develop LV thrombus. Furthermore, depend-
ing on thrombus morphology and the time of follow-up,
LV thrombus has in the past been associated with up to
a 22% risk of embolization
20–23
and a 37% risk of major
adverse cardiovascular events (MACEs).
17
Therefore, this AHA scientific statement was commis-
sioned with the goals of addressing 8 key clinical man-
agement issues (Table 1) related to the management of
patients at risk for and with LV thrombus.
METHODOLOGY
To develop this scientific statement, writing committee
members were identified and selected from a broad ar-
ray of relevant areas of expertise related specifically to
addressing the aforementioned clinical questions on LV
thrombus, including heart failure, coronary artery disease,
preventive cardiology, stroke, anticoagulation, pharmaco-
therapy, echocardiography, CMR, and guideline/scientific
statement methodology. The writing group searched for
studies on LV thrombus on PubMed, Google Scholar, and
other sources using such search terms as thrombus, an-
ticoagulation, warfarin, DOAC, echocardiography, CMR,
cardiomyopathy, heart failure, and MI. Relevant studies
were identified and reviewed.
In general, OAC was considered to be treatment with
a VKA with a target international normalized ratio (INR)
of 2 to 3 or full-dose DOAC (at doses used in contem-
porary trials for the prevention of cardioembolic event in
patients with atrial fibrillation and in trials comparing VKA
with DOAC for the treatment of LV thrombus). Except
for 1 trial that specifically studied the effect of low-dose
DOAC on LV thrombus, all studies in this scientific state-
ment address full-dose anticoagulation, and suggested
management strategies given should not be extrapolated
to low-dose DOAC.
Consistent with recent AHA guidance on scientific
statements, we have striven to keep this document
as concise and readable as possible while seeking to
address the many questions that caregivers may have
on this topic. For this scientific statement, we have con-
structed a Study Summary Tables Supplement, which
summarizes in greater detail the specifics of studies
discussed in this document and reviewed by the writ-
ing committee in formulating the text and conclusions.
For all sections, a primary author without relevant
relationships with industry and ≥1 secondary authors
drafted the initial text and conclusions. All sections,
suggested management, tables, and the key flow dia-
gram were then presented, reviewed, and discussed
by all writing group members, and the manuscript was
then revised according to those reviews and discus-
sions. Consensus was reached for all conclusions and
suggested management after 2 further conference
calls and additional vetting through group emails. The
manuscript was then reviewed by 3 external reviewers
and revised accordingly. The finalized manuscript was
approved by all writing group members.
PATHOPHYSIOLOGY
A commonly accepted paradigm (based on Virchow’s
triad of thrombogenesis) posits the pathogenesis of LV
thrombus as occurring as a result of the interplay of 3
factors: (1) stasis attributable to reduced ventricular func-
tion, (2) endocardial injury, and (3) inflammation/hyperco-
agulability (Figure 1). The relative contributions of each
of these factors to LV thrombus formation depend on the
cause of the myocardial dysfunction and its duration. Al-
though regional endocardial injury and inflammation may
be the dominant factors after an acute MI, stasis attribut-
able to globally reduced LV function may be the key factor
in DCM.
Traditionally, LV thrombus is considered to form in
the milieu of significant myocardial dysfunction with
low LV ejection fraction (LVEF). After anterior wall MI,
reduced LVEF is a significant risk factor for thrombus
formation, and most thrombi occur in the area of api-
cal wall motion abnormalities in hypokinetic, akinetic, or
Table 1. Eight Key Clinical Management Issues Related to
the Management of Patients at Risk for and With LV Thrombus
1. Is echocardiography adequate for detection of suspected LV thrombus, or
is CMR (or cardiac CT) indicated when there is concern for LV thrombus?
2. In the era of DAPT after ACS and PCI, which patients should be consid-
ered for OAC therapy after anterior/apical MI and akinesis, particularly
given the increased bleeding rates with combined OAC therapy and
antiplatelet therapy?
3. In those patients with acute MI with visualized LV thrombus, when (if
ever) can anticoagulation be stopped? Is a single echocardiogram after
3–6 mo of therapy not demonstrating LV thrombus enough to confidently
discontinue?
4. Which, if any, patients with DCM or HFrEF (not related to acute MI)
should be treated with preventive (prophylactic) OAC?
5. In those with DCM or HFrEF who form LV thrombus and thus may have
a predilection to do this, can OAC ever be stopped (even if a follow-up
echocardiogram demonstrates LV thrombus resolution)?
6. Is anticoagulation really indicated for laminated thrombus (not a more
mobile, round, mural thrombus)?
7. Is DOAC a reasonable alternative to warfarin for the prevention and treat-
ment of LV thrombus?
8. What management options are there in patients with persistent LV throm-
bus despite therapy?
ACS indicates acute coronary syndrome; AMI, acute myocardial infarction;
CMR, cardiac magnetic resonance; CT, computed tomography; DAPT, dual an-
tiplatelet therapy; DCM, dilated cardiomyopathy; DOAC, direct oral anticoagu-
lant; HFrEF, heart failure with reduced ejection fraction; LV, left ventricular; MI,
myocardial infarction; OAC, oral anticoagulant; and PCI, percutaneous coronary
intervention.
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dyskinetic (aneurysm) segments. Regional LV dysfunction
and reduced and abnormal kinetic energy flow patterns
within the LV can predispose to LV thrombus even in the set-
ting of only mild to moderate LV systolic dysfunction.
24,25
In the acute MI setting, the severity and extent of car-
diac injury increase the risk of developing an LV throm-
bus. LV thrombus is more common in STEMI compared
with non–STEMI. Larger injury (higher peak troponins),
delayed reperfusion attributable to late presentation, and
faint or no antegrade coronary flow (TIMI [Thrombolysis
in Myocardial Infarction] grade 0 or 1) after reperfusion
are other risk factors.
26
Monocytes and macrophages
play an important role in healing after acute MI, and pre-
liminary studies suggest that altered monocyte expres-
sion through compromised extracellular remodeling
(eg? abnormal collagen I production) and prolonged loss
of integrity of endocardium predispose to LV thrombus
formation.
27
After an anterior wall MI, higher mean platelet
volume, C-reactive protein, and fibrinogen levels also are
associated with LV thrombus formation.
28,29
Lower LVEF and the presence of scar (indicated by
the presence and extent of delayed gadolinium enhance-
ment by CMR) are risk factors for LV thrombus formation
in DCM.
30
Inflammation, hypercoagulability, and endo-
cardial involvement by specific disease processes (eg,
amyloidosis, eosinophilic myocarditis) are also important
pathophysiological mediators in DCM that may increase
the risk of LV thrombus formation.
31–36
However, data in
relation to specific DCM causes are sparse on both LV
thrombus risk and the impact on clinically relevant throm-
bus/thromboembolism.
The key relevant studies on LV thrombus pathophysi-
ology are summarized in the Study Summary Tables Sup-
plement.
IMAGING OF LV THROMBUS
The accurate detection of LV thrombus directly affects
treatment and clinical outcomes. Transthoracic echo-
cardiography is the standard imaging technique for the
detection of LV thrombus. The use of ultrasound-enhanc-
ing-agent during echocardiography may up to double the
sensitivity of LV thrombus detection.
15
Thus, it would seem
advisable to administer an echocardiography-enhancing
agent to increase sensitivity in patients in whom there
is concern for LV thrombus such as those with acute MI
with anteroapical akinesis (or dyskinesis) and in those
with suspected cardioembolic stroke. Transesophageal
echocardiography does not generally improve visualiza-
tion of the LV apex
16
and is not regarded as a useful
secondary imaging modality for the assessment of LV
thrombus.
Data on the use of cardiac computerized tomogra-
phy for the detection of LV thrombus are limited to case
reports and small series.
37
No studies have validated
cardiac computerized tomography–detected LV throm-
bus by pathology or clinical outcomes. Nevertheless, it is
recognized that computerized tomography, whether done
specifically as a cardiac study or for extracardiac indica-
tions, may incidentally identify LV thrombus.
Late gadolinium enhancement (LGE) imaging on
CMR has been validated as a technique to detect LV
thrombus through verification by pathology,
38
and the
finding of CMR-detected LV thrombus is associated
with increased short-term (6 months)
38
and long-term
(median, 3.3 years)
13
embolic events. Studies using LGE
CMR as the reference standard have demonstrated that
echocardiography has a low sensitivity for the detection
of LV thrombus. One meta-analysis of 3 studies compris-
ing a total of 431 patients with STEMI found a sensitiv-
ity of 29% for echocardiography with LGE CMR as the
reference standard.
12
Although the use of an ultrasound-
enhancing agent improves the sensitivity of echocardiog-
raphy, it is still substantially lower compared with LGE
CMR.
13–15
LV thrombi detected by LGE CMR but not by
echocardiography tend to be small in volume and mural
in morphology.
13,15
The superiority of LGE CMR to detect LV thrombus
is not simply related to the higher-resolution anatomic
imaging; it is also related to tissue characterization of
LV thrombus by LGE CMR, which, because of the lack
of vascularity of LV thrombus and thus lack of LGE, eas-
ily distinguishes it from the surrounding myocardium
(Figure 2).
13–15,38
CMR factors associated with increased risk for LV
thrombus include severe LV systolic dysfunction,
13,38
high
myocardial scar burden,
13,38
apical wall motion abnormali-
ties after an acute MI,
24
history of acute cardioembolic
event,
39
and LV aneurysm.
40
There are limited data on whether detection by CMR of
LV thrombi not diagnosed by echocardiography actually
leads to improved outcome. In 1 nonrandomized analysis
Figure 1. LV dysfunction, endocardial injury, and
inflammation/hypercoagulability (Virchow’s triad)
contribute to the formation of LV thrombus in different
cardiac conditions.
LV indicates left ventricular.
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of 110 patients found to have LV thrombus on CMR (89%
of whom were started or continued on an anticoagulant),
in those who had CMR- but not echocardiography-
detected LV thrombi, there was no statistically significant
difference in the incidence of the composite embolic
end point compared with those in whom LV thrombus
was detected by both echocardiography and CMR.
13
It is
unknown whether the patients with LV thrombus detected
by CMR but not by echocardiography were treated with
anticoagulation and? if not? whether they would have had
a higher risk of embolism than patients with LV throm-
bus confirmed by both CMR and echocardiography who
were treated.
CMR may be most appropriate (1) when there is the
suggestion of a possible LV thrombus on echocardio-
gram but echocardiography imaging (even with an ultra-
sound enhancing agent) is not diagnostic and (2) when
echocardiography does not demonstrate LV thrombus
but a clinical concern (eg, cardioembolic stroke) remains.
The key relevant studies on imaging of LV throm-
bus are summarized in the Study Summary Tables
Supplement.
PREVENTION OF LV THROMBUS AFTER
ACUTE MI
LV thrombus is a well-established complication of MI,
particularly for STEMI involving the anteroapical wall
with associated wall motion abnormalities, and is a po-
tential precursor to embolic events. The incorporation of
prompt reperfusion strategies, initially with thrombolysis
and subsequently with percutaneous coronary interven-
tion (PCI), into standard treatment algorithms for STEMI
seems to have reduced, but not eliminated, the risk of LV
thrombus formation.
Evidence for anticoagulation strategies to prevent
LV thrombus is limited and dated. In a meta-analysis
of 307 patients with anterior MI from 4 small trials in
the prereperfusion era (1980s), therapeutic anticoagu-
lation with intravenous heparin, VKA, or both, agents
reduced the incidence LV thrombus (odds ratio [OR],
0.32 [95% CI, 0.20–0.52]), but no data on safety events
were reported, and these trials were underpowered to
determine whether there was a beneficial reduction in
MACEs or systemic embolism.
41
Notably, these trials
were undertaken among patients who did not receive
reperfusion (PCI or thrombolysis), a P2Y
12
inhibitor, and
rarely received aspirin. Furthermore, the duration of anti-
coagulation in these trials was short (predominantly in-
hospital treatment only). A subsequent 1997 randomized
trial of dalteparin therapy in 776 patients with anterior
MI treated with thrombolytic therapy reported a reduced
incidence of a composite end point of LV thrombus for-
mation or systemic embolism but with increased rates of
major bleeding and without a reduction in arterial embo-
lism alone or death.
42
Participants in this trial received
aspirin (but not a P2Y
12
inhibitor), and the duration of
dalteparin treatment was again brief (mean follow-up, 9
days).
No published randomized trials specifically address
full-dose anticoagulation for the prevention of LV throm-
bus among patients with MI in the PCI era. Several
contemporary observational studies have suggested
that the addition of anticoagulation to DAPT to prevent
LV thrombus among patients with anterior MI is not
Figure 2. Examples of LV thrombus (red
arrows) visualized by both CMR and
echocardiography (patient A) and by only
CMR (patient B).
CMR indicates cardiac magnetic resonance;
and LV, left ventricular. Adapted with permission
from Velangi et al.
13
Copyright ? 2019 American
Heart Association, Inc.
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associated with a reduction in MACEs
43–45
and may in
fact increase major bleeding.
46–48
However, these obser-
vational studies are limited by significant biases, includ-
ing indication bias. Nonetheless, studies of combination
antiplatelet and anticoagulant therapy in patients with
other indications for OAC (most commonly atrial fibrilla-
tion) have clearly demonstrated a several-fold increased
risk of bleeding.
49,50
Collectively, historical clinical trials suggest that short-
term prophylactic anticoagulation may reduce the risk of
LV thrombus formation among patients with anterior MI,
although these trials were underpowered to determine
whether such prophylactic anticoagulation led to a clini-
cally relevant reduction in systemic embolism or MACEs.
The 2013 ACC/AHA STEMI guideline, based on Level
of Evidence C, gives a Class IIb indication (may be con-
sidered) for prophylactic anticoagulation among patients
with STEMI and anterior apical akinesis or dyskinesis at
risk for LV thrombus, with a duration that can be limited
to 3 months.
1
In our more current review of the literature,
we found few data that clearly support routine antico-
agulation in the current reperfusion/coronary stenting/
DAPT era, nor did we find data supporting this specific
duration of 3 months. Thus, factors such as perceived
risk of thrombus formation, bleeding risk with combined
antiplatelet and anticoagulant therapy, and patient pref-
erence should be taken into account when deciding on
whether to initiate prophylactic anticoagulation.
Recently, 1 modest-sized single-center, open-labeled
randomized trial of 279 patients specifically examined
whether low-dose anticoagulation (rivaroxaban 2.5
mg twice daily for 30 days) in addition to DAPT could
decrease the risk of LV thrombus compared with DAPT
alone.
51
The addition of low-dose rivaroxaban compared
with no such therapy lowered the risk of LV thrombus for-
mation (0.7% versus 8.6%; hazard ratio, 0.08 [95% CI,
0.01–0.62]), as well as net adverse clinical events, with-
out increased bleeding. In addition to other limitations of
the trial (eg, single center, open label), there was a high
rate of patient dropout (16.5%), and >75% of patients
had an LVEF>45%.
51,52
Although a practice of routine prophylactic anticoagu-
lation in all patients does not appear to be supported by
data, consideration of the pros and cons of prophylac-
tic anticoagulant therapy to prevent LV thrombus in this
setting on a patient-by-patient basis seems prudent. If
prophylactic anticoagulation is initiated after MI, we sug-
gest a 1- to 3-month duration because the risk of LV
thrombus formation is highest within the first month after
MI before declining.
53–55
The risk of LV thrombus formation after MI may be
greatest in the first 2 weeks, and several studies have
found increased incidence of LV thrombus detection by
transthoracic echocardiography (or CMR) when per-
formed 1 to 2 weeks after MI (compared with when per-
formed in the first several days after MI).
16,53–58
Therefore,
in patients after MI with anteroapical akinesis or dyski-
nesis in whom no LV thrombus is visualized in the first
or several days after MI and anticoagulation initiation is
not planned, a focused follow-up echocardiogram with
an intravenous ultrasound-enhancing agent (or CMR if
the echocardiography image quality is poor) might be
considered. The timing of such a limited follow-up echo-
cardiogram could be just before discharge in those with
prolonged (eg, >3–7 days) hospital stays or within sev-
eral weeks after MI (as has been suggested in a recent
review
16
) for those discharged within ≈3 days of presen-
tation. At present, however, it should be noted that there
are no good study data that such a strategy of repeat
imaging actually leads to a reduction in embolic events.
The key relevant studies on prevention of LV thrombus
after acute MI are summarized in the Study Summary
Tables Supplement.
TREATMENT OF LV THROMBUS AFTER
ACUTE MI
The formation of LV thrombus after acute MI is associated
with a 5.5-fold increased risk of embolic events compared
with no thrombus.
41
Untreated, the annual stroke or sys-
temic embolization rate is ≈10% to 15%. Protruding and
mobile thrombi are perceived to be more likely to embolize
than immobile, calcified, and laminated thrombi.
23,59–61
Limited evidence suggests that anticoagulation therapy
is more likely to resolve LV thrombus and to lower embolic
risk compared with no or subtherapeutic anticoagulation.
One small double-blind randomized controlled trial found
that complete thrombus resolution occurred more fre-
quently among those who received warfarin compared
with those who received no warfarin or antiplatelet ther-
apy (60% versus 10%; P<0.01). LV thrombus resolution
was also more common in individuals who received aspi-
rin at a higher dose than used in contemporary practice
(600 mg daily) compared with no warfarin or antiplatelet
therapy (45% versus 10%; P<0.01).
62
In a meta-analysis
of 7 observational studies including 270 patients with LV
anterior wall MI and LV thrombus, systemic anticoagula-
tion was associated with a lower risk of embolic events
(OR, 0.14 [95% CI, 0.04–0.52]).
41
In a more recent study,
among patients treated with warfarin, greater time in ther-
apeutic range (TTR) was associated with less systemic
thromboembolism (TTR ≥50%, 2.9%; TTR <50%, 19%;
P=0.036).
63
The magnitude of benefit with good antico-
agulation control (commonly defined when warfarin is used
with a TTR ≥70%) likely outweighs the potential increased
risk for bleeding among patients with LV thrombus, even in
the presence of antiplatelet therapy.
The optimal duration of anticoagulation for the treat-
ment of LV thrombus after MI is uncertain, with no ran-
domized controlled trials examining alternative durations
of therapy to date. The 2013 ACC/AHA STEMI guideline
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states that the duration of therapy can be limited to 3
months, although this appears to be more expert opinion
than based on clinical trial data. In contrast, in the AHA/
ASA “2021 Guideline for the Prevention of Stroke in
Patients With Stroke and Transient Ischemic Attack,” anti-
coagulation is recommended for ≥3 months, seemingly
on the basis primarily of 1 small 1987 study of patients
not treated with reperfusion therapy.
64
Until further data emerge, we favor repeat imaging at 3
months with the same modality of imaging (or better) that
was used to initially diagnose the LV thrombus. If there is
thrombus resolution, it seems reasonable to discontinue
OAC at that time. Because the risk of recurrent LV throm-
bus is reasonably high in the first 3 months after MI,
64
earlier discontinuation of anticoagulation on the basis of
imaging resolution of the initial thrombus alone could be
falsely reassuring if the LV function remains significantly
impaired or the initial wall motion abnormalities that pre-
disposed to LV thrombus formation persist. However, if
cardiac imaging is performed before 3 months for another
indication (eg, when considering placement of an implant-
able cardioverter defibrillator), earlier discontinuation of
anticoagulation might be reasonable if the thrombus has
resolved and the LV function and wall motion abnormali-
ties have improved (ie, no longer akinetic or dyskinetic).
LV thrombi may also develop in patients with a nonre-
cent (eg, >3 months) MI (or ischemic cardiomyopathy).
No clinical trial data exist to inform the duration of anti-
coagulation in this setting. It is the consensus of this writ-
ing group that anticoagulation (VKA or DOAC) should
be initiated for patients with LV thrombus in this setting
for at least 3 to 6 months. A shared decision-making
approach should be applied as to whether anticoagula-
tion should be continued indefinitely, factoring in a given
demonstrated milieu to form thrombus, improvement or
lack of improvement in LV systolic function, bleeding risk,
tolerability of OAC, and the patient’s risk tolerances of
possible stroke or bleeding complications.
In summary, therapeutic anticoagulation generally should
be initiated for the treatment of LV thrombus after acute MI,
typically for a duration of 3 months, with follow-up imaging at
this time point. For patients with a history of more distant MI
(or ischemic cardiomyopathy) who develop LV thrombus, we
suggest initiation of OAC for at least 3 to 6 months, with a
shared decision-making approach for indefinite therapy. The
issue of persistent LV thrombus despite OAC is addressed in
a subsequent section. The key relevant studies on treatment
of LV thrombus after acute MI are summarized in the Study
Summary Tables Supplement.
PREVENTION OF LV THROMBOSIS IN DCM
For the purposes of this document, the term DCM is used
to encompass those cardiomyopathies with depressed
LV systolic function not attributable to myocardial isch-
emia/MI. LV thrombus is reportedly less common in
DCM compared with ischemic cardiomyopathy, possibly
because of underdetection as the incidences of throm-
boembolic events have been found to be similar.
30,38
No
randomized controlled trials have addressed the primary
prevention of LV thrombus per se in patients with DCM.
Several randomized controlled trials have been conduct-
ed to evaluate the optimal antithrombotic regimen for the
prevention of major adverse events in patients with heart
failure in sinus rhythm.
HELAS (Heart Failure Long-Term Antithrombotic
Study) randomized 197 patients with heart failure with
reduced ejection fraction to warfarin, aspirin, or pla-
cebo.
65
The study results showed no significant differ-
ence in the incidence of thromboembolism between
groups. The WASH pilot trial (Warfarin/Aspirin Study in
Heart Failure) randomized 279 patients with heart fail-
ure with reduced ejection fraction (55% with nonisch-
emic causes of the cardiomyopathy) to warfarin, aspirin,
or placebo and found no significant difference between
the groups in the composite end point of death, stroke, or
MI.
66
The WATCH trial (Warfarin and Antiplatelet Therapy
in Chronic Heart Failure) randomized 1587 patients with
heart failure with reduced ejection fraction (27% with
DCM) to warfarin, aspirin, or clopidogrel but was termi-
nated early as a result of failure to reach target enrollment.
No significant difference among groups in the composite
end point of death, nonfatal MI, or nonfatal stroke was
observed in those who had been enrolled.
67
The WAR-
CEF trial (Warfarin versus Aspirin in Reduced Cardiac
Ejection Fraction) randomized 2860 patients with heart
failure with reduced ejection fraction (≈57% with DCM)
to warfarin or aspirin. The study results showed a ben-
efit with warfarin in terms of decreased risk of ischemic
stroke (0.72 events per 100 patient-years versus 1.36
events per 100 patient-years; hazard ratio, 0.52 [95%
CI, 0.33–0.82]; P=0.005). However, the warfarin group
had increased major bleeding compared with the aspirin
group (1.78 events per 100 patient-years versus 0.87
events per 100-patient years; P<0.001).
68
A recent Cochrane systematic review, which included
3 randomized trials, concluded that the available evi-
dence does not support the routine use of anticoagu-
lation in people with heart failure who remain in sinus
rhythm.
69
The 2012 American College of Chest Phy-
sicians guidelines on antithrombotic therapy and pre-
vention of thrombosis recommend against the use of
antiplatelet therapy or warfarin for patients with systolic
dysfunction without established coronary artery disease
and no LV thrombus (Grade 2C).
4
There are limited data on several specific types
of DCM and associated risk factors for LV thrombus
formation. These are discussed here and summarized
in Table 2.
Takotsubo syndrome (stress cardiomyopathy) has
been associated with a modest incidence of LV thrombus.
A meta-analysis of 21 observational studies comprising
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29 410 patients with takotsubo syndrome revealed a
pooled estimated LV thrombus rate of 1.8%.
70
Similarly,
multicenter international registry data of 541 patients
reported LV thrombus in 2.2%, with apical ballooning pat-
tern and troponin I levels >10 ng/mL associated with an
increased risk of LV thrombus formation.
71
The European
Society of Cardiology international expert consensus doc-
ument on takotsubo syndrome states that in patients with
LV dysfunction and apical ballooning, “although evidence
is lacking, anticoagulation with intravenous/subcutaneous
heparin would appear to be appropriate in such patients.”
5
LV noncompaction is characterized by excessive tra-
beculations and deep intertrabecular recesses. Studies
suggest an increased risk of thromboembolism in patients
with LV noncompaction related to LV thrombus formation
in the deep intertrabecular recesses.
72
A Heart Rhythm
Society expert consensus statement recommends that
anticoagulation may be reasonable with LV noncompac-
tion and LV dysfunction (Class of Recommendation IIb;
Level of Evidence B-NR).
6
However, the literature sup-
porting this recommendation is based on 1 small case
series without control subjects.
79
The AHA/ASA “2021
Guideline for the Prevention of Stroke in Patients With
Stroke and Transient Ischemic Attack” gives a Class IIa
recommendation that in patients with ischemic stroke or
transient ischemic attack (TIA) in the setting of LV non-
compaction, treatment with warfarin can be beneficial to
reduce the risk of recurrent stroke or TIA, although this is
based strictly on expert opinion.
2
Note, however, that this
is not really a recommendation for the primary prevention
of LV thrombus, nor is it based on the systematic detec-
tion of LV thrombus.
Several observational studies report a higher incidence
of LV thrombus and thromboembolism in patients with
peripartum cardiomyopathy.
36,74,75
The hypercoagulable
state associated with pregnancy likely increases the risk
of LV thrombus formation. A 2016 AHA scientific state-
ment on DCMs states that “anticoagulation is reasonable
in patients with peripartum cardiomyopathy and severe
LV dysfunction to prevent thrombus formation given the
risk of hypercoagulable state during pregnancy” (which
is based on Level of Evidence C data).
7
The European
Society of Cardiology Heart Failure Association recom-
mends heparin-based anticoagulation in acute peripar-
tum cardiomyopathy with LVEF ≤35% to decrease the
risk of thromboembolism.
8
Low-molecular-weight hepa-
rins are preferred antepartum when VKAs are generally
avoided because of the risk of teratogenicity and fetal
bleeding. Both low-molecular-weight heparins and VKAs
are reasonable choices postpartum.
8,78
A small number of case reports and case series of
LV thrombus have been reported in patients with other
forms of DCM, including hypertrophic cardiomyopathy,
chemotherapy-related cardiomyopathy, cardiac amyloi-
dosis, cardiomyopathy attributable to Chagas disease,
and eosinophilic myocarditis.
31–35
No prospective obser-
vational studies or randomized clinical trials have evalu-
ated the impact of anticoagulation in these patients for
the primary prevention of LV thrombus.
In summary, no prospective trials support the routine
use of OAC for the primary prevention of LV thrombus
in patients with DCM in sinus rhythm. On a case-by-
case basis? OAC could be considered in patients with
specific types of DCM at increased risk for LV throm-
bus formation such as those with takotsubo syndrome,
LV noncompaction, eosinophilic myocarditis, peripartum
cardiomyopathy, and cardiac amyloidosis. In such cases
in which OAC is implemented, the recommended dura-
tion of preventive OAC for these DCM subtypes is not
established; indefinite OAC might be considered unless
the LVEF improves or bleeding contraindication occurs.
The key relevant studies on the prevention of LV
thrombus in nonischemic cardiomyopathy are summa-
rized in the Study Summary Tables Supplement.
TREATMENT OF LV THROMBUS IN DCM
As noted, LV thrombus is observed less frequently in
DCM compared with ischemic cardiomyopathy. Con-
sequently, there are few data on the incidence of LV
thrombus and subsequent thromboembolic events in
patients with DCM or on the treatment of LV thrombus
once identified.
In a retrospective analysis of 159 patients with LV
thrombus, only 21.5% had a nonischemic cause.
17
Mean
LVEF was 32%, and the vast majority of LV thrombi
occurred in the LV apex. Most patients were treated
Table 2. Specific DCMs (Nonischemic) and Associated Risk
Factors for Which Anticoagulation for the Prevention of LV
Thrombus Might Be Considered
DCM
Risk factors associated with LV thrombus
formation
Takotsubo syndrome LV dysfunction with LVEF ≤30% and/or api-
cal ballooning
5,70,71
Left ventricular noncompaction History of stroke or TIA
2
and/or LV dysfunc-
tion
6,72,73
Peripartum cardiomyopathy Bromocriptine administration and/or LVEF
≤35%
7,8,36,74,75
Hypertrophic cardiomyopathy Apical aneurysm
31,76,77
Chemotherapy-related
cardiomyopathy
LV restrictive filling pattern and/or LVEF
≤30%
32
Cardiac amyloidosis AL type and/or LV restrictive filling pattern
33
Cardiomyopathy attributable
to Chagas disease
Apical aneurysm
34
Eosinophilic myocarditis Prior embolic episode
35
DCM indicates dilated cardiomyopathy; LV, left ventricular; LVEF, left ventricu-
lar ejection fraction; and TIA, transient ischemic attack.
Low-molecular-weight heparin is preferred antepartum when vitamin K an-
tagonists are generally avoided because of the risk of teratogenicity and fetal
bleeding. Both low-molecular-weight heparin and vitamin K antagonists are rea-
sonable choices postpartum.
78
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with OAC, with either a VKA or a DOAC, and 67% were
also treated with an antiplatelet agent. A total of 62.3%
achieved total LV thrombus regression over a median of
103 days. Thrombus recurrence or an increase in the
size of the LV thrombus occurred in patients with poor
medical adherence and in those with prothrombotic con-
ditions such as active cancer, inflammatory or hemato-
logical diseases, or chronic renal failure. It is important to
note that successful treatment of LV thrombus was asso-
ciated with improved survival and fewer MACEs. Patients
on anticoagulation for >3 months and with LVEF ≥35%
had fewer MACEs.
17
Clinical practice guidelines offer little discussion on
anticoagulation for the treatment of LV thrombus in the
setting of DCM and the duration of treatment. Further-
more, there is a paucity of study data on this. The most
recent AHA statement
7
on DCM suggests that VKA
therapy is probably indicated for patients with image-
proven intracardiac thrombus in the setting of cardiac
amyloidosis, although treatment duration was unspeci-
fied. The 2012 American College of Chest Physicians
guidelines on antithrombotic therapy and prevention of
thrombosis suggest at least 3 months of OAC therapy for
LV thrombus in DCM (Grade 2C).
4
The consensus of this writing group, which is based on
retrospective registry data and small, prospective obser-
vational studies, is for anticoagulation (VKA or DOAC) in
patients with LV thrombus in the setting of DCM for at least
3 to 6 months, with discontinuation if LVEF improves to
>35% (assuming resolution of the LV thrombus) or if major
bleeding occurs.
20,80,81
Whether anticoagulation should be
continued indefinitely, given the proven milieu or predis-
position to thrombus formation, even if follow-up imag-
ing demonstrates resolution of the LV thrombus, cannot
be determined but might be prudent in those in whom LV
systolic function does not improve with guideline-directed
therapies, in those who have persistent apical akinesis or
dyskinesis, and in patients with patients with proinflam-
matory or hypercoagulable states such as malignancy or
renal failure, assuming that such patients are able to toler-
ate OAC. This setting may be a particularly important case
of shared decision-making in which the risks of indefinite
anticoagulation (and increased pill burden plus additional
anticoagulation monitoring and drug-drug and drug-food
interactions in the case of warfarin) are balanced by the
patient and health care professional against a possible
(although theoretical) reduction in the risk of stroke.
The key relevant studies on treatment of LV thrombus
in DCM are summarized in the Study Summary Tables
Supplement.
MURAL (LAMINATED) THROMBUS
An LV thrombus is categorized as mural (laminated) if its
borders are mostly contiguous with the adjacent endocar-
dium, as opposed to protuberant if its borders are distinct
from the adjacent endocardium and it protrudes into the
LV cavity. Mural LV thrombi are often undetected by echo-
cardiography performed without intravenous administration
of an ultrasound-enhancing agent (eg, Definity, Optison,
Lumason). Although administration of an ultrasound-en-
hancing agent increases sensitivity, close approximation of
a small thrombus to the adjacent akinetic wall (which also
lacks enhancing agent uptake) can limit detection. Delayed-
enhancement CMR offers the best sensitivity and specific-
ity specifically for this thrombus subtype (Figure 3).
13
Studies using echocardiography have historically
identified mural LV thrombi to be associated with a lower
risk of embolism compared with protuberant or mobile
LV thrombi.
23,82
Despite a lack of correlative pathologi-
cal imaging studies, mural thrombi detected by imaging
are often considered organized (and thus with lower
thromboembolic potential than protuberant or mobile
thrombi). However, the risk of thromboembolism with
mural thrombus is not negligible. Up to 40% of thrombo-
embolic events in patients with LV thrombus occur in the
mural subtype.
82
In a large contemporary observational
study using CMR (with modern medical therapy and anti-
coagulation; n =155, 32% mural LV thrombus), the risk
of long-term embolic events (stroke, TIA, or extracranial
systemic arterial embolism) was not significantly differ-
ent between patients with mural and those with protu-
berant LV thrombi (P=0.39).
3
However, in this analysis,
the small number of patients limited the power to detect
significant differences, and protuberant thrombi had a
numerically higher risk of embolism.
Limited data also suggest that protuberant thrombi
may resolve earlier than mural thrombi (OR, 3.2 [95%
CI, 1.1–8.89]; P=0.026),
83
which may affect long-term
thromboembolic potential. Consistent with this, it is not
Figure 3. Example of an LV apical mural (laminar) thrombus
(red arrows) seen on gadolinium-enhanced CMR.
Note the adjacent white appearing areas indicating infarcted
myocardium. CMR indicates cardiac magnetic resonance; and LV, left
ventricular.
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uncommon for repeated echocardiograms over the
course of months or years to continue to show small
residual mural thrombus, which is likely well organized by
that point with a lower risk of thromboembolism.
This writing group suggests the following approach to
mural thrombus; based more on consensus than study
data. For a newly diagnosed mural thrombus, although the
risk of embolization may be less than for a protuberant
thrombus, it is likely not trivial, and it would be prudent to
anticoagulate for this thrombus similarly to a protuberant
thrombus. For persistent mural thrombus after a course
of OAC, particularly if organized or calcified, the risk of
embolization is likely low, and in such cases, a shared
decision-making approach seems appropriate, weighing
the small but likely nonzero risks of cardioembolic stroke
against the risks and inconveniences of OAC.
The key relevant studies on mural (laminated) LV
thrombus are summarized in the Study Summary Tables
Supplement.
DOAC AS AN ALTERNATIVE TO WARFARIN
FOR THE TREATMENT OF LV THROMBUS
VKAs, predominantly warfarin, have traditionally been
used and recommended for the prevention and treat-
ment of LV thrombus. OAC with warfarin, however, re-
quires dietary consistency, frequent INR monitoring,
and vigilance with regard to drug-food (and drug-drug)
interactions that can be challenging for many patients.
Failure to maintain a therapeutic INR (TTR <50%) ap-
pears to increase the risk of stroke in patients with LV
thrombus.
16,63
These challenges have led to increased
adoption of DOAC for oral anticoagulation treatment in
atrial fibrillation and venous thromboembolism.
84
In cur-
rent practice, some practitioners have extrapolated the
results of studies of DOAC for atrial fibrillation and ve-
nous thromboembolism to LV thrombus and are using
DOAC for such treatment.
The 2013 ACC/AHA STEMI guideline recommenda-
tion on anticoagulation for LV thrombus calls out a VKA
and does not mention DOAC, although this recommenda-
tion was formulated a decade ago.
1
The 2017 European
Society of Cardiology STEMI guideline on anticoagula-
tion for LV thrombus states simply that “anticoagulation
should be administered” but mentions neither warfarin
nor DOAC.
3
The 2021 AHA/ASA stroke guideline con-
tains a Class IIb recommendation that in patients with
stroke or TIA and new LV thrombus, the safety of anti-
coagulation with a DOAC to reduce risk of recurrent
thrombus is uncertain, citing 2 retrospective studies.
85,86
Thus, at present, there is little organizational guidance on
whether DOAC is a reasonable alternative to warfarin for
the treatment of LV thrombus.
Several retrospective studies, randomized trials, and
meta-analyses comparing DOAC with warfarin for the
treatment of LV thrombus provide some, although not
always consistent, results.
86–97
Three small random-
ized controlled trials found DOACs to be noninferior to
VKAs.
90–92
The major limitation of these trials was the
small sample size. A meta-analysis of these 3 random-
ized controlled trials, which consisted of a total of 139
patients, found DOACs to be noninferior to VKA with
respect to mortality, stroke, or LV thrombus resolution.
93
Pooled analysis also showed that major bleeding was sig-
nificantly lower with DOACs (2.86% with DOACs versus
13.2% with warfarin; OR, 0.16 [95% CI, 0.02–0.82]).
93
A
second meta-analysis, which included 8 randomized and
nonrandomized studies with a pooled sample of ≈1200
patients, also found DOACs to be noninferior to VKA,
again with lower bleeding rates.
94
Another meta-analysis,
consisting of 2 randomized trials and 16 cohort studies in
2666 patients, found a statistically significant reduction in
stroke with DOAC compared with VKA (OR, 0.63 [95%
CI, 0.42–0.96]; P=0.03).
95
However, no significant differ-
ence was noted in mortality, bleeding, systemic embolism,
and the combined end point of systemic embolism or
stroke and LV thrombus resolution. A meta-analysis of 8
retrospective studies with pooled data on 1955 patients
found that DOACs were noninferior to or at least as
effective as VKAs in the treatment of LV thrombus, but
no other benefit was found, including bleeding complica-
tions.
96
Yet another meta-analysis of 12 studies and 2322
patients found no difference between DOACs and VKAs
in the resolution of LV thrombus or bleeding complica-
tions.
97
Taken as a whole, these studies and meta-analy-
ses seem to suggest that DOACs is at least as good as
VKAs in terms of ischemic and bleeding events.
To further assess all available current data, we conducted
an updated and comprehensive meta-analysis compar-
ing the effectiveness and safety of DOACs and VKAs for
the treatment of LV thrombus (see Study Summary Tables
Supplement, Section IX for methodology and individual
studies). This analysis combined the data of randomized
clinical trials, prospective studies, and retrospective stud-
ies from inception to January 19, 2022. Pooled data from
these 21 studies included 3057 patients with LV thrombus,
of whom 824 were treated with DOAC and 2233 treated
with VKA. The median follow-up time (according to data
from 19 studies) was 12 months (interquartile range, 6–24
months). The median duration of anticoagulation in each
arm (provided in only 4 studies) was 222 days (interquartile
range,125.2–417 days) for DOAC and 345.5 days (inter-
quartile range, 253–575 days) for VKA. This meta-analysis
found no differences in therapeutic efficacy and safety in
the treatment of LV thrombus between DOAC and VKA
treatment in stroke or systemic embolization (OR, 0.94
[95% CI, 0.70–1.25]; P=0.65; Figure 4), as well as in all-
cause mortality (OR, 0.92 [95% CI, 0.64–1.30]; P=0.63),
thrombus resolution (OR, 1.21 [95% CI, 0.89–1.64];
P=0.22), and bleeding complications (OR, 0.79 [95% CI,
0.56–1.11]; P=0.17). (Additional forest plots of these 3
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analyses are given in Section VIII of the Study Summary
Tables Supplement). Separate meta-analyses using only
randomized controlled trials and randomized controlled tri-
als plus prospective studies did not find statistically sig-
nificant differences between the 2 treatment strategies in
therapeutic efficacy and favored DOAC in terms of bleed-
ing outcome (see Study Summary Tables Supplement).
Thus, according to all currently available data, DOACs
are considered by this writing group to be a reasonable
alternative to VKA in patients with LV thrombus and may
be particularly attractive as a therapy in patients in whom
a therapeutic INR range is difficult to achieve consis-
tently or in whom frequent INR checks are impractical
(eg, lack of transportation). At present, there are no data
on the use of DOACs for either prophylaxis or treatment
of LV thrombus in patients with end-stage renal disease.
Thus, the choice of OAC in such patients must be based
on best clinical judgment and shared decision-making.
The key relevant studies on DOACs as an alternative
to warfarin for the treatment of LV thrombus are summa-
rized in the Study Summary Tables Supplement.
OAC IN PATIENTS TREATED WITH
ANTIPLATELET THERAPY
Combining OAC and antiplatelet therapy significantly in-
creases bleeding risk.
98
Over the past decade, multiple
studies have explored the best treatment strategies in
patients undergoing PCI with an indication for antiplate-
let therapy and who also have an indication for OAC.
98
Although in these studies LV thrombus was rarely the in-
dication for OAC, it would seem reasonable to extrapolate
the results of these studies, as well as resultant expert and
organizational recommendations, to patients with indica-
tions for OAC for the prevention or treatment of LV throm-
bus. On the basis of these studies and consistent with
current practice and guideline recommendations,
99–101
when oral anticoagulation is added to antiplatelet therapy
in patients who have undergone PCI, a general strategy
of double (dual) therapy, with OAC (preferably a DOAC)
and a P2Y
12
inhibitor (preferably clopidogrel), after 1 to
4 weeks of triple therapy? is preferred over longer-term
triple therapy consisting of an OAC plus DAPT.
DAPT FOR THE PREVENTION OF LV
THROMBUS
The pathophysiology of thrombus formation provides
the rationale for the use of anticoagulants, rather than
antiplatelet drugs, for the prevention or treatment of LV
thrombus.
16,102
No randomized clinical trials have exam-
ined the impact of DAPT alone (without OAC) for the
prevention of LV thrombus after an acute MI. In a data-
base analysis of patients with anterior wall STEMI with
Figure 4. Updated meta-analysis of randomized studies of warfarin vs DOAC in patients with LV thrombus, with end points of
stroke and systemic thromboembolism.
Similar analyses for the end points of all-cause mortality, thrombus resolution, and bleeding are given in Section VIII of the Study Summary Tables
Supplement. DOAC indicates direct oral anticoagulant; IV, instrumental variable; and Vit-K, vitamin K.
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apical akinesis or dyskinesis (on echocardiography per-
formed within 7 days of hospitalization), those treated
with warfarin plus clopidogrel-based DAPT had a greater
incidence of composite ischemic and bleeding adverse
cardiac events than those treated with clopidogrel-based
DAPT alone; there was only 1 ischemic stroke in each
treatment group.
46
One observational study found that
ticagrelor-based DAPT was associated with a lower inci-
dence of LV thrombus compared with clopidogrel-based
DAPT.
103
A study comparing a treatment strategy of ti-
cagrelor-based DAPT at 1 hospital with triple antithrom-
botic therapy at another hospital in patients treated with
primary PCI for anterior STEMI with “apical dysfunction”
found no difference in a composite end point of ischemic
and bleeding events, although only 1 patient in the study
had a stroke or TIA.
104
There are overall insufficient high-
quality study data to assess whether DAPT alone has any
protective effects for the formation of LV thrombus or
whether a more potent P2Y
12
inhibitor such as ticagrelor
might be preferable if DAPT alone is used to treat pa-
tients at risk of LV thrombus formation.
FIBRINOLYSIS FOR LV THROMBUS
There are very limited data on the efficacy and safety of
fibrinolysis for LV thrombus. In 1 small series, 16 patients
with MI 3 to 12 weeks previously and found to have large
LV thrombi were treated with 2- to 8-day courses of uro-
kinase. Lyses of the thrombus were deemed successful
in 10 patients (predominantly in those with more recent
MI), with no evidence of embolic events in any patient.
All patients were subsequently treated with 6 months of
OAC.
105
A few small reports address the use of fibrinoly-
sis for the acute treatment of stroke in patients who also
had LV thrombus.
106–109
Although in most such cases no
clinical emboli resulted, at least 1 such case was well
documented, resulting in embolization of the LV throm-
bus and severe stroke in the hemisphere contralateral to
the initial stroke. The 2019 AHA/ASA guideline for the
early management of patients with acute ischemic stroke
states that in patients with major ischemic stroke likely
to produce severe disability and known LV thrombus,
treatment with IV alteplase may be reasonable (Class of
Recommendation IIb; Level of Evidence C-LD).
110
On the
basis of consensus opinion, given the very limited safety
data and small but likely nonzero risk of embolization, we
do not generally suggest fibrinolytic treatment for the pri-
mary purpose of treating LV thrombus.
SURGICAL EXCISION OF LV THROMBUS
There are only a few anecdotal reports and retrospective
small case series of surgical excision of LV thrombus.
111–115
Most such cases are in the setting of another indication
for cardiac surgery such as multivessel coronary artery
disease or aortic stenosis. At present, there are insufficient
data to recommend surgical excision (without other indi-
cations for surgery) for the treatment of LV thrombus. Be-
cause of the risks of surgery and lack of supportive data,
such an approach should be limited to rare circumstances
such as inability to tolerate anticoagulation therapy (other
than that briefly administered during surgery) when there
is perceived to be a high risk of embolization or cardioem-
bolic stroke despite anticoagulation.
LV THROMBUS SIZE, LV THROMBUS
REGRESSION, AND EMBOLIC RISK
Multiple studies have found that the most important risk
factor for LV thrombus embolization is a mobile or pro-
tuberant thrombus.
16,23,59–61,82
LV thrombus size rarely ap-
pears in studies as a risk factor for embolization, and when
it does, it is a lesser risk factor.
82
Thus, for most thrombi,
size per se should not factor strongly into decisions about
OAC. In 1 study, smaller baseline thrombus size was as-
sociated with a greater likelihood of LV thrombus regres-
sion, and total LV thrombus regression was associated
with a lower risk of mortality.
17
In a second study, failure of
initial thrombus resolution and thrombus recurrence were
independent predictors of stroke.
59
The management of
thrombi that do not resolve or regress in size with OAC is
addressed in the LV Thrombus Persistence Despite Anti-
coagulation Therapy section.
MANAGEMENT OF MASSIVE LV
THROMBUS
There are only a few anecdotal reports on the manage-
ment of giant, huge, massive, or obliterating thrombus,
including treatment with DOAC, fibrinolytic therapy,
and surgical resection.
116–120
In unusual circumstances,
thrombus size may affect diastolic ventricular volume or
obstruct either mitral inflow or aortic outflow. There are
insufficient data to preferentially recommend any one
approach to large or massive LV thrombi, and these rare
scenarios are best addressed with a multidisciplinary ap-
proach to therapeutic intervention.
LV THROMBUS PERSISTENCE DESPITE
ANTICOAGULATION THERAPY
LV thrombus persistence despite ongoing anticoagula-
tion and recurrence after completion of anticoagulation
are understudied phenomena. Observational research
suggests that persistence of LV thrombus is not uncom-
mon. In a contemporary report, 157 of 159 patients with
LV thrombus (79% of whom had coronary artery disease)
were treated with oral anticoagulation for a median of 1.4
years (VKA, DOAC, or heparin). Concomitant antiplatelet
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therapy was prescribed in 67.9%. Serial echocardiog-
raphy was conducted per usual clinical care. Complete
thrombus resolution was achieved in 62.3% (n=99)
at a median of 103 days (interquartile range, 32–392
days).
17
Recurrence of thrombus or an increase in LV
thrombus area was observed in 14.5% (n=23), a finding
associated with poor adherence, prothrombotic condi-
tions, and increased mortality.
17
In another report of 35 patients with STEMI compli-
cated by LV thrombus, a higher rate of resolution was
reported on serial echocardiography using a predefined
assessment protocol (65% resolution at 2 months, 87%
at 4 months, 81% at 12 months, and 100% at 18 months).
All participants received warfarin-based anticoagulation
(46% with concomitant clopidogrel) for at least 4 months
or until thrombus resolution. Again, there was a recur-
rence rate of 14% after OAC discontinuation.
121
Although trial data informing the treatment of persistent
or recurrent LV thrombus are lacking, prolonged anticoagu-
lation and repeated imaging assessment are generally rec-
ommended. Treatment adherence should be assessed, and
anticoagulation should generally be continued until resolu-
tion.
10
Although there are no good trial data on changing the
anticoagulation approach, we suggest, on the basis of con-
sensus opinion, a trial of an alternative OAC in some patients
with persistent LV thrombus, particularly a protruding or
Figure 5. Overview of suggested strategies for the prevention and management of LV thrombus.
CMR indicates cardiac magnetic resonance; D/C, discontinuation; DCM, dilated cardiomyopathy; HCM, hypertrophic cardiomyopathy; LMWH,
low-molecular-weight heparin; LV, left ventricular; LVEF, left ventricular ejection fraction; LVNC, left ventricular noncompaction; MI, myocardial
infarction; OAC, oral anticoagulation; and VKA, vitamin K antagonist. Trial of VKA if persistent LV thrombus despite dual OAC; trial of dual OAC if
persistent LV thrombus in the setting of consistent subtherapeutic international normalized ratio; and trial of LMWH if persistent LV thrombus in
the setting of consistent therapeutic international normalized ratio.
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mobile thrombus. For example, individuals who are com-
pliant with DOAC but have persistent LV thrombus could
be treated with a trial of VKA; those who are unable to
maintain therapeutic INRs with VKA and have persistent
LV thrombus could be treated with a trial of DOAC; and
patients with confirmed therapeutic INRs on VKA who
nonetheless have persistent LV thrombus might be treated
with a trial of low-molecular-weight heparin. On the other
hand, in patients with persistent mural (laminar) thrombus,
particularly if the thrombus becomes organized or calcified,
the risk of embolization may be low, and discontinuation of
OAC is not unreasonable after a risk/benefit discussion
with the patient.
10
However, given the lack of high-quality
data to confirm this opinion, decisions on mode and dura-
tion of anticoagulation should be on a case-by-case basis.
Last, there is no evidence that surgery for persistent LV
thrombus has net efficacy.
The key relevant studies on persistence of LV throm-
bus despite treatment are summarized in the Study Sum-
mary Tables Supplement.
PRACTICAL MANAGEMENT
SUGGESTIONS
Only AHA/ACC guidelines can in general make formal
recommendations. That said, so as not to make this docu-
ment merely an academic exercise, the writing group has
striven to generate some practical management sugges-
tions that are based on careful and critical review of ac-
tual study data, as well as existing guidelines and expert
opinion, that address the 8 key questions that served as
the rationale for this scientific statement and the assem-
bly of this multispecialty writing group. These suggestions
are given in Table 3 and summarized in Figure 5. Factors
to assess and reassess in patients with LV thrombus that
support the continuation of OAC and factors that may or
do not favor continued OAC are given in Table 4.
CONCLUSIONS
Despite advances in reperfusion therapy for acute MI and
pharmacological and device treatments for patients with
cardiomyopathy with depressed LVEF, LV thrombus con-
tinues to be a not uncommon and challenging medical
condition. In addition, despite decades of research, treat-
ment recommendations are often based on limited, often
noncontemporary studies, with a paucity of study data
in some settings to guide informed treatment. Accord-
ingly, contemporary clinical trials are needed to inform the
Table 3. Suggested Practical Management of Patients at
Risk for or With LV Thrombus
1. We suggest that CMR may be most appropriate when (1) there is the
suggestion of a possible LV thrombus on echocardiogram but echocar-
diography imaging even with an ultrasound-enhancing agent is not diag-
nostic and (2) echocardiography does not demonstrate LV thrombus but
a clinical concern remains (for example, cardioembolic stroke).
2. We suggest that, given the relatively weak data supporting prophylactic (pre-
ventive) OAC in patients with acute anteroapical STEMI treated with reperfu-
sion therapy (usually primary PCI) and anteroapical akinesis, any such consid-
eration of OAC should weigh and incorporate the perceived risk of thrombus
formation and bleeding and involve shared decision making. If OAC is initi-
ated, a treatment duration might be 1–3 mo, depending on bleeding risk.
3. We suggest that, on the basis of reasonable study data, post-MI pa-
tients with LV thrombus should be treated with OAC, typically for a
duration of 3 mo.
4. We suggest that, given reasonably randomized data, patients with DCM
should not be prophylactically treated with OAC, with the possible excep-
tion of those with specific cardiomyopathies (for example, takotsubo syn-
drome, LV noncompaction, eosinophilic myocarditis, peripartum cardiomy-
opathy, and cardiac amyloidosis) with associated factors that increase the
risk of LV thrombus formation, in which cases OAC could be considered.
5. We suggest that, on the basis of limited data, patients with NICM with
LV thrombus should be treated with OAC for at least 3–6 mo, with dis-
continuation if LVEF improves to >35% (assuming resolution of the LV
thrombus) or if major bleeding occurs. There are insufficient study data to
determine whether OAC should be continued indefinitely.
6. We suggest that, on the basis of limited data, it may be prudent to treat
patients with OAC for newly diagnosed mural (laminated) LV thrombus as
one would a patient with a protruding or mobile thrombus.
7. We suggest that, on the basis of supportive though insufficiently powered
randomized data, in patients with LV thrombus, DOAC seems to be a rea-
sonable alternative to warfarin.
8. We suggest that, on the basis of consensus opinion, in some patients
with persistent LV thrombus, particularly a protruding or mobile thrombus,
a trial of an alternative OAC or LMWH (for example, VKA if on DOAC,
DOAC if on VKA with repeatedly subtherapeutic INR, LMWH if on VKA
with therapeutic INRs) is not unreasonable. On the other hand, also on
the basis of consensus opinion, discontinuation of OAC in patients with
persistent mural (laminar) thrombus, particularly if the thrombus becomes
organized or calcified, is not unreasonable.
CMR indicates cardiac magnetic resonance; DCM, dilated cardiomyopathy;
DOAC, direct oral anticoagulant; INR, international normalized ratio; LMWH,
low-molecular-weight heparin; LV, left ventricular; LVEF, left ventricular ejection
fraction; MI, myocardial infarction; NICM, nonischemic cardiomyopathy; OAC,
oral anticoagulant; PCI, percutaneous coronary intervention; STEMI, ST-seg-
ment–elevation myocardial infarction; and VKA, vitamin K antagonist.
Table 4. Factors to Assess and Reassess in Patients With
LV Thrombus That Support the Continuation of OAC and Fac-
tors That May or Do Not Favor Continued OAC
Factors that favor continued OAC
Anteroapical MI with persistent akinesis
Protruding/mobile thrombus
Suspected or known cardioembolic event
Not high bleeding risk
Proinflammatory or hypercoagulable states
Recurrent LV thrombus
Factors that may or do not favor continued OAC
High bleeding risk
Concomitant antiplatelet therapy
Improvement in LVEF or focal akinesis
Persistent mural (laminated) thrombus, particularly if organized or calcified,
despite therapeutic OAC
LV indicates left ventricular; LVEF, left ventricular ejection fraction; MI, myo-
cardial infarction; and OAC, oral anticoagulant.
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outstanding uncertainty of whether the benefit of pro-
phylactic anticoagulation in reducing the incidence of LV
thrombus formation outweighs the risks in some settings.
Future research should investigate (1) the natural history
of mural (laminated) LV thrombus and whether the duration
of anticoagulation should be tailored to the morphology of
the LV thrombus; (2) the benefits of OAC in addition to an-
tiplatelet therapy in patients with STEMI who have under-
gone primary PCI; (3) whether indefinite anticoagulation
is merited in patients with DCM or with prior (not acute or
recent) MI who develop LV thrombus; and (4) the optimal
anticoagulants (eg, VKA, DOAC, low-molecular-weight
heparin) in specific clinical settings. As of this writing, sever-
al trials (NCT03764241, NCT04970381, NCT05028777,
NCT04970576, NCT03786757, NCT05077683) are in
progress that are investigating management issues ad-
dressed in this scientific statement, and future such trials
are strongly encouraged.
ARTICLE INFORMATION
The American Heart Association makes every effort to avoid any actual or poten-
tial conflicts of interest that may arise as a result of an outside relationship or a
personal, professional, or business interest of a member of the writing panel. Spe-
cifically, all members of the writing group are required to complete and submit a
Disclosure Questionnaire showing all such relationships that might be perceived
as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science
Advisory and Coordinating Committee on June 10, 2022, and the American
Heart Association Executive Committee on August 2, 2022. A copy of the
document is available at https://professional.heart.org/statements by using
either “Search for Guidelines & Statements” or the “Browse by Topic” area. To
purchase additional reprints, call 215-356-2721 or email Meredith.Edelman@
wolterskluwer.com.
The American Heart Association requests that this document be cited as
follows: Levine GN, McEvoy JW, Fang JC, Ibeh C, McCarthy CP, Misra A, Shah ZI,
Shenoy C, Spinler SA, Vallurupalli S, Lip GYH; on behalf of the American Heart
Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke
Nursing; and Stroke Council. Management of patients at risk for and with left
ventricular thrombus: a scientific statement from the American Heart Association.
Circulation. 2022;146:e???–e???. doi: 10.1161/CIR.0000000000001092
The expert peer review of AHA-commissioned documents (eg, scientific
statements, clinical practice guidelines, systematic reviews) is conducted by
the AHA Office of Science Operations. For more on AHA statements and
guidelines development, visit https://professional.heart.org/statements. Se-
lect the “Guidelines & Statements” drop-down menu, then click “Publication
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Permissions: Multiple copies, modification, alteration, enhancement, and/or
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at https://www.heart.org/permissions. A link to the “Copyright Permissions Re-
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Disclosures
Writing Group Disclosures
Writing group
member Employment Research grant
Other
research
support
Speakers’
bureau/
honoraria
Expert
witness
Ownership
interest
Consultant/
advisory board Other
Glenn N.
Levine
Baylor College of Medicine None None None None None None None
John W.
McEvoy
National University of Ireland
Galway (Ireland) and Johns
Hopkins Ciccarone Centre
for Cardiovascular Disease
Prevention
None None None None None None None
James C.
Fang
University of Utah None None None None None None None
Chinwe Ibeh Columbia University None None None None None None None
Gregory Y.H.
Lip
University of Liverpool,
Liverpool Centre for Cardio-
vascular Sciences Institute of
Ageing and Chronic Disease
(United Kingdom)
None None BMS/Pfizer;
Boehringer In-
gelheim; Daiichi-
Sankyo (no fees
are received by
him personally)?
None None BMS/Pfizer;
Boehringer In-
gelheim; Daiichi-
Sankyo (no fees
are received by
him personally)?
None
Cian P.
McCarthy
Massachusetts General Hos-
pital, Harvard Medical School
None None None None None None None
Arunima Misra Baylor College of Medicine None None None None None None None
Zubair I. Shah University of Kansas Medical
Center
None None None None None None None
Chetan
Shenoy
University of Minnesota Medi-
cal School
None None None None None None None
(Continued )
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Reviewer Employment Research grant
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board Other
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any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $5000 or
more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
Modest.
?Significant.
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