Download Natural history of left ventricular thrombi: Their appearance

JACC Vol . 15, No . 4
790
March 15,1990 :790-800
CLINICAL STUDIES
Thrombi-, Their Appearance and
Ventricular `'
Natural History
Resolution in the Posthospitallization Period of
Acute Myocardial Infarction
ANDRE KEREN, MD, SHMUEL GOLDBERG, MD, SHMUEL GOTTLIEB, MD,
JACOB KLEIN, MD, CLAUDIO SCHUGER, MD, AHARON MEDINA, MD,
DAN TZIVONI, MD, FACC, SHLOMO STERN, MD, FACC
Jerusalem . Israel
A series of 198 consecutive patients with acute myocardial
infarction were prospectively studied before hospital discharge and during 24 .0 t 8 .6 months of follow-up. A
predischarge i irombus was found In 38 (31%) of 124
patients with anterior Infarction but in none of 74 patients
with inferior infarction (p < 0 .001) . Early thrombolytic
therapy in 34 patients did not decrease the rate of thrombus
occurrence . Acute anterior infarction, ejection fraction
c35% and apical dyskinesia or aneurysm (but not akinesia)
were significantly related to the appearance of thrombus
during hospitalization by stepwise logistic regression anal .
ysis .
Echocardiographic follow-up of 159 patients for at least
6 months (mean 26 .6 ± 8 .4) revealed that thrombus
disappeared in 14 (48%) of 29 . Disappearance of thrombus
was related to predischarge apical akinesia (but not dyskinesla) and to warfarin therapy during the follow-up period .
A new thrombus first appeared after hospital discharge in
13 of 130 patients, and In 7 of the 13 it resolved during
further follow-up . Thus, 30% (13 of 42) of thrombi in these
patients appeared after discharge from the hospital .
Left ventricular thrombus occurs frequently in the course of
acute myocardial infarction and is associated with increased
embolic risk (1-6) . Acute anterior infarction and severe
apical asynergy have been uniformly correlated with formation of thrombus (7-19) . Clinical (8-10,18-21) and laboratory (15-17) markers of the extent of myocardial damage as
well as administration of anticoagulant (22-26) or fibrinolytic
From The Heiden Department of Cardiology . Bikur Cholim Hospital and
Hebrew University Hadassah-Medical School, Jerusalem . Israel .
Manuscript received July 5 . 1989 : revised manuscript received October
18, 1999 . accepted October 25 . 1989.
Address for reprints ; Andre Keren . MD. The Heiden Dar-rtment of
Cardiology, Bikur Cholim Hospital . P.O. Box 492. Jerusalem 91000 . Israel .
®1990 by the American College of Cardiology
Three factors were related to occurrence of new thrombi
during the follow-up period : deterioration in left ventricular ejection fraction, predischarge ejection fraction X35%
and ventricular aneurysm or dyskinesia. Systemic embolism occurred in six patients, all with a p ischarge
thrombus p < 0 .001) . Mobility of the thrombus was the
only variable significantly related to subsequent embolic
events (p = 0 .001) by logistic regression analysis. Thus, the
predischarge echocardiogram identifies patients with
thrombus and those at highest risk of embolic events . It can
indicate patients who are likely to have thrombus resolution
and those at risk of developing a new thrombus after
hospital discharge . Follow-up echocardiograms may help in
guiding the length of long-term anticoagulant therapy .
Four additional patients with a predischarge apical
mobile thrombus (not part of the consecutive series) received thrombolytic therapy . In two of the four, lysis of
thrombus was achieved without complications, but systemic
embolism occurred in the other two, and proved fatal in
one.
(J Am Coll Cordial 1990;15 :790-800)
(27-30) therapy during the acute phase of infarction have
been shown to have a variable influence on the incidence of
thrombi . A thrombus disappearance rate ranging from 20%
to 71% (8,10,11,19,20,27,31-33) and first appearance of left
ventricular thrombus after hospital discharge (8,13,20) have
been reported . Factors related to thrombus appearance in
the posthospitalization period and its embolic potential have
not been systematically evaluated in prospective studies .
Echocardiography is both sensitive and specific in the
detection and morphologic characterization of ventricular
thrombus (21,34-37) . Protrusion and mobility of the thrombus have been variably (13% to 83%) associated with increased risk of embolization (12-18), but it has been claimed
(18) that spontaneous variability in thrombus shape and
0735-10971901$3 .50
JACC Vol, 15. No. 4
March 15, 1990 :790-800
KEREN ET AL .
NATURAL HISTORY OF THROMBI
mobility significantly decreases the prognostic value of these
characteristics .
The present study prospectively investigated 198 consecutive patients with acute transmural myocardial infarction .
The patients had long-term clinical, echocardiographic and
nuclear angiographic follow-up evaluations to attempt to
define 1) factors related to the formation of thrombus during
the acute phase of infarction ; 2) factors related to disappearance of thrombus during the follow-up period ; 3) the frequency of and factors related to appearance of a new
thrombus during the follow-up period-, and 4) the risk of
embolization of thrombus detected either before or after
hospital discharge. Pertinent experience is reported in four
additional patients in whom fibrinolytic therapy was used
during the late phase of acute infarction to achieve lysis of a
mobile thrombus .
Methods
Study patients. The study group included 198 consecutive patients who survived an acute transmural myocardial
infarction, had technically adequate predischarge echocardiograms and had no additional cardiac or systemic illness
that could affect left ventricular function or long-term prognosis . They represented 93% of the 212 patients with acute
infarction discharged from the hospital between February
1985 and January 1987 . Excluded were 2 patients with
inadequate echocardiograms and 10 with primary myocardial or valvular heart disease, emergency surgery or coca .,nary angioplasty during hospitalization or a systemic ilip-2ss
that could affect long-term prognosis . Two additional patients with previous infarction and echocardiographic documentation of left ventricular thrombus < 12 h after their
hospitalization were excluded because thrombus appearance
could not be attributed with certainty to the new infarction
CW the 198 patients included in the study, 168 were men
and 30 were women ; the mean age was 62 .3 ± 11 .8 years
(range 32 to 86) . Echocardiography was performed 10 .6 ±
4.1 days (range 7 to 21) after the acute event . Transmural
myocardial infarction was diagnosed by typical history,
characteristic increase in serum creatine kinase, glutamic
oxaloacetic transaminase and lactic dehydrogenase enzyme
levels, and development of diagnostic Q waves on the
electrocardiogram (ECG) . The location of the infarction was
defined from the ECG (38) . Patients with lateral and with
combined acute anterior and inferior infarction were included in the group with anterior infarction .
Six weeks after hospital discharge, the patients had their
first clinical and echocardiographic follow-up evaluation,
and these examinations were repeated every 3 months
during the first year and every 6 months thereafter . Nuclear
angiography was also performed before hospital discharge,
every 6 months during the first year and every 12 months
thereafter .
791
Echocardiography . Two-dimensional echocardiography
was performed with use of a Hewlett Packard phased array
ultrasonograph and a medium and short focused 2 .5 or 3 .5
MHz transducer, or both . Patients with previous infarction
and those who received streptokinase shortly after admission had their first echocardiogram performed within 12 h of
hospitalization . Each study included all standard echocardiographic views (36) . In assessing the apical area, images
were recorded with different gain settings and angulations of
the transducer, and a short focused transducer was used in
each patient to minimize near field artifacts and to differentiate muscular trabeculae and aberrant bands from thrombus
(21,34,36) .
Left ventricular thrombus was defined as an echo-dense
mass, contiguous but distinct from the endocardium, located
in an area of asyne .,-gy that was seen in both systole and
diastole in at least two echucardiographic views (8,21,3436) . The agreement of two independent reviewers was required for diagnosis of thrombus and other echocardiographic variables . Theri-, was 96% interobserver agreement
for thrombus and 92% agreement for characteristics of wall
motion abnormalities adjacent to the cardiac mass . In cases
of disagreemem, a decision was reached by joint review of
the case .
A thrombus was classified as either mural (if the free
margin of the mass was concave following the curvature of
the endocardial surface) or protruding (if the free margin was
convex in relation to the adjacent endocardium) ; it was
considered mobile if any portion of it moved independent of
the underlying myocardium (6,12-15) . The area of the thrombus was defined by tracing its contour on a still frame image
(16) using the built-in calibrated measurement system of the
echocardiographic machine . During follow-up evaluations, a
? 50% change in thrombus area was considered to be a
significant change in thrombus size . Left ventricular aneurysm was defined as a localized area of akinesia or dyskinesia that deformed the ventricular contour in both systole and
diastole 16,15 .20) .
Wall inotion of the apical area, where most of the
thrombi predictably (6-16) occurred, was qualitatively
graded as normal . hypokinetic, akinetic or dyskinetic ; 90%
of dyskinetic segments were : located in the area of an apical
aneurysm . Therefore, apical dyskinesia and left ventricular
aneurysm (the latter associated in some cases with apical
akinesia) were analyzed as a single category for statistical
correlations . Akinesia without aneurysm was separately
evaluated . Changes from hypokinesia to akinesia or from
akinesia to dyskinesia were defined as deterioration in wall
motion, and improvement was diagnosed when the opposite
changes occurred .
Nuclear angiography . Left ventricular ejection fraction
was evaluated using multiple gated technetium blood pool
scans on an Elscint 400 Apex gamma camera . A change of
792
JACC Vol . 15, No. 4
March 15, 1990:790-800
KEREN ET AL.
NATURAL HISTORY OF THROMBI
>5% in ejection fraction was defined as deterioration or
improvement in global ventricular contractility (39) .
Early fibrinolytic and long-term anticoagulant therapy .
Thirty-four patients admitted to the emergency room within
4 h of the onset of typical chest pain, with ST segment
elevation in at least two ECG leads and lack of response to
sublingual nitrates received fibrinolytic therapy (27) . After
intravenous irnfusk i of hydrocortisone (100 mg), streptokinase (1 .5 million U) and heparin (15 IU/kg per h) were also
given intravenously . The hematologic effect of the medication was assessed by repeat fibs inogen level and partial
thromboplastin time measurements . After 24 h, the heparin
dose was adjusted to maintain the partial thromboplastin
time in the therapeutic range (70 to 140 s) . Successful
reperfusion was defined using clinical and angiugraphic
criteria (30) . Patency of the infarct-related artery was evaluated in each case on coronary arteriograms obtained 5 to 10
days after hospitalization . Before hospital discharge, oral
warfarin was started, and neparin administration was
stopped when the prothrombin time reached the therapeutic
range (20% to 30%) . Changes in the warfarin regimen and
bleeding complications were recorded .
Systemic embolism . The c iteria for systemic embolization were similar with those described in previous studies
(11,15-17) . The diagnosis of embolism to a limb required the
presence of sudden circulatory compromise and pathologic
confirmation. A cerebrovasculat embolic event was diagnosed in the presence of a sudden neurologic deficit in the
absence of a previous transient ischemic attack and a carotid
artery bruit, normal carotid Doppler recording and independent confirmation of the embolic ; nature of the event by a
neurologist . In patients with hypertension, nonlacunar cerebral infarction had to be demonstrated by computed tomography .
Statistical analysis . Clinical, echocardiographic and nuclear angiographic variables were evaluated by univariate
and multivariate analysis . Continuous variables were expressed as mean values ± SD . Differences between two
mean values were evaluated by a paired or unpaired twotailed Student t test . Differences among three mean values
were evaluated with one-way analysis of variance . Categoric
variables were tested by chi-square test or Fisher's exact
test where indicated .
Stepwise logistic regression analysis (40) was used to
define explanatory variables for four major events ("risk
groups") . 1) The risk of thrombus formation during hospitalization was evaluated in the original 198 patients ; 2) the
risk of systemic embolization was evaluated in 189 patients
(9 patients were lost to follow-up) who had a clinical followup period of 24 .0 ± 8 .6 months (range I to 48) ; 3) factors
related to the disappearance of thrombus ; and 4) the risk of
new thrombus appearance during the follow-up period were
evaluated in 159 patients with s6 months of echocardiographic follow-up study (range 6 to 48 months, mean 26 .6 ±
m134
at-86
n-74
0-0
n-94
Ttn-11(43!5)
m37(36%)
0066
LM
n∎0
Figure 1 . Myocardial infarction (Ml) location, therapy and presence
of left ventricular thrombus (LVT+) during initial hospitalization of
98 patients . Ant = anterior; Inf = inferior ; STK + = streptakinase
administered within 3 h of chest pain ; STK - = no streptokinase
administered .
8.4) . Thus, patients who had an echocardiographic follow-up
period of <6 months because of death, cardiac surgery or
coronary angioplasty performed before that time period
were excluded from this analysis .
The stepwise regression analysis defined the beta coefficient and its standard error as well as the corrected odds
ratio (comparing the risk and reference groups) for each
explanatory variable selected (40) .
Attempt to lyre left ventricular thrombi . After conclusion
of our study, four additional patients had a large protruding
mobile ventricular thrombus . Each received intravenous
streptokinase or urokinase in an attempt to achieve lysis of
tee thrombus. Streptokinase was given in doses usually
employed in patients with a thrombosed prosthetic valve
(41,42), namely, a 375,000IU bolus followed by 70,000 IU/h
and heparin, 1,000 U/h . Urokinase was given as previously
described by Kremer et al . (43), as a 250,000 IU bolus
followed by 75,000 IU/h and heparin, 1,000 U/h . After this,
warfarin therapy was started . Two of these patients have
been previously described (44,45), but the complications
noted and the relevance of these cases to those described in
the consecutive series warrant inclusion of this experience .
Results
Incidence and factors related to ventricular thrombus
before hospital discharge (Fig . 1) . A left ventricular thrombus was found on predischarge echocardiograms in 38 (31%)
of 124 patients with anterior and none of 74 patients with
inferior infarction (p < 0.001) . Of the 38 thrombi, 18 (47%)
were mural and 20 (53%) were protruding . Six (16%) of the
JACC Vol . t5 . No . 4
March 15, 1990:790-800
KEREN ET AL .
NATURAL HISTORY OF THROMBI
Table 1 . Predischarge Clii cal and Echocaruiographic
f virrelations in 124 Patients With Anterior Wall Myocardial
Infarction (univariate analysis)
showed similar findings in the two groups, except that
patients with a thrombus were younger (p = 0 .02) and had a
higher prevalence of left ventricular ejection fraction <35%
(p = 0 .01) . The incidence of hypokinetic apical contractility
was higher in patients without a thrombus (p = 0 .01),
whereas dyskinesia or left ventricular aneurysm, or both,
were more frequently found in patients with a thrombus (p =
0 .006) .
Stepwise logistic regression analysis (Table 2) showed
that anterior location of the infarct, decreased left ventricular ejection fraction (35%) and apical dyskinesia or aneurysm
had the highest association with left ventricular thrombus
during hospitalization .
Effect of early throw holytic therapy . Streptokinase was
given to 34 patients (Fig . 1) ; 26 had anterior infarction and 11
(42%) of these had an apical thrombus . Six (55%) of the 11
thrombi were mural, 4 (36%®) were protruding and 1(9%®) was
mobile . The mean thrombus size was 2 .7 ± 1 .9 cm' . None of
these patients had evidenced thrombus on the first echocardiogram performed within 12 h of hospitalization . Among
these 26 patients, thrombus was found in 5 (63%) of 8
patients without and in 6 (33%) of 18 patients with reperfusion (p = NS) . Among the 98 patients with anterior infarc .
Lion and no streptokinase therapy, 27 (28%) had a left
ventricular thrombus (p = NS compared with treated patients) . No significant differences were found among clinical
features, ejection fraction, type of thrombus or apical wall
motion between patients with and without streptokinase
therapy .
Left Ventricular
Thr,>mbus
Age (yr)
Male
Previous MI
Ant + inf MI
Maximal CK*
CHF
Arrhythmiast
Cardiogenic shock or CPR
LVEF (%)
LVEF =_?5%
Apical wall motion (echo)
Hypokinesia
Akincsia
Dyskinesia/aueurys n
Present
(n = 38)
Absent
(n = 86)
59 13
36(95%)
30%)
4(11%)
7.4 ± 3 .9
14(37%)
10 (26%)
4 (11°( t
32 ± 11
34 189x)
71 (83%)
22(26%)
1002%)
7.0 ± 4 .6
43150%)
21 (24%)
14(16%x)
40 ± 12
57(66%)
0 .02
NS
NS
NS
NS
NS
NS
NS
NS
0 .01
0
2-1 (587()
16(421/(, )
18 (21 1/c)
52 46fff)
16,19%)
0 .01
NS
0 .1N16
64 ± 11
793
p Value
*Multiples of upper normai limit of creatie kinase (CK) level . tAtrial
fibrillation, ventricular tachycardia or fibrillation, complete heart block . Ant
= anterior ; CHF = congestive heart failure : CPR = cardiopulmonary resustation ; echo = echocarliography : int' = inferior; LVEF = left ventricular
ejection fraction ; MI = myocardial infarction .
38 thrombi were mobile ; a,) 6 were of the protruding type .
Mean thrombus size was 3 .2 ± 1 .6 cm 2 (range 0 .5 to 7 .1) .
Comparison of clinical and laboratory data in patients
with anterior infarction with and i ;-ithout thro®nbaac (Table 1)
Table 2 . Results of Stepwise Logistic Itegre,s .,ion Analysis
Variable
Beta
Standard
Error
Odds Ratio
p Valu.
Predischarge LV thrombus
Anterior MI (Pre)
LVEF s35% (Pre)
Aneurysm (Pre)
2 .22
1 .49
1 .00
1 .08
0 .52
0.45
9 .20
4 .42
2 .73
0.04
0 .005
0.03
Follow-up new LV thrombus
:
Deterioration iii LV contractility (FU)
LVEF <_35% (Pre)*
Aneurysm (Pre)t
2 .46
1 .54
.46
1
0 .90
0.69
0.90
1) .80
4 .69
4 .31
0.006
0 .02
0.05
Follow-up; disappearance of LV thrombus
No dyskinesialaneurysm (Pre)*
Long-term anticoagulant therapy (FU)
1 .59
1 .38
0.80
0 .92
4 .90
? .00
0 .03
0 .04
Systemic embolism
LV thrombus mobility (Pre)§
6 .80
0.43
6 .10
0.001
*Because follow-up and predischarge left ventricular ejection fraction (LVEF) =_35% showed a high correlation
coefficient (r = 0.79), the model arbitrarily included one of these variables . because follow-up and predischarge
ventricular aneurysm showed a high correlation coefficient (r = 0 .81), the model arbitrarily also included one of these
variables . #Apical aneurysm during follow-up showed a negative correlation coefficient (r = -0 .98) with apical
akinesia and could replace it in the model . §Presence of presdischarge left ventricular thrombus showed a high
correlation coefficient (r = 0 .89) with thrombus mobility. FU = follow-up; LV = left ventricular ; Pre = predischarge ;
other abbreviations as in Table 1 .
JACC Vol . 15, No. 4
March 15, 1990:790-800
KEREN ET AL .
NATURAL HISTORY OF THROMBI
794
FQLt2W-1110 6E611111110
LYr MM LOCATION OF
ANI
n-159
Nat<..et
inf In
n∎95
n-64
I
s
nuam
-
1i
6YL
1~
n-29
n-66
n-64
it
LIE
n-10
no 3
L1
n-14
F
1~xti
Lwrt
n• 2
13/130(106)
s
LYr14/29(46%)
LYT+
6/130(4 .60
Figure 2 . Posthospitalization appearance (LVT+) and disappearance (LVT-) of left ventricular thrombus in 159 patients with at
least 6 months (mean 26 .6 ± 8.4) of echocardiographic follow-up .
*In two patients, thrombus recurred and resolved again during
further follow-up . Abbreviations as in Figure I .
Long-Term Echocardiographic
Follow-Up (Fig . 2)
An echocardiographic follow-up period of at least 6
months was accomplished in 159 patients . Predischarge
thrombus was foorid in 29 (31%) of the 95 patients with
anterior infarction and in none of the 64 patients with inferior
infarction .
Appearance of new left ventricular thrombus during follow-up (Fig. 2) . Of 130 patients without a predischarge
thrombus 13 (10%) had a new thrombus ; in 8 it was mural, in
5 it was protruding and in I of the latter it was mobile . The
mean size was 4.4 ± 4 .3 cm 2 (range 1 .0 to 15 .0) . The
thrombus was observed at a mean of 4 .6 ± 2 .1 months after
hospital discharge, but in four cases it first appeared at >6
months of follow-up . When compared by univariate analysis
with the 117 patients without a new thrombus, the 13
patients with a new thrombus hed a significantly higher
prevalence of previous myocardial infarction (p = 0 .005),
congestive heart failure during hospitalization and follow-up
(p < 0.05 for both), left ventricular aneurysm during hospitalization and follow-up (p = 0 .001 for both), decreased left
ventricular ejection fraction during hospitalization and follow-up (p < 0 .01 for both) and deterioration in left ventricular contractility during follow-up (p = 0 .001). Deterioration
in apical contractility from hypokinesia to akinesia or from
akinesia to dyskinesia was similar in the two groups (p =
0 .1) . Compared with the patients with a predischarge thrombus, those with a new thrombus after discharge showed a
higher incidence of previous infarction (p = 0 .006) .
Logistic regression analysis revealed three variables to
be related to occurrence of a new left ventricular thrombus
after discharge (Table 2) : 1) deterioration in overall left
ventricular contractility during the follow-up period, 2) predischarge left ventricular ejection fraction <_35%®, and
3) predischarge ventricular aneurysm or dyskinesia .
Disappearance and changes in morphology of predischarge
thrombus (Fig. 2). Three of the 38 patients with a predischarge thrombus were lost to follow-up study, 3 died and 3
underwent surgical procedures before repeat echocardiographic studies . The remaining 29 patients were followed up
by echocardiography for ~6 months . Fourteen (48%) of the
29 predischarge thrombi disappeared during 6 .5 ± 3 .7
months (range 2 to 13), and 10 of these 14 thrombi disappeared within 6 months . The thrombus persisted until the
end of the follow-up period in the other 15 patients (52%) .
and 13 (87%) of these showed no significant change in size .
The clinical features in the 14 patients with and the 15
without disappearance of thrombus were similar . However,
the predischarge echocardiogram disclosed apical akinesia in
11 (79%) of the 14 patients with disappearance but in only 6
(40%) of the 15 with persistence of thrombus (p = 0 .03) .
Apical aneurysm or dyskinesia was found in three patients
(21%) with thrombus disappearance and in nine (60%) of
those with thrombus persistence (p = 0 .03) . Improvement or
deterioration in left ventricular global and apical contractility
was similar in patients with and without persistence of
thrombus .
The morphology of the 14 thrombi that disappeared (6
mural, 6 protruding and 2 mobile) and their size were similar
to those of the thrombi that persisted .
Changes in shape and mobility could be evaluated in 27
thrombi (2 thrombi could not be detected on the first
echocardiographic study after discharge) . In 6 (22%) of the
27 thrombi, a change occurred in thrombus shape ; 5 protruding thrombi became of the mural type and I mural thrombus
evolved into the protruding type . In four patients, the
thrombus lost its mobility during follow-up .
Stepwise logistic regression analysis (Table 2) disclosed
that two variables were related to disappearance of predischarge thrombi : 1) apical akinesia on the predischarge
echocardiogram, and 2) long-term anticoagulant therapy .
Long-term anticoagulant therapy . This was administered
to 19 of 130 patients without a predischarge thrombus ; a
thrombus did not occur in the 16 patients who continued
receiving anticoagulant therapy until the end of the follow-up
period (Fig. 3) . Thrombus occurred in 13 (11%) of 114
patients without any or without continuous long-term anticoagulant therapy (p = NS) (Fig. 4) . Three of these 13
KEREN ET AL .
NAB ORAL HISTORY OF THROMBI
JACC Vol . VS, No . 4
March 15, 1990 :790-800
EQL
PREDISCUMSE
FOLLOW-UP
GAPME-Nn-AN-A
n469
km
nQ9
Aft9
j1q__
R-20
-11
719(78%)
7/20(36%)
k&-
_&__
n-16
n-114
795
patients had aneurysm and no thrombus while receiving
anticoagulant therapy for 3 to 21 months, but a thrombus did
occur 1 .5 to 3 months after cessation of anticoagulant
therapy . After diagnosis of a new thrombus, treatment with
warfarin was begun in all 13 patients, and the thrombus
resolved in I during a further follow-up period of 3 to 18
months (mean 6 .8 ± 4 .9) (Fig . 3 and 4) .
Among the 29 patients with a predischarge thrombus,
long-term anticoagulant therapy was administered to 9 (Fig .
3) . The thrombus disappeared in 7 (7890 of the 9 patients
To0/16(0%)
--AU-
n-13 L91°4
-Lifft6/114(5%)
Figure 3 . Correlation between changes in echocardiographic incin
dence of left ventricular thrombus and long-term anticoagulant
therapy during follow-up . Ac+ = long-term anticoagulants administered ; Ac- = no anticoagulant therapy given, other abbreviations
as in Figure 2 .
Figure 4 . Formation of a left ventricular thrombus after hospital
discharge . Upper panel : A, Patient with apical dyskinesia without
predischarge thrombus . B . Protruding thrombus (T) found 3 months
later . C . Resolution of the thrombus after 5 months of warfarin
therapy . Lower panel : A, Patient with left ventricular (LV) aneurysm (an) . Thrombus was not found before discharge and during 12
months of echocardiographic follow-up study while warfarin was
administered . B, A mobile thrombus (1) detected 3 months after
cessation of anticoagulant therapy, which resolved (C) within 2
months of renewed anticoagulant t herapy . L A = left atrium ; RA
right atrium : RV = right v ;mtricie .
796
JACC Vol . 15, No. 4
March 15, 1990:790-800
KEREN ET AL .
NATURAL HISTORY OF THROMBI
Table 3 . Use of Thrombolytic Agents for Lysis of Apical Mobile Thrombus During Acute
Myocardial Infarction in Four Patients
Thrombolytic Therapy
Patient No .
Age (yr)/
Gender
Day Post
Ml
Type
Duration
Ih)
Outcome
I
2
3
4
41/M
451M
591M
541M
23
10
8
8
UK
STK
STK
STK
36
14
64
54
Successful, no complications
Successful. no complications
Successful, transient diplopia
Stroke,* death
*Fifteen percent of the original thrombus persisted and embolized. M = male ; STK = streptokinase ; UK =
urokinase : other abbreviations as in Table I .
with and 7 (3517,)) of we 20 patients without anticoagulant
therapy (p < 0 .05) . In five patients (three with aneurysm and
two with apical akinesia), warfarin therapy was stopped 3 to
12 months after resolution of the thrombus . However,
thrombus recurred in two patients with aneurysm and disappeared again after renewal of anticoagulant therapy . In
none of the seven patients with thrombus resolution without
long-term anticoagulant therapy was recurrence of a thrombus seen .
Systemic embolism . Six (17%) of the 35 patients with a
thrombus on the predischarge evaluation had systemic embolism during the follow-up period . None of the 154 patients
without a thrombus had systemic embolism (p < 0 .001) .
Among the 13 patients who developed a new thrombus
during the follow-up period and received long-term anticoagulant therapy thereafter, none had systemic embolism .
The time interval between hospital discharge and embolization was 10 .9 ± 14.0 months (range I to 36), but four patients
had embolism within 6 months . Two, emboli were to a limb
and organized thrombus was retrieved at surgery . In four
patients, an ischemic type cerebrovascular accident was
diagnosed, and two of these patients died . Systemic embolism occurred in I (7%) of 14 patients with a predischarge
mural thrombus, 1 (7%) of 15 with a protruding nonmobile
thrombus and 4 (66%) of the 6 with a protracting mobile
thrombus (p < 0 .001) .
Long-term anticoagulant therapy . Twenty-one patients
(9 with thrombus on the predischarge echocardiogram and 13
with a new thrombus during follow-up period) received
long-term anticoagulant therapy and none had systemic
embolism. Of the 26 patients with a thrombus without
anticoagulant treatment, 6 (23%) had an emboik' event (p <
0 .02) . Stepwise logistic regression analysis (Table ?) related
subsequent embolic events to presence of a protruding
mobile thrombus (p = 0 .001).
Prognostic significance of a left ventricular thrombus .
Twenty-nine patients (15%) died among the 189 patients
observed during the 2 year follow-up period . Cause of death
was congestive heart failure in 12, recurrent myocardial
infarction in 5, sudden cardiac death in 8, cerebrovascular
accident in 2 and unknown in 2 . The mortality rate was 23%
(8 of 35) in those with anterior infarction associated with a
predischarge thrombus, 15% (13 of 84) in those with anterior
infarction without a thrombus and I 1 % (8 of 70) in those with
inferior infarction (p = NS) . There were no significant
complications related to warfarin therapy .
Thrombolytic therapy for apical mobile thrombus (Table
3). Urokinase or streptokinase was used in four patients
who were not part of the consecutive series described here ;
Data on patients I and 2 have been previously published
(44,45) . All four patients had anterior infarction with apical
akinesia or dyskinesia, and the diagnosis of thrombus was
made on days 5 to 16 . Ejection fraction ranged from 28% to
46% . After diagnosis of thrombus, systemic heparinization
was applied for 48 to 72 h . During heparin therapy, Patient I
had a transient ischemic attack, with disappearance of the
smallest of three apical thrombi originally found . Because
heparin therapy did not change thrombus size or mobility,
urokinase or streptokinase was started . In all four cases, a
significant decrease in size of the thrombus, together with a
marked increase in its mobility was seen 8 to 12 h later . In
Patients I and 2, the thrombus disappeared without complications . In Patient 3, diplopia occurred 9 h after the start of
streptokinase infusion . Heparin infusion was continued, but
streptokinase administration was stopped for 24 h until
complete resolution of diplopia. The renewed streptokinase
infusion led to complication-free resolution of the thrombus .
Patient 4 had a large protruding mobile apical thrombus
that decreased significantly in size after 52 h of uncomplicated infusion of streptokinase . One hour later, the patient
suddenly lost consciousness and developed signs of a right
hemispheric stroke . Disappearance of the apical thrombus
was documented by immediate echocardiography ; computed
tomography excluded cerebral hemorrhage and showed the
presence of extensive right hemispheric infarction (Fig . 5) .
The p.Atient died a few days later .
Patients 1, 2 and 3 were discharged on long-term anticoagulant treatment . During 20 to 32 months of follow-up,
thrombus recurred in one patient after cessation of warfarin,
but disappeared again after renewal of anticoagulant therapy .
JACC Vol, 15, No . 4
March 15 . 1990:790- 800
KEREN ET AL .
NATURAL HISTORY OF THROMBI
Figure 5 . Fatal cerebral embolism in a patient with a mobile apical
thrombus who received streptokinase . A, Echocardiogram showing
a large apical thrombus (T) (arrows) with a mobile protruding
portion . B, The thrombus after 52 h of uncomplicated sti optokinase
therapy . C, One hour later, signs of right hemispheric stroke
occurred and the thrombus disappeared . D, Computed tomography
showed extensive right hemispheric cerebral infarction (Cl) occupying the territory of the right middle cerebral artery . L = left ;
my = mitral valve ; R = right ; tv = tricuspid valve .
Discussion
Determinants of ventricular thrombus appearance before
hospital discharge. Logistic regression analysis showed that
anterior location of the infarction, left ventricular ejection
fraction :s35% and apical dyskinesia or aneurysm were the
major variables related to thrombus formation . The 31%
incidence rate of left ventricular thrombus in anterior infarction and its absence in inferior infarction are in agreement
with previous reports (8-14) . In anterior infarction, furt.`er
clinical variables (such as previous infarction, congestive
heart failure, cardiogeaic shock, maximal serum enzyme
levels) did not separate patients with and without predischarge thrombus . Thus, on the basis of clinical criteria, all
patients with anterior infarction should be considered at high
risk of thrombus formatio .j . Decreased ejection fraction was
an independent predictor of (46) but not a prerequisite for
(11) thrombus formation . Thrombus is rare in the presence of
797
a preserved or only mildly decreased left ventricular ejection
fraction, but may occur in patients with an apical aneurysm,
as seen in four patients in this series . Similar to find-ngs in
other studies (8,46), apical dyskinesia or aneurysm correlated better with thrombus occurrence by univariate (p =
UK (Table 1) or multivariate (p = (103) (Table 2) analysis
than did akinesia (p = NS) .
Effect of early fibrinolyfic therapy . This study did not
demonstrate a benefic ;al effect of early fibrinolytic therapy
on left ventricular ejection fraction and the incidence of
thrombus . Sharma et al . (29) observed thrombus within 24 h
of streptokinase administration . In the present study, thrombus was found only after the lytic phase, while patients were
fully anticoagulated . The unusually high incidence of thrombus (42%) found in our patients with anterior infarction
receiving streptokinase may be related to the small number
of patients evaluated . However, two randomized (28,30) and
one uncontrolled (29) study showed an incidence of 26% to
55% of thrombus in similar patients . In contrast, Eigler et al .
(27) compared 12 patients treated with and 10 patients
without early thrombolytic therapy and found a significant
improvement in both ejection fraction and thrombus incidence in the treated group . Our present study and a previous
study (30) showed a statistically nonsignificant trend toward
fewer thrombi in patients with successful reperfusion .
Appearance of ventricular thromLns during follow-up .
Prospective echocardiographic studies have shown that 33%
to 62% of thrombi detected during hospitalization are
present within 48 h of the acute event (18,20,24,27) and some
may be found at admission (20) . Few data (8, 18,20) are
available concerning the appearance of thrombi after hospitalization . In 13 (1017c) of our 130 patients . a thrombus first
developed during the follow-up period . This was found in
15% of patients with anterior and 5% of those with inferior
infarction . All patients with inferior infarction had either a
large inferior wall aneurysm or severe inferoapical asynergy .
The new thrombus occurred within 6 months of the infarction in 69% of cases, and in 38% of the cases, it was of the
protruding type (Fig . 4) . None of the 16 patients on continuous anticoagulant therapy developed a thrombus during the
follow-up period compared with 11% of patients without
anticoagulant therapy (p = NS) .
Logistic regression analysis showed three factors to be
related to the occurrence of thrombus after hospital discharge : 1) deterioration in left ventricular ejection fraction
during the f
P,:r ;-J . '.) iniiiall,' low ejection fraction,
and 3) ventricular aneurysm or dyskinesia during hospitalization or follow-up . Previous infarction and congestive
heart failure showed a significant correlation with the occurrence of thrombus by univariate but not by stepwise logistic
regression analysis .
Disappearance of thrombus during follow-up . Logistic
regression analysis revealed that the type of apical wall
motion before and warfarin therapy after hospital discharge
798
KEREN ET AL .
NATURAL HISTORY OF THROMBI
were the major factors associated with disappearance of
thrombus in 48% of the patients with a predischarge thrombus . Thrombus disappeared in 65% of patients with apical
akinesia but in only 25% of those with apical aneurysm or
dyskinesia (p = 0 .03) . Seven of the 13 new thrombi found
after hospital discharge disappeared during further follow-up
(Fig. 4) . Improvement in wall motion adjacent to the thrombus has been suggested as a possible mechanism for thrombus resolution (10) . The current study and others (20,22) do
not support this observation .
Thrombus disappeared in 78% of patients wcompared
w t only 35% of those without long-term anticoagulant
t erapy (p < 0 .05) . A randomized study (32) of warfarin
therapy in patients with thrombus after acute myocardial
infarction demonstrated 88% versus 24°j~ disappearance
rates in treated and untreated patients, respectively . In
nonrandomized studies (8,10,11,18 .20,27,33) thrombus disappearance rates have ranged from 42% to 84% with and
14% to 40% without long-term anticoagulant therapy . The
beneficial effect of long-term anticoagulant therapy has been
supported by indium-Ill platelet imaging, which showed
prolonged (months to years) surface activity of thrombi with
active platelet deposition (47,48) and inhibition of this activity by warfarin in some cases (48) . Furthermore, there are
reports (8,20) of thrombus reappearance after cessation of
anticoagulation therapy . to this study and another study
(20), thrombus recurred after cessation of anticoagulants
only in patients with aneursym or dyskinesia, not in those
with apical akinesia.
Systemic embolism . Previous studies (8-21,25,26,33)
have demonstrated systemic embolism in 147 (20%) of 746
patients (range 4% to 63%) with echocardiographically documented ventricular thrombus, but in only 16 of 785 patients
(2%, range 0 to 4%) without thrombus . In this study,
systemic embolism occurred in 6 (17%) of 35 patients with a
thrombus, but in none of the 154 patients without a predischarge thrombus (p < 0 .001) . Clinical and nuclear angiographic variables were not predictive of embolic events .
Although most embolic events occur within 6 months of
infarction, ventricular thrombus continued to represent an
increased risk for systemic embolism in the current and
previous (12-15) reports .
Thrombus mobility on predischarge echocardiographv
showed the best correlation with subsequent embolic events
(p < 0 .001), The incidence of embolism in patients with a
mobile thrombus has ranged from 13% to 83% (11-17) and, in
most cases, mobile thrombi were of the protruding type
(13-20) . The reported average rates of systemic embolism
were 55% (47 of 86) in protruding mobile, 18% (18 of 102) in
protruding nonmobile and 10% (25 of 255) in mural thrombi
(11-16,18) . Changes in thrombus shape and mobility were
common when evaluated from the first day of infarction (18),
but were rare in patients evaluated ?3 months after the acute
event (33) . In the present study, the morphologic character-
JACC Vol . 15, No . 4
March 15, 1990 :790-800
istics of persistent thrombus defined before hospital discharge remained relatively stable and were predictive of
subsequent embolic events . A thrombus formed after hospital discharge was not associated with systemic embolism .
However, in this group, there was only one patient with a
mobile thrombus, and long-term anticoagulant therapy was
given to all patients immediately after detection of thrombus .
Further studies are needed to evaluate the embolic potential
of thrombi formed during follow-up .
It has been suggested that long-term anticoagulant therapy is not indicated in patients with ventricular aneurysm
because of a low incidence of embolism (6,49-51) . In the
current series, three of six emboli occurred in patients with
a ventricular aneurysm . Moreover, cessation of anticoagulant therapy after periods of up to 2 years was associated
with either recurrence or first appearance of a new thrombus
only in patients with aneurysm . Similar to our results, other
investigators (12,15,17) found the same incidence of embolism in patients with and without aneurysm, and Reeder et
al . (52) demonstrated that in patients with aneurysm, the
frequency of systemic embolism decreased significantly with
longer periods of anticoagulant therapy .
Fibrinolytic therapy in patients with a mobile apical thrombus. Kremer et al . (43) reported lysis of a protruding thrombus in 10 of 16 patients after acute myocardial infarction . At
least three of their patients had a mobile thrombus . The
treatment was successful in eight of nine patients within 4
weeks of the acute infarction . None of the patients had
clinical embolism, and only in one was therapy discontinued
because of hematuria . Shenoy et al . (53) reported successful
lysis of an apical mural thrombus with streptokinase . Considering the foregoing discussion, we selectively applied this
therapy to four patients with a protruding mobile thrombus .
In the first two previously reported cases (44,45), lysis of
thrombus was achieved without complication . In the latter
two cases, however, systemic embolism occurred, with
transient diplopia in one and stroke followed by death in the
other. This experience confirms that fibrinolytic agents are
capable of lysing ventricular thrombi but suggests that the
risks of this therapy may be higher than previously assumed .
Limitations of the study . This was an observational study
in which anticoagulant and fibrinolytic therapies were not
controlled and were applied to a small number of patients .
Therefore, the results regarding these therapies are not
conclusive . The data regarding resolution and appearance of
a new thrombus during the follow-up period can be applied
only to long-term survivors on medical therapy because
echocardiographic follow-up of ?6 months was not available
in approximately 20% of the patients, mostly because of
death or operative interventions during that time period . The
results of univar9 .ate statistical .analysis should be considered
with caution given the multiple comparisons made . However, we also used logistic regression analysis, which eliminated fortuitous statistical significance .
JACC Vol . 15, No. 4
March 15,1990 :790-800
KEREN ET AL .
799
NATURAL HISTORY OF THROMBI
Clinical implications . The results of this study support
the view that echocardiography should be routinely performed before hospital discharge in all patients with acute
anterior myocardial infarction (54,55) to 1) diagnose patients
with ventricuiar thrombus and those with a protruding
mobile thrombus who are at especially high risk of embolization ; 2) define patients at risk of developing thrombus
after hospital discharge ; and 3) identify patients who may
undergo resolution of thrombus during follow-up . We did not
demonstrate a reduction in incidence of lentricular thrombus by early fib inoytiQ therapy and a full dose of anticoagulants during the acute phase of infarct'an . However, longterm anticoagulant therapy applied to a relatively small
number of patients in the posthospitalization period was
associated with an increased resolution rate of thrombus and
with prevention of systemic embolism in patients with documented thrombus . Long-term anticoagulant therapy under
echocardiographic guidance is probably indicated until resolution of the thrombus is seen on the follow-up echocardiogram . 1A eighing the risk-benefit ratio, long-term anticoagulant therapy may be given indefinitely to selected patients
with left ventricular aneurysm, decreased or deteriorating
left ventricular ejection fraction (that is, in the presence of
the factors that predispose to occurrence of a new thrombus
during the follow-up period) . Lysis of fresh thrombi with
thrombolytic agents is feasible, but may be associated with
death . More data are needed before thrombolysis is acceptea
as the therapy of choice in patients with a mobile thrombus
(56) .
We thank Richard L. Popp, MD of Stanford . California for reviewing the
manuscript and his valuable editorial comments . We thank Shaul Yalon for
technical help, and Hanna Sebag for preparation of the manuscript .
8.
singer RW . Mikell FL. Elsperger J . Hodges M . Incidence of leftvmoricular thrombosis after acute transmural myocardial infarction :
serial Avaluwion by two-dimensional echocardiography . N Engl I Med
198130 :197-302 .
9 . Friedman 011 ('srlson K . Marcus Fl . WcAfenden JM . Clinical correlations in patient, with acute myocardial infarction and left ventricular
thrombus detected by two-dimensional echocardiography . Am J Med
1982 :72 :894-8 .
10 . Keating EC . Gross SA, Schlamowitz RA, et al . Mural thrombi in
myocardial infarctions : prospective evaluation by two-dimensional echocardiography . Am J Med 19,93,74 :989-95 .
11 . Weinreich DJ . Burke JF, Pauletto FJ . Left ventricular mural thrombi
complicating acute myocardial infarction : long-term follow-up with serial
echocardiography . Ann intern Med 1984 :100 :789-94 .
12 . Haugland JM, Asinger RW, Mikell FL, Elspergcr J, Hodges M . Embolic
potential of left ventricular thrombi detected by two-dimensional echocardiography . Circulation 1984 :70 :588-98 .
13 . Meltzer RS, Visser CA, Kan G, Roelandt J . Two-dimensional echocardiographic appearance of left ventricular thrombi with systemic emboli
after myocardial infarction . Am J Cardiol 1984 :53 :1511-3 .
14 . Visser CA, Kan G, Meltzer RS, et al . Embolic potential of left ventricular
thrombus after myocardial infarction : a two-dimensional echocardiographic study of 119 patients . J Am Coll Cardiol 1985 :5 :1276-80 .
15 . Stratton JR . Resnick AD . Increased embolic risk in patients with left
ventricular thrombi . Circulation 1987 :75 :1004--11 .
16. Johannessen KA, Nordrehaug JE, von der Lippe G, Vollset SE . Risk
factors for embolisation in patients with left ventricular thrombi and acute
myocardial infarction . Br Heart J 1988 :60 :104-10 .
17 . Jugdutt BI . Sivaram CA, Wortman C, Trudell C . Penner P . Prospective
two-dimensional echocardiographic evaluation of left ventricular thrombus and embolism after acute myocardial infarction . J Am Coll Cardiol
1989 :13 :554-64 .
18. Domenicucci S, Bellotti P . Chiarella F . Lupi G . Vecchio C . Spontaneous
morphologic changes in left ventricular thrombi : a prospective twodimensional echocardiographic study . Circulation 1987 :75 :737-43 .
19. Spirito P, Bellotti P. Chiarella F, Domenicucci S . Sementa A . Vecc 'iio C
Prognostic significance and natural history of left ventricular thromft tit
patients with acute myocardial infarction : a two-dimensional echuc> -'
graphic study . Circulation 1985 -.72 :774-80,
References
20 . Visser CA . Kan G . Meltzer RS, Liek 1, Durrer D . Long-term follow-au, o•;.
left ventricular thrombus after acute myocardial infarction : a 'ovodimensional echocardiographic study in 96 patients . Chest 1984 ;86 :532-~ .
1 . Wright IS, Marple CD, Beck DF . Report of the Committee for the
Evaluation of Anticoagulants in the Treatment of Coronary Thrombosis
With Myocardial Infarction . Am Heart J 1948 ;36 :801-15 .
21 . Stratton JR, Lighty GW . Pearlman AS, Ritchie JL . Detection of I&
ventricular thrombus by two-dimensional echocardiography : sensitivity,
specificity, and causes of uncertainty . Circulation 1982 :66 :156-66 .
2 . Arnott WM, Bigs R, Gilchrist AR, et al . Assessment of short-term
anticoagulation administration after cardiac infarction : report of the
Working Party on Anticoagulant Therapy in Coronary Thrombosis to the
Medical Research Council . Br Med J 1969 :1 :335-42 .
22 . Nordrehaug JE . Johannessen KA, von der Lippe G . Usefulness of
high-dose anticoagulants in preventing left ventricular thrombus in acute
myocardial infarction . Am J Cardiol 1985 :55 :1491-3 .
3 . Veterans Administration Cooperative Study . Anticoagulants in acute
myocardial infarction : results of a cooperative clinical trial . JAMA
1973 ;225 :724-9 .
4 . Hellerstein HK, Martin JW . Incidence of thromboembolic lesions accompanying myocardial infarction . Am Heart 3 1947 :33 :443-52 .
5, Jordan RA, Miller RD, Edwards JE, Parker RL . Thromboembolism in
acute and healed myocardial infarction . Circulation 1952 :6 :1-6 .
6. Cabin HS, Roberts WC . Left ventricular aneurysm . intraaneurysmal
thrombus and systemic embolus in coronary heart disease . Chest 1980;
77 :585-90.
7 . DeMaria AN, Bommer W, Neumann A, et al . Left ventricular thrombi
identified by cross-sectional echocardiography . Ann Intern Med 1979 :90:
14-8.
23 . Davis MJ . Ireland MA . Effect of early anticongulation on the frequency of
left ventricular thrombi after anterior wall acute myocardial infarction .
Am J Cardiol 1986 :57 :1244-7 .
24 . Gueret P. Dubourg 0 . Ferrier A, Farcot JC, Rigaud M, Bourdarias JP .
Effects of full-dose heparin anticoagulation on the development of left
ventricular thrombosis in acute transmural myocardial infarction . J Am
Coil Cardio! 1986 :8 :419-26 .
25 . Aryan S, Boscha K . Prophylactic anticoagulation for left ventricular
thrombi after acute myocardial infarctior : a prospective randomized tri(4 .
Am Heart J 1987 :113 :688-93 .
26. Turpie AGG . Robinson JG, Doyle DJ, et al . Comparison of high-dose
with low-dose subcoatmous heparin to prevent left ventricular mural
thrombosis in patients w I acute transmural anterior myocardial infarction . N Engl J Med 1989 ;320 :352-7 .
800
KL:tEN ET AL .
NATURAL HISTORY OF THROMBI
JACC Vol . 15 . No . 4
March 15 . 1990 :790-800
27 . Eigler N. Maurer G . Shah PK . Effect of early systemic thrombolytic
therapy on left ventricular thrombus formation in acute anterior myocardial infarction . Am J Cardiol 1984 ;54:261-3 .
Besse PM . Acute thrombotic obstruction with disc valve prostheses :
diagnostic considerations and fibrinolytic treatment . J Am Coll Cardiol
1986 :7 :743-51 .
28 . Stratton JR. Speck SM. Caldwell JH, et al . Late effects of intracoronary
streptokinase on regional wall motion, ventricular aneurysm ind left
ventricular thrombus in myocardial infarction : results from the Western
Washington Randomized Trial . J Am Coll Cardiol 1985 :5 :1023-8 .
42 . Kurzrok S . Singh AK. Most AS, Williams DO. Thrombolytic therapy for
prosthetic cardiac valve thrombosis . J Am Coll Cardiol 1987 ;9 :592-8 .
29. Sharma B, Carvalho A, Wyeth R . Franciosa JA . Left ventricular thrombi
diagnosed by echocardiography in patients with acute myocardial infarction treated with intracoronary streptokinase followed by intravenot ;
heparin. Am J Cardiol 1985 ;56 :422-5.
30. Held AC, Gore JM, Paraskos J, et al . Impact of thrombolytic therapy on
left ventricular mural thrombi in acute myocardial infarction . Am J
Cardiol 1988 ;62 :310-1 .
31 . Meltzer RS . Guthaner D . Rakowski H . Popp RL . Martin RP. Diagnosis of
left ventricular thrombi by two-dimensional echocardiography . Br Heart
J 1979 ;42 :261-5 .
43 . Kremer P. Fiebig R, Tilsner V . Bleifeld W . Mathey DG . Lysis of left
ventricular thrombi with urokinase . Circulation 1985 ;72:112-8.
44. Keren A, M,dina A, Gottlieb S. Banai S, Stern S . Lysis of mobile left
ventricular thrombi during acute myocardial infarction with urokinase .
Am J Cardiol 1987 ;60 :1180-I .
45 . Keren A. Mazouz B . Moriel M . Tzivoni D, Stern S. Use of streptokinase
for lysis of a mobile left ventricular thrombus . report of a case and review
of the literature . Cardiology 1988;75 :444-7.
46 . Lamas GA, Vaughan DE . Pfeffer MA . Left ventricular thrombus forma .
tion after first anterior wall acute myocardial infarction . Am J Cardiol
1988 :62:31-5 .
32 . Tramarin R, Pozzoli M . Febo O. et al . Two-dimensional echocardiographic assessment of anticoagulant therapy in left ventricular thrombosis
early after acute myocardial infarction . Eur Heart J 1986-.7 :482-92,
47 . Ezekowitz MD, Wilson DA . Smith EO, el al . Comparison of indium- l I I
platelet scintigraphy and two-dimensional echocardiography in the diagnosis of left ventricular thrombi . N Engl J Med 1982 ;306 :1509-13 .
33 . Stratton JR . Nemanich JW . Johannessen KA . Resnick AD . Fate of left
ventricular thrombi in patients with remote myocardial infarction or
idiopathic cardiomyopathy . Circulation 1988 ;78 :1388-93 .
48 . Stratton JR. Ritchie JL. The effects of antithrombotic drugs in patients
with left ventricular thrombi : assessment with indium- I I I platelet imaging
and two-dimensional echocardiography . Circulation 1984 ;69:561-8.
34 . Asinger RW, Mikell FL, Sharma B, Hodges M . Observations on detecting
left ventricular thrombus with two-dimensional echocardiography : emphasis on avoidance of false positive diagnoses. Am J Cardiol 1981 ;47 :
145-56.
35 . Visser CA, Kan G . David GK, Lie K1, Duffer D . Two-dimensional
echocardiography in the diagnosis of left ventricular thrombus : a prospective study of 67 patients with anatomic validation . Chest 1983 ;83:228-32 .
36 . Keren A, Billingham ME . Popp RL . Echocardiographic recognition and
implications of ventricular hypertrophic trabeculations and aberrant
bands . Circulation 1984 :70:836-42 .
37 . Keren A, Takamoto T . Harrison DC . Popp RL. Left ventricular apical
masses : noninvasive differentiation of rare from common ones . Am J
Cardiol 1985 ;58:697-9.
38. Criteria Committee of the New York Heart Association . Nomet;ciaturc
and Criteria for Diagnosis of Disease of the Heart and Great Vessels . 7th
ed . Boston: Little .3rown, ±O73 :959.
39. Wackers FJT, Berger HJ . Jehnstone DE, et al . Multiple gated cardiac
blood pool imaging for left ventricular ejection fraction : validation of the
technique and assessment of variability . Am J Cardiol 1979 ;43 :1159-66.
40. Pregibond D. Logistic regression diagnostics . Ann Statist 1981 :9:705-24 .
41 . Ledain LD . Ohayon JP, Co!te JP. Lorient-Roudaut FM . Roudaut RP .
49 . Fuster V . Halperin JL . Left ventricular thrombi and cerebral embolism .
N EnglJ Med 1989 ;320:392-4.
50. Simpson MT. Oberman A . Kouchoukos NT, Rogers WJ . Prevalence of
mural thrombi and systemic embolization with left ventricular aneurysm :
effect of anticoagulation therapy . Chest 1980 ;77 :463-9.
51 . Lapeyre AC . Steele PM . Kazmier FJ, Chesebro JH, Vlietstra RE, Fuster
V . Systemic embolism in chronic left ventricular aneurysm : incidence and
the role of anticoagulation . J Am Coll Cardiol 1985 ;6:534-8 .
52. Reeder GS, Lengyel M, Tgjik AJ, Seward JB, Smith HC, Danielson GK .
Mural thrombus in left ventricular aneurysm : incidence, role of angiography, and relation between anticoagulation and embolization . Mayo Clin
Proc 1981 ;56:77-81 .
53 . Shenoy MM . Friedman SA . Dhar S . Berman P . Streptokinase lysis of
intraventricular thrombus and pulmonary emboli with resolution of acquired intracardiac shunt . Ann Intern Med 1985 :103:65-6.
54 . Nixon JV . Left ventricular mural thrombus . Arch Intern Med 1983 ;143 :
1567-71 .
55 . Kaplan K. Prophylactic anticoagulation following acute myocardial infarction. Arch Intern Med 1986 ;146:593-7.
56 . Gutt,:rman DD . Characterization of the acute left ventricular thrombus :
hermit or nomad? J Am Coll Cardiol 1989:13 :565-6.