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From Service de Cardiologie B et Hémodynamique, Hôpital
Cardiologique, Lille Cedex, France.
Correspondence to M.E. Bertrand, MD, Service de Cardiologie B, Hôpital Cardiologique, Boulevard du Professeur J Leclercq, 59037 Lille Cedex, France. E-mail bertrandme{at}aol.com
Methods and ResultsWe studied with angioscopy the
morphological characteristics of the infarct-related lesion in 56
patients between 24 hours and 4 weeks after MI. Forty of these patients
were initially treated with a thrombolytic agent. Most
lesions were complex (complex+ulcerated shape=54%). The predominant
color of the plaque was yellow in 79% of cases; only 6% were
uniformly white. Angioscopically visible thrombus was found in 77% of
cases. Despite angioscopic evidence of instability, only 7% of the
patients had post-MI angina. During the 1-month time window since the
occurrence of MI, there was no significant difference in the
angioscopic appearance of the plaque except for a slight increase in
uniformly white plaques (P=.07). The use of a
thrombolytic agent at the onset of MI was associated
with a reduction in thrombus size and less protruding thrombi
(P=.02) but not with a decreased frequency of plaque
containing thrombi. Furthermore, a trend for more frequently ulcerated
plaques (45% versus 16%, P=.06) was associated with
the use of a thrombolytic agent.
ConclusionsThese results suggest that healing of the
infarct-related lesion requires more than 1 month and that an
"unstable" yellow plaque with adherent thrombus is common during
that period. This finding may partly explain the unique behavior of
recent infarct-related lesions, which are more prone to occlude than
other lesions.
Coronary angioscopy provides direct visualization of the
intravascular lumen and permits a complete description of plaque
surface. This technique has been validated by the results of
histopathology4 and provides information that
cannot be obtained by angiography5 on plaque
shape and color and on the presence and the size of thrombi. To date,
several authors have described the angioscopic characteristics of the
infarct-related lesions early after MI.6 7 8 9 Few
data are available,8 10 however, on the
appearance and characteristics of the plaque during the subsequent
weeks, the time window within which most such occlusions occur. In
addition, while the effect of thrombolysis on the
angiographic morphology of the infarct-related lesion is well
characterized,11 12 there are few angioscopic
data. Indeed in the only published series that used angioscopy to
investigate the effect of thrombolysis on plaque
morphology, thrombolysis was not specifically performed
for acute MI but to study its effects on intracoronary thrombus
identified on angioscopy.9
The purpose of the study was (1) to describe the morphological
characteristics of the infarct-related lesion within 1 month of MI in a
large population of patients initially treated by
thrombolysis or conservative medical management; (2) to
describe the natural history of such lesions as a function of elapsed
time in the month after MI; and (3) to evaluate the effect of
thrombolytic therapy on the angioscopic characteristics
of the infarct-related lesion.
During the time period of the study (January 1992 to June 1994), 592
patients underwent PTCA of an infarct-related lesion between 24 hours
and 4 weeks after acute MI. All patients were considered potential
candidates for angioscopy, and the procedure was performed if the
following criteria were met: (1) patients had MI between 24 hours and 4
weeks before angiography; (2) the infarct-related artery; determined
from the entry ECG, ventriculographic contraction abnormalities, and
coronary angiography findings; was clearly identifiable; (3)
percutaneous or surgical
revascularization was not attempted before
coronary angioscopy; (4) the infarct-related lesion was
anatomically suitable for angioscopy (see below); and (5) angioscopy
equipment and staff skilled in angioscopy were available at the time of
PTCA. The protocol was approved by the Institutional Review Board of
our institution and informed consent was obtained from all patients
before angioscopy.
Thus angioscopy of the infarct-related lesion was performed in 56
patients between 24 hours and 4 weeks after an acute MI and before any
mechanical revascularization procedure (angioplasty
or coronary artery bypass grafting). For the purpose of the
study, patients were classified depending on whether or not they had
received thrombolytic therapy at the time of MI. They
were also classified as a function of the time elapsed between the MI
and the angioscopy procedure into early-recent MI (24 hours to day 10)
and late-recent MI(day 11 to day 30).
Angioscopy Procedure and Analysis
Coronary angioscopy was performed with the ImageCath system
(Baxter, Edwards LIS Division), which includes an angioscope catheter,
an irrigation system, a light source, and a video
system.13 Aspirin (500 mg IV) was given 2 hours
before the procedure. After administration of 10{ths}000 IU of
heparin, the lesion was crossed with a standard 0.014-in floppy
guidewire. The angioscopy catheter was then advanced over the guidewire
and an initial recording was obtained while the angioscope was
advanced through the lesion; subsequently, another recording
was obtained while the angioscope was withdrawn. The guidewire was left
in place and the angioscopy catheter was then exchanged for a standard
PTCA catheter.
All videotapes were reviewed jointly by two physicians who were unaware
of the angiographic findings. The definitions and classifications used
(Table 3
The angioscopic evaluation of the plaque before PTCA consisted of an
assessment of the shape of the narrowing, plaque color, and presence of
thrombus. The shape of narrowing was classified as smooth concentric,
smooth eccentric, complex, or ulcerated; a lesion was classified as
smooth eccentric if a segment of normal-appearing wall was visualized
at the site of the lesion; a complex narrowing was defined as an
irregular plaque with jagged edges; an ulcerated plaque was defined as
an area of lining red clot surrounded by irregular plaque. The color of
the plaque was classified as white or yellow. The "predominant"
color was defined as the color that made up >50% of the plaque
surface seen on angioscopy. The "darkest" color was defined as the
darkest zone seen in any part of the plaque. Angioscopic thrombus
(Figure
Angiographic Analysis
Quantitative computer-assisted angiographic measurements of the lesion
were performed on end-diastolic frames by a single
investigator unaware of the angioscopic findings with the CAESAR
(Computer Assisted Evaluation of Stenosis And
Restenosis) system.19 We routinely
perform angiography in at least two projections, after
intracoronary injection of isosorbide dinitrate (2 mg).
Reference diameter and minimal luminal diameter were measured and
percent stenosis was calculated for each lesion. Total
occlusion was defined as a TIMI grade
Statistical Analysis
The angiographic characteristics of the infarct-related lesion are
summarized in Table 2
The angioscopic characteristics of the lesions are summarized in Table 3
Angioscopic Variables According to the Time Elapsed Since
MI
Angioscopic Variables According to the Use of a
Thrombolytic Agent at the Time of MI
Diagnostic Value of Angiographic Criteria for
Intracoronary Thrombi
The results of the present study demonstrate that angioscopic
characteristics of plaque instability (complex morphology, yellow
color, thrombus) last during 1 month after MI, even in
asymptomatic patients and in patients initially treated
with thrombolysis. These findings provide a possible
explanation for the unique behavior of the infarct-related lesions that
are more prone to late occlusion than other lesions. In the era of new
and very potent antiplatelet therapies, and with expanding
indications for coronary stenting, these findings have
potential implications for the clinical management of patients after
MI.
The Present Study and Its Relation to Previous Studies
It is important to emphasize that the results of the present
study, as well as the results of Ueda et al,8 are
significantly different from those reported by Tabata et
al10 in a group of patients who underwent
angioscopy at a mean interval of 2 weeks after MI. In this study only
50% of the patients had yellow plaques and only 43% had lesions
containing thrombi. A possible explanation for the apparent discrepancy
relates to the high proportion of patients in their study in whom
revascularization was achieved by mechanical means
alone (34%); by contrast, this was the case in only 9% of patients in
the study by Ueda et al and in none of the patients in our study.
Angioscopic Findings: Relation to Symptoms
These results are significantly different from those of Tabata et
al,10 who found that thrombus, identified by
angioscopy, was highly predictive of clinical instability. As already
discussed, the population studied by Tabata et al was significantly
different from the population in the present study in that a high
proportion of patients were initially treated with balloon angioplasty
(34%); in addition, the clinical presentation at the onset
of MI was more frequently a nonQ-wave MI (10%), and a significantly
higher proportion of patients had post-MI unstable angina (33%).
Effect of Thrombolysis on Plaque Morphology and
Thrombus Burden
The use of thrombolysis was associated with a slightly
higher prevalence of ulcerated plaques (P=.17). Similarly,
the percentage of uniformly white plaques, a marker of plaque
stabilization, was lower in patients treated with
thrombolysis (P=.01; Table 5
These data provide new insights into residual plaque morphology
after thrombolysis for acute MI. They demonstrate that
thrombolysis is associated with a reduction in thrombus
mass but that, perhaps surprisingly, morphological characteristics of
plaque instability last for several weeks and are even more
frequent in patients treated with thrombolytic
agents.
Angiographic Versus Angioscopic Identification of Thrombus in
Recent MI
Therapeutic Implications of the Presence of Thrombus in Recent
MI
These results are also consistent with the observation that the
initial success of thrombolysis for acute MI, as
documented by vessel patency at angiography at 48 hours, is countered
by reocclusion within 3 months in almost 30% of
patients.1 2 Indeed the high rate of reocclusion
in this setting is associated with deleterious effects on both left
ventricular ejection fraction20 and
on clinical outcome.22
Study Limitations
Conclusions
Received June 19, 1997;
revision received September 5, 1997;
accepted September 25, 1997.
2.
Takens BH, Brügeman J, van der Meer J, den Heyer
P, Lie KI. Reocclusion three months after successful
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Siegel RJ, Ariani M, Fishbein MC, Chae JJ, Park JC,
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den Heijer P, Foley DP, Escaned J, Hillege HL, van
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6.
Mizuno K, Satomura K, Miyamoto A, Arakawa K, Shibuya
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N Engl J Med. 1992;326:287291.[Abstract]
7.
Mizuno K, Miyamoto A, Satomura K, Kurita A, Arai T,
Sakurada M, Yanagida S, Nakamura H. Angioscopic coronary
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8.
Ueda Y, Asakura M, Hirayama A, Komamura K, Hori M,
Kodama K. Intracoronary morphology of culprit lesions after
reperfusion in acute myocardial infarction: serial angioscopic
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9.
Feld S, Ganim M, Carell MZ, Kjellgren O, Kirkeeide RL,
Vaughn WK, Kelly R, McGhie AI, Kramer N, Loyd D, Anderson HV, Schroth
G, Smalling RW. Comparison of angioscopy, intravascular ultrasound
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patients. J Am Coll Cardiol. 1996;28:97105.[Abstract]
10.
Tabata H, Mizuno K, Arakawa K, Satomura K, Shibuya T,
Kurita A, Nakamura H. Angioscopic identification of coronary
thrombus in patients with postinfarction angina. J Am Coll
Cardiol. 1995;25:12821285.[Abstract]
11.
Ambrose JA, Winters SL, Arora RR, Haft JI, Goldstein J,
Rentrop KP, Gorlin R, Fuster V. Coronary angiographic
morphology in myocardial infarction: a link between the pathogenesis of
unstable angina and myocardial infarction. J Am Coll
Cardiol. 1985;6:12331238.[Abstract]
12.
Nakagawa S, Hanada Y, Koiwaya Y, Tanaka K. Angiographic
features in the infarct-related artery after intracoronary
urokinase followed by prolonged anticoagulation.
Circulation. 1988;78:13351344.
13.
Bauters C, Lablanche JM, McFadden EP, Hamon M, Bertrand
ME. Relation of coronary angioscopic findings at
coronary angioplasty to angiographic restenosis.
Circulation. 1995;92:24732479.
14.
den Heijer P, Foley DP, Hillege HL, Lablanche JM, van
Dijk RB, Franzen D, Morice MC, Serra A, De Scheerder I, Serruys PW, Lie
KI. The. `Ermenonville' classification of observations at
coronary angioscopy: evaluation of intra- and inter-observer
agreement. Eur Heart J. 1994;15:815822.
15.
Ambrose JA, Winters SL, Stern A, Eng A, Teicholz LE,
Gorlin R, Fuster V. Angiographic morphology and the pathogenesis of
unstable angina. J Am Coll Cardiol. 1985;5:609616.[Abstract]
16.
Levin DC, Fallon JT. Significance of the angiographic
morphology of localized coronary stenoses: histologic
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17.
Wilensky RL, Bourdillon PDV, Vix VA, Zeller JA.
Intracoronary artery thrombus formation in unstable angina: a
clinical, biochemical and angiographic correlation. J Am
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18.
The Thrombolysis in Myocardial Infarction
(TIMI) Study Group. The Thrombolysis in Myocardial
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19.
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Fadden EP. Discordant results of visual and quantitative estimates of
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Circulation. 1994;90:17061714.
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© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Coronary Angioscopic Findings in the Infarct-Related Vessel Within 1 Month of Acute Myocardial Infarction
Natural History and the Effect of Thrombolysis
![]()
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
BackgroundLimited angioscopic
information is available on the natural history of infarct-related
plaque after myocardial infarction (MI), in particular the effect
of thrombolysis.
Key Words: myocardial infarction thrombolysis angioplasty
![]()
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Recent
infarct-related lesions show a high propensity for reocclusion. In
patients treated with thrombolytic agents who have a
patent infarct-related artery at 48 hours, reocclusion occurs in the
ensuing 3 months in almost 30%.1 2 Furthermore,
after successful percutaneous transluminal
coronary angioplasty (PTCA) of the culprit lesion in the month
after myocardial infarction (MI), the restenosis (51%) and
occlusion (13%) rates at 6-month follow-up are excessively
high.3 The reason(s) for the high incidence of
late vessel reocclusion after MI are unclear.
![]()
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Patient Population
It is our institutional policy to perform coronary
angiography in all patients with recent MI in the absence of absolute
contraindications; ad hoc angioplasty of the infarct-related vessel is
performed, provided that the diameter stenosis is >50% and
that the overall anatomy of the coronary vessels does
not preclude angioplasty, for example, left main disease or lesions
judged to be unsuitable for angioplasty by the
operator.3
To be considered anatomically suitable for coronary
angioscopy, a lesion had to meet the following criteria: (1) the
culprit lesion was located more than 1.0 cm from the ostia to allow
inflation of the occlusion cuff, (2) the luminal diameter of the
coronary artery was >2.0 mm and <4.0 mm, (3) the
segment of the artery proximal to the lesion was not tortuous and had
no significant angulation, and (4) the site of cuff inflation was not
the site of a major side branch. The above criteria were designed to
ensure the safety of the procedure and to ensure a coaxial position of
the angioscope in order to optimize image acquisition.
) are adapted from the "simplified Ermenonville
classification" that was proposed by the European Working Group on
Coronary Angioscopy.14
View this table:
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Table 3. Angioscopic Variables
) was defined as a superficial
(lining) intraluminal, or protruding mass, adherent to the vessel
surface but clearly identified as a separate structure. Thrombus was
further classified by color (white, red, or mixed red and white). A
"pure" white thrombus was defined as a shaggy, irregular, and
cotton-woollike mass.

View larger version (23K):
[in a new window]
Figure 1. Coronary angioscopic findings A, Yellow plaque (P)
with a lining thrombus (T). B, Yellow plaque (P) with a large
protruding thrombus (T). C, Predominantly white plaque (P) with a
localized yellow area (arrow) and an adjacent lining thrombus (T). L
indicates lumen.
Two experienced interventional cardiologists performed the
qualitative analysis independently. Disagreements were resolved
by a further joint reading. Lesions were classified as concentric or
eccentric. Location (bifurcation), length (>10 mm), presence of
calcification, and irregular edges were also noted. Angiographic
criteria of intracoronary thrombus were recorded as
previously described:15 16 17 (1) an intraluminal
filling defect surrounded by contrast material, seen in multiple
projections; (2) unilateral or bilateral overhanging edges of the
lesion; (3) haziness; and (4) ulcerated borders. The
anterograde blood flow before angioplasty was graded with the
TIMI Study Group classification.18
1.
Data are presented as mean value±SD. Differences
between means were assessed using unpaired Student's t test
or ANOVA followed by Scheffe's F test when applicable.
Differences between proportions were assessed by chi-square
analysis or Fisher's exact test when applicable. A value of
P<.05 was considered to indicate statistical
significance.
![]()
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The baseline characteristics of the study population are detailed
in Table 1
. Most patients were men. Mean
age was 55±11 years. A thrombolytic agent was used in
two thirds of the patients at the time of acute MI; 98% of patients
were treated with oral aspirin (100 to 300 mg/daily) from admission and
100% of patients were treated with heparin infusion to achieve a
target activated clotting time for at least 72 hours after MI.
Seven percent of the population had post-MI unstable angina. The mean
interval between MI and angioscopy was 12.2±5.8 days. The culprit
lesion was located in the left anterior descending (50%), right
coronary (34%), and left circumflex artery (16%),
respectively.
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Table 1. Clinical Characteristics of the Study Population
. Lesions were
eccentric in 41% and ulcerated in 21% of the cases. The presence of
thrombus was suspected in 12% of the cases, using the most strict
angiographic definition (thrombus=filling defect), and in 54% of the
cases when we used a combination of classic criteria (see details in
Table 2
).15 16 17 The mean reference diameter of
the culprit vessel was 3.1 mm, the minimal luminal diameter at the
lesion site was 0.71 mm, and the mean percent stenosis was
76%. The artery was open in 79% of the cases (TIMI=3) and totally
occluded in 14% (percent stenosis=100, TIMI=0 or 1).
View this table:
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Table 2. Angiographic Variables
, and typical findings are shown in the
Figure
. A majority of lesions were complex (complex+ulcerated shape).
The predominant color of the plaque was yellow in 79% of the cases.
Fifteen percent were predominantly white with some yellow plaque
(Figure
); only 6% of the plaques were uniformly white (darkest
color=white). Seventy-seven percent of the patients had angioscopically
visible thrombus at the infarct-related lesion. Lining thrombi were
more frequent than protruding thrombi; thrombus color was mixed in 55%
of cases; and a cotton-woollike thrombus was observed in 18% of the
patients.
To analyze the relationship between the angioscopic
variables and the time elapsed between the MI and the angioscopic
procedure, patients were first divided into two groups as a function of
the median delay between MI and angioscopy (10 days): early-recent MI
(day 1 to 10) and late-recent MI (day 11 to 30). The plaque shape
(complex+ulcerated shape=46% versus 65%) did not differ between
groups. The predominant color of the plaque was similar in the two
groups (yellow=76% versus 81%): however, a trend toward a higher
frequency of uniformly white plaques (0% versus 12%,
P=.07) was observed in late-recent MI. The presence (79%
versus 75%) and the size (protruding thrombi=36% versus 43%) of
thrombi did not differ significantly between patients studied before or
after day 10. Furthermore, there was no difference in the color of the
thrombus (white, red, and mixed) between patients studied before or
after day 10. Similar results were obtained when the population was
divided into quartiles and tested for trends (Table 4
).
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Table 4. Relation of Angioscopic Characteristics to the Time
Elapsed Between Myocardial Infarction and Angioscopy
The relationship between the angioscopic variables and the
prior administration of a thrombolytic agent at the
time of myocardial infarction is presented in Table 5
. A trend for more complex+ulcerated
plaques was observed in patients treated with
thrombolysis (complex+ulcerated plaques=61% versus
38%, P=.16). The apparently higher proportion of complex
plaques in patients treated with thrombolytic therapy
was mainly due to a higher proportion of ulcerated plaques (ulcerated
plaques=45% versus 15%, P=.06). The dominant color of the
plaque was similar in the two groups (yellow=69% versus 82%), however
a higher frequency of completely white plaques (0% versus 12%,
P=.01) was observed in patients who had not received
thrombolytic therapy. The prevalence of thrombus was
slightly, but not significantly, higher in patients who had received
thrombolytic therapy compared with those who had not
(82% versus 63%, P=.12). However, the size of the observed
thrombus was significantly smaller in patients who had received
thrombolytic therapy (protruding thrombus=30% versus
70%, P=.02). No difference in the color of the thrombus
(white, red, or mixed) was detected.
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Table 5. Relation Between Angioscopic Characteristics and the
Prior Administration of Thrombolytic Therapy
In this study, an evaluation of the diagnostic value
of angiography for the detection of intracoronary thrombi
within 1 month after MI was performed with the use of classic
angiographic criteria (see "Methods" and Table 6
). Using the presence of a "filling
defect" as the only criterion, the specificity and positive
predictive value of angiography were very high (specificity=100%;
positive predictive value=100%). However, the sensitivity and negative
predictive value were very low (sensitivity=16%; negative predictive
value=27%). With the use of a combination of four criteria (filling
defect, overhanging edges, haziness, ulcerated borders) the specificity
and positive predictive value of angiography were slightly decreased
(specificity=85%; positive predictive value=93%). However, the
sensitivity and negative predictive value were much higher
(sensitivity=65%; negative predictive value=58%).
View this table:
[in a new window]
Table 6. Diagnostic Value of Angiographic
Criteria for the Detection of Intracoronary Thrombus
![]()
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
The recent infarct-related lesion has a high propensity for
spontaneous reocclusion in the weeks or months after
thrombolysis.1 2 Even when
successfully treated by balloon angioplasty, this propensity for
reocclusion persists.3 Occlusion of the
infarct-related vessel has a well-documented detrimental effect on left
ventricular function in the short
term.3 20 Furthermore, an occluded
infarct-related vessel has a detrimental effect on left
ventricular remodeling and survival in the long
term.21 22 Angiographic studies in patients with
recent infarction have not identified specific morphological
characteristics of the plaque that have a high predictive value for
reocclusion.23 24 25
The three important characteristics of the infarct-related
lesion observed within the first month of MI are thrombus (77%),
yellow plaque (79%), and complex morphology (54%), that is,
morphological aspects associated with plaque
instability.7 26 Within that period, these
findings are not dependent on the time elapsed since infarction, as
demonstrated by the lack of difference between the patients studied
before day 10 and those studied between day 11 and day 30 after MI. A
previous report by Mizuno et al7 suggests that
when angioscopy is performed in "old" MI (the mean time between MI
and angioscopy was more than 2 months) the plaque is usually healed
with 82% of white plaques and 0% of thrombus. The same authors showed
that when angioscopy is performed within hours or days after the onset
of MI there is a high frequency of yellow plaque and
thrombus6 7 ; these observations were
independently reported by others.8 9 The results
of the present study suggest that the healing process of the
infarct-related plaque requires more than 1 month. This extends the
findings of Ueda et al8 in a small series (10
patients) investigated 1 month after MI. They found yellow plaque in
all patients, thrombus in 6 patients (60%), and intimal flap in 4
patients (40%). The population studied was highly selected, as most
(n=7) had a combination of mechanical reperfusion and
thrombolysis. The results of our study extend their
findings to a much larger population of patients that is additionally
more representative of the general patient population
after MI.
Angioscopic characteristics of plaque instability, yellow plaque,
and plaque containing thrombus, are frequently associated with clinical
instability in patients without recent MI.7 26
After MI, our results show that angioscopic findings suggestive of
plaque instability are extremely frequent (75% to 80% of the study
population) even in the absence of clinical symptoms. Reported rates of
early post-MI unstable angina range from 6% to 21% of
patients27 28 29 (7% in the present study).
Thus after MI, clinical status is a poor predictor of plaque
stability.
The use of thrombolytic agents had a significant
impact on the thrombotic burden; only 30% of patients treated by
thrombolytic therapy had protruding thrombi versus 70%
of patients who had not received thrombolytic therapy
(P=.02). However, thrombolytic therapy did
not reduce the prevalence of thrombus as demonstrated by the fact that
thrombus was equally frequent in both groups (Table 5
).
). These effects
of thrombolysis probably reflect the fact that clot
lysis exposes an underlying ulcerated lesion.
Several studies have evaluated the diagnostic value of
angiography compared with angioscopy in the detection of
thrombus.5 26 However, these studies used a very
strict definition, the filling defect, as the angiographic criterion
for the presence of intracoronary thrombus. Furthermore, none
of these studies investigated patients with recent MI. In the
present report, the sensitivity of the angiographic "filling
defect" for the detection of intra coronary thrombus was
16%, consistent with the 19% to 27% sensitivity reported in
the two series referred to above.5 26 However,
using a combination of angiographic criteria previously associated with
intracoronary thrombus (filling defect, overhanging edge,
haziness, ulcerated borders),15 16 17 65% of
thrombi were suspected by angiography. While these results confirm that
angiography has a lower sensitivity than angioscopy, they show also
that careful analysis of the angiographic pattern can detect
two thirds of the thrombi observed by angioscopy. This compares
favorably with previously published data.5 26
Delayed PTCA of the culprit lesion in patients with a recent MI
initially treated by thrombolysis is a strategy
associated with a satisfactory clinical outcome.3
However, when such a procedure is performed, the restenosis
(51%) and occlusion (13%) rates at 6-month
follow-up3 are higher than those reported for
elective PTCA. Moreover, the latter complication is usually associated
with a deleterious effect on ejection fraction.3
The results of the present study together with those of a previous
report, demonstrating that the presence and the size of thrombus at the
angioplasty site are strong predictors of restenosis and
reocclusion at 6 months,13 suggest that the high
frequency of "silent" thrombus in the infarct-related lesion, even
after thrombolysis, may contribute to the worse 6-month
angiographic outcome when angioplasty is performed in this clinical
setting. The results of the present study need also to be
interpreted in the light of previous results by White et
al26 and by Feld et al9
demonstrating that the presence of thrombus at the angioplasty site, as
seen by angioscopy, is associated with a less favorable
early26 and late9 clinical
outcome.
Some study limitations need to be acknowledged. First, the fact
that all patients investigated underwent PTCA after angioscopy raises
the possibility of selection bias. However, the fact that during the
study period all patients in our institution undergoing
coronary angiography after a recent MI had ad hoc
angioplasty if lesion location and morphology was suitable suggests
that the population studied was representative of the
overall population of post-MI patients in our
institution.3 This is further corroborated by the
relatively low rates of "filling defect" seen at angiography (12%)
and post-MI angina (7%) in the present study. These rates are in
the lower range of those previously described in the general population
of patients with MI when studied during a similar period of
time.11 27 28 29 Second, since angioscopic
analysis was performed jointly by two physicians, data on
interobserver and intraobserver variability are not available. However,
the inherently subjective nature of angioscopy was minimized by the use
of a classification adapted from the "simplified Ermenonville
classification."14
This study suggests that the healing process of the
infarct-related lesion requires more than 1 month and that an
"unstable" yellow plaque with adherent thrombus and complex
morphology is a common finding during that period irrespective of the
clinical picture. In addition, thrombolytic therapy,
despite its documented beneficial effects on clinical outcome, has a
less dramatic effect on plaque stabilization. The persistence of plaque
instability, even in the absence of symptoms, provides a possible
explanation for the previously described higher rates of
restenosis and reocclusion when angioplasty is performed at
recent infarct-related lesions as well as the high rate of late vessel
occlusion after successful thrombolysis. In the era of
new and very potent antiplatelet agents and in the light of recent
progress in the field of coronary stenting, these findings
suggest that the use of such approaches could be useful in improving
the outcome of patients after MI.
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References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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angiographic study. Circulation. 1993;87:15241530.
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