(Circulation. 1996;93:223-228.)
© 1996 American Heart Association, Inc.
Articles |
Clinical Implications of the `No Reflow' Phenomenon
A Predictor of Complications and Left Ventricular Remodeling inReperfused Anterior Wall Myocardial Infarction
From the Division of Cardiology, Sakurabashi Watanabe Hospital, Osaka, Japan, and the First Department of Medicine, Osaka University School of Medicine (T.M., M.H.).
Correspondence to Hiroshi Ito, MD, Division of Cardiology, Sakurabashi Watanabe Hospital, 2-4-32 Umeda, Kita-ku, Osaka 530, Japan.
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Abstract |
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Background Recent studies demonstrated that the "no reflow" phenomenon after coronary reflow implies the presence of advanced myocardial damage. In this study, we verified the prognostic value of the detection of this phenomenon by studying complications, left ventricular morphology, and in-hospital survival after acute myocardial infarction (AMI).
Methods and Results The study population consisted of 126 patients with a first anterior AMI. All patients received coronary reflow within 24 hours of onset of symptoms and underwent myocardial contrast echocardiography (MCE) before and shortly after coronary reflow with an intracoronary injection of sonicated microbubbles. From contrast reperfusion patterns, patients were divided into two subsets: those with MCE no reflow (47 patients, 37%) and those with MCE reflow (79 patients). There was no difference in the frequency of arrhythmia or coronary events between the two subsets. Pericardial effusion and early congestive heart failure were observed more frequently in patients with MCE no reflow than in those with MCE reflow (26% versus 4%, P<.05; 45% versus 15%, P<.05, respectively). Congestive heart failure tended to be prolonged in those with MCE no reflow, and 3 patients (7%) of this subset died of pump failure. Left ventricular end-diastolic volume progressively increased in the convalescent stage in patients with MCE no reflow (early versus late, 145±43 versus 169±60 mL, P<.001), whereas it decreased in those with MCE reflow (154±42 versus 144±44 mL, P<.01).
Conclusions The substantial size of the MCE no reflow phenomenon at coronary reflow conveys useful information about an outcome of coronary intervention and left ventricular remodeling in individual patients with anterior wall AMI, although these are suggestive results in a limited number of patients.
Key Words: echocardiography • contrast media • myocardial infarction • reperfusion • microcirculation • prognosis • remodeling
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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In acute myocardial infarction (AMI), several variables have been proposed to identify the patients at high risk for death. They include advanced age, extent of ECG changes, evidence of acute failure of the left side of the heart, a history of previous infarction or concomitant diabetes mellitus, and patency of the infarct-related artery.1 2 In early clinical decision making, it would be much more valuable if we could identify individuals with a relatively good or an exceptionally unfavorable prognosis among the high-risk group. Several studies imply that coronary reperfusion generally improves left ventricular performance and patient prognoses; however, coronary reperfusion does not necessarily provide preserved left ventricular performance and good patient prognoses, and predicting high-risk patients among reperfused patients remains difficult.2 3 4 5
Although it is generally believed that the patent epicardial coronary vessel should guarantee flow at the microvascular beds in AMI, ischemic episodes may often break down the coronary microvasculature; thus, flow to the infarct myocardium may be markedly reduced despite the angiographic documentation of reflow in the infarct-related artery (the "no reflow" phenomenon).6 7 8 9 10 11 12 In our previous studies using myocardial contrast echocardiography (MCE), the recovery in myocardial contractile function was significantly worse in patients with substantial MCE no reflow than in those with MCE reflow.13 14 However, clinical outcomes of patients with and without no reflow are still unknown. Although a large myocardial infarction triggers left ventricular remodeling, which worsens patient morbidity and mortality,15 16 it is currently difficult to predict ventricular dilation in individual reperfused patients. Left ventricular remodeling or dilation may be predicted on the basis of the presence or absence of MCE no reflow in the early phase.
This study was attempted to verify the prognostic value of detecting MCE no reflow. Specifically, in-hospital survival, complications, and left ventricular morphology were related to the MCE reflow patterns in 126 consecutive patients with reperfused anterior wall AMI.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Study Population
MCE was performed in 140 consecutive patients who were admitted to the Coronary Care Unit of the Sakurabashi Watanabe Hospital for the first MI of the anterior wall from February 1989 through July 1994. The diagnosis of AMI was made on the basis of chest pain of
30
minutes' duration occurring within 6 hours of
presentation, ST-segment elevation of 2 mm in two
contiguous ECG leads, and more than a threefold increase in serum
creatine kinase activities. Fourteen patients were excluded from
analysis because of inadequate image quality (8 patients),
multivessel disease (4 patients), or inadequate coronary reperfusion
even after interventions (Thrombolysis in Myocardial Infarction Trial
[TIMI] grade 0, 1, or 2 flow; 2 patients). Therefore, this report is
based on the remaining 126 patients (96 men, 30 women; mean age, 55
years [range, 38 to 75 years]). Eight patients demonstrated a patent
coronary artery (TIMI grade 3 flow) at the initial
coronary angiography performed within 24 hours after the onset
of symptoms, and the intervention was not performed. The other 118
patients underwent intracoronary thrombolysis
(tissue plasminogen activator 1 200 000 U or
urokinase 480 000 to 960 000 U; 19 patients) or coronary
angioplasty (99 patients) to the culprit lesion and achieved successful
coronary reflow within 24 hours after the onset of chest pain.
Informed consent was obtained from each patient by an investigator. The
study protocol was approved by the hospital's Ethics Committee.
Protocol
In the early stage, catheterization was
performed by use of the femoral approach after the injection of 100
U/kg heparin. Each patient rested in the supine position. On completion
of the diagnostic coronary arteriography and left
ventriculography, 2 mL sonicated ioxaglate (Hexabrix-360, Tanabe)
containing microbubbles (mean size, 12 µm) was injected into the left
coronary artery for MCE as previously
described.13 14 A commercially available mechanical
sector
scanner (model SAL-38B, Toshiba; carrier frequency, 3.5 MHz) was used.
Imaging of the apical long-axis view was initiated about 10 seconds
before the contrast injection and was continued for an average of 30
seconds with a constant-gain setting. MCE images were recorded
on 1.25-cm videotape with a VHS recorder (model BR-6000, Victor).
MCE was repeated with the contrast injected into the right
coronary artery. MCE was repeated about 16 minutes (range, 10
to 24 minutes) after successful reflow was confirmed with
coronary arteriography. A II-lead ECG was continuously
monitored during and after MCE.
After coronary reflow, heparin was continued for 48 hours and was adjusted to maintain the activated clotting time to >180 seconds. All patients were maintained on a regimen of aspirin or ticulopidine and cumadine. If required, oral nitrates, calcium antagonists, ß-blockers, diuretics, and/or angiotensin-converting enzyme inhibitors were added and continued until the late-stage examination.
A lead V5–equivalent ECG was monitored continuously until a mean of 7 days after the infarction (range, 3 to 10 days) for the detection of arrhythmias. Two-dimensional echocardiography was performed before coronary reflow and at days 2, 3, 7, 14, and 28 of the infarction with a commercially available electrical sector scanner (model SSH-65A or SSH-260A, Toshiba; carrier frequency, 3.75 MHz). In each echocardiographic examination, parasternal long-axis and short-axis views at the levels of the mitral valve and midpapillary muscle and an apical long-axis view were recorded on 1.25-cm videotape with the same VHS recorder. The presence or absence of pericardial effusion was also evaluated.
Coronary arteriography, left ventriculography, and MCE were repeated at a mean of 25 days after the infarction (range, 24 to 29 days) by use of the right brachial approach. All medications were withdrawn at least 12 hours before cardiac catheterization.
Analysis of MCE Data
Echocardiographic images were analyzed
with a commercially available off-line computer system (model
LA-500, PIAS or Color Cardiology Workstation, TomTec
Imaging). End-diastolic
echocardiographic frames after contrast injection were
selected with synchronization to the peak of the R wave on the ECG. An
operator selected the echocardiographic images with the
best delineation between contrast-enhanced and nonenhanced
myocardium to determine risk area,17 18 which
was determined to be an area showing no contrast enhancement in the
prereflow MCE from injection into either the right or left
coronary artery. In cases of TIMI grade 3 flow at the initial
coronary angiography, the extent of abnormal contraction
segment of the left ventricle was considered the risk
area.18 MCE performed just after coronary reflow
was analyzed in the same fashion, and when the endocardial
length of the area showing residual contrast defect exceeded a fourth
of that of the risk area, myocardial reperfusion in the corresponding
segment was considered incomplete (MCE no reflow). Areas showing
contrast defects were always successfully defined, and measurements of
the size of the residual contrast defects were highly reproducible, as
mentioned previously.13
Analysis of Catheterization
Data
The right anterior oblique views of left ventriculograms in
baseline and the late stage were analyzed to measure left
ventricular end-diastolic volume and global
left ventricular ejection fraction with the area-length
method. The regional wall motion of the infarct zone was evaluated
quantitatively and expressed as SD per chord with the centerline
method.19 The percent diameter stenosis of the
infarct-related artery also was determined after reflow and at
follow-up. Collateral channels were graded in the initial
coronary arteriograms as follows: 0=no collaterals,
1=incomplete slow opacification in the distal vessel, 2=slow but
complete opacification of the distal vessel, and 3=distal vessel
opacified as well as the normal vessel. An angiographer blinded to
patient data analyzed the cinefilms in a random sequence.
In-Hospital Data Collection
The patients were followed up for
the occurrence of
complications until hospital discharge. Data on clinically relevant
in-hospital events (death from any cause and reinfarction) were
carefully collected in the study forms. Another investigator also
reviewed data on these patients. The type and frequency of
ventricular arrhythmia were evaluated by Holter
monitoring on the day of the infarction, and ECG monitors recorded
continuously until at least 5 days after the infarction. Malignant
arrhythmia was defined as ventricular
tachycardia (a minimum of three consecutive beats of
ventricular origin at a rate of >100 beats per minute) and
ventricular fibrillation observed at any time during
hospitalization. Left ventricular heart failure was defined
as the presence of clinical congestive heart failure (the presence of a
third heart sound, Killip class 2, Forrester subset of 2 or 4,
dyspnea, or evidence of pulmonary congestion on chest
radiographs). Early postinfarction angina was defined as angina
pectoris observed within 7 days after the onset of infarction.
Symptom-limited bicycle ergometer exercise test was performed at a
mean of 24 days after the infarction (range, 22 to 26 days) to evaluate
the presence of post-AMI ischemia (late postinfarction angina).
Pericardial effusion and cardiac tamponade were diagnosed on the basis
of clinical and echocardiographic findings.
Restenosis was defined as a loss of initial gain by 50% in
cases of coronary angioplasty and as an increase in the
American Heart Association classification of coronary
stenosis of more than one grade in cases of
intracoronary thrombolysis.
Statistical Analysis
All data are expressed as
mean±SD. Univariate
analyses of differences between reflow and no reflow groups
were performed with one-way ANOVA (Scheffé's F
test) for continuous outcome variables and by
2 tests for discrete outcome variables. If a
small number (less than five) was included, Fisher's exact test was
applied instead of 2 tests for the
analysis of discrete variables. Statistical
analysis of temporal changes in certain variables was
computed by ANOVA and Scheffé's F test for repeated
measures. The contribution of factors to early and late congestive
heart failure and left ventricular dilation was evaluated
by multivariate regression analysis as
explained later. Differences were considered significant at
P<.05.
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Results |
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Patient Characteristics
The risk area was well opacified in 79 patients as indicated by MCE performed shortly after coronary reflow (MCE reflow), whereas 47 patients (37%) demonstrated a substantial size of the residual contrast defects within the risk area (MCE no reflow). Table 1
summarizes patient characteristics of these two
subsets. There were no differences in age, sex, culprit lesion, time
from the onset of symptoms to reperfusion, angiographic collateral
grade, and frequency of coronary risk factors between the two
subsets. All patients with MCE no reflow subsequently developed Q waves
in 12-lead surface ECG, but 27 of 79 patients with MCE reflow (34%)
manifested non–Q-wave myocardial infarction. There were no significant
differences in the in-hospital medications between the two
subsets.
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Complications and In-Hospital Prognosis
Table
2 summarizes coronary events and
findings. There were no differences in the frequency of
restenosis, reocclusion, early and late postinfarction
angina, or recurrent ischemia (extension and recurrent
infarction) between the two subsets. Table 3 summarizes
in-hospital complications and survival of the two subsets.
Frequencies of malignant arrhythmias shortly after
coronary reflow and the total number of malignant
arrhythmia, excluding reperfusion arrhythmia, were
significantly higher in patients with MCE no reflow than those with MCE
reflow. Pericardial effusion was observed more frequently in patients
with MCE no reflow than in those with MCE reflow. Cardiac tamponade was
not observed in patients with MCE reflow but was observed in 6% of
patients with MCE no reflow. Congestive heart failure within 3 days of
the AMI was observed more frequently in the patients with MCE no reflow
than those with MCE reflow. Congestive heart failure, if it occurred,
tended to last beyond the third day in patients with MCE no reflow,
whereas remission of heart failure was observed within 3 days in most
patients with MCE reflow. There were, however, no differences in
hemodynamic variables and in-hospital
medications between the two subsets 1 month later (reflow versus no
reflow: pulmonary capillary wedge pressure, 9±5 versus 10±6
mm Hg; cardiac index, 3.3±0.6 versus 3.2±0.9
L·min-1·m-2).
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One patient with MCE reflow died in the hospital; the cause of death was a blowout-type cardiac rupture that occurred 2 hours after the reperfusion. In contrast, three patients (6%) with MCE no reflow died of congestive heart failure 12, 17, and 57 days after the AMI.
Left Ventricular Function and Morphology
Adequate left
ventriculograms were obtained in both the early and
late stages in 116 patients: 76 with MCE reflow and 40 with MCE no
reflow. Reasons for incomplete examinations were arrhythmia or
incomplete opacification during left ventriculography (5 patients),
in-hospital death (3 patients), and no left ventriculography in the
early stage (2 patients). Baseline regional contractile function was
better in patients with MCE reflow. A significant improvement in left
ventricular global function was observed in patients with
MCE reflow, but there was a little improvement in patients with MCE no
reflow (MCE reflow, 46±11% versus 57±13% [early versus
late],
P<.001; MCE no reflow, 38±11% versus 43±12%,
P<.05). Similarly, the regional contractile function in the
infarct zone was well preserved in the early stage and showed more
improvement in patients with MCE reflow compared with those with MCE no
reflow (MCE reflow, -3.0±0.6 versus -2.1±1.0 SD per
chord
[early versus late], P<.001; MCE no reflow,
-3.4±0.4 versus -3.0±0.7 SD per chord,
P<.01). Therefore, the patients with MCE reflow manifest
much better (P<.001) regional function than those with MCE
no reflow in both the early and late stages.
There were no differences
in left ventricular
end-diastolic and systolic volumes in a
baseline study between the two subsets (see the Figure).
In patients with MCE reflow, left ventricular
end-diastolic volume decreased significantly from
baseline to the late stage (154±42 versus 144±44 mL,
P<.01). In patients with MCE no reflow, however, left
ventricular end-diastolic volumes increased
significantly from baseline to the late stage (145±43 versus
169±60
mL, P<.001), implying left ventricular
remodeling. Thus, end-diastolic volume was greater in
patients with MCE no reflow than those with MCE reflow in the late
stage. In addition, substantial left ventricular dilation
(an increase in end-diastolic volume by >20%) was
observed in 17 of 40 patients with MCE no reflow and 6 of 76 patients
with MCE reflow. Therefore, sensitivity, specificity, and positive
predictive value of MCE no reflow for future substantial left
ventricular dilation are 43%, 92%, and 74%,
respectively.
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Factors Contributing to Heart Failure and Left
Ventricular Dilation
To evaluate the contribution of each factor to
early and late
congestive heart failure and left ventricular dilation (an
increase in left ventricular end-diastolic
volume by >20%), multiple logistic regression analysis was
performed. The variables shown in Table 4 were used
for the analysis. For multiple regression analysis,
factors showing a value P<.1 in univariate
analysis were selected. Multiple regression analysis
depicted MCE no reflow, preseptal occlusion (possibly related to the
size of the risk area), and age as significant variables to
determine early congestive heart failure. On the other hand, only MCE
no reflow contributed significantly to late congestive heart failure.
Similarly, MCE no reflow is only one factor that is a significant
variable for determining significant left ventricular
dilation. Therefore, MCE no reflow contributed significantly to these
clinical observations. Together, however, these variables could
explain <30% of the total effects of these clinical
observations.
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Discussion |
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The epicardial coronary vessel, even if patent, may not necessarily guarantee flow at the microvascular beds in patients with AMI because ischemic episodes may often break down the coronary microvasculature.10 12 14 15 20 21 A substantial no reflow area was observed shortly after successful coronary angiographic reflow in 37% of the patients with acute anterior AMI in this study. MCE no reflow not only resulted in poor functional recovery but also was associated more frequently with pericardial effusion, cardiac tamponade, and congestive heart failure that tended to last beyond 4 days compared with MCE reflow. In addition, the left ventricular cavity was dilated in the late stage despite the patent infarct-related artery in patients with MCE no reflow, whereas ventricular volumes decreased in the convalescent stage in patients with MCE reflow. Thus, our results documented that the MCE no reflow phenomenon strongly discriminates individual patients with poor outcomes and left ventricular remodeling from those with favorable outcomes.
No Reflow Phenomenon and Complications
It is important in the
decision of therapeutic strategy to predict
the severity and duration of left ventricular dysfunction
in the early stage of an AMI. In our patients with MCE no reflow,
clinical congestive heart failure was observed frequently on the day of
AMI and tended to last 4 days or longer, whereas heart failure, if
present, showed remission within 3 days of the AMI in most patients
with MCE reflow. The reason for the higher frequency of early
congestive heart failure in patients with MCE no reflow is still not
clear. Left ventricular contractile function before
coronary reflow was better in patients with MCE reflow than
those with MCE no reflow; this may at least partially account for the
difference in the frequency of early congestive heart failure. Multiple
regression analysis indicated that the no reflow phenomenon,
the culprit lesion reflecting the size of the risk area, and age are
related to early congestive heart failure. Congestive heart failure was
observed frequently beyond 4 days after reperfusion in patients with
MCE no reflow. Multiple regression analysis revealed that MCE
no reflow is the only factor contributing to late congestive heart
failure. AMI was larger in patients with MCE no reflow than in those
with MCE reflow; thus, it may take longer for the left ventricle to
adapt to a larger infarction. The differences in the frequency and
duration of congestive heart failure between the subsets may be
explained this way. The hemodynamic derangement was no
longer observed at the follow-up study (hemodynamic
data), possibly because the left ventricle successfully adapted in the
late stage in any patient with congestive heart failure at that
time.
Pericardial effusion and cardiac tamponade were observed frequently in patients with MCE no reflow. In any patient with cardiac tamponade, we successfully performed pericardial drainage, and bloody effusion was drained. Therefore, cardiac tamponade may be attributed to hemorrhagic infarction caused by coronary reperfusion, oozing rupture, or both. In contrast, all patients with pericardial effusion manifested clinical signs of pericarditis (friction rub or chest pain augmented by respiration and curable with antiinflammatory drugs). Although pericardial drainage was not performed, postinfarction pericarditis was a probable diagnosis. The transmurality of MI should contribute to the occurrence of pericarditis because Q-wave MI subsequently developed in all patients with MCE no reflow, whereas 34% of patients with MCE reflow manifested non–Q-wave infarction. It is well known that pericarditis is observed more frequently in cases of Q-wave than non–Q-wave MI. Transmural myocardial damage with intramural hemorrhage may lead to cardiac tamponade; however, no pathological data were obtainable in our patients to support our speculation.
We initially anticipated that coronary events (recurrent ischemia, early and late postinfarction angina, restenosis, and reocclusion) may be more frequent in patients with MCE no reflow than in those with MCE reflow because microvascular damage is likely to slow the epicardial coronary blood flow and because the stagnation of blood flow may accelerate local thrombus formation. However, there was no difference in the frequency of any coronary event between patients with and without MCE no reflow. Therefore, coronary microvascular damages may not necessarily increase the frequency of coronary events or augment the rate of coronary restenosis. These observations may be related to the following: coronary angioplasty performed in most of our patients with the residual coronary stenosis of <50% or adequate heparinization in the early stage, followed by adequate cumadination and antiplatelet therapy until the follow-up study.
In-Hospital Death
Four patients experienced cardiac death.
Three patients (6%) with
MCE no reflow died of congestive heart failure. In these patients,
substantial no reflow was observed despite the successfully recanalized
coronary artery. Congestive heart failure lasted beyond 4 days
and was resistant to intra-aortic counterpulsation,
diuretics, catecholamine, or load reduction
therapy. Thus, if the no reflow phenomenon is documented in the large
areas of the left ventricle, we should prepare ourselves for
intractable and prolonged congestive heart failure. In contrast, a
patient with MCE reflow died of a blowout-type cardiac rupture
observed 2 hours after successful coronary reflow. Although the
study population is limited, cardiac rupture may not be predictable on
the basis of postreflow MCE patterns.
Left Ventricular Remodeling
The progressive left ventricular
dilation is observed
sometimes during the early convalescent period of
AMI.16 22 Although this dilation appears to
represent a compensatory mechanism for suppressed
ventricular function, it may profoundly derange left
ventricular function and affect patient
prognoses.23 Although coronary reperfusion per se
might have a beneficial effect of preventing left
ventricular dilation,16 22 24 a
substantial
population (19% to 42%) of patients still manifests significant left
ventricular dilation, and predicting left
ventricular dilation in reperfused patients is still
difficult. Among factors that influence ventricular
dilation, the resultant size of the infarction or asynergy is
considered to be a major determinant of left ventricular
dilation in reperfused patients.15 16 Therefore, if
we
could estimate the size of the MI, we could predict the left
ventricular dilation in the early stage of the
infarction.
The results of our previous and present studies showed that MI as assessed with left ventricular ejection fraction, regional wall motion, and the extent of asynergy is significantly larger in patients with MCE no reflow than those with MCE reflow. Patients with MCE no reflow manifested significant left ventricular dilation from the early to late stage. In contrast, end-diastolic volume decreased in the late stage in patients with MCE reflow. These findings are compatible with our previous observations. Therefore, MCE no reflow seems to be a predictor of left ventricular dilation in patients with reperfused anterior wall MI.
Limitations
The results of this study should be considered in
light of several
limitations. First, our method depends heavily on
echocardiographic image quality. Second, contrast
intensity is influenced by many factors, including the size and number
of microbubbles; factors altering ultrasonic reflection such as gain
setting, depth of penetration, incident angle, axial and lateral
resolution; gray scale compression; and the nonlinearity of echo
amplitude signals. The timing of MCE after coronary reflow is
another factor affecting the size of the no reflow
phenomenon.12 Third, only patients with first anterior
wall MI were enrolled in this study. Therefore, the prognostic value of
MCE no reflow has not been established in patients with
inferior or posterior wall MI or recurrent MI. Finally, our
analysis was based on a comparison of in-hospital
complications and angiographic data only; survival and quality of life
in a longer follow-up period were not taken into consideration.
Clinical Implications
Assessment of microvascular perfusion
seems to be essential in
gaining further understanding of patient outcome and of the relation
between intervention and outcome. Neither the patency status nor the
severity of stenosis of the infarct-related artery
indicates the extent of microvascular integrity, and MCE may be the
only method currently available for assessment of the microvascular
integrity. Thus, we may use MCE to identify patients with good or poor
prognoses after AMI in a catheterization laboratory at
the time of diagnostic angiography. The prompt assessment
of both coronary anatomy and the quality of
microvascular perfusion (and hence myocardial viability) may aid in
decision making in individual patients. At present, however, the
demonstration of no reflow may have little clinical usefulness in the
management of these patients.
MCE assessment of reperfusion patterns provides a useful predictor of left ventricular remodeling in individual patients. If substantial no reflow is observed after coronary reflow, an advanced form of load reduction therapy is recommended to attenuate left ventricular dilation.25
MCE is inexpensive and can be performed in a catheterization laboratory in only a few minutes. However, obvious practical problems currently are connected with acquisitions of MCE in acute patients. Newly developed contrast media such as sonicated albumin solution can produce contrast enhancement of the left chambers and the myocardium through the contrast injection into the right or left atrium11 26 or the peripheral veins in canine experiments. Such new contrast media should expand the clinical application of MCE in the near future. With the advent of such contrast media, MCE can be performed to serially assess myocardial flow and viability after coronary reflow at bedside in the Intensive or Coronary Care Unit.
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Acknowledgments |
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We greatly acknowledge the excellent technical assistance of Yuzo Sakagami, Yoshiki Jonishi, and Masakazu Ueda, the excellent secretarial assistance of Rie Nishizawa, and the statistical advice of Dr Kusuoka (Osaka University).
Received January 23, 1995; revision received July 26, 1995; accepted August 25, 1995.
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A. P. Furber, F. Prunier, H. C. P. Nguyen, S. Boulet, S. Delepine, and P. Geslin Coronary Blood Flow Assessment After Successful Angioplasty for Acute Myocardial Infarction Predicts the Risk of Long-Term Cardiac Events Circulation, December 7, 2004; 110(23): 3527 - 3533. [Abstract] [Full Text] [PDF]
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K. Iwakura, H. Ito, S. Kawano, A. Okamura, K. Tanaka, Y. Nishida, Y. Maekawa, and K. Fujii Assessing myocardial perfusion with the transthoracic Doppler technique in patients with reperfused anterior myocardial infarction: comparison with angiographic, enzymatic and electrocardiographic indices Eur. Heart J., September 1, 2004; 25(17): 1526 - 1533. [Abstract] [Full Text] [PDF]
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A. Hansen, A. Kumar, D. Wolf, K. Frankenbergerova, A. Filusch, M.-L. Gross, S. Mueller, H. Katus, and H. Kuecherer Evaluation of cardioprotective effects of recombinant soluble P-selectin glycoprotein ligand-immunoglobulin in myocardial ischemia-reperfusion injury by real-time myocardial contrast echocardiography J. Am. Coll. Cardiol., August 18, 2004; 44(4): 887 - 891. [Abstract] [Full Text] [PDF]
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C. F. Azevedo, L. C. Amado, D. L. Kraitchman, B. L. Gerber, N. F. Osman, C. E. Rochitte, T. Edvardsen, and J. A.C. Lima Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging Eur. Heart J., August 2, 2004; 25(16): 1419 - 1427. [Abstract] [Full Text] [PDF]
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C. O. Costantini, G. W. Stone, R. Mehran, E. Aymong, C. L. Grines, D. A. Cox, T. Stuckey, M. Turco, B. J. Gersh, J. E. Tcheng, et al. Frequency, correlates, and clinical implications of myocardial perfusion after primary angioplasty and stenting, with and without glycoprotein IIb/IIIa inhibition, in acute myocardial infarction J. Am. Coll. Cardiol., July 21, 2004; 44(2): 305 - 312. [Abstract] [Full Text] [PDF]
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G. K. Lund, A. Stork, M. Saeed, M. P. Bansmann, J. H. Gerken, V. Muller, J. Mester, C. B. Higgins, G. Adam, and T. Meinertz Acute Myocardial Infarction: Evaluation with First-Pass Enhancement and Delayed Enhancement MR Imaging Compared with 201Tl SPECT Imaging Radiology, July 1, 2004; 232(1): 49 - 57. [Abstract] [Full Text] [PDF]
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C. M. Gibson and A. Schomig Coronary and Myocardial Angiography: Angiographic Assessment of Both Epicardial and Myocardial Perfusion Circulation, June 29, 2004; 109(25): 3096 - 3105. [Full Text] [PDF]
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A. J. Taylor, N. Al-Saadi, H. Abdel-Aty, J. Schulz-Menger, D. R. Messroghli, and M. G. Friedrich Detection of Acutely Impaired Microvascular Reperfusion After Infarct Angioplasty With Magnetic Resonance Imaging Circulation, May 4, 2004; 109(17): 2080 - 2085. [Abstract] [Full Text] [PDF]
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L. C. Amado, D. L. Kraitchman, B. L. Gerber, E. Castillo, R. C. Boston, J. Grayzel, and J. A. C. Lima Reduction of "no-reflow" phenomenon by intra-aortic balloon counterpulsation in a randomized magnetic resonance imaging experimental study J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1291 - 1298. [Abstract] [Full Text] [PDF]
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H. F.J Mannaerts, J. A van der Heide, O. Kamp, M. G Stoel, J. Twisk, and C. A Visser Early identification of left ventricular remodelling after myocardial infarction, assessed by transthoracic 3D echocardiography Eur. Heart J., April 2, 2004; 25(8): 680 - 687. [Abstract] [Full Text] [PDF]
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L. Bolognese, N. Carrabba, G. Parodi, G. M. Santoro, P. Buonamici, G. Cerisano, and D. Antoniucci Impact of Microvascular Dysfunction on Left Ventricular Remodeling and Long-Term Clinical Outcome After Primary Coronary Angioplasty for Acute Myocardial Infarction Circulation, March 9, 2004; 109(9): 1121 - 1126. [Abstract] [Full Text] [PDF]
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M. T Dirksen, G. Laarman, A. W.J van 't Hof, G. Guagliumi, W. A.L Tonino, L. Tavazzi, D. J.G.M Duncker, M. L Simoons, and on behalf of the PARI-MI Investigators The effect of ITF-1697 on reperfusion in patients undergoing primary angioplasty: Safety and efficacy of a novel tetrapeptide, ITF-1697 Eur. Heart J., March 1, 2004; 25(5): 392 - 400. [Abstract] [Full Text] [PDF]
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M. Takeuchi, Y. Nohtomi, H. Yoshitani, C. Miyazaki, K. Sakamoto, and J. Yoshikawa Enhanced coronary flow velocity during intra-aortic balloon pumping assessed by transthoracic doppler echocardiography J. Am. Coll. Cardiol., February 4, 2004; 43(3): 368 - 376. [Abstract] [Full Text] [PDF]
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J. Cortadellas, J. Figueras, M. Missorici, E. Domingo, J. Rodes, J. Castell, and J. Soler Soler ST segment elevation at 72 hours in patients with a first anterior myocardial infarction best correlates with pre-discharge and 1-year regional contractility and ventricular dilatation Eur. Heart J., February 1, 2004; 25(3): 224 - 231. [Abstract] [Full Text] [PDF]
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L Galiuto Optimal therapeutic strategies in the setting of post-infarct no reflow: the need for a pathogenetic classification Heart, February 1, 2004; 90(2): 123 - 125. [Full Text] [PDF]
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S. Kaul and H. Ito Microvasculature in Acute Myocardial Ischemia: Part II: Evolving Concepts in Pathophysiology, Diagnosis, and Treatment Circulation, January 27, 2004; 109(3): 310 - 315. [Full Text] [PDF]
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H. Kunichika, O. Ben-Yehuda, S. Lafitte, N. Kunichika, B. Peters, and A. N. DeMaria Effects of glycoprotein iib/iiia inhibition on microvascular flow after coronary reperfusion: A quantitative myocardial contrast echocardiography study J. Am. Coll. Cardiol., January 21, 2004; 43(2): 276 - 283. [Abstract] [Full Text] [PDF]
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R. A. Kloner and W. Dai Glycoprotein IIb/IIIa inhibitors and no-reflow J. Am. Coll. Cardiol., January 21, 2004; 43(2): 284 - 286. [Full Text] [PDF]
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R. H. Mehta, K. J. Harjai, D. Cox, G. W. Stone, B. Brodie, J. Boura, W. O'Neill, C. L. Grines, and Primary Angioplasty in Myocardial Infarction (PAMI Clinical and angiographic correlates and outcomes of suboptimal coronary flow inpatients with acute myocardial infarction undergoing primary percutaneous coronary intervention J. Am. Coll. Cardiol., November 19, 2003; 42(10): 1739 - 1746. [Abstract] [Full Text] [PDF]
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M. Nishino, H.-J. Youn, D. Gheorghevici, C. Zellner, T. M. Chou, K. Sudhir, and R. F. Redberg Effect of Intracoronary Estradiol on Postischemic Microvascular Damage in a Porcine Model: A Myocardial Contrast Echocardiographic Study Angiology, November 1, 2003; 54(6): 701 - 709. [Abstract] [PDF]
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C Coletta, A Sestili, F Seccareccia, R Rambaldi, R Ricci, A Galati, R Bigi, N Aspromonte, M Renzi, and V Ceci Influence of contractile reserve and inducible ischaemia on left ventricular remodelling after acute myocardial infarction Heart, October 1, 2003; 89(10): 1138 - 1143. [Abstract] [Full Text] [PDF]
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