From the Division of Cardiology, Department of Medicine (K.C.W., L.A.B.,
S.P.S., R.S.B., J.A.C.L.) and the Division of Diagnostic Imaging, Department
of Radiology (E.A.Z., C.H.L.), The Johns Hopkins University School of
Medicine, Baltimore, Md, and The Feinberg Cardiovascular Research Institute
(R.M.J.), Northwestern University Medical School, Chicago, Ill.
Methods and Results—Forty-four patients underwent MRI 10±6 days
after infarction. Microvascular obstruction was defined as
hypoenhancement seen 1 to 2 minutes after contrast injection. Infarct
size was assessed as percent left ventricular mass
hyperenhanced 5 to 10 minutes after contrast. Patients were followed
clinically for 16±5 months. Seventeen patients returned 6 months after
infarction for repeat MRI. Patients with microvascular obstruction
(n=11) had more cardiovascular events than those
without (45% versus 9%; P=.016). In fact,
microvascular status predicted occurrence of
cardiovascular complications (
Conclusions—After infarction, MRI-determined microvascular
obstruction predicts more frequent cardiovascular
complications. In addition, infarct size determined by MRI also relates
directly to long-term prognosis in patients with acute myocardial
infarction. Moreover, microvascular status remains a strong prognostic
marker even after control for infarct size.
Experimentally, the territory injured by prolonged ischemia is
composed primarily of nonviable myocardial tissue in which myocytes
perish first, followed eventually by necrosis of the
endothelial cells that line intramyocardial
capillaries.12 13 At the center of the infarcted
segment, however, myocytes and capillaries may undergo necrosis
simultaneously because of profound and sustained
ischemia. In that situation, capillaries become occluded by
dying blood cells and debris, to the degree that even with restoration
of epicardial blood flow, the infarct core will not promptly reperfuse.
This area of microvascular obstruction has been called the
"no-reflow" or "low-reflow" region.12 13
The presence of microvascular obstruction immediately after acute
infarction correlates with greater myocardial damage by
electrocardiography and
echocardiography6 and thus
poorer global ventricular function in the early
postinfarction phase.10 14 However, the long-term
prognostic significance of microvascular obstruction in patients with
acute myocardial infarction remains unknown. In addition, the
mechanisms linking microvascular obstruction to a greater risk of
postinfarction complications are unclear.
Infarct expansion with subsequent scar formation and
ventricular remodeling also contributes significantly to
the prognosis of patients surviving acute myocardial
infarction.15 16 17 Left ventricular
dilatation and volume-overload hypertrophy of noninfarcted
myocardium are the consequences of the remodeling
process.18 19 20 These changes in
ventricular architecture partly reflect infarct
extent16 19 21 but also depend on the rate of
infarct healing and the material properties of the infarcted segment
during the healing process.16 22 23 The benefit
of reperfusion, even without myocardial salvage, in limiting infarct
expansion and remodeling has been
demonstrated.24 25 26 However, despite patent
epicardial vessels by coronary angiography, myocardial
reperfusion may not occur at the microvascular
level.10 11 27 Previous studies indicate that the
presence of microvascular obstruction adversely affects early left
ventricular remodeling,14 perhaps by
impeding the beneficial effects of myocardial reperfusion on the
material properties of infarcted tissue, leading to greater infarct
expansion.
Contrast-enhanced MRI techniques allow the in vivo visualization of
regions of profound microvascular obstruction in patients with acute
myocardial infarction.6 These regions appear as
dark, subendocardial zones surrounded by hyperenhanced infarcted or
injured myocardium and correspond to experimentally
produced no-reflow regions.7 We conducted this
study to determine whether the presence of MRI microvascular
obstruction within human infarcts is a marker for long-term
cardiovascular complications. In addition, we measured
infarct extent by MRI and examined whether its interaction with infarct
core microvascular status had additional prognostic value. Finally, in
a subgroup of patients who had repeat imaging 6 months after
infarction, we tested the hypothesis that microvascular obstruction
relates to eventual transmural myocardial damage and late
ventricular remodeling.
All subjects had coronary angiography by standard techniques
4±4 days (range, 0 to 11 days) after infarction. Two independent
observers, blinded to clinical outcome, classified the angiograms
according to Thrombolysis in Myocardial Infarction (TIMI)
study group criteria.28 ECGs taken at this time
were also analyzed by two blinded, independent observers for
Q-wave presence and infarct location, defined by leads demonstrating Q
waves and/or ST-segment changes. "Acute" MRI occurred 10±6 days
after infarction. "Chronic" MRI studies were performed 180±51 days
after infarction.
MRI Protocol
MRI Data Analysis
The hyperenhanced areas (Fig 2
Chronic Studies
Acute and Chronic Studies
Clinical Study Outcomes
Statistical Analysis
For the chronic studies, changes in functional and anatomic indices
over time were assessed by paired t tests or
ANOVA.33 Logistic regression was used to
determine predictors of fibrous scar formation.33
To evaluate the relationship between MRI extent of hyperenhancement and
changes in functional and anatomic indices, linear regression was
used.33
Data are expressed as mean±SD. Values of P<.05 were
considered significant.
Clinical Significance of MRI-Defined Microvascular
Obstruction
MRI microvascular obstruction was a more potent marker for
postinfarction cardiovascular complications than
patency status of the infarct-related epicardial artery (assessed from
the most recent angiogram preceding MRI). Although infarct-related
artery status correlated with microvascular status (P<.05),
5 of the 11 patients with MRI microvascular obstruction in fact had
TIMI 3 flow (Table 2
Clinical Significance of MRI-Defined Infarct Size
Experimentally, large reperfused infarcts are more often associated
with regions of "no-reflow" produced by microvascular obstruction
than are small infarcts.13 In this study, MRI
microvascular obstruction and larger infarct sizes were clearly
related: patients with microvascular obstruction had an average infarct
size of 32.6±9.6% versus 22.9±10.0% in those without
(P<.005). By multiple regression analysis, the
presence of MRI microvascular obstruction remained a prognostic marker
of untoward permanent events when infarct size was controlled for
(
Prognostic Significance of Acute MRI Functional Indices
MRI Predictors of Transmural Myocardial Infarction and
Ventricular Remodeling
Acute infarct size, indexed as the extent of myocardial
hyperenhancement, also predicted eventual scar formation
(
MRI hypoenhanced areas correspond to experimentally produced no-reflow
regions and reflect myocardial microvascular
obstruction.7 34 The evidence corroborating this
is substantial. The pattern of hypoenhancement seen in our study
patients is identical to that produced in experimental animals in terms
of both spatial location and temporal occurrence after contrast
injection, as shown by time-intensity curves.7
Myocardial biopsies taken from regions of hypoenhancement in
experimental animals have demonstrated profound microvascular damage at
the infarct core, with microvascular obstruction by red blood cells and
necrotic debris.34 In the canine model, MRI
hypoenhanced regions are characterized by profoundly reduced blood
flow, as measured by radioactive
microspheres.7 These areas also
correspond to regions that do not take up the vital stain
thioflavin.7 Both of these characteristics
further support the close correlation between MRI hypoenhancement and
microvascular obstruction. Recent work investigating the time course of
MRI hypoenhancement development has further corroborated this
association with microsphere flow
measurements.35
This study demonstrates that early after infarction, patients with MRI
microvascular obstruction have larger regions of injured
myocardium than those without it, again correlating well
with previous experimental data.13 Our results
also concur with studies supporting the clinical importance of profound
alterations in microvascular integrity after coronary
occlusion.6 14 We have previously shown that
microvascular obstruction is associated with greater
echocardiographic regional dysfunction acutely, ECG Q
waves, and occluded infarct-related arteries by
angiography.6 The present study demonstrates
that such an MRI pattern predicts subsequent
cardiovascular complications, including cardiac death,
reinfarction, heart failure, and stroke. Although the prognostic value
of microvascular obstruction may arise partly because it reflects a
larger infarct, our findings suggest that its presence may
independently predict long-term cardiovascular
complications.
Other imaging modalities have been used to demonstrate postinfarction
alterations in microvascular integrity after reperfusion. Myocardial
contrast
echocardiography10 11 14 has
correlated the presence of contrast defects with poor functional
recovery of postischemic myocardium despite
restored infarct-related artery flow.10 11 Unlike
MRI, however, it currently requires intracoronary injection of
microbubbles, necessitating cardiac catheterization.
Furthermore, infarct size definition is unfeasible with contrast
echocardiography once flow in the infarct-related
artery is reestablished. In vivo microvascular integrity has also been
studied with techniques that use such radioactive tracers as
201Tl and
82Rb.36 37 However, no
echocardiographic or nuclear studies have related those
alterations to postinfarction long-term prognosis. Although our results
agree with those obtained by such techniques, we demonstrate the
clinical importance of microvascular obstruction by relating it to a
greater probability of cardiovascular complications
after acute infarction.
Another finding of our study is the direct relationship between
MRI-determined infarct size and the risk of developing
cardiovascular complications after infarction. Patients
with larger infarcts had worse clinical outcomes. MRI myocardial
hyperenhancement results from myocardial injury and/or necrosis and
correlates well with infarct size clinically and
experimentally.6 7 8 9 It also closely approximates
201Tl fixed perfusion defect
size.38 Like ours, previous studies have
correlated larger thallium perfusion defects with increased
cardiovascular complications.38
Likewise, predischarge infarct size by 99mTc
sestamibi appears to predict long-term left ventricular
function better than predischarge left ventricular ejection
fraction.39 Our range of MRI-determined infarct
sizes was comparable to that obtained by 99mTc
sestamibi.39 However, because sestamibi is a
relatively pure perfusion agent, direct comparisons with gadolinium may
not be possible.
This study highlights the merits of a method that directly assesses
myocardial injury after acute coronary artery occlusion. The
ability of MRI perfusion patterns to predict clinical outcome was
stronger than that of left ventricular function assessed
during the acute postinfarction period. The decreased predictive value
of early postinfarction ejection fraction can be explained by several
factors. Significant myocardial stunning can occur after infarction,
leading to an initial underestimation of left ventricular
ejection fraction.40 Conversely, hyperkinesis of
noninfarcted myocardium may occur, thereby preserving
overall ejection fraction in the face of significant myocardial loss
due to infarction.41 Finally, the ability of
ejection fraction to accurately reflect the extent of myocardial damage
early after acute infarction is also limited by its dependence on
global afterload conditions.42 For these reasons,
Califf et al43 have suggested that left
ventricular ejection fraction alone should not be used as a
clinical trials outcome, particularly in the acute postinfarction
period.
One limitation of our study was the small sample size, which
necessitated that we combine multiple clinical end points for
statistical analysis. Nonetheless, we were able to demonstrate
significant differences in clinical outcome in only 44 patients. To
maximize and highlight the value of our MRI parameters as
surrogates for clinical outcome, we chose to include not only
conventional postinfarction complications, such as cardiac death,
reinfarction, and heart failure, but also clinically relevant outcomes,
such as embolic cerebrovascular accident and unstable angina requiring
hospitalization. Embolic stroke complicates the early postinfarction
course of 0.7% to 4.7% of patients.44 45 The
risk of stroke is directly proportional to left ventricular
dysfunction in postinfarction patients.46
Furthermore, the devastating morbidity associated with such events led
us and others47 to identify stroke as an end
point after myocardial infarction. Nonetheless, even when stroke is
eliminated as a permanent clinical end point, the difference between
post-MI complication rates in patients with and without MRI
microvascular obstruction remains statistically significant. By
including only cardiac death, reinfarction, and congestive heart
failure, the event rates become 4 of 11 (36.4%) for patients with
microvascular obstruction versus 3 of 33 (9.1%) for those without
(
Other methodological limitations of this study should be discussed in
light of the potential advantages of MRI in examining postinfarction
patients. One potential limitation was using only four base-to-apex
short-axis cross sections to quantify infarct size. However, infarct
size can, in fact, be adequately assessed with three base-to-apex
short-axis slices.48 Current MRI technical
limitations precluded the attainment of useful scans for infarct size
determination in 6 patients. However, in all patients, images during
the first minutes after contrast were preserved, allowing the
assessment of microvascular integrity for the entire group. This
limitation related to difficulties in sustaining multiple breath-holds
combined with claustrophobia, an apparently more prevalent phenomenon
in postinfarction patients. Wider magnet
designs49 and solutions to the obstacles
associated with motion artifacts50 and the need
for breath-hold imaging51 will certainly minimize
patient apprehension and discomfort during the examination. Moreover,
the possibility of combining detailed studies of myocardial
function,52 perfusion,6 and
sodium metabolism53 with the
noninvasive assessment of coronary
anatomy54 and epicardial coronary
artery blood flow55 highlight the
diagnostic potential of MRI in coronary artery
disease.
The exact mechanisms whereby microvascular obstruction determines
postinfarction prognosis remain unknown. One potential explanation is
the relationship between presence of microvascular obstruction and
infarct size, documented previously in a canine
model13 and confirmed in this study. However,
controlling for infarct size did not eliminate the power of
microvascular obstruction to predict the occurrence of adverse
postinfarction events. Theoretically, early obstruction of microvessels
after reperfusion could result in altered material properties locally
relative to regions receiving adequate reperfusion. This concept is
supported by previous studies that related the presence of
microvascular obstruction documented by contrast
echocardiography to left ventricular
remodeling early in the postinfarction period.14
In addition, other investigators have shown that myocardial reperfusion
limits postinfarction ventricular
remodeling24 and improves patient prognosis even
without salvaging myocardium.24 25 26
Similarly, in our study, the presence of microvessel obstruction in the
acute postinfarction period was associated not only with a greater rate
of fibrous scar formation but also with greater ventricular
remodeling, in terms of both increased left ventricular
volumes and masses. Moreover, altered myocardial material properties as
a mechanism of worse ventricular remodeling should
theoretically be most important in patients with large infarcts who are
already at risk for greater postinfarction remodeling and heart
failure.17 19 56 In this regard, our results
support the notion that there may be an interaction between infarct
size and the presence of microvascular obstruction, resulting in
greater left ventricular enlargement and worse prognosis
after infarction. However, given the small sample size of the patient
group who underwent repeat MRI, our findings linking microvascular
obstruction to long-term left ventricular remodeling
require confirmation by future clinical or experimental studies.
Finally, it is possible that other mechanisms may predispose a patient
to developing microvascular obstruction over and above the contribution
of infarct size. The importance of platelet function in
coronary syndromes has recently been
demonstrated.57 Whether or not hematologic
alterations lead to more prolonged or extensive coronary
thrombosis and/or reperfusion injury13 also needs
further investigation. In any case, mechanistic possibilities linking
microvascular occlusion to postinfarction prognosis are important to
consider because they could lead to the development of new strategies
that limit myocardial damage after therapeutic myocardial reperfusion
in patients with acute infarction.
In conclusion, the presence of MRI microvascular obstruction acutely
predicts long-term prognosis in patients with myocardial infarction. In
addition, the extent of total myocardial ischemic injury
assessed by MRI also directly relates to the risk of
cardiovascular complications after infarction.
Moreover, microvascular status remains a strong prognostic marker even
after infarct size is controlled for. The ability to combine
microvascular perfusion studies with direct measurements of infarct
extent illustrates the potential of MRI to study the heart after acute
coronary thrombosis.
Received July 9, 1997;
revision received October 16, 1997;
accepted October 16, 1997.
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Clinical Investigation and Reports
Prognostic Significance of Microvascular Obstruction by Magnetic Resonance Imaging in Patients With Acute Myocardial Infarction
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The extent of
microvascular obstruction during acute coronary occlusion may
determine the eventual magnitude of myocardial damage and thus, patient
prognosis after infarction. By contrast-enhanced MRI, regions of
profound microvascular obstruction at the infarct core are hypoenhanced
and correspond to greater myocardial damage acutely. We investigated
whether profound microvascular obstruction after infarction predicts
2-year cardiovascular morbidity and mortality. 
2=6.46,
P<.01). The risk of adverse events increased with
infarct extent (30%, 43%, and 71% for small [n=10], midsized
[n=14], and large [n=14] infarcts, P<.05). Even
after infarct size was controlled for, the presence of microvascular
obstruction remained a prognostic marker of postinfarction
complications (2=5.17, P<.05). Among
those returning for follow-up imaging, the presence of microvascular
obstruction was associated with fibrous scar formation
(2=10.0, P<.01) and left
ventricular remodeling (P<.05).
Key Words: prognosis • microcirculation • magnetic resonance imaging
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Patient prognosis
after acute myocardial infarction relates directly to the extent of
myocardial injury produced during coronary
occlusion.1 2 Postinfarction
electrocardiography,
echocardiography, and contrast ventriculography are
often used to indirectly assess the degree of myocardial
damage,1 3 4 whereas radionuclide studies with
99mTc sestamibi and contrast-enhanced fast MRI
can measure infarct size directly.5 6 7 8 9 Recently,
in addition to the extent of infarcted myocardium, the
magnitude of microvascular obstruction sustained during acute
infarction has been related to clinical
outcome.10 11
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Study Patients
Forty-four patients were enrolled (Table 1
). Entry criteria included typical
symptoms of acute infarction with ECG changes, creatine phosphokinase
(CPK) elevation more than twice the upper limits of normal, and >5%
myocardium-specific bands. All patients gave informed
consent according to the Johns Hopkins Hospital Joint Committee for
Clinical Investigation standards. All but 2 received
thrombolytics or direct angioplasty: 1 had colon
cancer; the other presented for care >24 hours after
infarction. Data from 22 patients were published in a previous study
characterizing postinfarction MRI myocardial enhancement
patterns.6 Seventeen patients returned 6 months
after infarction for repeat MRI; these patients composed the long-term
follow-up group.
View this table:
[in a new window]
Table 1. Patient Characteristics
Images were acquired during multiple breath-holds on a 1.5-T
whole-body magnet (Signa, General Electric). Details of the pulse
sequence used in this study have been published
previously.29 It resembles inversion-recovery
turboFLASH30 in that pixel intensity is heavily
T1-weighted but minimizes T2 contamination by spoiling xy
plane magnetization. Use of a very short TE minimizes T2* effects.
Within each RR interval, 60 nonselective dummy radiofrequency pulses
are transmitted before imaging to drive magnetization to a steady
state. Thirty-two image phase encoding steps immediately follow,
acquired with TR of 6.5 ms, TE of 2.3 ms, and flip angle of
45°.29 Ninety-six phase-encoding steps per
image are acquired, such that each image is completed in three cardiac
cycles. K-space lines 1, 4, 7 ... etc; 2, 5, 8 ... etc; and
3, 6, 9 ... etc are obtained during the first, second, and third
beats, respectively. Matrix size was 256x96, field of view was 36 cm,
and voxel size was 1.4x3.7x10.0 mm. The imaging protocol
included four base-to-apex short-axis cross sections acquired with
prospective ECG gating during 12 heartbeat breath-holds. For the acute
studies, a bolus of Gadoteridol (ProHance, Squibb, 0.1 mmol/kg)
was administered by fast hand injection. Immediately after contrast,
images were acquired every 30 seconds for 5 minutes, then each minute
for the next 10 minutes. All perfusion images were obtained late in
diastole (diastasis). Studies lasted 
45 minutes, with no
adverse contrast reactions. A similar pulse sequence was used to obtain
short-axis and long-axis image planes at end diastole and
end systole to obtain functional and anatomic indices for both acute
and chronic MRI studies.
Acute Studies
Signal-intensity curves were generated with the aid of the
software package NIH IMAGE. The methodology has been
described.6 7 Regions of interest were defined
within the infarcted region, represented as an area of
hyperenhanced plus hypoenhanced signal in the territory perfused by the
angiographically determined infarct-related artery. Regions of interest
were also defined inside the noninfarcted myocardium and
the left ventricular cavity. In patients with hypoenhanced
subendocardium at the infarct core (Fig 1), the central region of interest was
defined within the dark zone, whereas other sample regions were taken
from areas of increased signal intensity surrounding the dark zone. The
pulse sequence produces dark, homogeneous precontrast
cardiac images.6 7 29 Signal intensity over time
from each image was quantified, and the curves generated for each
patient were expressed as the percent increase in signal intensity (SI)
over baseline precontrast signal intensity: normalized SI
(%)=100x(SI-baseline SI)/baseline SI (Fig 1B).
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Figure 1. MRI (A) and time-intensity curve (B):
microvascular obstruction. A is from patient with anteroseptal infarct
and extensive subendocardial microvascular obstruction (between
arrows). B, Corresponding time-intensity curves. Microvascular
obstruction ( 
) is characterized by low signal intensity early after
contrast followed by a gradual rise. Images 1 to 2 minutes after
contrast (arrow) best delineate such regions because of maximal signal
intensity differences between normal, noninfarcted
myocardium (
) and infarct core
microvascular damage. In infarct periphery (
), signal intensity
resembles that of noninfarcted myocardium initially but
then diverges, reflecting eventual hyperenhancement.) from the
four base-to-apex short-axis images obtained 5 to 10 minutes after
contrast were planimetered, with hypoenhanced regions included when
present.7 All hypoenhanced regions were
smaller than and circumscribed by hyperenhanced regions. Infarct size,
expressed as percent total LV mass, was then calculated from the
percentage of hyperenhancement plus hypoenhancement in each slice,
weighted according to slice cross-sectional
area.7 Thus, for all slices, infarct size=
(%
hyperenhanced plus hypoenhanced)x(cross-sectional
area)/(cross-sectional area). Two observers blinded to clinical
outcome determined microvascular status visually from scans obtained 1
to 2 minutes after contrast (Fig 1A
). The presence of microvascular
obstruction was corroborated by a characteristic time-intensity curve
(Fig 1B). There was complete consensus as to the MRI presence or
absence of microvascular obstruction. Infarct size was measured by two
blinded observers with good interobserver
(y=0.9x, r=.8) and intraobserver
(y=0.99x, r=.9) variability. Although
6 patients had technically limited studies precluding accurate
delineation of infarct extent, in all patients, microvascular status
could be determined because image quality was preserved at the earlier
time points (up to 2 to 5 minutes after contrast).
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Figure 2. MRI (A) and time-intensity curve (B):
hyperenhancement. A is from patient with anterolateral infarct. First
image, precontrast, shows homogeneous signal from
myocardium and intracavitary blood. Second image, taken
immediately after contrast (first arrow, B), shows bright
ventricular cavities before myocardial contrast
penetration. Third image was taken 520 seconds after contrast (second
arrow, B), at which time, intensity of infarcted area (between arrows)
resembles that of blood and is most discernible from noninfarcted
myocardium. B, Corresponding signal intensity curves.
On the 6-month scans, scar was defined according to published
criteria based on autopsy data.31 If the
myocardial segment shown to be hyperenhanced on the acute study was
thinned on the chronic images (end-diastolic wall thickness
<6 mm in three or more adjacent image planes), transmural scar
formation was diagnosed (Fig 3).
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Figure 3. MRI: fibrous scar formation. First image (acute
study), taken immediately after contrast, shows bright
ventricular cavities with homogeneous
myocardium. Second image (acute study), obtained 570
seconds after contrast, delineates inferior wall
hyperenhanced region. Six-month follow-up scan of same patient (third
image) depicts thinning of myocardial segment that was initially
hyperenhanced.
MRI studies were also analyzed for left
ventricular end-diastolic and
end-systolic volume, mass, and ejection fraction by standard
methods.32 Of the acute studies, 8 were
technically limited, precluding calculation of functional indices.
Patients were followed clinically for 16±5 months. Follow-up
was conducted through telephone interviews with the patient and/or his
or her physician and medical records review. Clinical end points
included cardiac death, defined by sudden death or death preceded by
typical chest pain; nonfatal myocardial reinfarction as determined by
typical chest pain with ECG changes and CPK elevation to more than
twice the upper limit of normal; congestive heart failure secondary to
left ventricular systolic dysfunction, diagnosed by
history and physical examination; ischemic cerebrovascular
accident corroborated by clinical criteria and neuroimaging; and
unstable angina requiring hospitalization, defined as typical chest
pain with ECG changes but no CPK elevation. For statistical purposes,
we defined permanent events as consisting of cardiac death,
reinfarction, congestive heart failure, or stroke. In every
analysis, all events were considered equivalent, and only the
first event was included in the calculation.
For the acute studies, patients were grouped by MRI
microvascular status and by MRI-determined infarct size: "small"
infarcts had <18% hyperenhancement; "intermediate," between 18%
and 30%; and "large," >30%. To compare complication rates after
infarction, the groups with and without microvascular obstruction were
analyzed with two-tailed Fisher's exact tests;
2 tests for trends were used for the three
infarct-size groups and the three ejection fraction
groups.33 The Kaplan-Meier technique was used to
compare time from acute infarct to clinical complication
occurrence.33 To examine individual and combined
effects of acute MRI microvascular perfusion pattern, MRI extent of
hyperenhancement, infarct-related artery patency, and MRI functional
indices on clinical outcome, logistic regression analysis was
used.33 The correlation between ejection fraction
and infarct size was assessed with linear regression
analysis.33
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Study Population Clinical Characteristics and Follow-up
Table 1 summarizes the patients' characteristics. Excluding the
10 who underwent rescue or direct angioplasty, patients had
coronary catheterizations 
48 hours after
infarction, at which time, 20 had coronary angioplasty.
Patients were followed for 16±5 months (range, 6 to 25 months).
Although 6 patients had multiple events, only the first event was
considered. Index clinical events occurred 14±6 months after
infarction (range, 0.3 to 25 months). These index events consisted of
cardiac death in 1 patient (2.3%); nonfatal reinfarction in 4 (9.1%);
congestive heart failure in 2 (4.5%); embolic stroke in 1 (2.3%); and
unstable angina requiring hospitalization in 11 (25%).
Eleven patients had microvascular obstruction on their acute MRI
scan; 33 did not. Of the 11 patients with microvascular obstruction, 5
(45%) experienced at least one permanent postinfarction complication
(cardiac death, reinfarction, congestive heart failure, or stroke)
versus only 3 (9%) of the 33 without obstruction (P=.016;
odds ratio for patients with obstruction, 5.7; 95% CI, 1.84 to 51)
(Fig 4). Moreover, univariate
regression analysis showed that microvascular status predicted
whether or not untoward permanent events occurred after infarction
(2=6.46, P<.01).
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Figure 4. Event-free survival (clinical course without
cardiovascular death, reinfarction, congestive heart
failure, or stroke) for patients with and without MRI microvascular
obstruction. ). Furthermore, by
regression analysis, the relationship between TIMI flow and the
rate of postinfarction complications was of only borderline statistical
significance (2=2.69,
.05<P<.1).
View this table:
[in a new window]
Table 2. Infarct-Related Artery Status Grouped by MRI
Microvascular Obstruction
Infarct size as determined by the extent of MRI hyperenhanced
tissue relative to total myocardium ranged from 4% to
54%. Ten patients had small (<18%), 14 had midsized (18% to 30%),
and 14 had large (>30%) infarcts. The risk of sustaining one of the
following complications increased with infarct size (P<.05)
(Fig 5): cardiac death, reinfarction,
congestive heart failure, stroke, or unstable angina requiring
hospitalization. Events occurred in 30% of the patients with small
infarcts, in 43% with medium infarcts, and in 71% with large infarcts
(Fig 5). When unstable angina was eliminated, a trend toward a higher
rate of permanent events with increasing infarct size persisted
(small, 10%; midsize, 14%; and large, 36%; .05<P<.1).
No differences were found when the rate of
revascularization (angioplasty and bypass surgery)
or unstable angina was considered independently. Infarct size did not
correlate with peak CPK or infarct-related artery patency.
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Figure 5. Event-free survival (clinical course without
cardiovascular death, reinfarction, congestive heart
failure, stroke, or unstable angina requiring hospitalization) for
patients grouped by MRI infarct size. 2=5.17, P<.05). In addition, the
predictive value of microvascular obstruction tended to vary with
infarct size. In the large-infarct group, the permanent event rate was
67% (4 of 6) in patients with obstruction versus 13% (1 of 8) in
those without (P=.09). Although no patients with small
infarcts had microvascular obstruction, among the midsized-infarct
group, patients with obstruction had a permanent event rate of 20%
(1 of 5) versus 11% (1 of 9) in those without
(P=NS).
When grouped by left ventricular ejection fraction
obtained in the acute postinfarction period, patients developed
permanent events at the following rates: 3 of 9 (33%) for the 
40%
group; 1 of 7 (14%) for the 40% to 55% group; and 4 of 20 (20%) for
the >55% group (2=0.92;
P=NS). If all events, including unstable angina requiring
hospitalization, are considered, complication rates are 7 of 9 (78%)
for the 40% group; 4 of 7 (55%) for the 40% to 55% group; and 8
of 20 (40%) for the >55% group
(2=3.78; .05<P<.1).
Left ventricular volumes and masses could not predict
clinical outcome. The correlation between ejection fraction and infarct
size was of borderline significance (F=3.60; P=.067).
Microvascular status in the acute period predicted the occurrence
of transmural myocardial damage with eventual scar formation 6 months
after infarction (2=10.0,
P<.01). Five (62.5%) of the 8 patients with microvascular
obstruction in the acute postinfarction period had
ventricular wall thinning consistent with scar
formation at 6 months, whereas none (0%) of the 9 patients without
microvascular obstruction developed fibrous scar (P<.03).
Furthermore, the presence of microvascular obstruction was associated
with greater increases in left ventricular volumes 6 months
after infarction. In patients with microvascular obstruction,
end-diastolic volumes rose by 89.0±77.8% versus
9.8±26.8% in patients without obstruction (P<.02).
Similarly, end-systolic volumes increased by 165.5±199.6% in
patients with microvascular obstruction compared with 3.0±19.8% in
those without (P<.04). Microvascular obstruction at 1 week
was also associated with a greater rise in left ventricular
systolic mass over 6 months (from 131.2±63.8 to 195.1±57.3 g)
compared with patients without obstruction (from 151.3±29.2 to
164.1±47.6 g) (P<.05). Left ventricular
ejection fraction was similar in the two groups acutely (48.8±20.0%
for patients with microvascular obstruction versus 54.3±12.0% for
those without, P=NS) and at 6 months (43.3±14.1% for
patients with microvascular obstruction versus 55.0±15.0% for those
without, P=NS). 2=5.9, P<.02).
Patients with MRI fibrous scars at 6 months after infarction had larger
acute infarct sizes than those who did not develop fibrous scar
(36.5±12.4% versus 21.9±9.6%, P<.03). More importantly,
the presence of microvascular obstruction remained predictive of
fibrous scar formation even when adjusted for infarct size
(2=10.85, P<.02).
Finally, acute infarct size was related to 6-month left
ventricular volumes. Chronic end-diastolic
volumes (P=.02) and chronic end-systolic volumes
(P=.044) correlated with infarct size acutely.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
This study is the first to demonstrate the relationship between
MRI contrast defects, which most likely reflect severe microvascular
obstruction, and long-term prognosis after infarction. The presence of
MRI microvascular obstruction correlates with a higher rate of
cardiovascular events in the first 2 years after acute
myocardial infarction. Infarct size, determined by MRI, is also
predictive of the risk of postinfarction complications. Although the
development of microvessel occlusion during coronary thrombosis
is related to infarct size, its presence remains a strong predictor of
adverse cardiovascular events even after the extent of
total myocardial damage is controlled for. 2=4.09,
.02<P<.05). When stroke is removed from the
analysis examining the predictive value of MRI-determined
infarct size on clinical outcomes, statistical significance is not
reached (2=2.79,
.05<P<.1). Nevertheless, the difference in event rates
remains high: 3 of 10 (30%) for patients with small infarcts, 6 of 14
(42.9%) for the medium-infarct group, and 9 of 14 (64.3%) for the
large-infarct group. We also chose to include unstable angina requiring
hospitalization as a clinical end point because of its impact on
patient outcome. All but 1 patient with such an episode required
revascularization to control the ischemic
event: 8 had coronary angioplasty and 2 had coronary
artery bypass surgery during the same hospital admission as their
unstable angina. Therefore, these hospitalizations not only were
significant in terms of patient morbidity but also led to costly
diagnostic and therapeutic interventions.
Acknowledgments
This study was supported by Grant-in-Aid 92–10-26–01 from the
American Heart Association, Dallas, Tex, and NHLBI grant HL-45090,
NIH, Bethesda, Md.
Footnotes
Reprint requests to João A.C. Lima, MD, Blalock 569, Division of Cardiology, the Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
The Multicenter Postinfarction Research Group.
Risk stratification and survival after myocardial infarction.
N Engl J Med. 1983;309:331–336.[Abstract]
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