REVIEW

Imaging
MRI in acute myocardial infarction
Martina Perazzolo Marra
1
*
, Joa o A.C. Lima
2,3
, and Sabino Iliceto
1
1
Division of Cardiology, Department of Cardiac, Thoracic, and Vascular Sciences, University of Padua Medical School, Via Giustiniani, 2, 35128 Padua, Italy;
2
Department of
Radiology, Johns Hopkins School of Medicine, Baltimore, USA; and
3
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, USA
Received 7 June 2010; revised 15 September 2010; accepted 15 October 2010; online publish-ahead-of-print 25 November 2010
Although acute myocardial infarction (AMI) is still one of the main causes of high morbidity in Western countries, the rate of mortality has
decreased signicantly. The main cause of this drop appears to be the decline of the incidence of ST-segment elevation myocardial infarction
(STEMI) along with an absolute reduction in case fatality rate once STEMI has occurred. Myocardial ischaemia progresses with the duration of
coronary occlusion and the delay in time to reperfusion determines the extent of irreversibile necrosis from subendocarial layers towards
the epicardium in accordance with the so-called wave-front phenomenon. Coronary artery recanalization, either by thrombolitic therapy or
primary percutaneous intervention, may prevent myocardial cell necrosis increasing salvage of damaged, but still viable, myocardium within
the area at risk. Magnetic resonance imaging (MRI) can provide a wide range of clinically useful information in AMI by detecting not only
location of transmural necrosis, infarct size and myocardial oedema, but also showing in vivo important microvascular pathophysiological pro-
cesses associated with AMI in the reperfusion era, such as intramyocardial haemorrhage and no-reow. The focus of this review will be on
the impact of cardiac MRI in the characterization of AMI pathophysiology in vivo in the current reperfusion era, concentrating also on clinical
applications and future perspectives for specic therapeutic strategies.
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Keywords Acute myocardial infarction Pathophysiology Magnetic resonance imaging
Introduction
Although acute myocardial infarction (AMI) is one of the major
causes of morbidity in Western countries,
1
mortality has
decreased signicantly and this drop appears to be the result of
the decline in the incidence of ST-segment elevation myocardial
infarction (STEMI) along with the absolute reduction of overall
mortality of AMI.
2
The reduction of mortality for AMI is due to
the efcacy of current therapeutic strategies focused on an early
reopening of the infarct-related artery, either by thrombolitic
therapy or primary percutaneous coronary intervention (PCI),
which represents the most effective way to limit infarct size (IS)
and reduce transmural extention of necrosis. Reperfusion
therapy modies traditional pathological features of AMI,
because coronary artery recanalization can prevent the transmural
progression of myocardial necrosis.
3,4
Indeed, reperfusion after
prolonged coronary occlusion may develop into reperfusion
injury associated with impairment of microcirculatory ow and
possible further deterioration due to intramyocardial haemor-
rhage. The pathological consequences of reperfusion strategies
can be currently detected in vivo by cardiac magnetic resonance
imaging (MRI), a non-invasive tool that allows the translation of
features previously studied only by experimental models from
bench to bedside. Cardiac MRI can provide a wide range of infor-
mation such as myocardial oedema (myocardium at risk), location
of transmural necrosis, quantication of IS and microvascular
obstruction leading also to intramyocardial haemorrage.
5
More-
over, cardiac MRI provides an accurate and reproducible modality
for the assessment of global ventricular volumes and function,
6
representing the most powerful phenotyping tool for a global
evaluation of post-infarction remodelling. This review will demon-
strate the impact of cardiac MRI in the in vivo assessment of the
pathophysiology of AMI in the current reperfusion era, focusing
also on clinical applications and future perspectives for therapeutic
strategies.
Technical advantages of cardiac
magnetic resonance
Cardiac MRI represents a non-invasive technique with increasing
applications in AMI providing the assessment of function, perfusion
and tissue characterization in a highly reproducible manner during
a single examination even in patients with acoustic window
* Corresponding author. Tel: +1 39 049 821 8642, Fax: +1 39 049 8761 764, Email: martina.perazzolomarra.1@unipd.it
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email: journals.permissions@oup.com.
European Heart Journal (2011) 32, 284293
doi:10.1093/eurheartj/ehq409
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limitations (Figure 1).
7
Cine MRI for evaluation of cardiac volumes,
mass, and systolic function is considered a gold standard com-
pared with other imaging modalities, since it does not apply geo-
metric assumptions.
6
The high values of reproducibility and
accuracy (standard error for left ventricular, LV, mass and
volume is about 5%) are particularly useful to reduce sample
size in clinical trials.
610
The steady-state free precession
sequences for cine images have replaced the older turbo gradient
echo due to increased natural contrast between blood and endo-
cardial border.
11,12
Consecutive breath-hold short axis of the
heart (temporal resolution of 50 ms or less) are used to obtain
functional assessment: after delineation of endocardial and epicar-
dial borders the summation of discs method is applied. New
three-dimensional MRI acquisition offers the advantage to cover
the entire myocardium with a single breath hold of 2030 s, but
with lower temporal resolution (100 ms).
7
Regional myocardial
function including wall thickening, evaluation and measures of
myocardial strain may be perfomed.
13
In patients with suspected coronary disease, myocardial per-
fusion reserve measured by cardiac MRI yields high diagnostic
accuracy for the detection of ow-limiting lesions.
12,14
Perfusion
MRI is performed at rest and again during a vasodilator stress
administration (i.e. adenosine, dipyridamole) using a rst-pass
technique with fast intravenous injection of a gadolinium-based
contrast agent.
15,16
The myocardial signal increases in normal well-
perfused myocardium, but not in the regions of myocardial
ischaemia.
17,18
Tissue characterization by cardiac MRI is due to the evaluation
of proton relaxation times T1 and T2. Currently T2 images are
used in non-contrast approaches, whereas T1 sequences are
used for contrast-enhanced studies (i.e. previous citied rst
pass). Increased myocardial water content increases signal on
T2-weighted images, such as inammation. Myocardial oedema in
the acute phase of myocardial infarction can be visualized as a
bright signal on T2-weighted images, dening myocardium at
risk.
1921
The major advantages of this technique are to distinguish
chronic from acute infarction,
22
and to quantify the proportion of
myocardial salvaged assessed retrospectively by comparing
T2-weighted oedematous size and late enhancement images.
23
Late gadolinium enhancement (LGE) images are T1-weighted
inversion recovery sequences acquired about 10 min after intrave-
nous administration of gadolinium and the inversion time is chosen
to null myocardial signal
24
using inversion time scout or look
locker sequences. Gadolinium is an extracellular agent, which
enhances its distribution volume in certain conditions such as
necrotic or brotic myocardium, assuming a bright signal (hyperen-
hancement), opposed to dark viable myocardium.
25
Cardiac MRI
highlights the region of scar or brosis as small as 0.16 g
26,27
and
the reproducibility is high with a coefcient of reproducibility
reported equal to+2.4% of LV mass in chronic setting.
28
The
pattern of LGE is useful to differentiate post-infarction necrosis
(subendocardial or transmural LGE) (Figure 2) from brosis in non-
ischaemic dilated cardiomyopathies (mid-wall LGE, subepicardial
LGE), or myocarditis (subepicardial or focal LGE) (Figure 3).
Delayed post-contrast sequences are currently used also to evalu-
ate persistent microvascular dysfunction/damage: in the context of
white LGE regions (infarcted myocardium) may coexist dark
hypoenhanced areas, traditionally referred to as microvascular
obstruction. Microvascular obstruction has been initially dened
as hypoenhancement at 12 min after gadolinium injection;
25,29,30
Figure 1 A complete cardiac magnetic resonance protocol is summarized in this gure taking into account the pathophysiological substrates
underlying different MRI ndings. SSFP indicates steady-state free precession; IR GRE, inversion recovery gradient echo; LV, left ventricle; RV,
right ventricle; AAR, area of myocardium at risk.
MRI in acute myocardial infarction 285
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however, persistent microvascular damage is currently evaluated
on delayed post-contrast sequences.
31
Myocardial ischaemia: area at risk
During the early phase of a coronary occlusion, the subsequent
discrepancy between myocardial oxygen supply and demand lead
to myocardial ischaemia, characterized by a specic pattern of
metabolic and ultrastructural alterations.
32
If ischaemia persists,
myocardial injury becomes irreversibile and the necrosis extends
from the subendocardium towards the subepicardium in accord-
ance with the wavefront phenomenon described initially by
Reimer and Jennings.
3,4
The nal IS depends mainly on the
extent of the so-called risk area, dened as the myocardial area
related to an occluded coronary artery with complete absence
of blood ow, either antegrade or collateral.
33
Up to now, myo-
cardium at risk has been measured by single photon emission
computer tomography (SPECT)
34
using the injection of a
Figure 2 Different extent of necrosis visualized by cardiac magnetic resonance. The patient represented on panel A shows a non-transmural
myocardial infarction detected by late gadolinium enhancement extending for 25% on the entire thickness of the antero-septal wall. On the
contrary, the T1 IR post-contrast sequence of patient B shows a transmural bright anterior and septal myocardial infarction.
Figure 3 Different late gadolinium enhancement patterns. The pattern of late gadolinium enhancement is useful to differentiate necrosis due
to myocardial infarction from brosis in different conditions. The patient presented in panels A and B shows a typical epicardial pattern of late
gadolinium enhancement in the inferior and infero-lateral wall, suggesting a myocarditis. The intramyocardial deposition of late gadolinium
enhancement on interventricular septum (mid-wall pattern) on panels C and D is typical for primary dilated cardiomyopathy.
M.P. Marra et al. 286
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technetium-based tracer before opening of the occluded vessel,
and by contrast echocardiography.
35
Recently, cardiac MRI is
used to visualize and to quantify the area at risk since increased
myocardial signal intensity depicted by T2-weighted sequences
are very sensitive to water-bound protons indicating an increased
water content with an active myocardial inammation and tissue
oedema. The concept of infarct-related oedema was initially eval-
uated on animal models of AMI, in which a linear correlation
between myocardial-free water content of the infarcted region
and prolongation of its T2 relaxation time is demonstrated.
19
Sub-
sequent experimental studies have shown that the area of high T2
signal abnormality closely matched the area at risk determined on
histology.
36,20
In particular, Aletras et al.
20
have demonstrated in an
animal model, with 90 min of coronary occlusion followed by
reperfusion, that the area at risk measured by microspheres was
comparable with the area of increased signal on T2-weighted
images 2 days later. At rst, the application of T2-weighted
imaging in the clinical setting is used to differentiate acute from
chronic myocardial infarction.
22
However, the most important
application of MRI ischaemia-related oedema regards the
evaluation of salvaged myocardium (Figure 4). Cury et al.
37
have
recently applied T2-weighted imaging to improve the accuracy in
the diagnosis of myocardial ischaemia in patients arriving to the
emergency room with acute chest pain, negative biomarkers and
inconclusive ECG. However, the most intriguing application is
the possibility to assess quantitatively the reversible and irrevers-
ible injury in reperfused AMI. Experimental data have shown that
in AMI the area with high T2 signal exceeds that of irreversible
injury. In fact, Choi et al.
38
have demontrated in a pig model the
high signal on T2-weighted images reects both irreversible and
reversibly injured, but essentially the viable, peri-infarct zone. On
this basis, Friedrich et al.
23
have compared T2-weighted images
with LGE to visualize reversible and irreversible myocardial
injury, respectively. Thereafter, many clinical studies have evaluated
the potential of MRI to assess myocardial oedema
3941
in compari-
son with well-established techniques.
42
However, the recent inter-
ventional study performed by Francone et al.
43
represents a
cornerstone for future investigation for the application of the
counterwise area of myocardium at risk in the clinical setting. In
this study,
43
the concept of reduction of total viable myocardium
Figure 4 Myocardium at risk represents the myocardial area related to an occluded coronary artery with complete absence of blood ow.
An example of risk area on septal wall (hyperenhancement) is described on panel A on T2-weighted images, the so-called remote myocar-
dium with normal blood ow appears dark, without signs of oedema, on the lateral wall. In the example B myocardial at risk (oedema) on
anterior, septal and inferior wall is shown: note inside the hyperenhancement on T2-weitghted images the presence of a hypoenhancement
core suggesting intramyocardial haemorrhage. Panels C and D represent a case of acute septal myocardial infarction. Panel C shows T2-weighted
images with transmural oedema extending toward all septal wall even partially in the inferior and anterior wall (black asterisk). Panel D shows
the same slice after delayed contrast injection: note that the bright signal intensity shows a late gadolinium enhancement extent of 75% of the
entire segment only in the anterior septal wall. Note the absence of late gadolinium enhancement in the previous areas involved by oedema
(white arrows), representing area of myocardium at risk.
MRI in acute myocardial infarction 287
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amount in proportion to the delay on time-to-reperfusion is
demonstrated in vivo: in particular, the salvaged myocardium (quan-
tied as the difference between area of increase T2 signal and area
of LGE) is markedly reduced (2.1%) when reperfusion occurs .
90 min after coronary occlusion in contrast with 8.5% in patients
with 90 min of delay.
Progression of necrosis: viability
According to the concept of wavefront phenomenon of myocardial
death,
4
IS increases, extending from the endo to the epicardium
with an increasing duration of coronary occlusion. If ischaemia per-
sists, myocardial injury becomes irreversible, usually between 20
and 45 min after coronary occlusion: a prompt coronary lumen
recanalization is able to prevent the progression of necrosis
leading in some cases to an aborted AMI. The major determinant
of nal transmural necrosis and microvascular damage is the dur-
ation of ischaemia, as recently demonstrated in vivo by MRI.
43,44
Beyond the potentially reversible events (ischaemia and
oedema), cardiac MRI can be used for assessment of the extent
of the irreverrsible necrosis using delayed contrast-hyperenhanced
images. Non-viable infarcted tissue is usually seen on MRI as a
hyperenhanced area after contrast injection, so-called LGE
(Figure 2). In the setting of AMI, the extracellular space is expanded,
also by oedema and inammation, and the contrast agent enters
the intracellular space through damaged cell membranes. The
LGE assessment has been validate against animal models
25
and rep-
resents a permanent memory of myocardial injury even after the
acute phase of infarction.
45
However, in the rst days after AMI,
LGE is more extensive compared with the chronic phase, when
the healing process is complete. Oshinski et al.
46
using a rat
model of AMI, showed that, immediately after contrast injection,
the enhanced region overestimates the true IS, on histology, by
2040%. Saeed et al.
47
have suggested that LGE does not occur
exclusively in regions with myocardial necrosis but also involves
the border zones of injured but viable myocardium surrounding
AMI. Other clinical studies have observed an initial overestimation
of IS that gradually decreases over time. Recently, Ingkanisorn
et al.
48
have found that IS on MRI appeared to diminish in size
on follow-up from 16 +12 to 11+9% (P , 0,003). The same
reduction on IS was noted by Hombach et al.
31
in a large popu-
lation study. Baks et al.
49
evaluating the effects of primary PCI on
early and late IS described a 31% decrease in LGE between
5 days and 5 months. More recently, LGE extent has been evalu-
ated during the hyperacute phase of STEMI: Larose et al.
50
have
performed in STEMI patients a cardiac MRI within 12 h of
primary PCI and at 6 months discovering a reduction in LGE
volume from 22 to 16% (P 0.01).
These observations are notable from a clinical point of view,
even if the measurement of IS by MRI is highly reproducible,
28
the chosen time of imaging along the healing process can yield
different results. The reduction of IS associated with the healing
process is 25% of initial size over 46 weeks. However, the
improved reproducibility of LGE with detection of smaller
changes in IS allows for substantial reduction in sample size for
clinical trials,
51
even when one takes into consideration variability
between patients.
52
Another technical issue to take into account when comparing
ISs in different AMI populations is the dose of gadolinium used.
In a recent international multicentre trial,
53
the sensitivity of LGE
rose with increased gadolinium dose, reaching 99 and 94% in
acute and chronic myocardial infarction, respectively, with the
0.3 mmol/kg dose.
The measurement of LGE seems to provide additive value as a
predictor of adverse outcomes after AMI above ejection fraction.
Before recent studies on AMI,
50,54
IS within 1 week from AMI
was directly related to LV remodelling and was a stronger predic-
tor of future events than measures of LV systolic performance.
55
More recently, Larose et al.
50
demonstrated that the occurrence
of LV dysfunction at 6 months invariably increased with greater
LGE: a cut-off of 23% LGE measured on hyperacute MRI
showed the best accuracy for late LV dysfunction (sensitivity
89%, specicity 74%).
After the healing process is completed and necrotic tissue has
been replaced by a scar,
56
MRI provides clinically relevant infor-
mation concerning viability. Cardiac MRI offers a unique tool to
assess multiple interrelated clinical markers of viability in a single
test with a limited time consumption, moreover considering that
LGE technique together with cine MRI takes no more than
30 min to perform. Scintigraphic techniques and stress echocardio-
graphy have been so far considered the mainstay of viability diag-
nosis. However, the role of MRI in the assessment of myocardial
viability is rapidly increasing as it has the advantage of being per-
formed under resting conditions, without exposing the patient to
radiation. Stress echocardiography with low dose of dobutamine
represents an inexpensive imaging tool for viability evaluation.
However, the high inter-observer variability and inter-individual
differences in image quality for echo-stress imaging explain the
lower sensitivity compared with LGE technique.
57
Moreover, in
the setting of AMI a pharmacological stress is not usually indicated.
Initially in an experimental model, Hillenbrand et al.
58
have demon-
strated that LGE is not detected in regions with severe but revers-
ible ischaemic injury and that there is an inverse relationship
between the transmural extent of necrosis and recovery of func-
tion. The rst clinical application of MRI to identify reversible myo-
cardial dysfunction has been made by Kim et al.
59
who have
determined the accuracy of MRI in predicting recovery in a
series of patients with chronic coronary artery disease and LV dys-
function undergoing myocardial revascularization. In the assess-
ment of myocardial viability in AMI patients, when the extent of
LGE is ,50% the likelihood for functional recovery is efcient.
60
Direct comparison with PET, as a gold standard, has shown excel-
lent results.
61,62
In particular, Klein et al.,
61
performing MRI and
PET within 1 week in patients with ischaemic disease and LV sys-
tolic dysfunction, have found a good correlation between the
two tests. Notably, more than half of subendocardial infarcts,
which have been detected by MRI, have been classied as
normal by PET. Kuhl et al.
62
have found similar results with 36%
of segments normal by PET, but showing subendocardial LGE on
MRI. When comparing SPECT imaging, the main advantage of
MRI LGE is its spatial resolution of 12 mm (in plane), contrary
to about 10 mm with SPECT scans.
63
Therefore, MRI can identify
subendocardial necrosis when perfusion by SPECT appears unal-
tered.
37,64
Wagner et al.
63
discovered the improvement in infarct
M.P. Marra et al. 288
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detection for LGE vs. SPECT with an elegant animal and clinical
study. Similar to animal data, this study has shown that SPECT
detection of LGE-evidenced infarcts varied according to transmural
extent: among segments with near transmural LGE (involving
.75% wall thickness), all show evidence of infarct by SPECT, on
the contrary segments with subendocardial LGE (involving
,50% wall thickness), SPECT detected infarct only in 53%.
Other studies have provided further evidence that LGE identies
myocardial infarctions that are undetected by SPECT.
65,66
Evaluat-
ing patients early after AMI, Ibrahim et al.
64
have compared MRI
with SPECT using troponin elevation as the reference standard,
and has discovered that cardiac MRI was signicantly more sensi-
tive than SPECT for the detection of small infarcts and infarction
in non-anterior region.
Reperfusion injury: no-reow
phenomenon, microvascular
obstruction and haemorrhage
Even if coronary artery ow recanalization represents the most
effective way to reduce IS, the process of reperfusion may itself
produce a series of consequences described in experimental
setting,
67
including myocyte death, microvascular damage with
no reow phenomenon, stunned myocardium and reperfusion
arrhythmias. The clinical relevance and also the most accurate
tool to visualize and quantify microvascular damage secondary or
not to reperfusion injury remains to be identied and so far,
there is no denitive consensus regarding the best imaging
modality. In this clinical scenario, it is reasonable to assume that
cardiac MRI may represent a cornerstone imaging tool yet vali-
dated against established traditional techniques (i.e.
contrast-echocardiography). In one of the rst experimental
studies Judd et al.
25
correlated the MRI ndings with pathology,
by thiavin-S staining, using a reperfused canine infarct model.
The authors demonstrated that hypoenhancement within bright
regions of LGE on delayed post-contrast sequences, so-called
dark zones, were areas of no-reow. In humans, Lima et al.
29
described a well-dened timeintensity curve of different areas
of enhancement occurring in human myocardial infarcts, on the
basis of the wash-in and wash-out kinetics of contrast agent. In
agreement with these observations, the assessment of microvascu-
lar damage had been performed using MRI rst-pass perfusion and
the delayed post-contrast sequences.
68
However, Lund et al.
69
found differences in sensitivity between rst-pass and delayed
hypoenhancement, which was conrmed by recent studies.
70
Cur-
rently, it is generally accepted that delayed hypoenhancement is
less sensitive than rst pass because small no-reow zones
become rapidly enhanced owing to diffusion of the extracellular
contrast medium from surrounding regions without impaired
microvasculature. Moreover, the persistence of a hypoenhance-
ment on delayed contrast sequences (1020 min after injection)
seems to characterize a persistent miscrovascular damage
31
(Figure 5). In conclusion, a complete protocol, including both tech-
niques, should be performed in the current evaluation of AMI by
cardiac MRI.
More recently, microvascular damage detected by MRI has been
evaluated in comparison with coronary Doppler ow reserve.
Hirsch et al.
71
found that the typical presence of early systolic ret-
rograde ow associated with no-reow on intracoronary ow
measurements was associated with the presence of microvascular
obstruction assessed on LGE images. Furthermore, multivariate
regression analysis revealed that the extent of microvascular
obstruction on MRI was the only independent factor related to
early systolic retrograde ow and diastolic deceleration rate.
Cardiac MRI features of reperfusion injury have been compared
also with well-known angiographic perfusion parameters like
TIMI (thrombolysis in myocardial infarction) ow and myocardial
blush grade (MBG). In a recent study by Appelbaum et al.
72
in
21 patients who underwent successful primary PCI and MRI, evi-
dence of impaired perfusion at rst pass was present in 90% of
cases with post-PCI myocardial perfusion grade (0/1/2), but only
in 18.2% with normal one. Porto et al.,
73
by analysing 27 patients
with AMI, found a linear correlation between decreasing MBG
and MRI signs of vascular obstruction, thus conrming the relation-
ship between post-PCI reperfusion index and MRI measures of
microvascular impairment. However, recently Nijveldt et al.
70
did
not nd any statistically signicant relationship between early or
late microvascular obstruction and TIMI ow or MBG in 60
patients with AMI treated with primary PCI. Larger multi-centre
population studies are needed to verify the relationship between
angiographic perfusion indexes and MRI for the detection of micro-
vascular damage.
Cardiac MRI features of no-reow also have prognostic signi-
cance in terms of clinical outcome
30,31
and changes in LV
volumes.
31,74
Even if the dark zones on MRI indicate poor prog-
nostic signicance, the real mechanism underlying these features
is not yet well understood in human AMI, since no-reow rep-
resents a complex time-sensitive phenomenon, which remains to
be fully understood. In fact, the no-reow phenomenon refers
to absent distal myocardial reperfusion after a prolonged period
of ischaemia, despite the culprit coronary arterys successful reca-
nalization,
75
and likely secondary to both luminal obstruction (i.e.
neutrophil plugging, platelets, atherothrombotic emboli) and exter-
nal compression by oedema and haemorrhage. The haemorrhagic
AMI reects the metamorphosis of ischaemic infarcts in the reper-
fusion era,
76
and are commonly observed after prolonged ischae-
mia once myocardial cell necrosis is well established.
Garcia-Dorado et al.
77
have discovered in an experimental model
that microvascular damage is an early event, and that intramyocar-
dial haemorrhage plays a role later in reperfusion injury. Microvas-
cular cell damage causes leakage of blood out of the injured vessel
and the subsequent healing process is characterized by haemo-
globin degradation. As for intracranial haemorrhage, MRI can
enhance tissue characterization through changes in relaxation
times T1 and T2, reecting changes in image signal intensity.
19
By
assessing the paramagnetic susceptibility effects of deoxyhemoglo-
bin, we have recently
78
conrmed previous experimental obser-
vations
79
in which dark areas on post-contrast inversion
recovery sequences indicate not only the presence of microvascu-
lar obstruction, but also of intramyocardial haemorrhage. As
shown in experimental models
80
the extent of the hemorrhagic
area correlates with the size of dark zones on LGE sequences;
MRI in acute myocardial infarction 289
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these preliminary results are conrmed by clinical studies
81,82
and
elucidate the clinical signicance of intramyocardial haemorrhage.
In a large population study, patients with haemorrhagic AMI have
shown a lower pre-PCI TIMI ow; moreover the area at risk, IS
and ratio of IS to area at risk were signicantly larger.
5
Further-
more, the size of dark zones on post-contrast images is
larger, and interestingly present in all patients with haemorrhagic
AMI. Recently, Beek et al.
83
have conrmed that the hypoenhance-
ment on T2-weighted images, suggesting intramyocardial haemor-
rhage, is present in the majority of patients with dark zones on LGE
and also closely related to markers of IS and function. However, it
has no prognostic signicance beyond delayed hypoenhancement.
Of note, in both studies, no differences in time from onset of
symptoms to revascularization between haemorrhagic and non-
haemorrhagic AMI patients has been found, suggesting that
factors such as the magnitude of collateral ow, preconditioning,
and others may inuence the nal outcome of myocardial revascu-
larization. In this regard, cardiac MRI is currently the only non-
invasive, reliable and reproducible imaging technique that may
detect the presence of haemorrhage. Despite emerging studies
about the presence of intramyocardial haemorrhage on
T2-hypoenhancement, experimental validation by histology is
lacking. Further studies with comparable protocols and reperfusion
strategies are necessary to clarify the clinical role of haemorrhage
beyond microvascular obstruction, since it still remains unclear
whether haemorrhagic AMI are at increased risk of rupture or
whether they are just a marker of myocardial reperfusion.
75
Signicance of MRI ndings to
ventricular remodelling
Delayed reperfusion therapy may increase IS and lead to adverse LV
remodelling due to infarct expansion, thinning of the necrotic
segment associated with dilatation, as well as compensatory hyper-
trophy of remote myocardium. Cardiac MRI measures of ventricular
volumes and mass are more accurate and reproducible than other
imaging techniques (Figure 6). In this regard, MRI is particularly suit-
able for the study of large infarcts with aneursimatic ventricular
chamber dilatation since LV volume and mass evaluations are inde-
pendent from geometric assumptions. Since the rst clinical
studies by Wu et al.
30
and Hombach et al.,
31
it has become clear
that IS, transmural infarction and persistent microvascular damage
on delayed post-contrast images are strong predictors of adverse
post-infarct remodelling over and above other clinical parameters.
Further clinical studies conrmed that IS was the main determinant
Figure 5 After a prolonged ischaemia the necrosis becomes transmural and as nal consequences a microvascular damage may appear inside
infarction. On T1 inversion recovery post-contrast sequences, the persistent microvascular damage appears dark (so-called dark zones) (white
asterisks) in the middle of late gadolinium enhancement, representing the myocardial necrosis on the inferior wall on panel A (note the involve-
ment of right ventricular inferior wall seen as an intense late gadolinium enhancement), and antero-spetal wall on panel B. Panels C and D show
the same patient: on C a transmural late gadolinium enhancement on the antero-septal wall with a dark zone is shown, smaller than example
B. Panel D represents the T2-weighted sequences of the same patient: inside the oedema (bright signal on anterior and septal wall) can be
detected a hypoenhancement core suggesting intramyocardial haemorrhage and corresponding to the dark zone on delayed post-contrast
sequence.
M.P. Marra et al. 290
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of LVvolumes.
84,85
In a 76 patient population
86
we have also demon-
strated that the (per patient) number of LV segments with trans-
mural necrosis have additional predictive value for early LV
remodelling independently of microvascular damage; by receiver
operating characteristic analysis, the presence of four LV segments
with transmural necrosis represents a powerful predictor of
adverse remodelling after primary PCI. Recently, Lund et al.
87
have
conrmed that IS on MRI is a stronger predictor of remodelling
than microvascular damage; on the contrary Nijveldt et al.
70
have
found that the presence of microvascular obstruction, and not its
extent, is the most powerful predictor of changes in global function
and LVend-systolic volume at follow-up. The more severe microvas-
cular damage indexed by intramyocardial haemorrhage on
T2-weighted images also has a prognostic role relative to adverse
remodelling. Indeed, Ganame et al.
5
have demonstrated on multi-
variate analysis that myocardial haemorrhage is an independent pre-
dictor of adverse LV remodelling, independently of the initial IS.
Novel cardiac MRI parameters have emerged as possible potential
indices of adverse remodelling, and the most attractive, from a
physiopathological point of view, is myocardial salvaged. So far,
the most widely practiced technique for measurement of myocardial
salvaged is SPECT.
88
However, using SPECT there are some limit-
ations, such as poor spatial resolution. Furthermore, this technique
requires the injection of the tracer immediately and the SPECT
imaging within a few hours after revascularization. Another tech-
nique may be contrast echocardiography with intravenous or intra-
coronary injection of microbubbles before revascularization of the
infarct-related artery.
89
Cardiac MRI is a simple one-stop-shop
tool to evaluate myocardium at risk and myocardial necrosis
during the same examination early after AMI, evaluating oedema
on T2-weighted images. Francone et al.
43
recently showed that
the presence and the extent of salvaged myocardium markedly
decreases when reperfusion occurs after . 90 min of coronary
occlusion. Therefore, only the patients reperfused early (within
90 min) have shown a signicant increase in LV ejection fraction.
Based on this concept, Masci et al.
90
have recently found in a
prospective cohort of 137 patients that myocardial salvage index
is independently associated with adverse LV remodelling. These nd-
ings remain unchanged after multivariate analysis and correction for
the occurrence of microvascular obstruction, infarct transmurality
and baseline ejection fraction. More recently, Eitel et al.
54
have con-
rmed that myocardial salvaged index is the strongest predictor of
major cardiac events and mortality at 6-months follow-up.
The capability of cardiac MRI to be a comprehensive phenotyp-
ing tool to demonstrate in vivo the complex pathophysiology of
AMI opens new perspectives in the evaluation of the efcacy of
novel reperfusion strategies and therapies.
Role of MRI on mechanical and
arrhythmic complications after
AMI
Cardiac MRI allows the possibility to detect the majority of mech-
anical complications following AMI. Isolated case reports have
dened the role of MRI in myocardial wall rupture detection
91
moreover, in clinical studies other complications such as pericar-
dial enhancement suggesting inammation, as well as pericardial
effusion have been described. Interestingly, LGE on MRI has
detected right ventricular involvement in association with inferior
AMI more frequently than current standard techniques:
92
this is
important because in these patients, the right ventricular ejection
fraction represents a signicant predictor of prognosis.
93
In addition, the detection of ventricular thrombi by MRI, in par-
ticular with early gadolinium enhancement is superior to that of
echocardiography, dening morphological delineation and spatial
extent (Figure 1). Application of LGE sequences for LV thrombosis
detection has been reported to be superior than cine MRI and echo-
cardiography.
94
In patients undergoing surgical LV reconstruction, a
complete cardiac MRI protocol has shown higher sensitivity (88%)
and specicity (99%) compared with transthoracic (23%, 96%) and
transoesophageal (40%, 96%) echocardiography. Long-inversion-
time imaging has been suggested to increase accuracy for thrombi
detection.
95
Moreover, the total amount of LGE by MRI has been
demonstrated to be a risk factor for thrombus deposition.
95
A novel potential application of MRI regards the identication of
possible arrhythmic risk areas. In preliminary clinical studies,
96,97
through MRI, the peri-infarct zone is portrayed by the visualization
of a grey border zone near the central infarcted core. This grey
zone has been related to post-infarction mortality as well as induci-
bility, during electrophysiological studies. Further studies in the acute
setting of AMI, possibly using novel molecular imaging techniques,
may clarify the role of the peri-infarct zone as an early predictor
of ventricular arrhythmias as well as giving a more complete under-
standing of the substrate for arrhythmias in the heterogeneous grey
zone including the potential roles of oedema and inammation.
Cardiac MRI value for differential
diagnosis assessment
Cardiac MRI may be very useful in the emergency room for the
rapid assessment of extra-cardiac causes of chest pain and
Figure 6 The adverse left ventricle remodelling after myocar-
dial infarction. Cardiac magnetic resonance shows a large apical
aneurism of left ventricle: the bright late gadolinium enhancement
delineates the thinned infarcted wall, note the massive thrombo-
sis inside the aneurism (white asterisk).
MRI in acute myocardial infarction 291
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mostly because it offers the opportunity to identify areas of in vivo
inammation and replacement brosis. Combining cine-images and
tissue characterization sequences (T1, T2 weighted), Assomull
et al.
98
have evaluated the role of cardiac MRI in patients with
chest pain, elevated troponins and unobstructed coronary arteries.
The most common diagnosis has been myocarditis (50%), followed
by myocardial infarction despite coronary angiography (11.6%),
thus providing a new diagnosis in 65% of patients, and excluding
signicant pathologies in the others. Recently, Bacchouche
et al.
99
have elucidated the diagnostic performance of MRI and
endomyocardial biopsy in patients with troponin-I positive acute
chest pain in the absence of signicant coronary artery disease.
In these 82 subjects a MRI diagnosis of myocarditis has been
made in 58%; typical LGE for infarction in 5%, 1% hypertrophic car-
diomyopathy, 1% dilated cardiomyopathy, and non-conclusive MRI
in 20%. Typical apical ballooning ndings without LGE deposition
have been found in 15% and have been considered diagnostic for
tako-tsubo cardiomyopathy. Moreover, comparison of diagnostic
MRI procedures with the corresponding diagnostic endomyocar-
dial biopsies have demonstrated a substantial match of diagnoses
(kappa 0.70).
Further studies to evaluate the accuracy of cardiac MRI vs. his-
tology and the prognostic signicance of LGE patterns in patients
with normal coronary arteries are needed to improve the clinical
impact of MRI.
Cardiac MRI safety implications
Cardiac MRI has been traditionally considered a non-invasive
imaging tool; however the presence of a magnetic eld and con-
trast administration involves even safety issues that need to be
explained. Also the MRI scanner room, with the presence of
static and gradient elds may interact with ferromagnetic objects
and this may cause electric currents. Finally, the body scanner
may transmit radiofrequency waves into the patients. Because of
these factors patients are screened for implanted cardiovascular
devices prior to undergoing MRI.
100
Potential complications of
MRI examinations in patients with pacemaker or implantable
cardioverter debrillator (ICD) include damage or movement of
the device, inhibition of the pacing output, induction of life-
threatening arrhythmias, cardiac stimulation, heating of the elec-
trode tips.
101103
Currently, an MRI terminology has been
intended to elucidate matters related to biomedical implants and
devices to ensure the safe use of MRI technology. This classication
includes the following denitions: (i) MRI safe, no hazards in all
magnetic resonance environments, (ii) MRI conditional, no
known hazards in a specic MRI environment with constraints
on the specic conditions of use, and (iii) MR unsafe, hazards in
all magnetic resonance environments.
104
Recently, a now commer-
cially available Advisa DR MRI
TM
MRI device (Medtronic, Inc., Min-
neapolis, MN) has been implanted, and it is the second generation
SureScan pacemaker designed to minimize the potential inter-
actions with the electromagnetic elds used for MRI systems.
Moreover, the patient positioning restriction for the Advisa MRI
SureScan Pacing System has been removed, allowing for the rst
time scans of the chest area. However, cardiac MRI examination
of patients with pacemakers is discouraged and the European
position paper specied a group at very high risk (pacemaker-
dependent) in which indication has to be re-considered, and
low-risk patients (pacemaker- non-dependent). Cardiac MRI exam-
ination in patients with ICD should not be performed unless the
centre is highly experienced and only when the benets expected
outweigh the risks taking into account even the possibility of arte-
facts due to device.
105
However, for both devices a full interrog-
ation prior and immediately after MRI scan has to be done and
repeated 1 week and 3 months later.
Finally, regarding coronary artery stents, data currently available
indicate that many of these could be considered as safe,
106,107
including drug-eluting stents.
108
The second important issue on safety regards contrast adminis-
tration related to nephrogenic systemic brosis (NSF) that may
occur after exposure to the extracellular non-ionic low osmolar
gadolinium-based contrast agent gadodiamide. Nephrogenic sys-
temic brosis is a systemic brosing disorder that principally
affects the skin, but can involve virtually any tissue in the human
body. In subjects with normal renal function, free gadolinium is
removed through the kidney with a half-life of approximately 3 h;
in patients with impaired renal function, this half-time is signicantly
longer.
109
So far, NSF has not been described in patients with pre-
served renal function. Current risk factors for NSF include princi-
pally acute or severe renal failure due to advanced chronic kidney
disease (glomerular ltration rate ,30 mL/min/1.73 m
2
). More-
over, other clinical characteristics possibly implied are severe
liver failure, peri-operative liver transplant, kidney transplant,
hepatorenal-syndrome, thrombophilia. Taking into account all
these risk factors and gadolinium exposure, the 1-year incidence
of NSF has been estimated to be between 1 and 4.6%.
7
Since a
therapy for NSF is not yet established, it is fundamental to evaluate
renal function in the context of AMI since patients treated with
primary PCI may have kidney failure for nephrotoxicity of iodine
contrast media.
Future perspectives:
developments and clinical
applications
Cardiac MRI represents a promising modality for a tissue charac-
terization of AMI, beyond traditional morpho-functional indexes.
Moreover, cardiac MRI parameters may in the future be used
with greater frequency as surrogate imaging end points of morbid-
ity and mortality for testing novel therapeutic strategies as in the
case of pharmacologic interventions and cellular-based therapies.
Another important question to address in the future is the
further determination of the true prognostic signicance of the
many parameters evaluated by MRI in patients with AMI. Prognos-
tic stratication is important for STEMI to better stratify patients at
risk of negative ventricular remodelling. However, even for non-ST
segment elevation acute coronary syndromes cardiac MRI rep-
resents a promising tool to identify new prognostic parameters
to select patients for an early invasive management.
110
The most well-recognized MRI features used to evaluate novel
therapies are IS and microvascular obstruction. For example, the
effect of cyclosporine, administrated at the time of reperfusion,
M.P. Marra et al. 292
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has been tested using IS and LV remodelling as end points of thera-
peutic intervention.
111
In addition, contrast-enhanced MRI has also
been used to dene the effect of intracoronary stem cell
therapy.
112
Similarly, MRI is applied to assess the next generation
of techniques utilized to manage no-reow, including the appli-
cation of devices to prevent distal microembolization. In this
regard, IS measured by MRI has been recently used to evaluate
the impact of a manual thrombectomy device.
113
Ongoing research will be directed to standardizing the cardiac
MRI protocol and to evaluating in large multi-centre population
studies the signicance of different imaging features for clinical
outcome, arrhythmogenic risk stratication and remodelling.
Finally, future technical improvements, such as molecular imaging,
will likely enable a better understanding of reperfusion injury and
the natural repair mechanisms following AMI as well as the biologic
determinants of LV remodelling including neovascularization
through angiogenesis.
114
Acknowledgements
The authors thank Barbara Hildenbrand for her professional
support and Dr Francesco Corbetti for the images obtained.
Conict of interest: none declared.
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