In contrast to the established nuclear imaging techniques magnetic res
onance imaging (MRI) is only in the early phase of its application to
detect viable myocardium after myocardial infarction. Although MRI tec
hniques have only recently been employed to assess residual myocardial
viability three approaches have been described to achieve this purpos
e: First, the use of signal intensity changes on spin-echo images with
and without the application of contrast media to define irreversible
injury to the myocardium in acute and subacute infarcts; second, measu
rement of metabolite concentrations within the infarct area using magn
etic resonance spectroscopy, and third quantitation of myocardial thic
kness and systolic wall thickening in chronic infarcts with and withou
t positive inotropic stimulation. When applying magnetic resonance tec
hniques to detect viable myocardium by imaging techniques, it is usefu
l to distinguish between acute infarcts and chronic infarcts that are
more than 16 weeks old. After this time, practically all infarcts have
healed and the necrotic myocardium has been transformed into scar tis
sue. MRI seems ideally suited to detect and characterize chronic myoca
rdial scar and distinguish it from viable but hibernating myocardium b
ecause it clearly depicts the regional wall thinning which is a typica
l feature of transmural infarcts (Figure 1). In contrast, more recent
infarcts, even if they are transmural and fail to show any contraction
during systole, may not yet exhibit myocardial thinning. Therefore, s
imply depicting the acutely injured myocardium by MRI is not sufficien
t to differentiate between necrotic and stunned, but viable myocardium
. On the other hand, an increase in signal intensity of acutely infarc
ted myocardium, which appears on T2 weighted spin-echo MR images only
a few hours after occlusion of a coronary artery, can be used to deter
mine the extent of irreversible myocardial damage (Figure 2). It is no
t clear, however, whether this area of increased myocardial signal int
ensity that is seen within the first week after the event only represe
nts necrotic myocardium or incorporates some edematous viable myocardi
um in the infarct border zone. After three weeks, true infarct size ma
y be more closely approximated by the area of increased signal intensi
ty because the edema surrounding the infarct has presumably regressed
and signal abnormalities are restricted to the pathologically determin
ed infarct area. More recently, new pulse sequences and high field mag
nets permit separate observation of the endocardial and epicardial por
tion of the left ventricular wall. This may further improve the detect
ion of residual viable cells which are preferentially located near the
epicardium. Magnetic resonance spectroscopy (MRS) may be more helpful
in the setting of acute myocardial infarction without wall thinning t
han in chronic infarcts, because a certain volume of myocardium is nec
essary to perform spectroscopic measurements of cell metabolism. Theor
etically, completely infarcted myocardium should not contain any measu
rable amount of phosphocreatine and ATP and could thus be distinguishe
d from myocardium which still harbours ischemic but surviving myocardi
al cells. It has been shown in vivo in animal models using coils direc
tly applied to the surface of the heart that phosphocreatine recovers
after a brief coronary occlusion and reperfusion. If these measurement
s could be performed noninvasively, they would be helpful to confirm t
he presence of residual viable cells in the infarct area. However, qua
ntification of metabolites by MRS still poses problems and further dev
elopment of the technique is needed to determine the mass of viable ce
lls within a region of interest. In conclusion, MRI relies on indirect
signs of viability such as signal characteristics, wall thickening an
d wall thickness but is not able to directly demonstrate preserved myo
cardial metabolism in the region of interest. Nevertheless, comparativ
e studies with FDG-PET and MIBI-SPECT indicate the potential of MRI to
correctly identify regions containing chronic scar which would be hel
pful to decide against revascularization of that particular region (Fi
gures 3 to 5). Moreover initial results from comparative studies betwe
en dobutamine-MR] and thallium-201-reinjection and FDG-PET demonstrate
d a good agreement between dobutamine induced wall motion in basally a
kinetic myocardial regions with preserved diastolic wall thickness and
criteria of viability as defined by FDG-PET and thallium-201 scintigr
aphy. Contrast media with a selective uptake into viable cells would b
e desirable and helpful to directly visualize hibernating myocardium b
ut have not yet been developed. MRS is a very promising technique for
demonstrating residual viability mainly in acute and subacute infarcts
but is presently clinically limited to large areas of interest. Furth
er research in animal models of acute and chronic infarcts will be nec
essary to establish the full potential of MR techniques and additional
clinical studies comparing MR techniques with established imaging mod
alities have to define the role of MRI and MRS in clinical problem sol
ving.