MAGNETIC-RESONANCE-IMAGING TECHNIQUES FOR THE ASSESSMENT OF RESIDUAL MYOCARDIAL VIABILITY

Citation
Fm. Baer et al., MAGNETIC-RESONANCE-IMAGING TECHNIQUES FOR THE ASSESSMENT OF RESIDUAL MYOCARDIAL VIABILITY, Herz, 19(1), 1994, pp. 51-64
Citations number
65
Categorie Soggetti
Hematology
Journal title
HerzACNP
ISSN journal
03409937
Volume
19
Issue
1
Year of publication
1994
Pages
51 - 64
Database
ISI
SICI code
0340-9937(1994)19:1<51:MTFTAO>2.0.ZU;2-C
Abstract
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.