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1Unité Mixte de Recherche-Centre National de la Recherche Scientifique 5515, Centre de Recherche et d'Applications en Traitement de l'Image et du Signal, Lyon; 2Centre d'Exploration et de Recherche Médicales par Emission de Positrons, Lyon; 3Université Claude Bernard, Lyon; and 4Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Lyon, France
Submitted 21 July 2003 ; accepted in final form 7 January 2004
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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40% of regions vs. 52% in mismatch viable, P < 0.05), but the extent of the increase after dobutamine was lower in infarcted regions (P = 0.06). Within each PET pattern, regions were grouped according to their Ecc values at rest into three categories (high, intermediate, and low contractile performance). In mismatch viable (hibernation), the inotropic reserve was similar among the three categories, but in the other PET patterns the presence and extent of the inotropic reserve was higher in those regions with lowest Ecc (without significant differences in perfusion). In severe CAD, the presence of the inotropic reserve assessed by midmyocardial changes under dobutamine does not relate to resting perfusion. At a similar level of perfusion, the presence of the inotropic reserve is inversely related to contractile performance at rest, but our results suggest that it may not be true for hibernating myocardium.
tagged magnetic resonance imaging; positron emission tomography; myocardial perfusion; coronary artery disease
In the present study, we investigated whether in severe CAD the presence of the inotropic reserve evaluated by intramyocardial changes under dobutamine relates to myocardial perfusion at rest. Thus we evaluated in severe CAD patients the relationship between PET patterns of perfusion and glucose uptake and the corresponding tagged MRI values of midmyocardial strains under low-dose dobutamine.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Patients were studied with institutional review board approval (according to the declaration of Helsinki) and with their written informed consent. We studied 18 patients with angiographically documented atherosclerosis (
70% diameter stenosis) in two or three coronary arteries and left ventricular dysfunction [left ventricular ejection fraction (LVEF) <50%] who were scheduled for surgical revascularization (Table 1). All patients underwent tagged MRI (at rest and after 10 µg·kg–1·min–1 dobutamine) and PET (perfusion and glucose uptake evaluation) on consecutive days.
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MRI
Patients were examined on a 1.5-T MR unit (Vision, Siemens Medical Systems; Erlangen, Germany) with a gradient amplitude of 25 mT/m and a phased array chest coil. After localization of the long axis of the left ventricle using an ungated multiplane localizing image set, short-axis cine views were first obtained to assess global cardiac function parameters at rest. Cine-MR acquisitions were obtained using an end-inspiratory breathhold-segmented k-space echo-gradient sequence. Imaging parameters were as follows: 28-cm field of view, 8-mm slice thickness, 8-mm slice spacing, repetition time = 80 ms, echo time = 4.8 ms, 20° fl ip angle, 5- to 7-line segmentation, and 256 x 140 image matrix interpolated to 256 x 256 for display; one signal was acquired using echo sharing.
Tagged MR acquisitions were performed at three short-axis locations: basal, midventricular, and apical. These locations were selected on a end-diastolic two-chamber long-axis cine view.
Tagged MR images at rest were obtained using a breathhold segmented k-space tagged turboflash sequence with a grid tagging pattern. Imaging parameters were the same as cine-MRI acquisition using a 7-mm tag line separation. Each breathhold acquisition took 16–25 heartbeats. After a 10- to 15-min dobutamine infusion at 10 µg·kg–1·min–1, cine-MR and tagged MRI were then repeated using the same imaging protocol. Single-lead ECG, blood pressure, and pulse oxymetry were monitored during the study. MRI studies lasted 45 min.
LVEF assessment. The first frame in each series was determined as the end-diastolic frame, and the image with the smallest ventricular volume was defined as the end-systolic frame. For LVEF calculation, the endocardial and epicardial contours of the end-diastolic and end-systolic frames of the left ventricle were traced using the Argus software version VA50A (Siemens).
PET Imaging
PET studies were performed on a Siemens/ECAT EXACT HR+ 63 slices whole body tomograph.
Perfusion assessment. H 152O (185 MBq) was injected intravenously over 10 s. Acquisition lasted 5 min, and emission scans were reconstructed in a 128 x 128 matrix using a Hanning filter with a cutoff frequency of 0.15 mm–1. Scan sequence consisted of 22 frames: 10 images x 4 s, 2 images x 10 s, 6 images x 20 s, and 4 images x 30 s.
Glucose uptake assessment. 18FDG studies were performed under hyperinsulinemic euglycemic clamp (8). One hour after H 152O studies, 18FDG (2 MBq/kg) was administered as an intravenous bolus. 18FDG emission scans were reconstructed in a 128 x 128 matrix using a Hanning filter (cutoff frequency of 0.18 mm–1). Transaxial resolution was 8 mm at the center of the field of view. 18FDG reconstruction provided a dynamic series: 6 images x 10 s, 12 images x 30 s, 13 images x 60 s, and 20 images x 120 s. Static 18FDG images were reconstructed from 45- to 60-min slices.
Image Analysis
Tagged images (Fig. 1) were processed using the Findtags software on a Silicon Graphics workstation.
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We reported strain changes between the reference state (end diastole) and the deformed state (end systole) with the use of the fractional changes (%) in length for normal strain in the circumferential direction [circumferential shortening (Ecc)]. A positive value stands for compression between two material points (shortening), whereas negative values reflect strain elongation (stretching). Midmyocardial transmural location was chosen to evaluate systolic function at each of the three predefined short-axis locations (apical, midventricular, and basal).
Factor analysis of medical image sequences (FAMIS) (12) was applied to H 152O PET dynamic series to obtain myocardial factor images, which represent relative perfusion (1, 17) (Fig. 2d). FAMIS computation was performed on H 152O short-axis slices resulting from the addition of three slices of 2.5 mm. To apply FAMIS to these resulting slices, aggregates were generated as square clusters 2 x 2 pixels wide. Three factor images were systematically extracted and corresponded to the right and left ventricular cavities and left myocardium (Fig. 2d).
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Image Registration
H 152O and static 18FDG PET volumes were realigned to generate short-axis slices suitable for matched correlation with the three short-axis MR images at rest.
Registration was performed on PET slices resulting from the addition of three slices of 2.5 mm. Circumferential registration (inplane registration) between MR strain slices (8 mm) and PET slices (7.5 mm) (Fig. 2, b–d) was carefully achieved taking into account relative apex to base location (from long-axis localizer view; Fig. 2a) and by matching landmark locations such as right ventricular insertion sites and papillary muscle location.
Data Analysis and Interpretation
Data analysis was performed on four sets of images: tagged MRI images at rest and under dobutamine (for functional analysis) and myocardial factor images and static 18FDG images (for perfusion and glucose uptake). Therefore, for each patient, a regional profile of function as well as perfusion and glucose uptake was available at the three short-axis locations (Fig. 2, bottom).
Twelve regions per short-axis slice were drawn on the corresponding static 18FDG image (Fig. 2c) using an automated sectorization procedure. These regions were then superimposed on the corresponding myocardial factor image (Fig. 2d).
Ecc in the midmyocardial transmural location was evaluated at rest and under dobutamine in the 12 PET corresponding regions at each of the three short-axis locations.
To compute the relative perfusion (%H 152O) and relative glucose uptake (%18FDG), two to three regions per patient were selected as controls using the information from angiography, Ecc, and perfusion. Selection of control regions was restricted to basal and midventricular slices, and only territories with no angiographic stenosis on the supplying artery were considered. Among all studied regions in a given patient, regions selected as controls had to belong to the group of the seven regions with best Ecc and perfusion. Moreover, perfusion normality was checked in the preselected control regions by computing absolute myocardial blood flow using a one-compartment kinetic model (2).
Regions were classed according to previously described classical PET patterns (3, 32): normal (%18FDG 90, %18FDG 
%H 152O 
1.2), match viable (55 %18FDG < 90, %18FDG %H 152O 1.2), infarcted (%18FDG < 55, %18FDG %H 152O 1.2), and mismatch viable (%18FDG %H 152O > 1.2).
The percentage of variability (3) between two tagged MRI repeated measures of Ecc in myocardial regions from healthy volunteers (n = 4) ranged between 4 and 10%. A threshold of twice the Ecc represented by the percentage of variability (i.e., 2% changes in Ecc) was used to define the presence of inotropic reserve under dobutamine (Eccdobu – Eccat rest 2%).
Statistical Analysis
Linear regressions were fitted by the least-squares method. A paired t-test was used to compare LVEF values. Normal distribution of data and SD were tested using the Kolmogorov-Smirnov test and the equal variance test, respectively. ANOVA and subsequently a Tukey test for multiple comparisons were performed to compare mean values. If the normality test failed when comparing mean values, a Kruskal-Wallis ANOVA on ranks was performed. In this case, the median instead of the mean of the groups was displayed.
Proportions were analyzed using a 2 goodness of fit test.
Data are displayed as means ± SD. P < 0.05 was interpreted as statistically significant.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Eighteen patients underwent tagged MRI and PET examinations (Table 1). Seven of eighteen patients had three-vessel disease and 11 patients had two-vessel disease (Table 1); 10 patients had diabetes, 9 had hypertension, and 7 had hypercholesterolemia. No patient had a history of recent myocardial infarction, and all patients were clinically stable at the time of the study.
At rest, the rate-pressure product at the initiation of the tagged MRI study (9,826. ± 1,550 mmHg·beats·min–1) differed significantly from that recorded 10 min after the beginning of 10 µg·kg–1·min–1 dobutamine infusion (12,838 ± 3,281 mmHg·beats·min–1, P < 0.01).
Circumferential Shortening at Rest and PET Patterns
Of 648 regions in 18 patients (36 regions/patient), 616 (95%) were suitable for comparative tagged MRI and PET analysis. On the basis of PET images, 175 regions were defined as normal, 159 as match viable, 146 as infarcted, and 136 as mismatch viable. In the 41 control regions, absolute perfusion at rest averaged 0.98 ± 0.24 ml·g–1·min–1 and Ecc at rest was 17 ± 4% (vs. 17 ± 5% after dobutamine, not significant).
Among normal, match viable, and infarcted regions, a positive linear correlation was found between regional values of Ecc at rest and both perfusion (r = 0.49, P < 0.01) and glucose uptake (r = 0.58, P < 0.01). To reduce statistical variability, these regions were divided according to normalized glucose uptake into seven groups: 40% (n = 91), 41–50% (n = 38), 51–60% (n = 45), 61–70% (n = 30), 71–80% (n = 41), 81–90% (n = 60), and 90% (n = 175). The mean Ecc at rest for each group showed a positive linear correlation with both the mean in perfusion (r = 0.95, P < 0.01; Fig. 3A) and mean in glucose uptake (r = 0.96, P < 0.01; Fig. 3B). Mismatch viable regions were considered as a separate group and showed, as expected, high levels of glucose uptake and depressed function (Fig. 3).
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At rest, Ecc ranged from 12 ± 6% to 8 ± 5% in normal and match viable regions, respectively (P < 0.05), and was 4 ± 4% in infarcted regions (P < 0.05 vs. normal and match viable). Ecc for mismatch viable regions (7 ± 5%) differed significantly from both normal and infarcted regions (P < 0.05).
Inotropic Reserve at Different PET Patterns
Of the 616 regions in 18 patients, 262 (42.5%) demonstrated an inotropic reserve during low-dose dobutamine infusion (Ecc increased by 2% from resting values). The proportion of regions with an inotropic reserve differed significantly as a function of PET patterns (2 = 7.9; degree of freedom = 3; P = 0.048): the highest proportion was observed in mismatch viable regions (0.52), whereas the proportion did not differ significantly among normal (0.40), match viable (0.38), and infarcted (0.41) regions. The dobutamine response among PET patterns was also evaluated using an Ecc increase of 4% from resting values to define the presence of an inotropic reserve: as previously found with a threshold of 2%, the proportion of regions with an inotropic reserve did not differ among normal (0.21), match viable (0.25), and infarcted regions (0.18), whereas it was higher (0.38) in mismatch viable regions (2 = 18.0; df. 3; P < 0.01).
In regions with an inotropic reserve, Ecc at rest was 12 ± 7%, 6 ± 4%, 3 ± 3%, and 7 ± 6% for normal, match viable, infarcted, and mismatch viable regions, respectively (P < 0.01) (Fig. 4). In these regions, the extent of the functional changes after dobutamine (Eccdobu – Ecc at rest) showed a trend toward lower values in infarcted regions (median = 3% vs. 4% for normal and 5% for match viable and mismatch viable, P = 0.06; Fig. 4).
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The 354 regions without inotropic reserve had, for each PET pattern, similar Ecc at rest compared with those with a demonstrable inotropic reserve (13 ± 6, 8 ± 4%, 5 ± 4%, and 8 ± 5% for normal, match viable, infarcted, and mismatch viable regions, respectively), and the extent of the changes after dobutamine did not differ significantly among PET patterns (median = –1% for each of them).
Inotropic Reserve Within Each PET Pattern
Within each PET pattern, regions were divided according to contractile performance at rest into three categories: the 25% of regions showing highest Ecc (High category), the 25% of regions showing lowest Ecc (Low category), and the 50% of regions showing intermediate Ecc (Intermediate category). For each PET pattern, we analyzed the presence of the inotropic reserve and the extent of changes after dobutamine in each of the three categories. For normal, match viable, and infarcted regions, the proportion of regions with an inotropic reserve was higher in the category showing lowest Ecc (Low category; Fig. 5 and Table 2). Moreover, the extent of the changes after dobutamine was higher in Low category (Table 2). Conversely, in mismatch viable regions, no differences were found among the three categories regarding both the presence of an inotropic reserve and the extent of changes after dobutamine stimulation (Fig. 5 and Table. 2). For each PET pattern, no differences in perfusion were found among categories (Table 2).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Inotropic Reserve at Different PET Patterns
In this study, two thresholds were used to determine the presence of intramyocardial inotropic reserve, and, in both cases, the proportion of regions with inotropic reserve did not differ among normal, match viable, and infarcted regions. These regions were characterized by different perfusion (and glucose uptake, by definition), and we concluded that in regions with normal or concomitant reductions in perfusion and glucose uptake, the presence of the inotropic reserve assessed by midventricular changes in Ecc does not relate to myocardial perfusion at rest. Yet, the extent of the changes under dobutamine showed a trend toward lower values in severely injured regions, suggesting that it likely depends on resting perfusion.
Our results show that ischemic midmyocardial tissue is able to preserve cellular integrity and to respond to inotropic stimulation. The ability to retain cellular integrity even in severely hypoperfused regions was anticipated in a tagged MRI study in patients with first anterior infarction. In this population of patients, Bogaert et al. (3) studied Ecc after reperfusion in two transmural levels defined as subendocardial and subepicardial. One week after reperfusion, the functional damage of the myocardium in match PET regions was found to be similar for all layers. Moreover, they observed a large recovery in subepicardial layers of severely injured match regions (blood flow <50% by PET) (3). These findings suggest the presence of viable tissue even in regions with a high degree of transmural infarction, not detectable by PET, where preserved contractile material could likely respond to inotropic stimulation.
No studies investigated whether the presence of an intramyocardial inotropic reserve relates to myocardial perfusion at rest in CAD. Conversely, some works attempted to evaluate the relationship between full wall thickening changes after inotropic stimulation and the level of regional perfusion at rest. Dobutamine echocardiography studies in conjunction with either PET (19, 22) or single photon emission computed tomography (21) showed that a positive inotropic response is more likely to occur in regions with preserved rather than reduced perfusion. On the contrary, the inotropic reserve detected by MRI during low-dose dobutamine was not associated with myocardial perfusion measured in terms of the technetium-99m sestamibi uptake (9). All these results were obtained among large dysfunctional regions and using myocardial thickening scores. Importantly, echocardiographic works were done in chronic CAD patients, whereas MRI evaluations were done soon after first myocardial infarction. Because full wall thickening results from an interaction between epicardial and endocardial fibers (cross-fiber shortening phenomenon) (25, 33), it is conceivable that such an interaction could be greatly modified in the set of chronic CAD in which alterations in the connective tissue matrix are well established (6).
Inotropic Reserve Within Each PET Pattern
A significant linear correlation was shown between Ecc at rest and the level of regional perfusion. In normal and match regions, such a correlation reflects that contractile performance relies to the oxygen supply and to the amount of necrosis caused by an insufficient oxygen supply (in match regions). Thus, despite the considerable scatter in this correlation, it could be stated that in general contractile performance at rest is "settled" by myocardial perfusion. The inotropic reserve after inotropic stimulus has to depend on the presence of regional flow response (14) and the amount of necrotic tissue (29). Among regions with similar perfusion at rest a similar amount of necrotic tissue could be expected and, therefore, it could be assumed that the open window for a sustained contractile response under dobutamine infusion is settled by the regional capacity to raise perfusion. Consequently, our findings let hypothesize that in regions having a relative high contractile performance at rest for a given level of regional perfusion, only little room remains for improvement under dobutamine. Such reasoning could explain why a positive contractile response is more likely to be present in regions with lowest contractile performance at rest and, moreover, the fact that the extent of the inotropic changes in those regions was higher.
In our study, mismatch viable regions (a reliable PET sign of hibernation) showed similar perfusion and contractile performance at rest than match viable regions but a higher presence of an inotropic reserve. Moreover, in mismatch viable regions, the presence of an inotropic reserve and the extent of changes under dobutamine were not related to resting Ecc. In fact, we found a relatively high proportion of hibernating regions with an inotropic reserve whatever the level of contractile performance was. Such a difference with match regions could be explained if hibernation is considered as a protective mechanism. This mechanism helps to maintain cellular integrity by downregulating contractile performance as an adaptation to reduced perfusion. Differently to match regions in which hypoperfusion leads to necrosis and contractile dysfunction, in hibernating myocardium the hypoperfusion leads to contractile dysfunction as a way to minimize necrosis (10, 13). This downregulated contractile performance in hibernating myocardium could lead to a larger open window for a functional improvement under dobutamine. Moreover, it has been reported that in hibernating myocardium glucose uptake is increased during dobutamine infusion (30), which represents an additional source of metabolic energy available during inotropic stimulation. These considerations could help to explain why a similar proportion of mismatch dobutamine-responsive regions could be seen at different levels of contractile performance.
Comparison With Previous Studies
In this study, a significant number of normal PET regions did not show an inotropic reserve, whereas a significant number of infarcted PET regions did.
Our results showing an extensive abnormal dobutamine response in normal PET regions appear consistent with the previous tagged MRI findings of Geskin et al. (15) in patients with one single CAD. These authors found that the extent of the changes in Ecc under dobutamine was twofold higher in dysfunctional regions than in the group of normally contracting regions (such a group may have partially contained normal PET regions). Moreover, many echocardiographic works (19, 26, 29–31) have also reported an attenuated or absent inotropic response in a nonnegligible proportion of normal PET regions. Thus it has been observed that 45% of dysfunctional regions with normal perfusion and glucose uptake were not able to normally respond to dobutamine stimulation (19, 26). In CAD patients with severe left ventricular dysfunction, normal regions supplied by nonstenotic vessels have been found to shown a decreased myocardial blood flow reserve, increased left ventricular wall stress, and the absence of an inotropic reserve in 59% of them (31). Skopicki et al. (29) focused on the study of normal PET regions with normal resting wall motion in severe CAD. They observed that the amount of these regions supplied by a patent coronary vessel did not differ significantly between those that contracted normally with dobutamine and those that did not, which is concordant with our observation of no significant changes under dobutamine in control regions supplied by patent arteries. These authors concluded that the absence of the dobutamine response is only partially explained by the inability of normal regions to increase blood flow (29), and they attributed a major role to the tethering effect (16) to explain this lack.
In infarcted PET regions, the presence of an inotropic reserve by tagged MRI was found higher than that usually reported by echocardiography (19, 20). In a recent work, Kramer et al. (18) compared the qualitative response to dobutamine by echocardiography with the quantitative response of tagged MRI after reperfused myocardial infarction. These authors used a high threshold (5% in Ecc under dobutamine) to define the presence of an inotropic reserve in regions showing depressed Ecc at rest (4 ± 1%), and they observed that more regions were identified as viable by dobutamine-tagged MRI than by dobutamine echocardiography (18). Therefore, it is conceivable that the evaluation of intramyocardial changes under dobutamine as well as the use of a more sensitive technique (i.e., tagged MRI) could detect a great functional improvement in severely injured regions. It is also possible that such results could partially be explained by some methodological shortcomings, such as the inability of PET to determine the wall transmurality of infarction and the lower reliability of PET measurements in thinned regions with low tracer activity. Finally, a positive dobutamine response in the midmyocardium of regions having subendocardial damage could contribute to the discrepancy between the presence of an inotropic reserve and the presence of necrosis by PET (28).
Technical Considerations and Limitations
Few studies (15, 18) have examined the use of low-dose dobutamine-tagged MRI in patients with less extensive CAD. In patients with single-vessel CAD and recent reperfused myocardial infarction, Geskin et al. (15) evaluated the ability of low-dose dobutamine-tagged MRI to predict functional recovery at 8 wk. In contrast to our study, their analysis was centered on dysfunctional regions at rest, and they considered the mean normal response in Ecc under dobutamine (5%) to detect the inotropic reserve (15). In our study, the analysis was related to regional PET patterns independently of the regional functional performance, and a moderate threshold was considered to define the presence of the inotropic reserve. Thus our analysis design was intended to address the entire PET spectrum and to overcome the difficulty of a consistent definition of "normal function" in CAD. In addition, the evaluation of some functional increase under dobutamine is a more useful endpoint as some myocardial regions (e.g., infarcted) are very unlikely to have a normal inotropic reserve.
Ecc was chosen to evaluate systolic function because 1) it is the most widely used tagged MRI parameter and the variability of the measure is less than that of the others parameters, and 2) it provides the largest contribution to LVEF (4).
The computation of Ecc from tagged images was done at the midmyocardial layer location, which contribute to achieve a robust measurement by avoiding potential segmentation errors that can occur near to endocardial and epicardial interfaces. In addition, this choice was intended to achieve correct matching between MRI and PET data.
A potential limitation is the use of a single low dose of dobutamine, which could theoretically mask the biphasic response using high doses. However, two tagged MRI works (24, 27) evaluating the effect of dobutamine in normal subjects found that Ecc as well as other functional parameters increased uniformly from rest to 10 µg·kg–1·min–1 dobutamine infusion and then did not increase further. Thus, even if this pattern of dobutamine response could be somewhat altered in CAD, these findings suggest that the use of low-dose dobutamine did not greatly distort the accuracy of our results.
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ACKNOWLEDGMENTS |
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GRANTS
This work was supported by the Hospices Civils de Lyon (Lyon, France).
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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