(Circulation. 1997;96:2859-2867.)
© 1997 American Heart Association, Inc.
Articles |
Multislice MRI in Assessment of Myocardial Perfusion in Patients With Single-Vessel Proximal Left Anterior Descending Coronary Artery Disease Before and After Revascularization
From Helsinki University Central Hospital, Department of Radiology and Cardiovascular Laboratory (K.S.V.), Department of Medicine.
Correspondence to Kirsi Lauerma, MD, Helsinki University Central Hospital, Radiology, FIN 00290 Helsinki, Finland. E-mail kirsi.lauerma{at}helsinki.fi
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Abstract |
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Background Our purpose was to use multislice MRI for detection of reversible myocardial ischemia and assessment of the effect of revascularization on tissue perfusion in patients with coronary artery disease.
Methods and Results Eleven patients with single-vessel proximal left anterior descending coronary artery disease were studied with MRI and thallium scintigraphy before and 3 months after revascularization. All patients had a reversible perfusion defect by scintigraphy before treatment. With a 1.5-T MR imager, IR-prepared turboflash images were acquired in three left ventricular short-axis planes during 0.05 mmol/kg Gd-DTPA bolus at rest and with dipyridamole-induced stress. Before treatment, stress increased enhancement slope in normal (6.4±4.4 to 7.4±5.0 s-1, P<.04) and decreased it in underperfused (5.4±3.7 to 2.6±1.4 s-1, P<.02) regions, resulting in a contrast-to-noise ratio of 6.87±3.09 in underperfused myocardium. Revascularization normalized enhancement patterns of the formerly underperfused myocardium and decreased defect size both in scintigraphy (66±53° to 8±12°, P<.001) and MRI sections (49±41° to 9±8°, P<.001). Agreement of 85% in detection and correlation of 0.86 (SEE, 21°, P<.001) in sizing perfusion defects was found between MRI and scintigraphy.
Conclusions Multislice contrast-enhanced MRI can be used to detect myocardial perfusion defects in patients with coronary artery disease and in assessment of the effect of treatment on myocardial perfusion.
Key Words: magnetic resonance imaging • perfusion • revascularization
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Introduction |
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Coronary artery disease is the major diagnostic challenge in cardiology, and the measurement of myocardial perfusion is the goal in many cardiac imaging techniques. Coronary x-ray angiography is considered the reference standard for the assessment of anatomic abnormalities within the coronary arteries, but the physiological significance of any particular lesion requires additional techniques for measurement of end-organ perfusion. Currently, several diagnostic tests, including stress echocardiography, thallium scintigraphy, and positron emission tomography, are used for detection of abnormalities in perfusion, metabolism, or function. Application of the ultrafast first-pass approach to MRI techniques1 offers the benefit of high spatial resolution and the possibility to image any desired plane with little invasiveness and without ionizing radiation.
Clinical cardiac MRI is used primarily to obtain anatomic information. In animal studies, both reversible and irreversible regional myocardial perfusion disturbances have been detected by combined use of exogenous contrast material and fast MRI.2 3 4 5 6 7 8 9 10 11 12 In patients with coronary artery disease, most MR perfusion studies have been performed by imaging one anatomic plane repeatedly during contrast agent injection.13 14 15 Coronary vasodilators, such as dipyridamole, have been used to induce a perceptible imbalance in perfusion between normal and hypoperfused myocardium.16 In MRI studies, pharmacological stress has been shown to increase differences in delivery of the contrast agent to myocardial regions perfused by normal and diseased arteries.2 5 6 11 14 15 17 18 19 Because low-molecular-weight MR contrast agents distribute to some extent from vascular to extracellular space during the first-pass circulation,20 only fast imaging sequences can capture regional myocardial perfusion differences. To be clinically useful in localization and sizing of perfusion defects, several LV planes must be covered during the same imaging session. If only one slice is imaged, 90% of the LV is neglected. If three slices are imaged, one third of the myocardial volume is encompassed.12 18 21 Acquisition of images of the entire heart with adequate temporal resolution will likely require echoplanar imaging.22 Our goal was to determine whether multislice first-pass MRI can detect myocardial perfusion defects during pharmacological stress in patients suffering from coronary artery disease and whether the effect of revascularization could be determined by this technique.
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Methods |
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Study Protocol
The study protocol was approved by the local ethics committee. Eleven consecutive patients with single-vessel proximal LAD stenosis
75% or occlusion detected in angiography and need
of revascularization based on clinical findings and
angiography were included. Thallium scintigraphy and MR
perfusion studies were performed within 1 week. All patients underwent
either balloon angioplasty (n=7) or bypass surgery (n=4) after imaging.
Three months after revascularization, both thallium
scintigraphy and MR perfusion study were repeated.
Patients
Informed consent was obtained from all 11 patients before they
entered the study. Mean age of the patients was 56 years (range, 40 to
68 years); 6 were men. All patients belonged to group III according to
the NYHA functional classification; the mean duration of symptoms
before the study had been 5 months (range, 3 to 12 months). None of the
patients had a history of myocardial infarction. In addition to
coronary artery disease, the patients suffered from
arterial hypertension (n=2),
hypercholesterolemia (n=1), mitral
insufficiency (n=1), and diabetes mellitus (n=1).
Coronary Angiography
Coronary angiography was performed with 6F high-flow
Judkins or Amplatz catheters and filming in multiple projections.
LV cineangiography was documented in the 30° right anterior oblique
projection. The studies were interpreted visually by experienced
angiographers (K.S.V. and P.H.). Coronary artery luminal
diameter reduction 75% was considered significant. LV ejection
fraction was calculated by the single-plane ellipsoid area-length
method.23
Thallium Scintigraphy
Multislice diagrams of gated single photon emission computed
tomography 201Tl myocardial perfusion studies were obtained
from all patients before and 3 months after
revascularization with Elscint Apex 425 ECT
equipment. Before the test, cardioactive drugs were discontinued for 7
plasma half-lives, and the patients were not allowed to drink
caffeinated drinks. Dipyridamole was infused at a dose
of 0.56 mg/kg IV over a period of 4 minutes, and 2 mCi
[201Tl]thallium chloride was injected within 2 minutes of
the end of the dipyridamole infusion. The acquisition
for the first projection was started 5 minutes after the
201Tl injection.
Thirty views were acquired by 180° rotation at 6° intervals for 20 minutes with a single-head low-energy all-purpose collimator (Elscint APC-3). The redistribution images were obtained 3 hours later. Routine uniformity and radius-of-rotation checks were performed. A 64x64 matrix with pixel size of 0.6x0.6 cm and 0.6-cm slice thickness was used.
Images were reconstructed by a minicomputer (Apex F1, Elscint) from the early systolic and late diastolic phases of the gated frames. Three transaxial scintigraphy levels were selected to correlate the LV short-axis MR slices by determining their distance from the apex on LV long-axis MRIs and stacks of scintigraphy sections. Circumferential profiles of myocardial thallium uptake were generated by plotting transmural mean pixel intensity against the location of each 3° radius.24 Analysis of the sections and profiles was performed without knowledge of the presence or absence of perfusion defect on MR images. The profiles were normalized to the maximum pixels, and intensity <75% of the maximum was classified as reduced perfusion.25 The size of the perfusion defect was assessed for each section as degrees of the 360° circle.
MRI Protocol
MR perfusion imaging study was performed on all patients before
and 3 months after revascularization. Cardioactive
drugs and caffeinated drinks were discontinued as before
scintigraphy. An 18-gauge catheter was inserted into the
antecubital vein for injection of dipyridamole and
contrast agent. Extension tubing was loaded with contrast agent to
permit injections outside the bore of the magnet. Patients were
positioned supine in the body coil of a 1.5-T Siemens Magnetom Vision
imager. Imaging was performed with the body coil used as receiver.
Coronal and LV long-axis scout images were obtained to determine the
final imaging plane to the LV short axis.
To monitor the first transit of bolus-injected contrast agent, ECG-gated IR-prepared turboflash images were acquired on three LV short-axis planes with the following parameters: TR/TE, 3.3/1.4 ms; matrix, 128x128; field of view, 350 mm; and flip angle, 8°. An inversion time of 400 ms was chosen to provide null myocardial signal before contrast administration. Perfused with Gd-DTPA, myocardium would therefore show relatively increased SI because of the predominant T1 shortening.
LV short-axis orientation was selected for MRI to minimize partial
volume effect, to allow comparison between myocardial regions perfused
by different arteries and between MR and thallium
scintigraphy sections. Images were acquired from three
slices (1 cm thick, 0.5 cm apart); the basal slice was set at the level
of the papillary muscles. Sets of 60 images were acquired, with the
three slices imaged repeatedly. The set of three slices was obtained
every four to six RR intervals (
4 seconds), and one IR preparation
pulse was followed by an imaging sequence for a single slice.
After the LV short-axis planes were localized, the transit of contrast agent was monitored at rest. During IR-prepared turboflash imaging, after the third set of the three slices, Gd-DTPA (0.05 mmol/kg) was injected intravenously at a speed of 5 mL/s. After the transit study, the washout of the contrast agent from the myocardium was monitored by repeated sets of IR-turboflash images every 5 minutes. As myocardial intensity came close to zero at 20 to 30 minutes after the contrast injection, the pharmacological stress was induced. The patient bed was withdrawn from the bore of the magnet, and care was taken not to move the patient. Dipyridamole (0.56 mg/kg) was infused over a period of 4 minutes during continuous monitoring of one ECG lead and blood pressure. Three minutes after the end of dipyridamole infusion, the patient was placed in the original imaging position, and a set of IR-prepared turboflash images was repeated during the injection of the second bolus of 0.05 mmol/kg Gd-DTPA. If chest pain appeared, the patient was treated with intravenous aminophylline immediately after imaging.
MRI Analysis
The effect of Gd-DTPA injection was quantified by measurement of
SI changes from right ventricular and LV chamber blood,
myocardial areas representing the perfusion beds of the
three coronary arteries, subcutaneous fat, and the SD of the
background noise.10 The ROI for the perfusion bed of the
LAD was located at the anteroseptal, that for the LCx at the lateral,
and that for the RCA at the posterior myocardial wall18 19
(Fig 1
). The ROI for the subcutaneous fat
was placed at the anterior thoracic wall close to the heart, and the SD
of the background noise was obtained from the ROI drawn outside the
body along the phase-encoding direction. All three slice positions of
both rest and stress image sets were analyzed with the three
myocardial ROIs. Regional SI values (arbitrary units) were measured
with the image analysis program NIH Image 1.59. Owing to the
displacement of the heart during breathing, placement of ROIs was
individually traced from image to image. ROI size and shape were kept
constant throughout the analysis of each section and myocardial
area. Values from the LAD ROI represented underperfused
myocardium, and the mean of the LCx and RCA ROIs, normal
myocardium. SI-time curves were generated for each section
and used for further analysis.
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Signal-to-noise ratio was calculated from the SI of normal myocardial region divided by the SD of background noise. The CNR of the underperfused myocardium was calculated from the formula CNR=(SI of normally perfused region-SI of LAD region)/SD of background noise. The SI change rate of normally perfused myocardium and the perfusion bed of diseased artery was assessed from the upslope of SI-time curves of each perfusion study and calculated as described by Matheijssen et al19 from the formula SI change rate=SI increase/time (ms). The ratio of SI change rate of underperfused to normal myocardium was calculated from these values. Heart rate during each imaging set was taken into account in analysis of the SI change rate and in the comparison of results between rest and stress studies.
The sizes of perfusion defects were assessed from stress images with
the largest myocardial CNR. A circumferential ROI of three pixel
thickness (7 mm) was drawn on the myocardium; care was
taken to avoid pixels in the blood pool or epicardial fat. The SI
profile was produced by plotting the mean SI of the three pixels
against the angular position to correlate the profiles generated from
the scintigraphy images. The mean and SD of SI of the
normal myocardium in the posterolateral myocardial region
were calculated for each section, and the pixels with SIs of 2 SD below
the mean were classified to represent the areas with reduced
perfusion. The size of underperfused region on each section was
presented as degrees of the circumferential profile. Anterior
and septal LV segments on scintigraphy
sections25 were considered to correspond to the LAD ROI
positioned on the anterior interventricular sulcus on MR
images (Fig 1
). The sections were compared to determine the presence or
absence and size of perfusion deficit. CNR was also calculated for
residual deficits detected either on scintigraphy or MR
sections after revascularization by use of values
obtained from MR circumferential profiles.
Statistical Analysis
All values were expressed as mean±SD. The significance of
differences in SI-time curves was determined by repeated-measures ANOVA
with multiple comparison of mean values by Scheffé's F test. The
paired two-tailed Student's t test was used to determine
the differences in CNR and SI change rate at rest and during stress
before and after revascularization and perfusion
defect sizes that were obtained from scintigraphy and MR
images. Also, the paired two-tailed Student's t test was
used to compare baseline heart rate and mean blood pressure with the
values obtained after dipyridamole injection and
between scintigraphy and MRI. The unpaired two-tailed
Student's t test was used to compare patient groups with
complete coronary artery occlusion and stenosis. The
mean difference in perfusion defect sizes was obtained by subtracting
defect size on MR sections from scintigraphy sections and
calculating the mean of the differences, as suggested by Bland and
Altman.26 Linear regression analysis was used to
compare the perfusion defect sizes on MR and scintigraphy
sections and to compare the myocardial SI change rates with the
relative myocardial intensity on scintigraphy. A
significance level of P<.05 was used.
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Results |
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Coronary Angiography and Thallium Scintigraphy
At coronary angiography, four patients had complete occlusion of the LAD. Seven patients had LAD stenosis with diameter reduction of 90±8% (range, 80% to 99%). All patients had normal LV function in cineangiography, and ejection fraction was 65±6% (range, 55% to 73%). Before treatment, at scintigraphy, all patients had reversible perfusion defects anteroseptally on at least one section. The size of perfusion defects was 66±53° (range, 0° to 166°) of the circumferential profile of each section.
All patients underwent revascularization in 2 to 8 weeks after coronary angiography. Four patients with a complete LAD occlusion were treated surgically with the native left internal thoracic artery used as bypass graft. In the rest, balloon angioplasty resulted in residual stenosis of 19±11% (range, 0% to 30%). In control scintigraphy, three months after revascularization, the defect sizes had decreased to 8±12° (range, 0° to 39°), P<.001 compared with the defect sizes before treatment. There were no resting deficits on scintigraphy sections before or after treatment.
MR Imaging
Before revascularization, at rest, contrast
injection was followed by rapid SI increase in chamber blood and slower
enhancement of myocardium (Fig 2a). Myocardial signal-to-noise ratio was
6±3 before contrast enhancement, 18±4 at the peak of the bolus, and
16±3 at the end of the image set. No statistical difference in SI
curves representing areas perfused by diseased and normal
arteries was detected (Fig 2a). However, an increase in CNR and a
difference in SI change rate between the myocardial regions was
observed (Tables 1 and 2).
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During pharmacologically induced stress, before contrast enhancement,
there was no difference in the myocardial SI between the areas perfused
by the diseased and normal arteries (Figs 2b and 3). A significant difference in the
myocardial regional SI lasted over seven images (28 seconds),
starting from the second image of the upslope of the myocardial
enhancement curve (Fig 2b). CNR increased after enhancement and
declined toward the end of the image set. The peak CNR was greater in
image sets acquired at stress than at rest (Table 1). The ratio of the
SI change rates measured in the myocardial areas perfused by diseased
to normal arteries was lower in the images acquired at stress than at
rest (Table 2). There was no statistical difference in CNR or SI change
rate values in patients with complete occlusion compared with patients
with coronary artery stenosis either at rest or at
stress.
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The effect of revascularization on myocardial MR
perfusion images is illustrated in Fig 4.
After revascularization, the SI alterations, CNR,
and SI change rates were not different in image sets acquired at rest
and at stress. All these values were comparable to the values obtained
from the images acquired at rest before
revascularization (Fig 2c, Tables 1 and 2). CNR was
higher at the peak of the contrast compared with the end of the image
set acquired at stress, but both values were within the range of noise
level.
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Before treatment, perfusion defect size on MRI sections was 49±41°
(range, 6° to 144°) of the circumferential profile.
Revascularization decreased the size to 9±8°
(range, 0° to 22°), P<.001. No resting deficits were
observed on MRI sections before or after treatment. The agreement on
the presence or absence of perfusion deficits between
scintigraphy and MRI sections was 85% (n=66 sections), and
that between scintigraphy and MRI sessions, 95% (n=22
cases, 11 patients imaged before and after treatment). After treatment,
three perfusion defects were detected only on scintigraphy
and eight only on MRI sections. The three deficits seen only on
scintigraphy had a size range of 6° to 39°, thallium
count 61% to 74% of maximum, and CNR on MR images of 1.20 to 1.96.
The eight deficits seen only on MR images had a size range of 4° to
22°, thallium count 76% to 85% of maximum, and CNR in the center of
the deficit 2.46 to 5.97. In the rest deficit, size was 5° to 22°
on MR and 3° to 39° on scintigraphy, thallium count
68% to 74% of maximum, and CNR in the center of the deficit 3.05 to
5.70. Correlation coefficient between the perfusion defect sizes
measured with scintigraphy and MRI was.86, and SEE was
21.3°, P<.001 (Fig 5).
Defect sizes were 7±23° smaller on MR than on
scintigraphy sections, P=.008.
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CNR and SI change rates of the LAD ROIs were not different in sections
with complete recovery compared with the sections with remaining small
regional defects. The CNR, SI change rates, and size of residual
perfusion defects were not statistically different between the patients
who had been treated with balloon angioplasty and bypass surgery.
Relative regional myocardial intensity on scintigraphy
sections and SI increase rate on the corresponding regions on MRI had a
correlation of r=.66 (Fig 6).
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Dipyridamole infusion increased heart rate from 56±7 to 71±10 bpm, and no significant change in mean blood pressure (105±14 mm Hg) was observed. There was no statistical difference in cardiovascular responses between scintigraphy and MRI. With slower heart rates, each MR slice was imaged every fourth heartbeat, and with faster heart rates (during pharmacological stress), every sixth heart beat, averaging into mean temporal resolution of 4.3±0.6 seconds (range, 3.4 to 6.0 seconds). There was no significant difference between rest (4.3±0.5 seconds) and stress (4.6±0.6 seconds) studies in temporal resolution, P=.06.
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Discussion |
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The purpose of this study was to use multislice pharmacologically stressed contrast enhanced IR-turboflash imaging (1) for detection and sizing of reversible myocardial ischemia in patients with proximal LAD disease and (2) in the assessment of the effect of revascularization on myocardial perfusion. Three slices were imaged repeatedly to cover a larger part of the myocardium than in single-slice studies. A body coil was used as receiver to allow the comparison of regional enhancement during the bolus injection of Gd-DTPA. Pharmacological stress was applied to increase the perfusion gradient between the myocardial areas. Data obtained from stress and rest studies were compared. The responses to bypass surgery and angioplasty were assessed and compared 3 months after revascularization.
Dipyridamole infusion was followed by increased CNR of myocardial perfusion defect and decreased ratio in SI change rates of underperfused to normal myocardial regions. The differential signal enhancement of normal and underperfused myocardial regions lasted >28 seconds, which allowed 85% agreement between scintigraphy and MRI on detection of the perfusion defects on all three myocardial sections. Relative regional myocardial intensity on scintigraphy sections correlated with SI increase rate on MRI. Revascularization decreased the size of the regional perfusion defects on scintigraphy and MRI sections. After revascularization, the enhancement patterns were identical in normal regions, in regions treated with angioplasty, and in regions treated with bypass surgery.
In conclusion, a close correlation was found between dipyridamole thallium scintigraphy and contrast-enhanced multislice MRI in detection and sizing of the regional myocardial perfusion defects. We suggest that multislice MR perfusion stress testing could be used to assess the effect of revascularization on regional myocardial perfusion.
In multislice myocardial perfusion imaging, good spatial resolution has been achieved with a surface coil as receiver, but uneven MRI signal has prevented quantitative analysis between anatomically different myocardial regions.18 We obtained images with the body coil as receiver, which allowed comparison both between the myocardial regions on the same MRI section and between the numerical results attained at rest and stress before and after revascularization. Also, sizing of perfusion defects was feasible from MRI sections. We selected a T1-weighted imaging sequence for the detection and sizing of myocardial perfusion defects, because myocardial signal-to-noise ratio on T2*-weighted images is low and the effect of bolus on myocardial signal is shorter.10 Multislice first-pass transit IR-prepared imaging has been able to locate acute myocardial ischemia in canine heart in vivo,12 and recent reports have outlined the feasibility of clinical MR imagers in multislice dynamic imaging of the human heart.17 18 21
The paramagnetic compound Gd-DTPA shortens T1 relaxation time, leading to increase in SI on T1-weighted MR images. Although in the first pass, 30% of the extracellular contrast agent enters the interstitium,20 27 myocardial Gd-DTPA concentration is determined primarily by coronary flow within 5 minutes of a bolus injection.28 Dipyridamole induces vasodilatation and flow in a normal more than in a diseased coronary artery,29 which generates contrast between normal and underperfused myocardial regions. After peripheral bolus injection, calculation of myocardial flow from the mean transit time curves is not feasible,30 but linear fit of SI increase is a sensitive parameter in discriminating underperfused from normally perfused myocardial regions.19 Consequently, in our study, the SI differences between the myocardial regions perfused by normal and diseased arteries were related to but did not exactly measure myocardial perfusion at the time of the bolus injection.
Before treatment, at rest, during peak enhancement of myocardium, we found an increase in contrast between regions perfused by diseased and normal coronary arteries and greater SI change rate in normal than in underperfused territory. In analysis of individual curves of each patient, baseline CNR was calculated from images with zero myocardial intensity (as a result of inversion time 400 ms). Peak CNR was derived from images with the largest contrast between the myocardial areas. In analysis of the mean curves of all patients, no statistical difference was found, possibly because the peak CNR appeared at divergent time points after the beginning of the enhancement and lasted only for two or three images. We suggest that the low peak CNR value indicates a small perfusion gradient between the myocardial areas at rest. Our finding is in agreement with the results of Manning et al,13 who used a single-slice IR-turboflash sequence and observed myocardial enhancement differences at rest in coronary artery disease patients. In multislice MR perfusion studies, comparison between regions has been prevented by either the use of surface coil17 18 or poor temporal resolution.17 In dogs, coronary artery occlusion but not stenosis has produced contrast between myocardial regions during bolus injection at rest.10 11 We suggest that in our patients, gradual development of coronary artery occlusion has induced collateral circulation to the underperfused area, which prevented differentiation between occlusion and stenosis.
Before treatment, during pharmacologically induced stress and peak
enhancement of myocardium, we observed a significant
increase in myocardial CNR. After dipyridamole
infusion, the SI change rate of normal myocardium increased
and that of underperfused region decreased (Table 2), indicating a
coronary steal phenomenon. This finding is in agreement with
other reports on stress-test first-pass MRI in animal
models2 5 6 11 and in coronary artery
patients.14 15 17 18 21 The best CNR was detected during
the upslope and peak of enhancement of normally perfused
myocardium, which implies that with careful timing, the
images with best contrast could be acquired during a single breathhold
of 30 seconds.
After revascularization, contrast enhancement patterns in the myocardial regions were indistinguishable both at rest and at stress. Manning et al13 discovered a significant increase in SI peak but no change in SI increase rate in the revascularized myocardial segments at rest after bypass surgery. In our study, CNR and SI change rates did not allow any differentiation of the formerly underperfused and normal myocardial regions. Enhancement properties in the revascularized myocardium were not dependent on the method of the therapy.
We observed linear correlation in defect sizing between MRI and thallium scintigraphy. Discrepancy with a canine study, with histochemical morphometry for comparison, could be explained by homogeneous defect size induced by artificial coronary stenosis in dogs.11 Perfusion defects were 7° smaller on MRI than on scintigraphy sections, with considerable differences (SD, 23°) compared with scintigraphy values. Although treatment decreased perfusion defect sizes in our patients, small residual defects were identified, of which three were seen only on scintigraphy and eight only on MR sections. As suggested by the normal enhancement curves obtained from the myocardial LAD ROIs drawn on the revascularized regions, low-intensity areas with size <10° could represent the lowest 2.5% of the normal myocardial intensity variation. Second, discrepancy between the two imaging methods in detection of small and sizing of large perfusion defects could rely on different data collection procedures. In MRI, the defects were seen during the 20-second upslope of myocardial enhancement, which in scintigraphy images were obtained during 20 minutes. Third, myocardial enhancement during first pass on MRI is a result of inflow of the enhancing agent from vasculature to myocardial extracellular space28 and water exchange rate in the tissue.31 In comparison, myocardial 201Tl content is controlled by coronary blood flow and the ability of myocytes to extract 201Tl from the blood (Na,K-ATPase pump).32 We suggest that the relatively poor correlation between bolus tracking MRI and thallium scintigraphy in evaluation of myocardial blood flow could be attributed to the differences in uptake and distribution of the tracers.
Our data were based on a strictly limited patient population with a homogeneous disease pattern. All patients had LAD disease, which prevented blinded comparison of deficit localization between the imaging methods. No patients with less severe coronary artery disease, multiple stenoses, or previous myocardial infarction were included. Our goal, however, was to assess the feasibility of multislice MRI stress test on evaluation of reperfusion therapy. More extensive studies on larger patient populations with variable myocardial ischemic disease are needed before MRI can be used clinically for assessment of myocardial ischemia and reperfusion.
In conclusion, pharmacologically stressed multislice MRI has a potential in detection of reversible myocardial perfusion defects in patients with coronary artery disease and in assessment of the effect of revascularization on regional perfusion.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by grants from the Foundations of Ida Montin and P.O. Klingendahl, the Radiological Society of Finland, the Finnish Medical Society Duodecim, the Helsinki University Central Hospital Research Funds, the Paavo Nurmi Foundation, and the Juselius Foundation.
Received April 8, 1997; revision received June 11, 1997; accepted June 14, 1997.
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