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T2-prepared Steady-State Free Precession Blood Oxygen Level–Dependent MR Imaging of Myocardial Perfusion in a Dog Stenosis Model¹

¹ From the Departments of Biomedical Engineering (S.M.S., X.B., D.L.), Radiology (S.M.S., D.S.F., B.E.S., X.B., R.A.O., D.L.), and Preventive Medicine (J.H.), Northwestern University, Evanston, Ill. From the 2003 RSNA Annual Meeting. Received February 21, 2004; revision requested April 30; final revision received October 6; accepted October 12. Supported in part by National Institutes of Health grant no. HL57484 and by Siemens Medical Solutions, Erlangen, Germany. Address correspondence to D.L., 448 E Ontario St, Suite 700, Chicago, IL 60611 (e-mail: d-li2{at}northwestern.edu).

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION References

 
PURPOSE: To assess the ability of a T2-prepared steady-state free precession blood oxygen level–dependent (BOLD) magnetic resonance (MR) imaging sequence to depict changes in myocardial perfusion during stress testing in a dog stenosis model.

MATERIALS AND METHODS: Study was approved by the institutional Animal Care and Use Committee. A hydraulic occluder was placed in the left circumflex coronary artery (LCX) in 10 dogs. Adenosine was administered intravenously to increase coronary blood flow, and stenosis was achieved in the LCX with the occluder. A T2-prepared two-dimensional steady-state free precession sequence was used for BOLD imaging at a spatial resolution of 1.5 x 1.2 x 5.0 mm³, and first-pass perfusion images were acquired for visual comparison. Microspheres were injected to provide regional perfusion information. Mixed-effect regression analysis was performed to assess normalized MR signal intensity ratios and microsphere-measured perfusion differences. For the same data, 95% prediction intervals were calculated to determine the smallest perfusion change detectable. Means ± standard deviations were calculated for myocardial regional comparison data. A two-tailed Student t test was used to determine if significant differences (P < .01) existed between different myocardial regions.

RESULTS: Under maximal adenosine stress, MR clearly depicted stenotic regions and showed regional signal differences between the left anterior descending coronary artery (LAD)–fed myocardium and the stenosed LCX-fed myocardium. Visual comparisons with first-pass images were also excellent. Regional MR signal intensity differences between LAD and LCX-fed myocardium (1.24 ± 0.08) were significantly different (P < .01) from differences between LAD and septal-fed myocardium (1.02 ± 0.07), which was in agreement with microsphere-measured flow differences (LAD/LCX, 3.38 ± 0.83; LAD/septal, 1.26 ± 0.49). The linear mixed-effect regression model showed good correlation (R = 0.79) between MR differences and microsphere-measured flow differences.

CONCLUSION: On T2-prepared steady-state free precession BOLD MR images in dogs, signal intensity differences were linearly related to flow differences in myocardium, with a high degree of correlation.

Supplemental material: radiology.rsnajnls.org/cgi/content/full/236/2/503/DC1

© RSNA, 2005

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION References

 
Measurement of myocardial perfusion reserve has become integral in the diagnosis and treatment of coronary heart disease. Several magnetic resonance (MR) imaging techniques have been developed to measure myocardial perfusion reserve—most notably, first-pass imaging by using an injection of gadolinium-based contrast agent (1,2). First-pass MR imaging typically exhibits good contrast between regions of different flow, but to effectively track the bolus of contrast agent through the myocardium, temporal resolution must be relatively high, and background signal intensity must be suppressed. These constraints limit the spatial resolution and overall coverage of the heart for first-pass techniques. Furthermore, the technique is less effective as contrast agent accumulates in the tissue, thereby limiting contrast agent dose or imaging runs. Blood oxygen level–dependent (BOLD) MR imaging is an interesting alternative because it relies on the endogenous contrast mechanism of deoxyhemoglobin. This removes the need for a tracer (gadolinium) and consequently temporal resolution requirements, allowing for higher spatial resolution and greater coverage of the heart.

Most cardiac BOLD studies have focused on T2*-weighted MR sequences because previous research in the brain has shown that T2* changes are greater than T2 changes when oxygen saturation is altered (3). These sequences have shown the ability to depict T2* changes caused by flow differences in the myocardium, from either selective vasodilation or the presence of stenosis, but they are not without problems. Low signal-to-noise ratios result in BOLD signal intensity changes that are not much greater than the noise level (4,5). Additionally, long echo times (>20 msec) result in severe flow artifacts from blood flow and increase the acquisition window during the cardiac cycle, making the sequence more sensitive to cardiac motion (6). Major problems occur in areas of the heart with local field inhomogeneities (7,8) because of the susceptibility weighting of gradient-echo sequences with long echo times (5,9,10). All of these problems have hampered BOLD MR imaging from progressing into a clinical technique.

Detection of the BOLD effect by using T2 weighting may be more feasible than T2* weighting in the heart. T2-weighted sequences are less susceptible to off-resonance effects associated with local field inhomogeneities. Additionally, T2-weighted sequences are more resistant to flow- and motion-induced artifacts and typically have higher signal-to-noise ratios than T2*-weighted sequences. The most common choice for T2-weighted sequences has always been spin echo. For cardiac imaging, however, spin echo has several downsides. Almost all cardiac spin-echo sequences, because of long echo times, require black-blood preparation to null the blood signal in the cardiac chambers to prevent flow artifacts. Effective black-blood preparation, though, often requires electrocardiographic triggering on every other heartbeat to allow for T1 recovery, thereby doubling the imaging time for the sequence. Long echo times also make spin-echo sequences more susceptible to motion artifacts and prolonged imaging times, even with fast spin-echo-type readouts. A unique alternative is to use T2 preparation (11) before acquiring data with another sequence structure, such as fast low-angle shot or steady-state free precession. Both fast low-angle shot and steady-state free precession have seen widespread use in cardiac imaging because their characteristically short repetition times maximize data acquisition efficiency and are less susceptible to motion artifacts. Previous cardiac BOLD research has already successfully involved use of the T2-prepared fast low-angle shot sequence to depict regional flow differences in an animal model (12). However, a T2-prepared steady-state free precession sequence may be more suited to BOLD imaging because steady-state free precession sequences have begun to replace fast low-angle shot sequences in cardiac imaging applications as a result of significantly higher signal-to-noise and contrast-to-noise ratios (13–16).

Previous results with T2-prepared fast low-angle shot (12) and T2-prepared steady-state free precession (17) MR sequences showed good correlation between signal intensity and myocardial flow differences in a selective coronary vasodilation animal model. However, these experiments did not simulate scenarios that would normally be seen in patients with coronary heart disease. Adenosine administration was intracoronary, not systemic, thereby increasing the factors of flow that could be obtained (approximately three to five) without substantially affecting heart rate and myocardial oxygen demand. In clinical practice, flow increases of this order may not be encountered—myocardial imaging studies with pharmacologic stress agents typically only increase flow by a factor of two to three. An animal stenosis model would better approximate conditions seen in human subjects and would allow measurement of the effectiveness of T2-prepared steady-state free precession in the detection of disease. The goal of this work was to assess the ability of a T2-prepared steady-state free precession BOLD MR sequence to depict differences in myocardial perfusion in a dog coronary artery stenosis model.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION References

 
Surgical Preparation of Animals
Ten mongrel dogs (19–24 kg, seven female and three male) were studied with approval from our institutional Animal Care and Use Committee. The animals were intubated and ventilated, and gas anesthesia was administered (2.0%–2.5% isoflurane and 100% oxygen). By using a sterile technique, a left lateral thoracotomy was performed between the 8th and 9th ribs to expose the heart (B.E.S.). The pericardium was opened and sewed into a cradle, and the left circumflex coronary artery (LCX) was identified. An external hydraulic occluder was placed around the LCX 1.0–1.5 cm from the bifurcation of the left main coronary artery for the purpose of inducing reversible stenoses within the LCX. A Doppler ultrasonographic flow probe (Crystal Biotech, Northborough, Mass) was placed circumferentially around the LCX 2–3 cm downstream from the occluder to measure LCX blood velocity. Catheters were implanted surgically into the left and right atria and were left in situ for the delivery of normal saline (0.9%), adenosine, and fluorescent microspheres during MR experiments. Another catheter was implanted in the aorta and left in situ for the measurement of aortic pressure in the laboratory setting. At the end of the surgical procedure, the chest was closed, and the animals were allowed to recover for 7 days before MR imaging was performed.

On the first day of imaging, dogs were examined in the laboratory setting to determine the intravenous response to doses of adenosine. Doppler velocity in the LCX and aortic pressure were measured at rest and during infusion of adenosine through the right atrial catheter. The adenosine dose was started at 0.14 mg/kg/min and then increased gradually until Doppler velocity stopped increasing or aortic pressure decreased significantly. The adenosine dose was higher (18,19) than the standard clinical dose (20) because of differences between dog and human physiology.

MR Sequence Design and Parameters
BOLD images were acquired by using an electrocardiographically triggered two-dimensional segmented steady-state free precession sequence with T2 preparation in each cardiac cycle (Fig 1). The T2-preparation scheme was described previously by Brittain et al (11) and was designed to be nonselective and insensitive to flow and B₀/B₁ inhomogeneous field effects. An /2 pulse ( = flip angle) and 20 dummy cycles were applied before image acquisition to reduce signal intensity oscillations within the steady-state free precession sequence (16). The parameters for each examination were as follows: repetition time msec/echo time msec, 3.0/1.3; flip angle, 70°; readout bandwidth, 930 Hz/pixel; T2 preparation time, 40 msec; field of view, 150 x 300 mm²; lines per heartbeat, 5–15; in-plane resolution, 1.5 x 1.2 mm²; section thickness, 5 mm; number of signals acquired, four; trigger delay, 350–450 msec (adjusted to acquire image data during mid-diastole); and breath-hold duration, 20–30 seconds. Asymmetric sampling was employed to reduce repetition time, with the echo center occurring at the 64th point in a 256-point readout period (21). Phase-encoding lines were acquired centrically.

View larger version (13K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Diagram of the T2-prepared steady-state free precession MR sequence. After the trigger delay, T2 preparation (T2-Prep) is applied, followed by an /2 preparation pulse and 20 dummy cycles before data acquisition. TE = echo time, TR = repetition time.

Three short-axis sections were acquired with the BOLD T2-prepared steady-state free precession sequence during rest conditions. We injected 3 x 10⁶ polystyrene fluorescent microspheres (Molecular Probes, Eugene, Oregon) through the left atrial catheter to provide regional myocardial perfusion information. Next, adenosine was infused into the right atrial catheter to vasodilate the entire coronary arterial tree. After flow velocity increases were confirmed with Doppler measurements, stenosis was achieved in the LCX by using the hydraulic occluder, and BOLD images were acquired. Microspheres were again injected to determine perfusion. Afterward, the pressure was released in the occluder, and the flows were allowed to return to baseline conditions. The same imaging and microsphere protocols could then be repeated by using different stenosis sizes by varying the inflation of the occluder.

During the final stenosis examination in each study, saturation-recovery steady-state free precession first-pass images (22) were acquired after microsphere injection to provide visual comparisons with the BOLD images. Saturation-recovery steady-state free precession image parameters were as follows: 3.0/1.5; field of view, 150 x 300 mm²; matrix, 64 x 128; section thickness, 5 mm; and breath-hold duration, approximately 30 seconds. We injected 0.075 mmol/kg gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Montville, NJ) intravenously, followed by a 10-mL saline flush. Four sections were acquired every two heart beats during contrast material injection. At the end of the examination, delayed-enhancement images were acquired to ascertain whether irreversible injury (infarction) had occurred (23). Animals were typically studied on two separate dates, an average of 5 days apart (range, 3–11 days). Seven different colors of microspheres were used in each animal. At the end of the last experiment, animals were euthanized with an overdose of pentobarbital, followed by potassium chloride injection, and the heart was removed for microsphere analysis.

After excising the heart, the left ventricle was separated from the rest of the organ (B.E.S., R.T.). Approximately 0.5 cm of the apex and basal portions were discarded before slicing the ventricle into four equal rings. Each ring was then sliced into eight equal segments. Each segment was weighed and dissolved for 96 hours in 4 mol/L of potassium hydroxide. After filtration and dissolution in 2-ethoxyethyl acetate, each segment was analyzed spectrophotometrically (Perkin Elmer, Wellesley, Mass) for fluorescence that reflected microsphere concentrations (B.E.S.).

Data Analysis
T2-prepared steady-state free precession BOLD images were analyzed with the aid of Argus software (Siemens Medical Solutions). Inner and outer contours were drawn around the myocardium of the short-axis sections and then divided into eight segments to correspond with microsphere measurements (S.M.S.). Signal intensities were recorded for each image segment. The signal intensities from images acquired during adenosine stress and stenosis (hereby referred to as stress-stenosis) were divided by the signal intensities from images acquired at baseline to normalize any differences due to coil sensitivities. Three regional comparisons were then made for each stress-stenosis image by dividing normalized signal intensities from one segment to another (S.M.S., D.S.F.). Two comparisons were made between myocardial segments fed by the left anterior descending coronary artery (LAD) and LCX-fed myocardial segments (hereby referred to as LAD/LCX), and the other comparison was made between LAD and septal-fed myocardial segments (hereby referred to as LAD/septal). Results were then matched to microsphere results on the basis of anatomic landmarks (S.M.S.).

Statistical Analysis
Analysis of the normalized comparison data was restricted to microsphere perfusion measurements (and corresponding MR measurements) that showed less than a 5:1 flow difference. Statistical tests were performed by using SAS software for Windows, version 8.2 (SAS Institute, Cary, NC) and Excel 2000 (Microsoft, Redmond, Wash). Means ± standard deviations were calculated for LAD/LCX and LAD/septal data for both microsphere and MR measurements. A two-tailed Student t test assuming unequal variances was used to determine if significant differences existed between the LAD/LCX and LAD/septal groups. Power analysis was performed to justify the sample size used in this study. A linear mixed-effect regression model was used to assess the relationship between the normalized MR signal intensity ratios and the microsphere-measured perfusion differences. The mixed-effect model was selected to account for within-cluster correlations. For the same data, 95% prediction intervals for future observations were calculated to determine the smallest perfusion change that could be detected with the T2-prepared steady-state free precession BOLD sequence. P values less than .01 were considered to indicate a statistically significant difference for all tests.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION References

 
A total of 16 MR imaging studies were performed in 10 dogs. Two MR imaging studies from one dog were eliminated because delayed-enhancement images and heart sectioning showed evidence of infarction. Two other MR imaging studies from another dog were also eliminated because of poor image quality. Image quality was excellent in the other animals studied. The remaining animals did not show any evidence of infarction, and 15 separate adenosine stress-stenosis studies were performed in these animals.

BOLD MR imaging results showed regional signal intensity differences between the LAD-fed myocardium and the stenosed LCX-fed myocardium. A comparison of BOLD T2-prepared steady-state free precession images obtained during rest conditions and adenosine stress-stenosis clearly outlined regions affected by stenosis in both the long-axis and short-axis views (Fig 2). This can be seen more clearly if the rest and stress-stenosis images are looped into a movie, as seen in Movie 1 (radiology.rsnajnls.org/cgi/content/full/236/2/503/DC1). BOLD images corresponded well with first-pass images (Figs 2, 3) and microsphere flow maps (Fig 2), as the same regions showed relative signal intensity loss due to stenosis. Figure 3 gives several more clear examples of perfusion differences in short-axis sections from different dogs with T2-prepared steady-state free precession imaging. Signal intensity increased in the lateral and anterior regions of the myocardium because of vasodilation from the rest to stress-stenosis images, while the stenosed posterior myocardial region showed no substantial differences in signal intensity.

View larger version (81K): [in this window] [in a new window] [Download PPT slide]   Figure 2. Comparison of BOLD MR images (steady-state free precession, 3.0/1.3, 40-msec T2 preparation) at rest (top and middle left images) and during stress-stenosis (top and middle right images), with corresponding first-pass image (bottom left) (saturation recovery steady-state free precession, 3.0/1.5) and microsphere flow image (bottom right). Arrows indicate the region of reduced perfusion due to stenosis in the BOLD stress-stenosis and first-pass images. Note the clear delineation of the myocardial region fed by the stenosed artery in the BOLD images, as well as the excellent match-up of the stress-stenosis BOLD image with the first-pass image and microsphere flow map. (The microsphere flow map was generated by calculating flow ratios in each segment in relation to one reference segment. Scale indicates black for 0 flow ratio and white for a five-fold flow ratio.)

View larger version (139K): [in this window] [in a new window] [Download PPT slide]   Figure 3. Three short-axis sections from three dogs that underwent T2-prepared steady-state free precession BOLD imaging (3.0/1.3, 40-msec T2 preparation) at rest and during stress-stenosis. Arrows indicate regions of reduced perfusion due to stenosis in each section. First-pass (saturation-recovery steady-state free precession, 3.0/1.5) images (right column) showed similar reduced perfusion regions, albeit with lower spatial resolution.

View larger version (24K): [in this window] [in a new window] [Download PPT slide]   Figure 4. Plot of normalized microsphere flow differences versus normalized MR signal intensity differences. Solid line indicates the linear mixed-effect regression model fitted to the data, and dashed lines are 95% prediction intervals for future observations. Data showed excellent correlation (R = 0.79) between MR signal intensity differences and microsphere flow differences, indicating that T2-prepared steady-state free precession BOLD MR imaging demonstrated perfusion differences.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION References

 
The T2-prepared steady-state free precession BOLD MR sequence demonstrated the ability to acquire high-spatial-resolution artifact-free images that provided perfusion-related information within the heart. The characteristically short repetition times (approximately 3.0 msec) of steady-state free precession sequences was resistant to flow artifacts and allowed data acquisition to be restricted to mid-diastole, thereby minimizing cardiac motion. T2-prepared steady-state free precession images also did not have susceptibility artifacts in the posterior-septal and posterior-lateral regions of the heart, a common problem with long-echo-time T2*-weighted sequences. Most important, unprocessed T2-prepared steady-state free precession BOLD images showed significant signal intensity differences due to flow perfusion defects; previous cardiac BOLD studies often required the calculation of T2 or T2* maps or the subtraction and/or division of stress-stenosis and rest images. This is a major advantage for application in a clinical setting.

Overall, the BOLD images exhibited good correlation with the microsphere-measured flow results. A comparison of this regression model (MR = [0.075 · SPHERE] + 0.96, R = 0.79) with previous work (17) in a selective coronary vasodilation animal model (MR = [0.081 · SPHERE] + 0.95, R = 0.79) showed similar results, indicating that the data were reproducible. Variation around the regression line may be due to differences between animals or imperfect registration of MR and microsphere signal measurements. The regression model showed a linear relationship between signal intensity differences and flow, indicating that T2-prepared steady-state free precession BOLD imaging could allow differentiation between varying degrees of stenosis. As was stated earlier, T2-prepared steady-state free precession BOLD imaging was capable of depicting a minimum perfusion difference of 2.6:1.0, which corresponds, on the average, to 75% stenosis (24).

Both the T2-prepared steady-state free precession BOLD and first-pass images accurately demonstrated areas of flow change due to stenosis. The T2-prepared steady-state free precession BOLD technique did not require the use of MR contrast media, however, and a single section could be acquired over a number of cardiac cycles. First-pass techniques involve trade-offs between spatial resolution, cardiac coverage, and accurately defining the passage of contrast agent through the myocardium. One parameter is always sacrificed to enhance another. The T2-prepared steady-state free precession BOLD sequence enabled images to be acquired at high spatial resolution (1.5 x 1.2 x 5.0 mm³) with adequate coverage of the entire heart, including several different section orientations, a clear advantage over first-pass imaging techniques.

There were limitations to this study. Potential problems, such as breath-hold quality and arrhythmias, were not factors because the animal was anesthetized and receiving ventilation. Stenoses were induced by using a hydraulic occluder, which may differ from stenoses caused by atherosclerotic plaques in human subjects. The length of time to acquire one section (20–30 seconds) will have to be reduced to cover the entire heart within the 3–6 minutes that adenosine is normally infused during human stress studies (20). Possible solutions may be to reduce the number of signals acquired or to move to three-dimensional imaging with breath holding or navigator-echo free breathing.

Future improvements to the BOLD technique are also warranted to detect smaller perfusion differences. One possible solution is to image at higher field strengths. Signal-to-noise ratio has been shown to increase linearly with field strength and, more important, BOLD signal changes have also increased with field strength (25–27), both of which should improve the detection of regional flow differences in the myocardium. The recent Food and Drug Administration approval of 3-T whole-body imagers may make this much more feasible in the near future.

In general, the T2-prepared steady-state free precession BOLD MR images accurately demonstrated regions of reduced perfusion due to stenosis in this animal model. Signal intensity differences were shown to be linearly related to flow differences in the myocardium, with a high degree of correlation. Visual comparisons with first-pass images were also excellent, indicating that T2-prepared steady-state free precession BOLD imaging should be considered an alternate MR technique for measurement of myocardial perfusion differences.

Practical application: T2-prepared steady-state free precession BOLD MR imaging is potentially useful for identification of myocardial perfusion defects in human subjects. Because it relies on an endogenous contrast mechanism, studies do not require contrast agent injection and can be repeated if necessary. More important, the technique is based on the BOLD effect, from which a measurement of myocardial oxygen extraction could be determined (28). Human studies will be necessary to determine the clinical feasibility of T2-prepared steady-state free precession BOLD MR imaging.

	ACKNOWLEDGMENTS

 
The authors thank Richard Tang, MD, for his help with the animal surgical model.

	FOOTNOTES

 

Abbreviations: LAD = left anterior descending coronary artery • LCX = left circumflex coronary artery

Author contributions: Guarantor of integrity of entire study, D.L.; study concepts, S.M.S., D.S.F., R.A.O., D.L.; study design, S.M.S., D.S.F., B.E.S., R.A.O., D.L.; literature research, S.M.S., D.S.F., X.B., D.L.; experimental studies, S.M.S., D.S.F., D.L.; data acquisition, S.M.S., B.E.S., X.B., D.L.; data analysis/interpretation, S.M.S., D.S.F., J.H., D.L.; statistical analysis, S.M.S., D.S.F., J.H., D.L.; manuscript preparation, S.M.S., D.L.; manuscript definition of intellectual content, S.M.S., D.S.F., R.A.O., D.L.; manuscript editing, S.M.S., D.L.; manuscript revision/review and final version approval, all authors

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