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Coronary Artery Disease: Assessment with a Comprehensive MR Imaging Protocol—Initial Results¹

¹ From the BHF Cardiac MRI Unit (S.P., T.R.J., T.N.B., M.U.S.) and Department of Medical Physics (J.P.R.), Leeds General Infirmary, Great George St, Rm 170, D-floor, Jubilee Building, Leeds LS1 3EX, England. Received August 27, 2001; revision requested October 17; revision received December 10; accepted January 29, 2002. S.P. supported by a British Heart Foundation Junior Research Fellowship. Address correspondence to S.P. (e-mail: sven.plein@leedsth.nhs.uk).

View larger version (63K): [in a new window]   Figure a, Patient 9.  Data acquired in a 62-year-old woman with prior inferior wall MI and angina. (a) Gradient-echo MR images in the left ventricular short-axis orientation at midventricular level in (left) diastole and (middle) systole and (right) corresponding MR image with delayed contrast enhancement. Gradient-echo MR images were acquired with a balanced fast field-echo sequence, and MR images with delayed contrast enhancement were acquired with a T1-weighted turbo field-echo sequence with a nonselective 180° prepulse. There is thinning of the inferior wall with absent wall thickening (solid arrows) and corresponding transmural hyperenhancement of the inferior wall (dotted arrow). (b) Myocardial perfusion MR images were acquired with a saturation-recovery T1-weighted turbo field-echo sequence in the left ventricular short-axis orientation at the midventricular level. Corresponding MR images were acquired (left) at rest and (right) during adenosine stress. A partly fixed, partly inducible inferior wall defect (solid arrows) and an inducible subendocardial anteroseptal defect (dotted arrows) are demonstrated. (c) (left) Coronary MR angiograms (3D navigator-gated acquisition) in double oblique orientation and (right) corresponding conventional angiograms. The RCA is occluded (solid arrows), and there is a moderate stenosis in the proximal LAD coronary artery (dotted arrows). The patient had more severe disease in the distal LAD coronary artery (not shown) that was probably the cause for the anteroseptal perfusion defect. The position of this section of the MR angiographic data set does not allow analysis of the LCX coronary artery. The signal intensity in the distal RCA is caused by backfilling from the left coronary artery system.

View larger version (82K): [in a new window]   Figure b, Patient 9.  Data acquired in a 62-year-old woman with prior inferior wall MI and angina. (a) Gradient-echo MR images in the left ventricular short-axis orientation at midventricular level in (left) diastole and (middle) systole and (right) corresponding MR image with delayed contrast enhancement. Gradient-echo MR images were acquired with a balanced fast field-echo sequence, and MR images with delayed contrast enhancement were acquired with a T1-weighted turbo field-echo sequence with a nonselective 180° prepulse. There is thinning of the inferior wall with absent wall thickening (solid arrows) and corresponding transmural hyperenhancement of the inferior wall (dotted arrow). (b) Myocardial perfusion MR images were acquired with a saturation-recovery T1-weighted turbo field-echo sequence in the left ventricular short-axis orientation at the midventricular level. Corresponding MR images were acquired (left) at rest and (right) during adenosine stress. A partly fixed, partly inducible inferior wall defect (solid arrows) and an inducible subendocardial anteroseptal defect (dotted arrows) are demonstrated. (c) (left) Coronary MR angiograms (3D navigator-gated acquisition) in double oblique orientation and (right) corresponding conventional angiograms. The RCA is occluded (solid arrows), and there is a moderate stenosis in the proximal LAD coronary artery (dotted arrows). The patient had more severe disease in the distal LAD coronary artery (not shown) that was probably the cause for the anteroseptal perfusion defect. The position of this section of the MR angiographic data set does not allow analysis of the LCX coronary artery. The signal intensity in the distal RCA is caused by backfilling from the left coronary artery system.

View larger version (168K): [in a new window]   Figure c, Patient 9.  Data acquired in a 62-year-old woman with prior inferior wall MI and angina. (a) Gradient-echo MR images in the left ventricular short-axis orientation at midventricular level in (left) diastole and (middle) systole and (right) corresponding MR image with delayed contrast enhancement. Gradient-echo MR images were acquired with a balanced fast field-echo sequence, and MR images with delayed contrast enhancement were acquired with a T1-weighted turbo field-echo sequence with a nonselective 180° prepulse. There is thinning of the inferior wall with absent wall thickening (solid arrows) and corresponding transmural hyperenhancement of the inferior wall (dotted arrow). (b) Myocardial perfusion MR images were acquired with a saturation-recovery T1-weighted turbo field-echo sequence in the left ventricular short-axis orientation at the midventricular level. Corresponding MR images were acquired (left) at rest and (right) during adenosine stress. A partly fixed, partly inducible inferior wall defect (solid arrows) and an inducible subendocardial anteroseptal defect (dotted arrows) are demonstrated. (c) (left) Coronary MR angiograms (3D navigator-gated acquisition) in double oblique orientation and (right) corresponding conventional angiograms. The RCA is occluded (solid arrows), and there is a moderate stenosis in the proximal LAD coronary artery (dotted arrows). The patient had more severe disease in the distal LAD coronary artery (not shown) that was probably the cause for the anteroseptal perfusion defect. The position of this section of the MR angiographic data set does not allow analysis of the LCX coronary artery. The signal intensity in the distal RCA is caused by backfilling from the left coronary artery system.