| Purpose To assess the application of CMR (Cardiac magnetic resonance ) hi coronary artery disease (CAD) compared with conventional coronary angiography. Material and Methods 26 cases of clinically suspected CAD were examined on a 1.5 T scanner (Twin Speed, GEMS) with dual gradients (40 mT/m and 23mT/m maximum amplitude for each) under zoom mode. The cardie phase array coil was used for FGRE-ET and FGRE delay enhancement sequences. All three sequences were acquired whole-heart coveraged in short axis planes with thickness of 10 mm. Contrast agent (Magnevist, Schering Company) was administered intravenously by power injector at the injection rate of 3ml/s, 3.5ml/s, 4ml/s, respectively in dosage of O.lmmol/kg. Conventional coronary angiography confirmed 21 of 26 cases as stenotic disease, one-vessel disease in 6, two-vessel in 7, and three-vessel in 8 cases, separately.There were 40 vessels involved. And also 5 cases were confirmed having normal coronary arteries. Results 14 LADs were stenotic confirmed on angiography. 10 (more than 90% of stenosis) out of 14 displayed abnormalities within the corresponding region on CMR, with 9 of 10 demonstrating hypoperfusion defects on FPMR and hyperenhanced intensity on delay enhancement sequence, and the other one showing hypoperfusion on FPMR within apex. Only 4 out of 14 with 85% stenosis displayed no abnormalities within the corresponding region on CMR. 16 RCAs showed stenotic changes on conventional coronary angiography. 13 of 16 showed narrowing more than 85%, with 8 revealing abnormal signal intensity on both FPMR and delay enhancement sequences, while 1 having hyperintensity on delay enhanced sequence and the remaining two showing no abnormality on CMR. 3 LADs were narrowed less than 85%, and two of these three showed no abnormalities and the other one had hypoperfused area on FPMR. 10 LCXs were stenotic on angiography, 9 of 10 with more than 70% stenosis. 5 of these 9 LCXs demonstrated abnormal signal intensity on both FPMR and delay enhancement sequences, and 1 had perfiision defect on FPMR and another one hadhyperenhanced intensity on delay enhancement sequence. One LCX with 90% stenosis and one with 85% stenosis showed no abnormality on these two sequences, respectively. 14 (93.3%) of 15 with severe steontic or occluded coronary arteries with collateral flow establishment had hyperenhancement on delay enhancement sequences, while for those with moderate stenotic disease only 12(48.0%) cases had same abnormalities. There was a significant difference between these two groups (F=0.005). On FPMR, low signal intensity within the subendocardial region of the segment 3, 4, and 5 were detected in 8 cases. For the group of 6 patients having both stenotic RCAs and LCXs and the other group of 8 patients having stenotic RCA or LCX or normal coronary vessels, abnormal signal intensity was demonstrated in 4 cases separately in each group. Thus, there was no significant difference between these two groups (F= 1.000). The low signal intensity within the entire subendocardial and/or region of myocardium was also detected on FPMR in two patients having stenotic middle segment and the branch of RCA, respectively, and also in two normal controls. There was no corresponding hyperintensity on delay enhancement sequence to thesetwo low signal intensities on FPMR. A round high signal was displayed within the subendocardial region of the segment 2 in the patient having 50% stenosis in middle segment of RCA confirmed on coronary angiography. Conclusion: For more than 80% of hemodynamically significant stenoses, the sensitivity of both FGRE-ET and delay enhancement sequence was 74.2% and 67.7%, retrospectively. Combining these two sequences, the sensitivity was 80.6%. CMR can reveal the abnormality induced by more than 90% stenosis of LAD and more than 85% stenosis of RCA. Combining FPMR and delay enhancement sequences, 70% stenotic LCX can be demonstrated with sensitivity of 78%. Those perfusion defect within the subendocardial region without accompanying hyper...
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