QUANTIFICATION OF AREA AT RISK DURING CORONARY-OCCLUSION AND REPERFUSION BY MEANS OF MR PERFUSION IMAGING

Purpose: Considerable clinical interest has focused on the size of isc hemic myocardium. Fast MR imaging in conjunction with MR contrast medi a has the potential to identify hypoperfused and infarcted myocardium. This study used MR perfusion imaging to detect and quantify reperfuse d ischemic myocardium during a brief coronary occlusion and reperfusio n, and to characterize the spatial extent of ischemic and reperfused i schemic myocardium relative to the ''true'' size of the area at risk a s defined in histochemical morphometry at post mortem. Material and Me thods: The left circumflex (LCX) coronary artery in 8 dogs was occlude d for 15 min followed by reperfusion in order to produce regional reve rsible myocardial ischemia. Perivascular Doppler probes were used to m easure blood flow in the left anterior descending (LAD) and LCX corona ry arteries. Fast inversion recovery-prepared gradient-recalled-echo i mages were acquired to delineate the ischemic area during occlusion, a nd the area of reversible ischemic injury at 1 and 30 min of reperfusi on. The size of ischemic and reperfused ischemic myocardium were compa red with the area at risk as determined by histochemical morphometry a t post mortem. Results: During LCX occlusion, LCX flow decreased from 16+/-1 to 0.2+/-0.1 ml/min. On contrast-enhanced images, ischemic myoc ardium was evident as a zone of relatively low signal intensity (SI) c ompared to normal myocardium. The size of the ischemic region was sign ificantly smaller (30+/-2%) than at post mortem (36+/-3%; p<0.05). Imm ediately after reperfusion, LCX flow increased to 83+/-11 ml/min and t he contrast medium caused greater enhancement in the reperfused ischem ic region than in the normal myocardium (69+/-3 vs 42+/-3 arbitrary un its; p<0.05). The increase in regional SI correlated closely with the increase in regional blood flow (r=0.73). At 1 min of reperfusion, the size of the reperfused ischemic myocardium was larger (48+/-3%, p<0.0 5) than the area at risk measured at post mortem. At 30 min of reperfu sion, when the flow returned to baseline values (16+/-2 ml/min), contr ast bolus produced no differential enhancement between the 2 myocardia l territories. Conclusion: MR perfusion imaging has the potential to d etect and quantify the size of ischemic myocardium and the region of p ost-occlusive hyperemia in the early reperfusion period. There is a si gnificant direct linear relationship between the regional contrast enh ancement of reperfused ischemic myocardium and the blood flow during p ost-occlusive hyperemia. The difference in the size of the area at ris k at MR perfusion imaging and at histochemical morphometry may reflect an influence of coronary collateral circulation.