Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction.
BACKGROUND
Contrast medium-enhanced magnetic resonance images of acute, reperfused infarcts have shown hypoenhanced and hyperenhanced regions in areas of injured myocardium. The precise mechanisms that lead to these altered enhancement patterns are unknown. This study was designed to evaluate possible mechanisms and to relate altered enhancement patterns to myocardial perfusion and viability.


RESULTS
Thirteen rabbits underwent in situ coronary artery occlusion and reperfusion followed by isolated perfusion with cardioplegic solution. T1-weighted spin-echo images were acquired continuously during step changes in perfusate Gd-DTPA concentration. Regional blood flow was also measured by use of radioactive microspheres in all rabbits. There were marked differences in Gd-DTPA wash-in and washout time constants (wash-in, 0.8 +/- 0.1, 2.1 +/- 02, and 16.3 +/- 2.4 minutes, P < .001; washout, 1.6 +/- 0.1, 4.8 +/- 0.5, and 31.1 +/- 3.3 minutes, P < .001) in normal, infarct rim, and infarct core regions, respectively, resulting in differential enhancement of these regions. Microsphere flows in the infarct rim and core were 42.9 +/- 4.0% and 12.0 +/- 1.6% of normal myocardium and correlated well with washout time constants (r = .86, y = 0.77x - 0.002, P < .001), suggesting that these time constants index the severity of microvascular damage. In addition, spatial maps of washout time constants were produced. The extent of regions with abnormal time constants correlated well with triphenyltetrazolium chloride-determined infarct size (r = .94, y = 0.95x + 4.17, P < .001).


CONCLUSIONS
In contrast-enhanced magnetic resonance images of acute, reperfused rabbit infarcts, differential image intensity is primarily due to regional differences in contrast agent wash-in and washout time constants. These regional differences in time constants also indicate the extent and severity of myocardial injury.
Kim
R J
RJ
Department of Medicine, Johns Hopkins Hospital, Baltimore, Md 21287-6568, USA. rkim@mri.jhu.edu
Chen
E L
EL
Lima
J A
JA
Judd
R M
RM
D000704:Analysis of Variance; D000818:Animals; D004487:Edema; D005682:Gadolinium / Q000493:pharmacokinetics; D019786:Gadolinium DTPA; D006470:Hemorrhage / Q000473:pathology; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008854:Microscopy, Electron; D008863:Microspheres; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology*; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D009942:Organometallic Compounds / Q000493:pharmacokinetics*; D004369:Pentetic Acid / Q000031:analogs & derivatives* / Q000493:pharmacokinetics; D011817:Rabbits; D012016:Reference Values; D013997:Time Factors
D009942:Organometallic Compounds; D004369:Pentetic Acid; D005682:Gadolinium; D019786:Gadolinium DTPA