Purpose: To demonstrate the advantages of signal intensity percent-infarct-mapping (SI-PIM) using the standard delayed enhancement (DE) acquisition in assessing viability following myocardial infarction (MI). SI-PIM quantifies MI density with a voxel-by-voxel resolution in clinically used DE images.
Materials and Methods:In canines (n¼ 6), 96 hours after reperfused MI and administration of 0.2 mmol/kg Gd(DTPA), ex vivo DE images were acquired and SI-PIMs calculated. SI-PIM data were compared with data from DE images analyzed with several thresholding levels using SI remoteþ2SD , SI remoteþ6SD , SI full width half maximum (SI FWHM ), and with triphenyl-tetrazolium-chloride (TTC) staining. SI-PIM was also compared to R1 percent infarct mapping (R1-PIM).Results: Left ventricular infarct volumes (IV) in DE images, IV SIremoteþ2SD and IV SIremoteþ6SD , overestimated (P < 0.05) TTC by medians of 13.
Conclusion:We have shown here, ex vivo, that SI-PIM has the same advantages as R1-PIM, but it is based on the scanning sequences of DE imaging, and thus it is obtainable within the same short scanning time as DE. This makes it a practical method for clinical studies.
BackgroundStandard extracellular cardiovascular magnetic resonance (CMR) contrast agents (CA) do not provide differentiation between acute and older myocardial infarcts (MI). The purpose of this study was to develop a method for differentiation between acute and older myocardial infarct using myocardial late-enhancement (LE) CMR by a new, low molecular weight contrast agent.Dogs (n = 6) were studied in a closed-chest, reperfused, double myocardial infarct model. Myocardial infarcts were generated by occluding the Left Anterior Descending (LAD) coronary artery with an angioplasty balloon for 180 min, and four weeks later occluding the Left Circumflex (LCx) coronary artery for 180 min. LE images were obtained on day 3 and day 4 after second myocardial infarct, using Gd(DTPA) (standard extracellular contrast agent) and Gd(ABE-DTTA) (new, low molecular weight contrast agent), respectively. Triphenyltetrazolium chloride (TTC) histomorphometry validated existence and location of infarcts. Hematoxylin-eosin and Masson's trichrome staining provided histologic evaluation of infarcts.ResultsGd(ABE-DTTA) or Gd(DTPA) highlighted the acute infarct, whereas the four-week old infarct was visualized by Gd(DTPA), but not by Gd(ABE-DTTA). With Gd(ABE-DTTA), the mean ± SD signal intensity enhancement (SIE) was 366 ± 166% and 24 ± 59% in the acute infarct and the four-week old infarct, respectively (P < 0.05). The latter did not differ significantly from signal intensity in healthy myocardium (P = NS). Gd(DTPA) produced signal intensity enhancements which were similar in acute (431 ± 124%) and four-week old infarcts (400 ± 124%, P = NS), and not statistically different from the Gd(ABE-DTTA)-induced SIE in acute infarct. The existence and localization of both infarcts were confirmed by triphenyltetrazolium chloride (TTC). Histologic evaluation demonstrated coagulation necrosis, inflammation, and multiple foci of calcification in the four day old infarct, while the late subacute infarct showed granulation tissue and early collagen deposition.ConclusionsLate enhancement CMR with separate administrations of standard extracellular contrast agent, Gd(DTPA), and the new low molecular weight contrast agent, Gd(ABE-DTTA), differentiates between acute and late subacute infarct in a reperfused, double infarct, canine model.
The phenomenological tissue kinetics of Gd(ABE-DTTA) was investigated in myocardial infarction (MI). Reperfused infarction was generated by balloon catheter in closed-chest canines (N ؍ 11). Forty-eight hours thereafter, inversion-recovery (IR)-prepared fast gradient-echo control images were acquired with varying inversion times (TIs). Precontrast R 1 maps were calculated from the TI dependence of signal intensity (SI) using nonlinear curve fitting. Then 0.05 mmol/kg Gd(ABE-DTTA) was administered I.V. In 11 dogs postcontrast R 1 maps were generated at 24 hr and 48 hr postcontrast. In five dogs measurements were also repeated at 108 hr and 12 days. In one dog early measurement was carried out at 4 hr. ⌬R 1 values for blood and viable and infarcted myocardium were calculated at each time point by subtracting the precontrast R 1 from the postcontrast R 1 . Gd(ABE-DTTA) showed significant, progressive accumulation into infarcts during the first 2 days (k in ؍ 0.39 hr -1 ) and a delayed clearance (k out ؍ 0.005 hr -1 ). Among the time points sampled, the maximum infarct ⌬R 1 was detected at 48 hr
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