Identification of Myocardial Cell Death in Reperfused Myocardial Injury Using Dual Mechanisms of Contrast-Enhanced Magnetic Resonance Imaging

Jean Francois H. Geschwind, Michael F. Wendland, Maythem Saeed, Kirsi Lauerma, Nikita Derugin, Charles B. Higgins

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Rationale and Objectives. Because the magnitude of dysprosium-induced signal loss depends on the microheterogeneity of its distribution (exclusion from intracellular space), we proposed that loss of myocardial cell integrity would be reflected by decreased potency of dysprosium in the injured compared with normal myocardium. We measured the effect of dysprosium on magnetic resonance (MR) imaging signal intensity of reperfused infarcted and nonischemic myocardium and related it to tissue concentration of the contrast media. Methods. Rats were subjected to 1 hr coronary artery occlusion followed by 1 hr reperfusion. After 45 min of reflow, group 1 (n = 9) received 1.0 and 0.2 mmol/kg dysprosium diethylenetriamine pentaacetic acid-bismethylamide (Dy-DTPA-BMA) and gadodiamide (GdDTPA-BMA), respectively. Group 2 (n = 7) received no contrast agents. Excised hearts were imaged with spinecho T1- and T2-weighted sequences. After imaging, hearts were stained (triphenyltetrazolium chloride) to define the injured zones. Concentrations of Dy-DTPA-BMA and Gd-DPTA-BMA in regional myocardial tissue were determined by induction coupled plasma-atomic emission spectrometry. Separate groups received one or the other contrast medium alone to control for potential error from the mixed effects of the two agents. Results. Gd-DTPA-BMA delineated reperfused infarcted myocardium as a bright zone on T1-weighted images, thus indicating delivery of the agent and reperfusion at the tissue level. Dy-DTPA-BMA delineated the reperfused infarction as a bright region by decreasing the signal intensity of nonischemic myocardium significantly more than that of injured myocardium, despite being present in greater concentration (by 2.46-fold) in the injured myocardium. Conclusion. These findings are consistent with the hypothesis that the failure of myocardial cells to exclude the dysprosium compound is responsible for the diminished potency of dysprosium to cause MR imaging signal intensity loss in reperfused myocardial infarction. The combination of the two contrast media may define reperfusion of the myocardium at the tissue level (Gadolinium distribution) and the presence and extent of myocardial necrosis (diminished dysprosium effect) in reperfused myocardial infarctions.

Original languageEnglish (US)
Pages (from-to)319-325
Number of pages7
JournalAcademic radiology
Issue number4
StatePublished - 1994
Externally publishedYes


  • Reperfused myocardial infarction
  • contrast media
  • magnetic resonance imaging
  • myocardial cell viability

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging


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