Volume 13 Supplement 1

Abstracts of the 2011 SCMR/Euro CMR Joint Scientific Sessions

Open Access

Manganese kinetics demonstrated a double contrast in acute but not in chronic infarction in a mouse model of myocardial ischemia reperfusion

  • Bénédicte MA Delattre1,
  • Vincent Braunersreuther2,
  • Stephany Gardier1,
  • Jean-Noël Hyacinthe1,
  • Lindsey A Crowe1,
  • François Mach2 and
  • Jean-Paul Vallée1
Journal of Cardiovascular Magnetic Resonance201113(Suppl 1):P164

DOI: 10.1186/1532-429X-13-S1-P164

Published: 2 February 2011

In this study we investigated whether Manganese (Mn2+) wash-in kinetics can add new information regarding a myocardial infarct characterization in particular if it can differentiate an acute infarct from a chronic scar.

Manganese (Mn2+) is considered as a specific MRI contrast agent that enters viable cardiomyocytes through calcium pathways. Compared to extracellular Gadolinium based contrast agents, it has the potential to assess cell viability and has already shown its ability to accurately measure infarct size with late enhancement imaging. So far, only information from the wash out phase after recirculation has been used for the detection and characterization of myocardial infarct.

In this study, we used a model of 60min ischemia followed by reperfusion on C57/BL6 mice. MRI exam was performed on a clinical 3T scanner, either 24 hours (n = 10) or 8 days (n =12) after reperfusion (acute and chronic infarct respectively). Mn2+-induced signal intensity (SI) kinetics were measured into three distinct areas, remote, infarction and left ventricular blood pool and compared to ex vivo TTC and Masson’s trichrome.

For both infarction types (acute and chronic) the SI kinetics showed a fast entry of the contrast agent into the blood pool followed by a slower wash-out corresponding to the recirculation phase of Mn2+. The SI into the remote area increased slowly from the start of the Mn2+ infusion to still 45 minutes later when a plateau was reached. We observed fast entry of Mn2+ into acute infarction followed by a recirculation phase that lead to a double contrast between infarction and “remote”, whereas the entry of Mn2+ into chronic infarction was slow and SI stayed lower than in “remote” (see figure 1). As a main hypothesis, extracellular space is largely enhanced in acute infarction due to cell membrane rupture (necrosis) and interstitial edema, whereas scar tissue is densely composed of collagen fibers that reduce the distribution volume of free Mn2+ ions.
Figure 1

Time course of normalized SI after MnCl2 infusion in different areas of the myocardium (remote, infarct and left ventricular blood pool), for mice with acute (left) or chronic (right) infarction. Bold lines are mean SI and thin lines are SEM.

In addition to its ability to depict accurately the infarcted area at late enhancement, Mn2+ is also able to discriminate acute versus chronic injury by the observation of double-contrast wash-in kinetics in a mouse model of ischemia reperfusion.

Authors’ Affiliations

University of Geneva, Geneva University Hospital
Geneva University Hospital


© Delattre et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.