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016 Uspio-enhanced CMR comprehensive methodological investigation and application in acute MI
  1. Jakub Lagan1,2,
  2. David Clark1,
  3. Anna Reid1,
  4. Gavin Lewis1,
  5. Josephine Naish2,
  6. James Fildes2,
  7. Andrew Trafford2,
  8. William Critchley2,
  9. Erik B Schelbert3,
  10. Matthias Schmitt1,
  11. Phillip Foden1,
  12. Christopher A Miller1,2
  1. 1University Hospital of South Manchester, UK
  2. 2University of Manchester, UK
  3. 3University of Pittsburgh, UK


Introduction Quantification of active myocardial inflammation may improve diagnosis, guide management and provide trial end-points for novel therapies. Ultrasmall particles of iron oxide (USPIO) are phagocytosed by activated leukocytes and USPIO-enhanced CMR is increasingly used to assess tissue inflammation. We aimed to; 1. Compare T2* imaging with T1 mapping, which is proposed as an alternative for ‘native’ cardiac iron measurement; 2. Determine whether imaging at a single time point post-USPIO is sufficient to detect active accumulation in tissue; 3. Determine whether USPIO signal from infarct and remote zones in acute myocardial infarction (MI) reflects active myocardial accumulation or passive ‘wash-through’ in oedematous myocardium.

Methods Four healthy volunteers and six patients with acute MI underwent 1.5T CMR, including T1 and T2* mapping, before and at multiple time points following 4 mg/kg ferumoxytol.

Results Normalised T2* of spleen, an organ with high active leukocyte activity, dropped post-USPIO and remained low over the study period (Figure 1), with no correlation seen between spleen T2* and blood T1 (rho=−0.43, p=0.875). In comparison, T1 recovery in spleen correlated strongly with T1 recovery in blood (rho=0.924, p<0.001). In healthy myocardium, an organ with low leukocyte activity, T1 and T2*recovery both correlated strongly with blood T1 (rho=0.953, p<0.001; rho=0.935, p<0.001 respectively).

In MI, absolute T2* values dropped and remained significantly lower in infarcted (15 vs 27ms, p<0.001, 22 vs 38 ms, p=0.001) and remote myocardium (21 vs 27ms, p=0.05, 28 vs 38 ms, p=0.024) compared to healthy controls. T2* and T1 recovery curves post-USPIO were significantly different in both infarcted (p=0.028) and remote myocardium (p=0.004; Figures 2).

Conclusions 0T2* is sensitive to active tissue accumulation of USPIO, likely because T2* reflects field gradients, such as those generated by compartmentalised (phagocytosed) USPIO. T1, which is due to short range dipolar interactions that reduce as USPIOs wash-out, simply tracks passive wash-through. T1 is therefore less suitable for detecting active leukocytes. Measuring T2* at a single time point post-USPIO is insufficient to determine tissue accumulation from passive wash-through. USPIO signal from infarct and remote zones in acute MI appears to genuinely reflect active myocardial accumulation, presumably due to phagocytosis by activated leukocytes.

Abstract 016 Figure 1

T1 and T2* in healthy volunteers normalised to baseline values.

Abstract 016 Figure 2

a. T1 and T2* in infarcted myocardium (acute MI patients) standardised to myocardium of healthy controls. b. T1 and T2* in remote myocardium (acute MI patients) standardised to myocardium of healthy controls.

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