1348869 - T2 Mapping in Acute Infarct Characterization at 0.55 T

Contemporary low magnetic field strength (B0) MR systems aim to enhance imaging availability and accessibility [1]. Myocardial transverse (T2) relaxation time is elevated with edema and inflammation, and quantitative T2 mapping has been used to characterize elevated T2 with acute myocardial infarction (MI) at higher field [2]. The present study assesses feasibility of quantitative T2 mapping in acute MI on a clinical 0.55 T system.

Methods:

Five pigs underwent 90 minute balloon occlusion followed by reperfusion of either the left anterior descending (n = 4) or left circumflex coronary artery (n =1). The animals were imaged at two time points: 5-19 days (n = 5) and 33-34 days (n = 4) post MI on a 0.55 T clinical system (MAGNETOM Free.Max, Siemens Healthcare, Erlangen, Germany), having maximum gradient amplitude and slew rate of 26 mT/m and 45 T/m/s. Prototype cardiac imaging sequences, including breath-held T2 prepared single-shot bSSFP for quantitative myocardial T2 mapping and breath-held inversion recovery prepared segmented bSSFP [3] for late gadolinium enhanced imaging (LGE, acquired post injection of 0.15 mmoL/kg of Gadavist, Bayer Healthcare, Whippany, NJ, USA) were acquired in three short-axis slices. To boost SNR and to account for longer T2 relaxation time at low field, the standard T2 mapping protocol was modified to acquire T2 preparation times of 0, 25, and 60 ms four times, i.e., 12 source images. Representative imaging parameters are listed in Table 1. An AHA 16 segment based mean T2 and full width half maximum percent signal enhancement on LGE were measured in suiteHEART (Neosoft LLC, Pewaukee, WI, USA). The animals were sacrificed at the end of the second imaging time point, and digital photographs of the sliced ex-vivo heart were obtained. Myocardial T2 in the AHA segments were grouped into remote and infarct regions based on LGE results.  

Results:

Figure 1 shows example T2 and LGE images from an animal at the two imaging time points; the corresponding ex-vivo image visually confirms the location and extent of infarct. As shown in Figure 2, myocardial T2 in the infarct regions was significantly elevated compared to remote myocardium at approximately one week (mean T2: 76.3 ± 8.9 vs 63.1 ± 5.4 ms, p < 0.001) and one month post MI (78.3 ± 12.0 vs 63.0 ± 4.8 ms, p< 0.001). LGE burden remained relatively stable over the two imaging points (13.5% at 1 month vs 13.9% at 1 week). Global myocardial T2 was 60.1 ± 1.3 ms in data available from three animals without MI.

Conclusion:

We have demonstrated a quantitative T2 mapping protocol that may be suitable for myocardial evaluation on a low field system with limited gradient performance. The protocol successfully characterized elevated T2 associated with acute infarct in an animal model. Future research studies in human subjects – healthy and with cardiovascular disease - will further serve to establish sensitivity and specificity of quantitative T2 at low field.