BackgroundT2-Weighted (T2W) magnetic resonance imaging (MRI) pulse sequences have been used to detect edema in patients with acute myocardial infarction and differentiate acute from chronic infarction. T2W sequences have suffered from several problems including (i) signal intensity variability caused by phased array coils, (ii) high signal from slow moving ventricular chamber blood that can mimic and mask elevated T2 in sub-endocardial myocardium, (iii) motion artifacts, and (iv) the subjective nature of T2W image interpretation. In this work we demonstrate the advantages of a quantitative T2 mapping technique to accurately and reliably detect regions of edematous myocardial tissue without the limitations of qualitative T2W imaging.MethodsMethods of T2 mapping were evaluated on phantoms; the best of these protocols was then optimized for in vivo imaging. The optimized protocol was used to study the spatial, view-dependent, and inter-subject variability and motion sensitivity in healthy subjects. Using the insights gained from this, the utility of T2 mapping was demonstrated in a porcine model of acute myocardial infarction (AMI) and in three patients with AMI.ResultsT2-prepared SSFP demonstrated greater accuracy in estimating the T2 of phantoms than multi-echo turbo spin echo. The T2 of human myocardium was found to be 52.18 ± 3.4 ms (range: 48.96 ms to 55.67 ms), with variability between subjects unrelated to heart rate. Unlike T2W images, T2 maps did not show any signal variation due to the variable sensitivity of phased array coils and were insensitive to cardiac motion. In the three pigs and three patients with AMI, the T2 of the infarcted region was significantly higher than that of remote myocardium.ConclusionQuantitative T2 mapping addresses the well-known problems associated with T2W imaging of the heart and offers the potential for increased accuracy in the detection of myocardial edema.

OBJECTIVES To evaluate the utility of rapid, quantitative T2 mapping compared with conventional T2-weighted imaging in patients presenting with various forms of acute myocardial infarction. BACKGROUND T2-weighted cardiac magnetic resonance (CMR) identifies myocardial edema before the onset of irreversible ischemic injury and has shown value in risk-stratifying patients with chest pain. Clinical acceptance of T2-weighted CMR has, however, been limited by well-known technical problems associated with existing techniques. T2 quantification has recently been shown to overcome these problems; we hypothesized that T2 measurement in infarcted myocardium versus remote regions versus zones of microvascular obstruction in acute myocardial infarction patients could help reduce uncertainty in interpretation of T2-weighted images. METHODS T2 values using a novel mapping technique were prospectively recorded in 16 myocardial segments in 27 patients admitted with acute myocardial infarction. Regional T2 values were averaged in the infarct zone and remote myocardium, both defined by a reviewer blinded to the results of T2 mapping. Myocardial T2 was also measured in a group of 21 healthy volunteers. RESULTS T2 of the infarct zone was 69 ± 6 ms compared with 56 ± 3.4 ms for remote myocardium (p < 0.0001). No difference in T2 was observed between remote myocardium and myocardium of healthy volunteers (56 ± 3.4 ms and 55.5 ± 2.3 ms, respectively, p = NS). T2 mapping allowed for the detection of edematous myocardium in 26 of 27 patients; by comparison, segmented breath-hold T2-weighted short tau inversion recovery images were negative in 7 and uninterpretable in another 2 due to breathing artifacts. Within the infarct zone, areas of microvascular obstruction were characterized by a lower T2 value (59 ± 6 ms) compared with areas with no microvascular obstruction (71.6 ± 10 ms, p < 0.0001). T2 mapping provided consistent high-quality results in patients unable to breath-hold and in those with irregular heart rhythms, in whom short tau inversion recovery often yielded inadequate imaging. CONCLUSIONS Quantitative T2 mapping reliably identifies myocardial edema without the limitations encountered by T2-weighted short tau inversion recovery imaging, and may therefore be clinically more robust in showing acute ischemic injury.

Background T2-weighted cardiac magnetic resonance (CMR) is useful in diagnosing acute inflammatory myocardial diseases such as myocarditis and tako-tsubo cardiomyopathy (TTCM). We hypothesized that quantitative T2 mapping could better delineate myocardial involvement in these disorders vs. T2-weighted imaging. Methods and Results Thirty patients with suspected myocarditis or TTCM referred for CMR who met established diagnostic criteria underwent myocardial T2 mapping. T2 values were averaged in involved and remote myocardial segments, both defined by a reviewer blinded to T2 data. In myocarditis, T2 was 65.2±3.2ms in the involved myocardium vs. 53.5±2.1 in remote myocardium (p<0.001). In TTCM, T2 was 65.6±4.0ms in the involved myocardium vs. 53.6±2.7ms in remote segments (p<0.001). T2 values were similar across remote myocardial segments in patients and all myocardial segments in controls (p>0.05 for all). T2 maps provided diagnostic data even in patients with difficulty breath-holding. A T2 cutoff of 59ms identified areas of myocardial involvement with sensitivity and specificity of 94% and 97%, respectively. T2 mapping revealed regions of abnormal T2 beyond those identified by wall motion abnormalities or LGE-positivity. Conventional T2-weighted short tau inversion recovery (T2W-STIR) images were uninterpretable in 7 patients due to artifact and unremarkable in 2 who had elevated T2 values. T2-prepared steady state free precession (T2p-SSFP) images showed areas of signal hyperintensity in only17/30 patients. Conclusions Quantitative T2 mapping reliably identifies myocardial involvement in patients with myocarditis and TTCM. T2 mapping delineated greater extent of myocardial disease in both conditions compared to that identified by wall motion abnormalities, T2W-STIR, T2p-SSFP or LGE. Quantitative T2 mapping warrants consideration as a robust technique to identify myocardial injury in patients with acute myocarditis or TTCM.

Background— Acute rejection is a major factor impacting survival in the first 12 months after cardiac transplantation. Transplant monitoring requires invasive techniques. Cardiac magnetic resonance (CMR), noninvasive testing, has been used in monitoring heart transplants. Prolonged T2 relaxation has been related to transplant edema and possibly rejection. We hypothesize that prolonged T2 reflects transplant rejection and that quantitative T2 mapping will concur with the pathological and clinical findings of acute rejection. Methods and Results— Patients were recruited within the first year after transplantation. Biopsies were graded according to the International Society for Heart Lung Transplant system for cellular rejection with immunohistochemistry for humoral rejection. Rejection was also considered if patients presented with signs and symptoms of hemodynamic compromise without biopsy evidence of rejection who subsequently improved with treatment. Patients underwent a novel single-shot T2-prepared steady-state free precession 4-chamber and 3 short axis sequences and regions of interest were drawn overlying T2 maps by 2 independent blinded reviewers. A total of 74 (68 analyzable) CMRs T2 maps in 53 patients were performed. There were 4 cellular, 2 humoral, and 2 hemodynamic rejection cases. The average T2 relaxation time for grade 0R (n=46) and grade 1R (n=17) was 52.5±2.2 and 53.1±3.3 ms (mean±SD), respectively. The average T2 relaxation for grade 2R (n=3) was 59.6±3.1 ms and 3R (n=1) was 60.3 ms (all P value <0.05 compared with controls). The T2 average in humoral rejection cases (n=2) was 59.2±3.3 ms and the hemodynamic rejection (n=2) was 61.1±1.8 ms ( P <0.05 versus controls). The average T2 relaxation time for all-cause rejection versus no rejection is 60.1±2.1 versus 52.8±2.7 ms ( P <0.05). All rejection cases were rescanned 2.5 months after treatment and demonstrated T2 normalization with average of 51.4±1.6 ms. No difference was found in ventricular function between nonrejection and rejection patients, except in ventricular mass 107.8±10.3 versus 127.5±10.4 g ( P < 0.05). Conclusions— Quantitative T2 mapping offers a novel noninvasive tool for transplant monitoring, and these initial findings suggest potential use in characterizing rejections. Given the limited numbers, a larger multi-institution study may help elucidate the benefits of T2 mapping as an adjunctive tool in routine monitoring of cardiac transplants.