Direct T2 quantification of myocardial edema in acute ischemic injury

Abstract

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.

Figure 1. Quantitative T2 in Infarct Zone, Remote and Healthy Control Myocardium

Box plot displays the distribution of quantitative T2 values measured within the infarct zone, remote myocardium, and myocardium of healthy controls. Whisker lengths define the distance between the 25th and the 75th percentiles.

Figure 2. T2 Maps, T2-STIR, and LGE Images in Patients With AMI

(A) A 53-year-old male patient admitted with ST-segment elevation myocardial infarction (STEMI) in the circumflex artery territory. Quantitative T2 in the infarct region was 72 ms compared with 56 ms in remote myocardium. (B) A 75-year-old-male patient presenting with left anterior descending artery territory STEMI. T2 of the infarct zone measured by T2 mapping was 66 ms compared with 51 ms in remote myocardium. (C) Basal short-axis slice in a 58-year-old female patient presenting with non-STEMI in the right coronary artery territory. T2 measured within the region of the infarct was 71 ms compared with 58 ms in remote myocardium. (D) A 62-year-old male patient admitted with a STEMI in the left anterior descending artery territory. Quantitative T2 of the infarcted segments was 73 ms. By T2 mapping, a rim with high signal intensity circumferential to the left ventricle is seen (*), consistent with post-infarct pericardial effusion. The region of infarct is indicated by arrowheads. AMI = acute myocardial infarction; LGE = late gadolinium enhancement; T2-STIR = T2-weighted short tau inversion recovery.

Figure 3. T2 Maps and LGE Images in Circumflex Artery Territory STEMI

Cardiac magnetic resonance was performed in this 51-year-old patient shortly after percutaneous revascularization. With LGE imaging, a large area of microvascular obstruction (red arrows) was observed, which corresponded to relatively low T2 values measured by quantitative T2 analysis. Vertical long-axis (VLA) view: T2 region 1, 57 ms; T2 region 2, 65 ms; T2 region 3, 54 ms. Mid-ventricular short-axis (Mid SAX) view: T2 region 1, 59 ms; T2 region 2, 54 ms. Abbreviations as in Figure 2.

Figure 4. Quantitative T2 in MO and Infarct Tissue Beyond MO

Box plot comparing T2 values observed in areas of microvascular obstruction (MO) and infarct tissue outside the area of MO. Whisker lengths define the distance between the 25th and the 75th percentile. Asterisks indicate outliers.

Figure 5. Matching T2 Maps, T2-STIR, and LGE Images in Patients With AMI and No Obvious Edema by T2-STIR

The region of infarct is indicated by arrowheads. (A) A 62-year-old male patient with non–ST-segment myocardial infarction (NSTEMI) (chest pain and minimally increased troponin I levels on admission). Findings on the coronary angiogram were initially interpreted as negative, but on further review (because of LGE images indicating a small region of infarct scar, [red arrowheads]), a lesion was found at the ostium of the third marginal branch of the right coronary artery. Findings on T2-STIR images were negative, but the T2 maps demonstrated focal tissue edema in the mid-inferolateral segment (T2 = 67 ms), involving the posteromedial papillary muscle. (B) A 60-year-old male patient presenting with NSTEMI; LGE images demonstrated a subendocardial infarct in the circumflex artery territory, corresponding to a focal “hotspot” by T2 mapping (T2 within the infarct = 68 ms). T2-STIR images could not definitively demarcate the area of injury due to subendocardial bright signal caused by stagnant blood. (C) A 45-year-old female patient with STEMI, undergoing percutaneous coronary intervention of the mid-circumflex artery territory shortly after onset of symptoms. Early successful revascularization resulted in the absence of irreversible myocardial injury by LGE 2 days later. T2-STIR images showed no enhancement; T2 maps, however, unequivocally indicated edema in the mid-inferolateral segment (T2 = 69 ms). Abbreviations as in Figure 2.

Figure 6. Bland-Altman Plots of Interobserver T2 Measurement Agreement

Bland-Altman plots for the measurement of quantitative T2 in infarcted myocardium (A), remote myocardium (B), and healthy controls (C), showing good interobserver agreement. Sample size in (C) = 21, with overlapping data causing dots standing for >1 data point.

Figure 7. T2 Maps, T2-STIR, and Single Heartbeat LGE Images Acquired With Free Breathing

This 48-year-old patient with AMI due to thrombotic occlusion of the right coronary artery was allowed to breath freely during the cardiac magnetic resonance examination. T2-STIR images were heavily degraded by motion artifacts, but T2 maps remained diagnostic, showing injury in the inferolateral segments (arrowheads). Quantitative T2 measured in the infarct zone outside the MO area (*) was 67 ms. Mid/apical SAX = mid ventricular/apical short-axis view; 3-Ch = 3-chamber view; other abbreviations as in Figure 2.