T1 mapping and T2 mapping at 3T for quantifying the area-at-risk in reperfused STEMI patients

Abstract

Background: Whether T1-mapping cardiovascular magnetic resonance (CMR) can accurately quantify the area-at-risk (AAR) as delineated by T2 mapping and assess myocardial salvage at 3T in reperfused ST-segment elevation myocardial infarction (STEMI) patients is not known and was investigated in this study.

Methods: 18 STEMI patients underwent CMR at 3T (Siemens Bio-graph mMR) at a median of 5 (4-6) days post primary percutaneous coronary intervention using native T1 (MOLLI) and T2 mapping (WIP #699; Siemens Healthcare, UK). Matching short-axis T1 and T2 maps covering the entire left ventricle (LV) were assessed by two independent observers using manual, Otsu and 2 standard deviation thresholds. Inter- and intra-observer variability, correlation and agreement between the T1 and T2 mapping techniques on a per-slice and per patient basis were assessed.

Results: A total of 125 matching T1 and T2 mapping short-axis slices were available for analysis from 18 patients. The acquisition times were identical for the T1 maps and T2 maps. 18 slices were excluded due to suboptimal image quality. Both mapping sequences were equally prone to susceptibility artifacts in the lateral wall and were equally likely to be affected by microvascular obstruction requiring manual correction. The Otsu thresholding technique performed best in terms of inter- and intra-observer variability for both T1 and T2 mapping CMR. The mean myocardial infarct size was 18.8 ± 9.4 % of the LV. There was no difference in either the mean AAR (32.3 ± 11.5 % of the LV versus 31.6 ± 11.2 % of the LV, P = 0.25) or myocardial salvage index (0.40 ± 0.26 versus 0.39 ± 0.27, P = 0.20) between the T1 and T2 mapping techniques. On a per-slice analysis, there was an excellent correlation between T1 mapping and T2 mapping in the quantification of the AAR with an R(2) of 0.95 (P < 0.001), with no bias (mean ± 2SD: bias 0.0 ± 9.6 %). On a per-patient analysis, the correlation and agreement remained excellent with no bias (R(2) 0.95, P < 0.0001, bias 0.7 ± 5.1 %).

Conclusions: T1 mapping CMR at 3T performed as well as T2 mapping in quantifying the AAR and assessing myocardial salvage in reperfused STEMI patients, thereby providing an alternative CMR measure of the the AAR.

Fig. 1

Matching T1 maps, T2 maps and LGE short axis CMR images from base to apex of a patient presenting with an acute inferior STEMI reperfused by PPCI. Both T1 and T2 maps delineate the AAR (black arrows) and the LGE images show a small subendocardial myocardial infarct (red arrows)

Fig. 2

Representative mid left ventricular short axis T1 maps, T2 maps and LGE short-axis images from three patients demonstrating varying degrees of myocardial salvage. In patient A, both the T1 and T2 maps delineate a large area of myocardial edema in the left anterior descending (LAD) territory (black arrow), corresponding to the AAR, with no significant myocardial infarct on LGE image (red arrow), indicating complete myocardial salvage. In patient B, the T1 and T2 maps again delineate an area of myocardial edema in the LAD territory (black arrow), with a subendocardal myocardial infarct on the LGE image (red arrow), indicating some myocardial salvage. In patient C, the T1 and T2 maps delineate an area of myocardial edema in the right coronary artery territory (black), with a transmural myocardial infarct containing some microvascular obstruction (hypoenhancement on T2 map and LGE images) on the LGE image (red arrow), indicating minimal myocardial salvage

Fig. 3

Performance of three different thresholding techniques for delineating the AAR on T1 and T2 maps. The AAR by the 2 standard deviation (2SD) technique was significantly larger than that delineated by the manual and Otsu thresholding techniques. There was no difference between the manual and Otsu techniques for both T1 and T2 mapping in delineating the AAR. *denotes significant statistical difference with P < 0.001

Fig. 4

Correlation and agreement between T1 and T2 mapping to delineate the AAR. Both on a per-slice (a and b) and per-patient analysis (c and d), there was an excellent correlation and agreement between T1 and T2 mapping technique to delineate the AAR. The interrupted lines in a and c represent reference lines with a slope of 1

Fig. 5

ROC curve showing the diagnostic performance of T1 mapping against T2 mapping to detect acute myocardial necrosis. Both T1 and T2 mapping performed equally well to detect acute myocardial necrosis. The AUC was 0.87 ± 0.02 for T1 and 0.86 ± 0.02 for T2, P = 0.96