This study demonstrates that T2-STIR performed up to 1 week after reperfusion can accurately determine myocardium at risk as it was before opening of the occluded artery. CMR can also quantify salvaged myocardium as myocardium at risk minus final infarct size.

BackgroundT2-weighted cardiovascular magnetic resonance (CMR) has been shown to be a promising technique for determination of ischemic myocardium, referred to as myocardium at risk (MaR), after an acute coronary event. Quantification of MaR in T2-weighted CMR has been proposed to be performed by manual delineation or the threshold methods of two standard deviations from remote (2SD), full width half maximum intensity (FWHM) or Otsu. However, manual delineation is subjective and threshold methods have inherent limitations related to threshold definition and lack of a priori information about cardiac anatomy and physiology. Therefore, the aim of this study was to develop an automatic segmentation algorithm for quantification of MaR using anatomical a priori information.MethodsForty-seven patients with first-time acute ST-elevation myocardial infarction underwent T2-weighted CMR within 1 week after admission. Endocardial and epicardial borders of the left ventricle, as well as the hyper enhanced MaR regions were manually delineated by experienced observers and used as reference method. A new automatic segmentation algorithm, called Segment MaR, defines the MaR region as the continuous region most probable of being MaR, by estimating the intensities of normal myocardium and MaR with an expectation maximization algorithm and restricting the MaR region by an a priori model of the maximal extent for the user defined culprit artery. The segmentation by Segment MaR was compared against inter observer variability of manual delineation and the threshold methods of 2SD, FWHM and Otsu.ResultsMaR was 32.9 ± 10.9% of left ventricular mass (LVM) when assessed by the reference observer and 31.0 ± 8.8% of LVM assessed by Segment MaR. The bias and correlation was, -1.9 ± 6.4% of LVM, R = 0.81 (p < 0.001) for Segment MaR, -2.3 ± 4.9%, R = 0.91 (p < 0.001) for inter observer variability of manual delineation, -7.7 ± 11.4%, R = 0.38 (p = 0.008) for 2SD, -21.0 ± 9.9%, R = 0.41 (p = 0.004) for FWHM, and 5.3 ± 9.6%, R = 0.47 (p < 0.001) for Otsu.ConclusionsThere is a good agreement between automatic Segment MaR and manually assessed MaR in T2-weighted CMR. Thus, the proposed algorithm seems to be a promising, objective method for standardized MaR quantification in T2-weighted CMR.

AimsTo determine the myocardial salvage index, the extent of infarction needs to be related to the myocardium at risk (MaR). Thus, the ability to assess both infarct size and MaR is of central clinical and scientific importance. The aim of the present study was to explore the relationship between T2-weighted cardiac magnetic resonance (CMR) and contrast-enhanced steady-state free precession (CE-SSFP) CMR for the determination of MaR in patients with acute myocardial infarction.Methods and resultsTwenty-one prospectively included patients with first-time ST-elevation myocardial infarction underwent CMR 1 week after primary percutaneous coronary intervention. For the assessment of MaR, T2-weighted images were acquired before and CE-SSFP images were acquired after the injection of a gadolinium-based contrast agent. For the assessment of infarct size, late gadolinium enhancement images were acquired. The MaR by T2-weighted imaging and CE-SSFP was 29 ± 11 and 32 ± 12% of the left ventricle, respectively. Thus, the MaR with T2-weighted imaging was slightly smaller than that by CE-SSFP (−3.0 ± 4.0%; P < 0.01). There was a significant correlation between the two MaR measures (r2= 0.89, P < 0.01), independent of the time after contrast agent administration at which the CE-SSFP was commenced (2–8 min).ConclusionThere is a good agreement between the MaR assessed by T2-weighted imaging and that assessed by CE-SSFP in patients with reperfused acute myocardial infarction 1 week after the acute event. Thus, both methods can be used to determine MaR and myocardial salvage at this point in time.