The role of regional myocardial topography post-myocardial infarction on infarct extension.

Infarct extension involves necrosis of healthy myocardium in the border zone (BZ), progressively enlarging the infarct zone (IZ) and recruiting the remote zone (RZ) into the BZ, eventually leading to heart failure. The mechanisms underlying infarct extension remain unclear, but myocyte stretching has been suggested as the most likely cause. Using human patient-specific left-ventricular (LV) numerical simulations established from cardiac magnetic resonance imaging (MRI) of myocardial infarction (MI) patients, the correlation between infarct extension and regional mechanics abnormality was investigated by analysing the fibre stress-strain loops (FSSLs). FSSL abnormality was characterised using the directional regional external work (DREW) index, which measures FSSL area and loop direction. Sensitivity studies were also performed to investigate the effect of infarct stiffness on regional myocardial mechanics and potential for infarct extension. We found that infarct extension was correlated to severely abnormal FSSL in the form of counter-clockwise loop at the RZ close to the infarct, as indicated by negative DREW values. In regions demonstrating negative DREW values, we observed substantial fibre stretching in the isovolumic relaxation (IVR) phase accompanied by a reduced rate of systolic shortening. Such stretching in IVR phase in part of the RZ was due to its inability to withstand the high LV pressure that was still present and possibly caused by regional myocardial stiffness inhomogeneity. Further analysis revealed that the occurrence of severely abnormal FSSL due to IVR fibre stretching near the RZ-BZ boundary was due to a large amount of surrounding infarcted tissue, or an excessively stiff IZ.

Computational Modelling of the Effect of Infarct Stiffness on Regional Myocardial Mechanics.

Ventricular remodeling after myocardial infarction increases the rate of mortality and is highly associated with the extent of infarct transmurality. It is hypothesized that infarct stiffness alters regional mechanics and affects the likelihood of human ventricular remodeling. However, this is yet to be studied in detail. In this paper, we present simulations from an actively-contracting left ventricular model to investigate the effects of transmural infarct stiffness on myofiber regional mechanics. Results show that higher infarct stiffness reduces systolic stress at the infarct and border zones, minimizing infarct bulging but increasing the diastolic stress at the endocardial border zone. Determining a proper amount of infarct stiffness is required to achieve a balanced regional mechanics across the cardiac cycle that may be useful in therapy, such as myocardial hydrogel injection to adjust its stiffness and reduce stress to prevent ventricular remodeling.

Segmentation of left ventricle in late gadolinium enhanced MRI through 2D-4D registration for infarct localization in 3D patient-specific left ventricular model.

PURPOSE: To evaluate a 2D-4D registration-cum-segmentation framework for the delineation of left ventricle (LV) in late gadolinium enhanced (LGE) MRI and for the localization of infarcts in patient-specific 3D LV models. METHODS: A 3-step framework was proposed, consisting of: (1) 3D LV model reconstruction from motion-corrected 4D cine-MRI; (2) Registration of 2D LGE-MRI with 4D cine-MRI; (3) LV contour extraction from the intersection of LGE slices with the LV model. The framework was evaluated against cardiac MRI data from 27 patients scanned within 6 months after acute myocardial infarction. We compared the use of local Pearson's correlation (LPC) and normalized mutual information (NMI) as similarity measures for the registration. The use of 2 and 6 long-axis (LA) cine-MRI scans was also compared. The accuracy of the framework was evaluated using manual segmentation, and the interobserver variability of the scar volume derived from the segmented LV was determined using Bland-Altman analysis. RESULTS: LPC outperformed NMI as a similarity measure for the proposed framework using 6 LA scans, with Hausdorrf distance (HD) of 1.19 ± 0.53 mm versus 1.51 ± 2.01 mm (endocardial) and 1.21 ± 0.48 mm versus 1.46 ± 1.78 mm (epicardial), respectively. Segmentation using 2 LA scans was comparable to 6 LA scans with a HD of 1.23 ± 0.70 mm (endocardial) and 1.25 ± 0.74 mm (epicardial). The framework yielded a lower interobserver variability in scar volumes compared with manual segmentation. CONCLUSION: The framework showed high accuracy and robustness in delineating LV in LGE-MRI and allowed for bidirectional mapping of information between LGE- and cine-MRI scans, crucial in personalized model studies for treatment planning.

Assessment of infarct-specific cardiac motion dysfunction using modeling and multimodal magnetic resonance merging.

PURPOSE: To propose a cardiac motion tracking model that evaluates wall motion abnormality in postmyocardial infarction patients. Correlation between the motion parameter of the model and left ventricle (LV) function was also determined. MATERIALS AND METHODS: Twelve male patients with post-ST elevation myocardial infarction (post-STEMI) and 10 healthy controls of the same gender were recruited to undergo cardiac magnetic resonance imaging (MRI) using a 1.5T scanner. Using an infarct-specific LV division approach, the late gadolinium enhancement (LGE) MRI images were used to divide the LV on the tagged MRI images into infarct, adjacent, and remote sectors. Motion tracking was performed using the infarct-specific two-parameter empirical deformable model (TPEDM). The match quality was defined as the position error computed using root-mean-square (RMS) distance between the estimated and expert-verified tag intersections. The position errors were compared with the ones from our previously published fixed-sector TPEDM. Cine MRI images were used to calculate regional ejection fraction (REF). Correlation between the end-systolic contraction parameter (αES ) with REF was determined. RESULTS: The position errors in the proposed model were significantly lower than the fixed-sector model (P < 0.01). The median position errors were 0.82 mm versus 1.23 mm. The αES correlates significantly with REF (r = 0.91, P < 0.01). CONCLUSION: The infarct-specific TPEDM combines the morphological and functional information from LGE and tagged MRI images. It was shown to outperform the fixed-sector model in assessing regional LV dysfunction. The significant correlation between αES and REF added prognostic value because it indicated an impairment of cardiac function with the increase of infarct transmurality. LEVEL OF EVIDENCE: 3 J. Magn. Reson. Imaging 2017;45:525-534.

Regional assessment of LV wall in infarcted heart using tagged MRI and cardiac modelling.

A segmental two-parameter empirical deformable model is proposed for evaluating regional motion abnormality of the left ventricle. Short-axis tagged MRI scans were acquired from 10 healthy subjects and 10 postinfarct patients. Two motion parameters, contraction and rotation, were quantified for each cardiac segment by fitting the proposed model using a non-rigid registration algorithm. The accuracy in motion estimation was compared to a global model approach. Motion parameters extracted from patients were correlated to infarct transmurality assessed with delayed-contrast-enhanced MRI. The proposed segmental model allows markedly improved accuracy in regional motion analysis as compared to the global model for both subject groups (1.22-1.40 mm versus 2.31-2.55 mm error). By end-systole, all healthy segments experienced radial displacement by ~25-35% of the epicardial radius, whereas the 3 short-axis planes rotated differently (basal: 3.3°; mid: -1° and apical: -4.6°) to create a twisting motion. While systolic contraction showed clear correspondence to infarct transmurality, rotation was nonspecific to either infarct location or transmurality but could indicate the presence of functional abnormality. Regional contraction and rotation derived using this model could potentially aid in the assessment of severity of regional dysfunction of infarcted myocardium.