Regional assessment of in vivo myocardial stiffness using 3D magnetic resonance elastography in a porcine model of myocardial infarction.

PURPOSE: The stiffness of a myocardial infarct affects the left ventricular pump function and remodeling. Magnetic resonance elastography (MRE) is a noninvasive imaging technique for measuring soft-tissue stiffness in vivo. The purpose of this study was to investigate the feasibility of assessing in vivo regional myocardial stiffness with high-frequency 3D cardiac MRE in a porcine model of myocardial infarction, and compare the results with ex vivo uniaxial tensile testing. METHODS: Myocardial infarct was induced in a porcine model by embolizing the left circumflex artery. Fourteen days postinfarction, MRE imaging was performed in diastole using an echocardiogram-gated spin-echo echo-planar-imaging sequence with 140-Hz vibrations and 3D MRE processing. The MRE stiffness and tensile modulus from uniaxial testing were compared between the remote and infarcted myocardium. RESULTS: Myocardial infarcts showed increased in vivo MRE stiffness compared with remote myocardium (4.6 ± 0.7 kPa versus 3.0 ± 0.6 kPa, P = 0.02) within the same pig. Ex vivo uniaxial mechanical testing confirmed the in vivo MRE results, showing that myocardial infarcts were stiffer than remote myocardium (650 ± 80 kPa versus 110 ± 20 kPa, P = 0.01). CONCLUSIONS: These results demonstrate the feasibility of assessing in vivo regional myocardial stiffness with high-frequency 3D cardiac MRE. Magn Reson Med 79:361-369, 2018. © 2017 International Society for Magnetic Resonance in Medicine.

Cardiotropin-1 and myocardial strain change heterogeneously in cardiomyopathy.

BACKGROUND: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. MATERIALS AND METHODS: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. RESULTS: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). CONCLUSION: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.