S. Ourselin, D. Rueckert, and N. Smith (Eds.): FIMH 2013, LNCS 7945, pp. 216–223, 2013. © Springer-Verlag Berlin Heidelberg 2013 Changes in In Vivo Myocardial Tissue Properties Due to Heart Failure Vicky Y. Wang 1 , Alistair A. Young 1,2 , Brett R. Cowan 3 , and Martyn P. Nash 1,4 1 Auckland Bioengineering Institute, University of Auckland, New Zealand {vicky.wang,a.young,martyn.nash}@auckland.ac.nz 2 Department of Anatomy and Radiology, University of Auckland, New Zealand 3 Centre for Advanced MRI, University of Auckland, New Zealand {b.cowan}@auckland.ac.nz 4 Department of Engineering Science, University of Auckland, New Zealand Abstract. A clinical image data driven mechanics analysis was used to quantify changes in tissue-specific passive and contractile material properties for groups of normal and HF patients. We have developed an automated mechanics modelling framework to firstly construct left ventricular (LV) mechanics models based on shape information derived from non-invasive dynamic magnetic resonance images, then to characterise passive tissue stiffness and maximum contractile stress by matching the simulated LV mechanics with data from the dynamic cardiac images. Preliminary statistical analysis revealed that patients with hypertrophy or non-ischemic heart failure exhibited increased passive myocardial stiffness compared to the normals. Elevated maximum contractile stress was also observed for hypertrophic patients. Tissue-specific parameter estimation analysis of this kind can potentially be applied in the clinical setting to provide a more specific disease measure to assist with stratification of HF patients. Keywords: In vivo passive myocardial stiffness, in vivo maximal active myocardial stress, hypertrophy, non-ischemic heart failure. 1 Introduction More than half of the patients diagnosed with heart failure (HF) exhibit preserved systolic function (i.e. normal ejection fraction, EF). This disease phenotype is commonly termed HF with preserved EF (HFPEF) [1][2] and reflects the impaired relaxation and filling during diastole [3][4]. Patients with HFPEF, often present with concentric left ventricular (LV) hypertrophy. A hypertrophic heart is a result of compensatory remodelling, but eventually becomes incapable of working efficiently. This type of remodelling is characterised by a normal or increased LV wall mass, normal or increased LV wall volume (with exceptions), normal LV end-diastolic (ED) volume, increased LV ED pressure, wall thickness, and a higher wall thickness to radius ratio [5]. At the microscopic level, the diameter of the myocytes is increased