Background: Cardiac remodelling is a set of cellular, tissue and organ changes that develop as a consequence of various injuries to the heart, such as myocardial infarction (MI). Global remodelling can be assessed by echocardiography, magnetic resonance or computed tomography imaging, however combining information on both cellular and entire organ level is still not possible by currently available imaging techniques. (1, 2) A prominent technique under research is Synchrotron X-ray Phase Contrast Imaging (X-PCI) that can be used for both 3D analysis of whole hearts, as well as cardiomyocytes (CMCs) without tissue processing or destruction. In basic and translational science rodent animal models are frequently used for myocardial ischemia research.

Methods: MI was induced by LAD ligation via a left thoracotomy in an established model of adult (8-11 week-old) Wister rats. The animals were sacrificed after 2 weeks when the hearts were extracted and imaged by X-PCI at TOMCAT beamline (Swiss Light Source, Paul Scherer Institute, Switzerland) using an energy of 20 keV with two different voxel sizes in selected regions of interest. 3D datasets obtained by this technique allowed calculation of ventricular volumes, mass and cavity dimensions, fibre orientation analysis, as well as analysis of individual cardiomyocytes (cross sectional area (CSA) calculation). We quantified global left ventricular (LV) remodelling in 4 post-MI rat hearts, and in a control healthy rat heart. In 2 post-MI hearts, the cardiomyocytes were analysed in the area of the MI (preserved cells adjacent to the fibrotic post-MI myocardium - peri-MI zone), and in the contralateral region (the non-affected myocardium). Cardiomyocytes of corresponding areas were analysed in the healthy heart alike. CSA was expressed as the mean value with standard deviation of measurements of 10 CMCs per area.

Results: Table 1 shows indices of global myocardial remodelling confirming wall thinning and increase in size and mass of the LV in post-MI rat hearts. The results of CSA calculations (Table 1) indicate significant (p<0.001) differences in CSA between peri-MI and non-MI areas of ischemic hearts, as well as compared to the healthy rat, indicating compensatory hypertrophy pronounced in the peri-MI area as opposed to contralateral region.

Conclusion: X-PCI provides results consistent with previous research in the field but obtained by one single technique that proves it valuable for quantifying both global and cellular myocardial remodelling.