{'fraction_non_alphanumeric': 0.041922290388548056, 'fraction_numerical': 0.02283571915473756, 'mean_word_length': 4.953346855983773, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
P2476Non-invasive left ventricular stiffness measurements for assessing diastolic myocardial properties after orthotopic heart transplantation


 
 
 After orthotopic heart transplantation (HTx), allografts undergo characteristic alterations including myocardial fibrosis. These histologic changes contribute to functional impairment, especially to increased passive myocardial stiffness (MS), which is an important pathophysiological determinant of left ventricular diastolic dysfunction (DF). However, the transplanted heart is affected by many factors that make the interpretation of diastolic echocardiographic parameters difficult. Echocardiographic shear wave (SW) elastography is an emerging approach for measuring MS in vivo. Natural SWs occur after mechanical excitation of the myocardium, e.g. after mitral (MVC), and their propagation velocity is directly related to MS, thus providing an opportunity to assess stiffness at end-diastole (ED).
 
 
 
 The aim was to evaluate the relationship between MS and diffuse myocardial fibrosis as mechanism of DF in HTx patients.
 
 
 
 We prospectively enrolled 33 patients (10.3±6.3 years after HTx) that underwent right heart catheterization (all) and CMR (n=18) during their annual check-up. We performed SW elastography in parasternal long axis views of the LV using a fully programmable experimental scanner (HD-PULSE) equipped with a clinical phased array transducer (Samsung Medison P2–5AC) at 1100±250 frames per second. Tissue acceleration maps were extracted from an anatomical M-mode line along the midline of the LV septum. The ED SW propagation velocity was measured as the slope in the M-mode image (Figure A). Right heart catheterization was performed on the same day. HTx patients were assumed to have diastolic dysfunction (DDF) if the pulmonary capillary wedge pressure (PCWP) exceeded 18mmHg (n=9). All other patients were assumed to have normal diastolic function (NDF, n=24). Native T1 and extracellular volume (ECV) were measured to evaluate diffuse myocardial fibrosis.
 
 
 
 Positive correlations were found between SW velocities at ED and PCWP (r=0.61, p<0.001; Figure B), between SW velocities at ED and T1 (r=0.80, p<0.001; Figure D), and between SW velocities at ED and ECV (r=0.66, p=0.004). SW propagation velocities at ED were significantly higher in DDF than in NDF (8.05±1.85 vs. 3.77±1.02 m/s; p<0.001; Figure C), and corresponded to the T1 values (as illustrated in Figure D).
 
 
 
 
 End-diastolic shear wave velocity – as a measurement of passive myocardial stiffness – showed a good correlation with CMR defined myocardial fibrosis. High PCWPs were consistent with the increase in SW velocities, reflecting the fibrous changes in the ventricle. These findings thus suggest that cardiac shear wave elastography has the potential to become a powerful tool for the assessment of diastolic myocardial properties in cardiac transplant recipients.
