Key result
Shear wave imaging identifies infarcted versus stunned myocardium, showing ~7-fold increased stiffness post-reperfusion.
Why the study?
Does shear wave imaging noninvasively quantify passive diastolic myocardial stiffness in an ovine model of ischemic cardiomyopathy?
Does shear wave imaging noninvasively quantify passive diastolic myocardial stiffness in an ovine model of ischemic cardiomyopathy?
Shear wave imaging is a novel noninvasive ultrasound-based technique capable of quantifying passive diastolic myocardial stiffness and discriminating between stunned and irreversibly infarcted myocardium.
Enables stiffness quantification in ovine ischemic injury; leaves open clinical adoption pending human validation.
OBJECTIVES: The aim of this study was to investigate the potential of shear wave imaging (SWI), a novel ultrasound-based technique, to noninvasively quantify passive diastolic myocardial stiffness in an ovine model of ischemic cardiomyopathy. BACKGROUND: Evaluation of diastolic left ventricular function is critical for evaluation of heart failure and ischemic cardiomyopathy. Myocardial stiffness is known to be an important property for the evaluation of the diastolic myocardial function, but this parameter cannot be measured noninvasively by existing techniques. METHODS: SWI was performed in vivo in open-chest procedures in 10 sheep. Ligation of a diagonal of the left anterior descending coronary artery was performed for 15 min (stunned group, n = 5) and 2 h (infarcted group, n = 5). Each procedure was followed by a 40-min reperfusion period. Diastolic myocardial stiffness was measured at rest, during ischemia, and after reperfusion by using noninvasive shear wave imaging. Simultaneously, end-diastolic left ventricular pressure and segmental strain were measured with a pressure catheter and sonomicrometers during transient vena caval occlusions to obtain gold standard evaluation of myocardial stiffness using end-diastolic strain-stress relationship (EDSSR). RESULTS: In both groups, the end-systolic circumferential strain was drastically reduced during ischemia (from 14.2 ± 1.2% to 1.3 ± 1.6% in the infarcted group and from 13.5 ± 3.0% to 1.9 ± 1.8% in the stunned group; p <0.01). SWI diastolic stiffness increased after 2 h of ischemia from 1.7 ± 0.4 to 6.2 ± 2.2 kPa (p < 0.05) and even more after reperfusion (12.1 ± 4.2 kPa; p < 0.01). Diastolic myocardial stiffening was confirmed by the exponential constant coefficient of the EDSSR, which increased from 8.8 ± 2.3 to 25.7 ± 9.5 (p < 0.01). In contrast, SWI diastolic stiffness was unchanged in the stunned group (2.3 ± 0.4 kPa vs 1.8 ± 0.3 kPa, p = NS) which was confirmed also by the exponential constant of EDSSR (9.7 ± 3.1 vs 10.2 ± 2.3, p = NS). CONCLUSIONS: Noninvasive SWI evaluation of diastolic myocardial stiffness can differentiate between stiff, noncompliant infarcted wall and softer wall containing stunned myocardium.
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Pernot et al. (2016) studied Ischemic cardiomyopathy (ovine model) (n=10). Shear Wave Imaging (SWI) vs. Baseline measurements / Sonomicrometry and pressure catheter (gold standard) was evaluated on Passive diastolic myocardial stiffness (SWI ED stiffness) (p=<0.01). Noninvasive shear wave imaging successfully differentiated infarcted myocardium (stiffness increased from 1.7 to 12.1 kPa after reperfusion, p<0.01) from stunned myocardium.
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