Shear Wave Imaging (SWI), a novel ultrasound-based technique, successfully evaluated myocardial stiffness, distinguishing between stiff, non-compliant infarcted wall from softer wall containing stunned myocardium in an ovine model of ischemic cardiomyopathy.

Findings were published in JACC: Cardiovascular Imaging.

As the researchers explained, distinguishing between infarcted and stunned myocardium is “of upmost importance because in [the] clinical setting, it is still challenging to differentiate these 2 types of ischemia only by strain echocardiographic evaluation of the regional active systolic function at rest.”

Continue Reading

SWI works via remote generation of shear waves in soft tissue by acoustic radiation force, combined with ultrasound, ultrafast imaging of shear wave propagation using the same ultrasonic transducer.

SWI was performed in 10 open-chest sheep (stunned group: n=5; infarcted group: n= 5). To induce acute myocardial ischemia, researchers performed ligation of a diagonal of the left anterior descending coronary artery in both groups—the stunned group for 15 minutes and the infarcted group for 2 hours, both of which were followed by a 40-minute reperfusion period.

Simultaneously, a pressure catheter and sonomicrometers measured end-diastolic left-ventricular pressure and segmental strain during transient caval occlusions in order to obtain “gold standard evaluation” of myocardial stiffness using the end-diastolic strain-stress relationship (EDSSR).

SWI measured diastolic myocardial stiffness at rest, during ischemia, and after reperfusion.

Both groups experienced a drastic reduction of end-systolic circumferential strain during ischemia (infarcted group: 1.3% ± 1.6% vs 14.2% ± 1.2% and stunned group: 1.9% ± 1.8% vs 13.5% ± 3.0%; P<.01). In the infarcted group, SWI diastolic stiffness increased from 1.7 ± 0.4 kPa to 6.2 ± 2.2 kPa (P<.05) 2 hours after ischemia, but not in the stunned group (after 15 minutes; 2.1 ± 0.6 kPa). The infarcted group experienced an even bigger increase after reperfusion (12.1 ± 4.2 kPa; P<.01).

During reperfusion, the infarcted group experienced a reduction in segmental systolic function (1.3% ± 1.7%; P<.01) while the stunned group recovered partial function (6.2% ± 4.7%; P<.01).

The exponential constant coefficient of the EDSSR confirmed diastolic myocardial stiffening, which increased from 8.8 ± 2.3 to 25.7 ± 9.5 (P<.01), although SWI diastolic stiffness did not change in the stunned group (2.3 ± 0.4 kPa vs 1.8 ± 0.3 kPa). This again was confirmed by the exponential constant of the EDSSR (9.7 ± 3.1 vs 10.2 ± 2.3).

“We demonstrated that reperfused infarcted myocardium has markedly increased diastolic myocardial stiffness which persisted after reperfusion,” researchers wrote. “In addition, we showed that stunned myocardium has preserved tissue compliance with no significant change of diastolic myocardial stiffness. As opposed to stiffness regional systolic myocardial function significantly decreased in both groups.”

However, they noted several study limitations, particularly that the open-chest experiment and sonomicrometry crystals may affect myocardial deformation and the choice to use 2 extremes (stunned and infarcted) to validate SWI. “More studies are necessary to relate myocardial stiffness to infarct transmurality,” researchers stated.

Nonetheless, they expect that SWI will be used in a clinical setting in post myocardial infarction for revascularization, following further investigation.


Pernot M, Lee W-N, Bel A, et al. Shear wave imaging of passive diastolic myocardial stiffness: stunned vs infarcted myocardium. JACC Cardiovasc Imag. 2016. doi:10.1016/j.jcmg.2016.01.022.