Background-Left ventricular (LV) torsion is due to oppositely directed apical and basal rotation and has been proposed as a sensitive marker of LV function. In the present study, we introduce and validate speckle tracking echocardiography (STE) as a method for assessment of LV rotation and torsion. Methods and Results-Apical and basal rotation by STE was measured from short-axis images by automatic frame-to-frame tracking of gray-scale speckle patterns. Rotation was calculated as the average angular displacement of 9 regions relative to the center of a best-fit circle through the same regions. As reference methods we used sonomicrometry in anesthetized dogs during baseline, dobutamine infusion, and apical ischemia, and magnetic resonance imaging (MRI) tagging in healthy humans. In dogs, the mean peak apical rotation was Ϫ3.7Ϯ1.2°(ϮSD) and Ϫ4.1Ϯ1.2°, and basal rotation was 1.9Ϯ1.5°and 2.0Ϯ1.2°by sonomicrometry and STE, respectively. Rotations by both methods increased (PϽ0.001) during dobutamine infusion. Apical rotation by both methods decreased during left anterior descending coronary artery occlusion (PϽ0.007), whereas basal rotation was unchanged. In healthy humans, apical rotation was Ϫ11.6Ϯ3.8°and Ϫ10.9Ϯ3.3°, and basal rotation was 4.

-There is a need for better methods to quantify regional myocardial function. In the present study, we investigated the feasibility of quantifying regional function in terms of a segmental myocardial work index as derived from strain Doppler echocardiography (SDE) and invasive pressure. In 10 anesthetized dogs, we measured left ventricular (LV) pressure by micromanometer and myocardial longitudinal strains by SDE and sonomicrometry. The regional myocardial work index (RMWI) was calculated as the area of the pressure-strain loop. As a reference method for strain, we used sonomicrometry. By convention, the loop area was assigned a positive sign when the pressure-strain coordinates rotated counterclockwise. Measurements were done at baseline and during volume loading and left anterior descending coronary artery (LAD) occlusion, respectively. There was a good correlation between RMWI calculated from strain by SDE and strain by sonomicrometry (y ϭ 0.73x ϩ 0.21, r ϭ 0.82, P Ͻ 0.01). Volume loading caused an increase in RMWI from 1.3 Ϯ 0.2 to 2.2 Ϯ 0.1 kJ/m 3 (P Ͻ 0.05) by SDE and from 1.5 Ϯ 0.3 to 2.7 Ϯ 0.3 kJ/m 3 (P ϭ 0.066) by sonomicrometry. Short-term ischemia (1 min) caused a decrease in RMWI from 1.3 Ϯ 0.2 to 0.3 Ϯ 0.04 kJ/m 3 (P Ͻ 0.05) and from 1.3 Ϯ 0.3 to 0.5 Ϯ 0.2 kJ/m 3 (P Ͻ 0.05) by SDE and sonomicrometry, respectively. In the nonischemic ventricle and during short-term ischemia, the pressure-strain loops rotated counterclockwise, consistent with actively contracting segments. Long-term ischemia (3 h), however, caused the pressure-strain loop to rotate clockwise, consistent with entirely passive segments, and the loop areas became negative, Ϫ0.2 Ϯ 0.1 and Ϫ0.1 Ϯ 0.03 kJ/m 3 (P Ͻ 0.05) by SDE and sonomicrometry, respectively. A RMWI can be estimated by SDE in combination with LV pressure. Furthermore, the orientation of the loop can be used to assess whether the segment is active or passive.sonomicrometry; pressure-strain loop STRAIN DOPPLER ECHOCARDIOGRAPHY (SDE) has been introduced as a new clinical method to measure regional myocardial function (2, 5, 18). As a measure of systolic function, one may use peak systolic strain, recorded either in the LV long axis as shortening strain or in the short axis as thickening strain. However, peak systolic strain is load dependant and therefore may not reflect systolic function when there are changes in loading conditions (18). This is analogous to the problem with load dependency of LV ejection fraction. In the latter case, one may use LV pressure-volume relations to differentiate between load-induced changes in function and changes in intrinsic myocardial contractility. Assessment of regional pressure-dimension loops, however, has not been feasible in clinical studies. In animal models, however, one may analyze regional function from pressure-segment length loops obtained from micromanometers and implanted sonomicrometric crystals (1,3,7,10,14,15,17). Similar to sonomicrometry, SDE provides a continuous measure of changes in regional dimension, and regional press...

Speckle tracking echocardiography provides accurate and angle-independent measurements of LV dimensions and strains and has potential to become a clinical bedside tool for quantifying myocardial strain.

Background-Postsystolic shortening in ischemic myocardium has been proposed as a marker of tissue viability. Our objectives were to determine if postsystolic shortening represents active fiber shortening or passive recoil and if postsystolic shortening may be quantified by strain Doppler echocardiography (SDE). Methods and Results-In 15 anesthetized dogs, we measured left ventricular (LV) pressure, myocardial long-axis strains by SDE, and segment lengths by sonomicrometry before and during LAD stenosis and occlusion. Active contraction was defined as elevated LVP and stress during postsystolic shortening when compared with the fully relaxed ventricle at similar segment lengths. LAD stenosis decreased systolic shortening from 10.4Ϯ1.2% to 5.9Ϯ0.9% (PϽ0.05), whereas postsystolic shortening increased from 1.1Ϯ0.3% to 4.2Ϯ0.7% (PϽ0.05). In hypokinetic and akinetic segments, LV pressure-segment length and LV stress-segment length loop analysis indicated that postsystolic shortening was active. LAD occlusion resulted in dyskinesis, and postsystolic shortening increased additionally to 8.2Ϯ1.0% (PϽ0.05). After 3 to 5 minutes with LAD occlusion, the dyskinetic segment generated no active stress, and the postsystolic shortening was attributable to passive recoil. Elevation of afterload caused hypokinetic segments to become dyskinetic, and postsystolic shortening remained partly active. Postsystolic shortening by SDE correlated well with sonomicrometry (rϭ0.83, PϽ0.01). Conclusions-Postsystolic shortening is a relatively nonspecific feature of ischemic myocardium and may occur in dyskinetic segments by an entirely passive mechanism. However, in segments with systolic hypokinesis or akinesis, postsystolic shortening is a marker of actively contracting myocardium. SDE was able to quantify postsystolic shortening and might represent a clinical method for identifying actively contracting and hence viable myocardium.

This study demonstrates that assessment of regional and global strain at 1.5 h after reperfusion therapy correlates with size and transmural extent of myocardial infarction as determined by contrast-enhanced MRI. The novel global strain parameter is a valuable predictor of the total extent of myocardial infarction and may therefore be an important clinical tool for risk stratification in the acute phase of myocardial infarction.