Myocardial strain is a principle for quantification of left ventricular (LV) function which is now feasible with speckle-tracking echocardiography. The best evaluated strain parameter is global longitudinal strain (GLS) which is more sensitive than left ventricular ejection fraction (LVEF) as a measure of systolic function, and may be used to identify sub-clinical LV dysfunction in cardiomyopathies. Furthermore, GLS is recommended as routine measurement in patients undergoing chemotherapy to detect reduction in LV function prior to fall in LVEF. Intersegmental variability in timing of peak myocardial strain has been proposed as predictor of risk of ventricular arrhythmias. Strain imaging may be applied to guide placement of the LV pacing lead in patients receiving cardiac resynchronization therapy. Strain may also be used to diagnose myocardial ischaemia, but the technology is not sufficiently standardized to be recommended as a general tool for this purpose. Peak systolic left atrial strain is a promising supplementary index of LV filling pressure. The strain imaging methodology is still undergoing development, and further clinical trials are needed to determine if clinical decisions based on strain imaging result in better outcome. With this important limitation in mind, strain may be applied clinically as a supplementary diagnostic method.

-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...

Background-Myocardial strain is a measure of regional deformation, and by definition, negative strain means shortening and positive strain, elongation. This study investigates whether myocardial strain can be measured by Doppler echocardiography as the time integral of regional velocity gradients, using sonomicrometry as reference method. Methods and Results-In 13 anesthetized dogs, myocardial longitudinal strain was measured on apical images as the time integral of regional Doppler velocity gradients. Ultrasonic segment-length crystals were placed near the left ventricular (LV) apex and near the base. Apical ischemia was induced by occluding the left anterior descending coronary artery (LAD), and preload was increased by saline.

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.