Novel Estimation of Left Ventricular Filling Pressure Using 3-D Speckle-Tracking Echocardiography: Assessment in a Decompensated Systolic Heart Failure Model.

E/e' allows for the non-invasive estimation of left ventricular (LV) filling pressure; however, Doppler malalignment can make the estimation unreliable, especially in dilated systolic failing hearts. The ratio of peak early diastolic filling rate to peak early diastolic global strain rate (FRe/SRe), which is a parameter derived from 3-D speckle-tracking echocardiography to estimate filling pressure, may be better applied in dilated systolic failing hearts because it can be obtained without the Doppler method. We investigated whether FRe/SRe could provide a better estimation of filling pressure than E/e' in 23 dogs with decompensated systolic heart failure induced by microembolization. FRe/SRe had better correlation coefficients with LV end-diastolic pressure (0.75-0.90) than did E/e' (0.40). The diagnostic accuracy of FRe/SRe in distinguishing elevated filling pressure was significantly higher than that of E/e'. This study indicates that FRe/SRe may provide a better estimation of LV filling pressure than E/e' in dilated systolic failing hearts.

Noninvasive assessment of intraventricular pressure difference in left ventricular dyssynchrony using vector flow mapping.

Diastolic intraventricular pressure difference (IVPD) reflects left ventricular (LV) diastolic function. The relative pressure imaging (RPI) enables the noninvasive quantification of IVPD based on vector flow mapping (VFM) and visualization of regional pressure distribution. LV dyssynchrony causes deterioration of cardiac performance. However, it remains unclear how IVPD is modulated by LV dyssynchrony. LV dyssynchrony was created in ten open-chest dogs by right ventricular (RV) pacing. The other ten dogs undergoing right atrial (RA) pacing set at the similar heart rate with RV pacing were used as controls. Echocardiographic images were acquired at baseline and during pacing simultaneously with LV pressure measurement by a micromanometer. Pressure difference (ΔP) was computed between the apex and the base of the LV inflow tract during a cardiac cycle by RPI and ΔP during isovolumic relaxation time (ΔPIRT), a parameter of diastolic suction, and that during early filling phase (ΔPE) were measured. During RV pacing, stroke volume (SV) and ΔPIRT decreased significantly, while ΔPE did not change compared to the baseline. During RA pacing, SV, ΔPIRT and ΔPE did not change significantly. ΔPIRT tended to correlate with -dP/dtmin and end-systolic volume, and significantly correlated with ejection fraction. IVPD during isovolumic relaxation time was decreased by LV dyssynchrony, while IVPD during early filling phase was not. A reduction of diastolic suction is observed in LV dyssynchrony and is significantly related to a decrease in SV.

Assessment of Myocardial Ischemic Memory Using Three-Dimensional Speckle-Tracking Echocardiography: A Novel Integrated Analysis of Early Systolic Lengthening and Postsystolic Shortening.

BACKGROUND: Persistence of subtle abnormal myocardial deformation such as postsystolic shortening (PSS) after transient ischemia can be used to diagnose a history of myocardial ischemia (myocardial ischemic memory). Furthermore, early systolic lengthening (ESL) has recently attracted attention as another marker of myocardial ischemia. However, it is unclear whether the persistence of such abnormal deformation can be detected by three-dimensional (3D) speckle-tracking echocardiography, which has relatively low spatial and temporal resolution compared with two-dimensional echocardiography. The aim of this study was to evaluate the diagnostic accuracy of myocardial ischemic memory and its spatial extent using 3D speckle-tracking echocardiography. METHODS: The left circumflex coronary artery was occluded for 2 min, followed by reperfusion, in 33 dogs. Their hemodynamic and 3D echocardiographic data were chronologically acquired. Peak systolic strain, early systolic strain index as a parameter of ESL, postsystolic strain index as a parameter of PSS, and myocardial dysfunction index as a combined parameter of ESL and PSS were analyzed in all left ventricular segments. RESULTS: At the center of the risk area, early systolic strain index and postsystolic strain index significantly increased until 20 min after reperfusion compared with baseline, although peak systolic strain recovered by 20 min. Myocardial dysfunction index significantly increased for >20 min after reperfusion and allowed better diagnostic accuracy of ischemic memory than the other parameters. In the 147 risk segments, abnormal values of myocardial dysfunction index remained in 49 segments (33%) at 20 min after reperfusion, whereas abnormal peak systolic strain was observed in only 13 segments (9%). CONCLUSIONS: ESL and PSS persisted after transient ischemia and could be detected by 3D speckle-tracking echocardiography. Integrated analysis of ESL and PSS provided higher diagnostic accuracy of ischemic memory. This method may be useful for detecting transient ischemic insults in patients after the disappearance of anginal attack.

Assessment of Left Atrial Work During Acute Coronary Occlusion.

Left atrial (LA) work can be measured through speckle tracking echocardiography by calculating LA pressure-strain loop area, which includes two distinct phases of active contraction/relaxation (A-work) and passive dilation/emptying (V-work). Echocardiographic and hemodynamic data were acquired at baseline and during occlusions of left anterior descending (LAD: n = 7) and left circumflex (LCx: n = 9) coronary arteries in dogs. Left ventricular (LV) circumferential strain was decreased and mean LA pressure was increased in both occlusions. Doppler-derived stroke volume was maintained during LAD occlusion, but it decreased during LCx occlusion. A-work increased during LAD occlusion, but it did not change during LCx occlusion. V-work decreased during LCx occlusion more than during LAD occlusion. The compensatory mechanism of LA function was limited during LCx occlusion, but this occurred during LAD occlusion. This study provided insight into a role of LA function in variable hemodynamic consequences in acute myocardial infarction.

Assessment of myocardial ischemic memory using speckle tracking echocardiography.

OBJECTIVES: The aim of this study was to evaluate which regional myocardial parameters derived from speckle tracking echocardiography could demonstrate myocardial ischemic memory in a brief ischemia-reperfusion dog model. BACKGROUND: Myocardial ischemic memory imaging, denoting the visualization of abnormalities provoked by ischemia and sustained even after restoration of perfusion, can convey important clinical information. We previously reported that post-systolic shortening (PSS) remains in the risk area after recovery from brief ischemia. However, it is still unclear whether abnormalities in other regional deformation parameters persist after relief from brief ischemia. METHODS: Echocardiographic data were chronologically acquired from 11 dogs during 2 min of coronary occlusion followed by reperfusion. Regional systolic and diastolic deformation parameters, including parameters related to PSS, were measured from radial and circumferential strain and from strain rate analyzed in the risk and normal areas. Strain imaging diastolic index (SI-DI), which had been proposed as a parameter for assessing ischemic memory, was also calculated. RESULTS: Peak systolic strain, end-systolic strain, and peak systolic strain rate decreased in the risk area during occlusion but recovered to the baseline level immediately after reperfusion. Strain rate during early diastole decreased during occlusion; however, the decrease did not persist after reperfusion. Post-systolic strain index (PSI) and time-to-peak strain index, which are parameters of PSS, increased during occlusion. These increases persisted until 10 to 20 min after reperfusion (circumferential PSI: 0.02 ± 0.04 [baseline] vs. 0.08 ± 0.04 [20 min], p < 0.05). SI-DI did not show a significant change during occlusion because of a large variation. CONCLUSIONS: Although abnormalities of PSS-related parameters alone persisted after recovery from 2-min occlusion, abnormalities of other deformation parameters, such as strain rate during early diastole, did not. These data suggest that assessment of PSS by speckle tracking echocardiography is useful for detecting myocardial ischemic memory.

Assessment of myocardial ischemic memory using persistence of post-systolic thickening after recovery from ischemia.

OBJECTIVES: We sought to investigate the time course of post-systolic thickening (PST) and systolic abnormality after recovery from brief myocardial ischemia. BACKGROUND: Myocardial ischemic memory imaging, denoting the visualization of abnormalities provoked by ischemia and sustained even after restoration of perfusion, is desirable and allows after-the-fact recognition of ischemic insult. PST offers a sensitive marker of myocardial ischemia, but whether this abnormal thickening remains after relief from brief ischemia is unclear. METHODS: Tissue strain echocardiographic data were acquired from 27 dogs under 2 different conditions of myocardial ischemia induced by either brief coronary occlusion (15 or 5 min) followed by reperfusion (Protocol 1) or by dobutamine stress during nonflow-limiting stenosis (Protocol 2). Peak systolic strain and post-systolic strain index (PSI), a parameter of PST, were analyzed. RESULTS: In Protocol 1, peak systolic strain was significantly decreased in the risk area during occlusion. This decrease in peak systolic strain in the 15-min group did not completely recover to baseline levels even 120 min after reperfusion, whereas the decrease in the 5-min group recovered immediately after reperfusion. We found that PSI was significantly increased during occlusion, but increased PSI in the 5-min group remained until 30 min after reperfusion (-0.19 +/- 0.18 [baseline] vs. 0.19 +/- 0.14 [30 min], p < 0.05) despite the rapid recovery of peak systolic strain. In Protocol 2, increased PSI was sustained until 20 min after the end of dobutamine infusion (-0.26 +/- 0.11 [baseline] vs. -0.16 +/- 0.10 [20 min], p < 0.05), although peak systolic strain recovered by 5 min after the end of dobutamine infusion. CONCLUSIONS: PST remained longer than abnormal peak systolic strain after recovery from ischemia. Assessment of PST may be valuable for detecting myocardial ischemic memory.

Assessment of dyssynchronous wall motion during acute myocardial ischemia using velocity vector imaging.

OBJECTIVES: The purpose of this study was to investigate the diagnostic value of velocity vector imaging (VVI) for detecting acute myocardial ischemia and whether VVI can accurately demonstrate the spatial extent of ischemic risk area. BACKGROUND: Using a tracking algorithm, VVI can display velocity vectors of regional wall motion overlaid onto the B-mode image and allows the quantitative assessment of myocardial mechanics. However, its efficacy for diagnosing myocardial ischemia has not been evaluated. METHODS: In 18 dogs with flow-limiting stenosis and/or total occlusion of the coronary artery, peak systolic radial velocity (V(SYS)), radial velocity at mitral valve opening (V(MVO)), peak systolic radial strain, and the percent change in wall thickening (%WT) were measured in the normal and risk areas and compared to those at baseline. Sensitivity and specificity for detecting the stenosis and occlusion were analyzed in each parameter. The area of inward velocity vectors at mitral valve opening (MVO) detected by VVI was compared to the risk area derived from real-time myocardial contrast echocardiography (MCE). Twelve image clips were randomly selected from the baseline, stenosis, and occlusions to determine the intra- and inter-observer agreement for the VVI parameters. RESULTS: The left circumflex coronary flow was reduced by 44.3 +/- 9.0% during stenosis and completely interrupted during occlusion. During coronary artery occlusion, inward motion at MVO was observed in the risk area. Percent WT, peak systolic radial strain, V(SYS), and V(MVO) changed significantly from values at baseline. During stenosis, %WT, peak systolic radial strain, and V(SYS) did not differ from those at baseline; however, V(MVO) was significantly increased (-0.12 +/- 0.60 cm/s vs. -0.96 +/- 0.55 cm/s, p = 0.015). Sensitivity and specificity of V(MVO) for detecting ischemia were superior to those of other parameters. The spatial extent of inward velocity vectors at MVO correlated well with that of the risk area derived from MCE (r = 0.74, p < 0.001 with a linear regression). CONCLUSIONS: The assessment of VVI at MVO permits easy detection of dyssynchronous wall motion during acute myocardial ischemia that cannot be diagnosed by conventional measurement of systolic wall thickness. The spatial extent of inward motion at MVO suggests the size of the risk area.

Quantitative assessment of microcollateral recruitment during coronary occlusion using real-time intravenous myocardial contrast echocardiography.

BACKGROUND: Residual collateral-derived myocardial blood flow (MBF) (A x beta) is important to protect against myocardial ischemia after acute coronary occlusion. METHODS: Recruitment of microcollateral was assessed in 22 dogs with left circumflex coronary artery occlusion by analysis of MBF and regional wall thickening (WT) using real-time myocardial contrast echocardiography. RESULTS: Video intensity and WT at the center of risk area were significantly lower than those at the border of risk area. The video intensity, A value, beta value, and MBF correlated well with WT after left circumflex coronary artery occlusion. The WT of the area with above 25% of normal MBF was preserved and was higher than that at below 25%. However, the deterioration of WT was not distinguished according to A value. CONCLUSION: Real-time myocardial contrast echocardiography is a useful noninvasive method to evaluate collateral-derived MBF, which can be a reliable index of protection against myocardial ischemia.

Noninvasive quantification of regional ventricular function in rats: assessment of serial change and spatial distribution using ultrasound strain analysis.

BACKGROUND: The optimal method for quantitative assessment of regional ventricular function in rats remains unclear. The goal of this study was to investigate the use of ultrasonic strain rate (SR) and strain analysis in evaluating the serial change and spatial distribution of regional contractile function in rats. METHODS: In all, 22 anesthetized rats underwent incremental dobutamine infusion (protocol 1) for assessment of serial change or underwent coronary ligation (protocol 2) for assessment of spatial distribution. For protocol 1, the serial change of systolic SR and strain during dobutamine was measured in the posterior myocardium on the short-axis view, and the systolic strain was compared with the percent change in wall thickening. For protocol 2, the spatial distribution of strain profile was analyzed in normal, peripheral ischemic, and central ischemic regions that were identified by myocardial contrast echocardiography. RESULTS: In protocol 1, the incremental dobutamine infusion resulted in a gradual increase in peak systolic SR. In contrast, peak systolic strain increased with low-dose dobutamine but tended to decrease for higher doses of dobutamine. Further, the serial change of peak systolic strain corresponded to changes in percent change in wall thickening, but the strain values were always lower than percent change in wall thickening. In protocol 2, the strain profile indicated postsystolic thickening in the peripheral ischemic region and indicated systolic wall thinning in the central ischemic region. CONCLUSIONS: Ultrasonic determination of SR and strain is an accurate and noninvasive method of quantitation of the serial change and spatial distribution of regional contractile function in rats.