Kasumi Masuda

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.

Energy loss in the left ventricle obtained by vector flow mapping as a new quantitative measure of severity of aortic regurgitation: a combined experimental and clinical study.

AIMS In aortic regurgitation (AR), energy loss (EL) produced by inefficient turbulent flow may be a burden to the heart predicting decompensation. We attempted to quantify EL in AR induced in an acute dog model and in patients with chronic AR using novel echocardiographic method vector flow mapping (VFM). METHODS AND RESULTS In 11 anaesthetized open-chest dogs, AR was induced by distorting the aortic valve with a pigtail catheter, in totally 20 cases. Regurgitant fraction was determined using pulsed Doppler echocardiography, <30% considered mild to moderate (Group 1, n = 11) and ≥30% moderate to severe (Group 2, n = 9). The clinical study consisted of 22 patients with various degrees of AR; 11 mild to moderate (Group 1) and 11 moderate to severe (Group 2), and compared with 12 normals. VFM is based on continuity equation applied to colour Doppler and speckle tracking velocities, acquired from apical long-axis image. EL was calculated frame by frame, averaged from three beats. In the dog study, diastolic EL increased significantly with severity of AR (baseline vs. Group 1 vs. Group 2: 3.8 ± 1.6 vs. 13.0 ± 5.0 vs. 22.4 ± 14.0 [J/(m s)], ANOVA P = 0.0001). Similar to dogs, diastolic EL also increased in humans by the severity of AR (control vs. Group 1 vs. Group 2: 2.8 ± 1.5 vs. 14.3 ± 11.5 vs. 18.6 ± 2.3 [J/(m s)], ANOVA P = 0.001). CONCLUSION VFM provides a promising method to quantify diastolic EL in AR. Diastolic EL increases in AR proportional to its severity. EL may be useful to determine the severity of disease from the aspect of cardiac load.

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.

Effects of mechanical limitation of apical rotation on left ventricular relaxation and end-diastolic pressure.

Left ventricular (LV) twist is thought to play an important role in cardiac function. However, how twist affects systolic or diastolic function is not understood in detail. We acquired apical and basal short-axis images of dogs undergoing open-chest procedures (n = 15) using a GE Vivid 7 at baseline and during the use of an apical suction device (Starfish) to limit apical rotation. We measured LV pressure and stroke volume using a micromanometer-tipped catheter and an ultrasonic flow probe, respectively. Peak radial strain, peak rotation, peak twist, peak systolic twisting rate (TR), peak untwisting rate during isovolumic relaxation period (UR(IVR)), and peak early diastolic untwisting rate after mitral valve opening (UR(E)) were determined using speckle tracking echocardiography. Immobilizing the apex with gentle suction significantly decreased apical rotation (-50 ± 27%) and slightly increased basal rotation, resulting in a significant decrease in twist. The time constant of LV relaxation (τ) was prolonged, and LV end-diastolic pressure increased. TR and UR(IVR) decreased. LV systolic pressure, peak positive and negative first derivative of LV pressure (±dP/dt), stroke volume, radial strain, and UR(E) were not changed. The correlation between τ and UR(IVR) (r = 0.63, P = 0.0006) was stronger than that between peak +dP/dt and TR (r = 0.46, P = 0.01). Diastolic function was impaired with reduced apical rotation and UR(IVR) when the apex of the heart was immobilized using an apical suction device.

Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase.

Afterload mismatch can cause acute decompensation leading to an occurrence of acute heart failure. We investigated how the left atrium (LA) and left ventricle (LV) react to acute increases in afterload using speckle tracking echocardiography (STE). LA strain and volume were obtained by STE in 10 dogs during banding of descending aorta (AoB). Simultaneously, LA pressure was measured by a micromanometer-tipped catheter. LA peak negative strain during LA contraction, strain change during LA relaxation (early reservoir strain), and that during LA dilatation (late reservoir strain) were obtained from LA longitudinal strain-volume curves. From pressure-strain curves, the areas of A-loop and V-loops were computed as the work during active contraction and relaxation (A-work) and that during passive filling and emptying (V-work). AoB increased LV systolic pressure (105 ± 15 vs. 163 ± 12 mmHg, P < 0.01) and mean LA pressure (3.8 ± 1.2 vs. 7.1 ± 2.0 mmHg, P < 0.01). LV global circumferential strain decreased (-18.8 ± 3.5 vs. -13.2 ± 3.5%, P < 0.01), but LV stroke volume was maintained (8.4 ± 2.3 vs. 9.6 ± 3.6 ml). LA peak negative strain (-2.9 ± 2.3 vs. -9.8 ± 4.0%, P < 0.01) and early reservoir strain (4.5 ± 2.1 vs. 7.7 ± 2.4%, P < 0.05) increased by AoB, but late reservoir strain did not change (8.9 ± 3.4 vs. 6.1 ± 3.4%). A-work significantly increased (3.2 ± 2.0 vs. 19.2 ± 15.1 mmHg %, P < 0.01), whereas V-work did not change (13.3 ± 7.1 vs. 13.1 ± 7.7 mmHg %). In conclusion, LA external work during active contraction and relaxation increased as compensation for LV dysfunction during aortic banding. Atrial dysfunction may lead failure of this mechanism and hemodynamic decompensation.

Different implication of elevated B-type natriuretic peptide level in patients with heart failure with preserved ejection fraction and in those with reduced ejection fraction.

There have been no reports that show significant direct relationship between echocardiographic parameters and B‐type natriuretic peptide (BNP) level. This could be due to the heterogeneous pathophysiology of heart failure and a lack of appropriate echocardiographic parameters. We sought to determine the best echocardiographic parameter that described elevated BNP level in patients with heart failure with and without systolic dysfunction.

Mapping of left ventricle wall thickness in mice using 11.7-T magnetic resonance imaging.

BACKGROUND The left ventricle (LV) wall thickness is an important and routinely measured cardiologic parameter. Here we introduce three-dimensional (3D) mapping of LV wall thickness and function using a self-gated magnetic resonance (MR) sequence for ultra-high-field 11.7-T MR cine imaging of mouse hearts. METHODS AND RESULTS Six male C57BL/6-j mice were subjected to 11.7-T MR imaging (MRI). Three standard views-short axis, long axis four-chamber, and long axis two-chamber-and eight consecutive short axis scans from the apex to base were performed for each mouse. The resulting 11 self-gated cine images were used for fast low-angle shot analysis with a navigator echo over an observation period of approximately 35min. The right ventricle (RV) and LV were identified in the short axis and four-chamber views. On 3D color-coded maps, the interventricular septum wall (diastole: 0.94±0.05mm, systole: 1.20±0.09mm) and LV free wall (diastole: 1.07±0.15mm, systole: 1.79±0.11mm) thicknesses were measured. CONCLUSION This 3D wall thickness mapping technique can be used to observe regional wall thickness at the end-diastole and end-systole. Self-gated cine imaging based on ultra-high-field MRI can be used to accurately and easily measure cardiac function and wall thickness in normal mouse hearts. As in the preclinical study, this versatile and simple method will be clinically useful for the high-field-MRI evaluation of cardiac function and wall thickness.

Longitudinal observations of progressive cardiac dysfunction in a cardiomyopathic animal model by self-gated cine imaging based on 11.7-T magnetic resonance imaging

The purpose of this study was to longitudinally assess left ventricular function and wall thickness in a hamster model of cardiomyopathy using 11.7-T magnetic resonance imaging (MRI). MRI were performed for six cardiomyopathic J2N-k hamsters and six J2N-n hamsters at 5, 10, 15, and 20 weeks of age. Echocardiography was also performed at 20 weeks. The ejection fraction (EF) at 15 and 20 weeks of age in J2N-k hamsters showed a significant decrease compared with those in controls. Conversely, the end-systolic and end-diastolic volumes in cardiomyopathic hamsters showed a significant increase compared with those in controls. Moreover, the heart walls of J2N-k hamsters at 15 and 20 weeks were thicker than those of controls at end-systole; however, there were no significant differences at end-diastole. Optical microscopy with Masson’s trichrome staining depicted no fibrosis in the control myocardium, although it showed interstitial fibrosis in the 20-week-old J2N-k cardiomyopathic myocardium. There were no differences in EF and the wall thickness observed on MRI and those observed on echocardiography. These results indicate the presence of systolic dysfunction in cardiomyopathic hamsters. Self-gated cine imaging based on 11.7-T MRI can be used for serial measurements of cardiac function and wall thickness in a cardiomyopathic model.

Application of three-dimensional speckle tracking echocardiography to assess left ventricular regional work using wall tension-regional area loop

Three-dimensional (3-D) speckle tracking echocardiography allows us to track a change in regional endocardial surface area. The change of regional area during a cardiac cycle should be useful for assessing left ventricular regional work. We investigated the feasibility of assessing regional work, calculated as the area within the wall tension-regional area (T-A) loop using 3-D echocardiography. Three-dimensional full-volume images were acquired using 3-D echocardiography (Artida, Toshiba) at baseline and during brief occlusion of the left circumflex coronary artery in eight dogs. Wall tension was calculated according to Laplaces law for a spherical model. Area change ratio (in %) determined by area tracking was transformed into a change of regional area (in cm(2)) by a custom software. We calculated the area within the T-A loop (TAA) in the area under transient ischemia (risk area) and the remote area as regional work and validated the T-A loop method by comparing the global integral of TAA with the total work assessed by the pressure-volume loop. During coronary occlusion, regional work for the risk area significantly decreased (baseline vs. occlusion, 26.8 ± 10.7 vs. 18.4 ± 7.8 mmHg·cm(3); P < 0.05), whereas that for the remote area did not change. The global integral of TAA closely correlated with the total work assessed by the pressure-volume loop (r = 0.91, P < 0.0001). The wall T-A loop reflected regional dysfunction caused by myocardial ischemia. This analysis using 3-D speckle tracking echocardiography might be useful to quantify left ventricular regional work.