ABSTRACT
The myocardial viability after myocardial infarction was evaluated by intravenous myocardial contrast echocardiography. Intravenous real-time myocardial contrast echocardiography was performed on 18 patients with myocardial infarction before coronary revascularization. Follow-up echocardiography was performed 3 months after coronary revascularization. Segmental wall motion was assessed using 18-segment LV model and classified as normal, hypokinesis, akinesis and dyskinesis. Viable myocardium was defined by evident improvement of segmental wall motion 3 months after coronary revascularization. Myocardial perfusion was assessed by visual interpretation and divided into 3 conditions: homogeneous opacification; partial or reduced opaciflcation or subendocardial contrast defect; contrast defect. The former two conditions were used as the standard to define the viable myocardium. The results showed that 109 abnormal wall motion segments were detected among 18 patients with myocardial infarction, including 47 segments of hypokinesis, 56 segments of akinesis and 6 segments of dyskinesis. The wall motion of 2 segments with hypokinesis before coronary revascularization which showed homogeneous opacification, 14 of 24 segments with hypokinese and 20 of 24 segments with akinese before coronary revascularization which showed partial or reduced opaciflcation or subendocardial contrast defect was improved 3 months after coronary revascularization. In our study, the sensitivity and specificity of evaluation of myocardial viability after myocardial infarction by intravenous real-time myocardial contrast echocardiography were 94.7% and 78.9%, respectively. It was concluded that intravenous real-time myocardial contrast echocardiography could accurately evaluate myocardial viability after myocardial infarction.
ABSTRACT
Speckle tracking imaging (STI) was employed to investigate the effect of right ventricular (RV) volume and pressure overload on left ventricular (LV) rotation and twist in 35 patients with atrial septal defect (ASD), 18 of which with pulmonary hypertension, and 21 healthy subjects serving as controls. The peak rotations of 6 segments at the basal and apical short-axises and the average peak rotation and interval time of the 6 segments in the opposite direction during early systolic phase were measured respectively. LV twist versus time profile was drawn and the peak twist and time to peak twist were calculated. LV ejection fraction (EF) was measured by Biplane Simpson. Compared to ASD patients without pulmonary hypertension and healthy subjects, the peak rotations of posterior, inferior and postsept walls at the basal level were lower (P<0.05), and the average counterclockwise peak rotation of 6 segments at the basal level during early systolic phase was higher (P<0.05), and the average interval time was delayed (P<0.05). LV peak twist was also lower (P<0.05), and had a significant negative correlation with pulmonary arterial systolic pressure (r=-0.57, P=0.001). No significant differences were found in LVEF among the three groups. It was suggested that although RV volume overload due to ASD has no significant effects on LV rotation and twist, LV peak twist is lower in ASD patients with pulmonary hypertension. Thus LV twist may serve as a new indicator of the presence of pulmonary hypertension in ASD patients.
ABSTRACT
This study evaluated the application of quantitative tissue velocity imaging (QTVI) in assessing regional myocardial systolic and diastolic functions in dogs with acute subendocardial ischemia. Animal models of subendocardial ischemia were established by injecting microspheres (about 300 μm in diameter) into the proximal end of left circumflex coronary artery in 11 hybrid dogs through cannulation. Before and after embolization, two-dimensional echocardiography, QTVI and real-time myocardial contrast echocardiography (RT-MCE) via intravenous infusion of self-made microbubbles, were performed, respectively. The systolic segmental wall thickening and subendocardial myocardial longitudinal velocities of risk segments before and after embolization were compared by using paired t analysis. The regional myocardial video intensity versus contrast time could be fitted to an exponential function: y=A-(1-exp-β-t), in which the product of A and β provides a measure of myocardial blood flow. RT-MCE showed that subendocardial normalized A.β was decreased markedly from 0.99±0.19 to 0.35±0.11 (P<0.05) in 28 left ventricular (LV) myocardial segments after embolization, including 6 basal and 9 middle segments of lateral wall (LW), 8 middle segments of posterior wall (PW) and 5 middle segments of inferior wall (IW). However, there was no statistically significant difference in subepicardial layer before and after embolization. Accordingly, the ratio of A.β of subendocardial myocardium to subepicardial myocardium in these segments was significantly decreased from 1.10±0.10 to 0.31±0.07 (P<0.05). Although the systolic wall thickening did not change 5 min after the embolization in these ischemic segments (29%+_3% vs 31%±5%, P>0.05), the longitudinal peak systolic velocities (Vs) and early-diastolic peak velocities (Ve) recorded by QTVI were declined significantly (P<0.05). Moreover, the subendocardial velocity curves during isovolumic relaxation predominantly showed positive waves, whereas they mainly showed negative waves before the embolization. This study demonstrates that QTVI can more sensitively and accurately detect abnormal regional myocardial function and post-systolic systole causedby acute subendocardial ischemia.