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Background: Both real-time three-dimensional echocardiography (RT3DE) and myocardial contrast echocardiography (MCE) are novel imaging techniques. The purpose of this study was to confirm the feasibility and accuracy of RT3DE combined with MCE for quantitative evaluation of myocardial perfusion defects., Methods: Thirteen dogs underwent ligation of the left anterior descending artery (LAD, n = 6) or distal branch of the left circumflex artery (LCX, n = 7) under general anaesthesia. Three to four ml of a perfluoropropane (C3F8) microbubble contrast agent was injected intravenously to assess the resulting myocardial perfusion defects with a commercially available Philips SONOS-7500 ultrasound system. After removal of the dog hearts, Evans blue dye was injected via the left and right coronary arteries to stain the myocardium at risk. In vitro anatomic measurements of myocardial mass after removal of the animals' hearts were used as controls., Results: Left ventricular (LV) mass determined by RT3DE ranged 36.7 - 68.9 g [mean, (54.6 +/- 9.6) g] before coronary artery ligation, and correlated highly (r = 0.99) with in vitro measurement of LV mass [range, 38.9 - 71.1 g; mean, (55.6 +/- 9.3) g]. There was no significant difference between RT3DE and in vitro measurements of LV mass [range, 36.7 - 68.9 g; mean, (51.3 +/- 12.5) g. Or range, 38.9 - 71.1 g; mean, (53.7 +/- 12.3) g, respectively] and under-perfused mass [range, 0 - 21.4 g; mean, (12.0 +/- 6.9) g. Or range, 0 - 19.8 g; mean, (10.8 +/- 6.3) g, respectively] after the LAD ligation (P > 0.05). Likewise, no significant difference was present between RT3DE and in vitro measurements of LV mass [range, 50.1 - 65.4 g; mean, (57.5 +/- 5.9) g. Or range, 51.5 - 65.8 g; mean, (57.3 +/- 6.4) g, respectively] and under-perfused mass [range, 0 - 25.6 g; mean, (13.3 +/- 9.6) g. Or range, 0 - 22.7 g; mean, (12.8 +/- 8.1) g, respectively] after the LCX ligation (P > 0.05). For all the animals with coronary ligation, LV mass measured by RT3DE ranged 35.9 - 68.6 g [mean, (54.8 +/- 10.0) g] and there was no significant difference between RT3DE and in vitro measurements of LV mass and under-perfused mass (P > 0.05, r = 0.99). Further, the under-perfused mass derived from RT3DE [range, 0 - 25.6 g; mean, (12.7 +/- 8.2) g] correlated strongly with the in vitro measurements [range, 0 - 22.7 g; mean, (11.9 +/- 7.2) g] (r = 0.96)., Conclusion: RT3DE with MCE is a rapid and accurate method for estimating LV myocardial mass and quantifying perfusion defects.

Background: Left ventricular (LV) dysfunction in patients with coronary artery disease is shown by strain and strain rate imaging. However, left atrium (LA) function in patients with coronary artery disease (CAD) has not been assessed by this method. Methods and Results: In 34 CAD patients, including 17 patients with enlarged LA (LA diameter ≤ 4.0 cm) and 17 with normal-size LA (LA diameter ≤ 4.0 cm), two-dimensional strain echocardiographic imaging (2DSE) was performed. Twenty healthy subjects as a control group were included. Both conventional parameters and strain parameters, such as LA peak systolic strain (LAs S/SR), preatrial contraction strain (LAa S), peak systolic (LAs SR), early diastolic strain rate (LAe SR) and late diastolic strain rate (LAa SR), were measured. Conventional parameters were abnormal in CAD patients with enlarged LA (ELA), but there were no significant differences between CAD with normal-size left atrium (NLA) and control groups. LAs S/SR and LAe SR were lower in patients than in normal controls, and were even lower in CAD-ELA group (P < 0.05). LAa S/SR were lower in CAD patients with ELA (P < 0.05), but without a significant difference between CAD-NLA and control groups. A significant correlation was observed between LAs S/SR and LA emptying fraction (r = 0.85, P < 0.05; r = 0.72, P < 0.05, respectively). LAa S/SR related well to LA ejection fraction (r = 0.68, P < 0.05; r = 0.61, P < 0.05, respectively). LAs SR was most accurate in identifying both CAD patients with NLA from controls and CAD patients from controls (area under the curve: 0.91; 0.95, respectively). Conclusions: LA diastolic dysfunction occurs prior to LA systolic dysfunction in CAD patients, and LAs SR is the most accurate index in identifying patients with CAD. (Echocardiography 2011;28:1095-1103) [ABSTRACT FROM AUTHOR]

Abstract Disruption of carotid vulnerable atherosclerotic plaque is responsible for acute ischemic stroke (AIS) and the early detection and intervention approach are greatly limited. Undertaking a microarray of microRNAs (miRNAs) in the plasma of AIS patients with carotid vulnerable plaques, miR-23a-5p was markedly elevated and was positively correlated with the plaque progression and vulnerability. Correspondingly, we found that miR-23a-5p expression was significantly increased in both plasma and macrophages from atherosclerosis mice. Bioinformatics analysis and in vitro knockdown experiments identified that ATP-binding cassette transporter A1/G1 as a novel target of miR-23a-5p. Luciferase reporter assays showed that miR-23a-5p repressed the 3′ untranslated regions (UTR) activity of ABCA1/G1. Moreover, functional analyses demonstrated that transfection of miR-23a-5p inhibitor enhanced cholesterol efflux and decreased foam cell formation through upregulating ABCA1/G1 expression levels. Furthermore, long term in vivo systemically delivered miR-23a-5p antagomir significantly increased ABCA1/G1 expression in the aorta of ApoE−/− mice. Importantly, the miR-23a-5p antagomir therapy significantly reduced atherosclerosis progression and promoted plaque stability. Our observations indicate that miR-23a-5p promotes macrophage-derived foam cell formation and might be a key regulator contributing to atherosclerotic plaque progression and vulnerability. Highlights • miR-23a-5p is significantly elevated in the plasma of patients with vulnerable plaque and is positively correlated with plaque instability. • miR-23a-5p binds to complementary sequences in the 3′ untranslated region of the ABCA1/G1 mRNA, resulting in down-regulation of ABCA1/G1 protein levels and cholesterol efflux in macrophages. • Silencing of miR-23a-5p attenuates atherosclerosis progression and promotes plaque stability in vivo. [ABSTRACT FROM AUTHOR]