Assessment of left ventricular energy loss using vector flow mapping in patients with stages 1-3 chronic kidney disease.

BACKGROUND: Patients with chronic kidney disease (CKD) experience abnormality of intracardiac blood flow status during early-stages of disease. Left ventricular energy loss (EL) derived from vector flow mapping (VFM) represents fluid energy lost as heat in left ventricle and had been used to detect intracardiac blood flow efficiency. We aimed to evaluate the left ventricular EL in stage 1-3 CKD patients, and explored whether hypertension, a main cardiovascular risk, deteriorate the abnormality of intracardiac blood flow status. METHODS: Transthoracic echocardiography was performed in 41 controls and 48 patients with stages 1-3 CKD. CKD patients consisted a subgroup with no hypertension, a subgroup with well-controlled hypertension and a subgroup with poorly controlled hypertension. The EL were calculated in the left ventricle using VFM analysis from the apical 3-chamber view. Furthermore, the correlation and stepwise multiple regression analysis were used to explore the potential independent predictors of left ventricular EL. RESULTS: Compared with controls, stage 1-3 CKD patients showed increased left ventricular EL during total diastole, late diastole, total systole, isovolumic contraction and ejection. CKD patients with poorly controlled hypertension had higher left ventricular EL compared to the other CKD subgroups. Additionally, the ratio of mitral early filling wave peak velocity and early mitral annular peak velocity on septal side, mitral early filling wave peak velocity, and left ventricular mass index were independent predictors of the diastolic EL; whereas systolic blood pressure and left ventricular mass index were independent predictors of the systolic EL. CONCLUSIONS: Left ventricular EL was a useful echocardiographic parameter to evaluate the impaired intracardiac blood flow efficiency in patients with stages 1-3 CKD. Hypertension was a crucial contributor for intracardiac blood flow abnormality. This study might provide valuable clinical data to discern cardiac dysfunction and reduce the cardiovascular risk in early-stage CKD.

A novel methodology for rat aortic pulse wave velocity assessment by Doppler ultrasound: validation against invasive measurements.

There is still lack of a simple, accurate, and noninvasive method for rat aortic pulse wave velocity (PWV) measurement, especially the transit distance cannot be accurately measured. Thus, we aimed to derive an equation for aortic transit distance as a function of the nose-to-rump length (L) and to test the hypothesis that aortic PWV measured by new equation combined with Doppler ultrasound (the "equation method") may have stronger correlation with invasive measurements than traditional "body surface method." Two-hundred male Sprague-Dawley (SD) rats (age ranged 5-24 wk) were included in protocol 1, and the aortic transit distances were measured postmortem. In protocol 2, heart-femoral PWV and carotid-femoral PWV were measured by equation method (hfPWVE, cfPWVE) and also by traditional body surface method (hfPWVS, cfPWVS) in another 30 young and 28 old rats. These measurements were then validated against invasively measured hfPWVI and cfPWVI from the same animal. Protocol 1 showed that the heart-femoral transit distance could be calculated by 0.6086 × L - 1.6523, and the carotid-femoral transit distance by 0.4614 × L + 1.8335. In protocol 2, in young rats, the Pearson r between hfPWVE, cfPWVE, hfPWVS, and cfPWVS and their corresponding invasive measurement were 0.8962, 0.8509, 0.8387, and 0.7828, respectively (all P < 0.0001). In the old group, the results were 0.8718, 0.7999, 0.8330, and 0.7112, respectively (all P < 0.0001). The hfPWVE and cfPWVE showed better agreement with hfPWVI and cfPWVI and lower intra- and interobserver variability compared with hfPWVS and cfPWVS in both groups. These findings demonstrate that this novel methodology provides a simple and reliable method for rat noninvasive aortic PWV measurement.NEW & NOTEWORTHY First, when measuring aortic PWV in SD rat models, the heart-femoral transit distance can be estimated by 0.6086 × L - 1.6523, and the carotid-femoral distance transit distance can be estimated by 0.4614 × L + 1.8335, where L (in mm) is nose-to-rump length. Second, this novel methodology for aortic PWV measurement was validated with a closer correlation with the invasive measurements than traditional approach in young and old rats. Third, this study provides a simple and reliable method for rat noninvasive aortic PWV measurement.

Annexin V conjugated nanobubbles: A novel ultrasound contrast agent for in vivo assessment of the apoptotic response in cancer therapy.

In vivo assessment of apoptotic response to cancer therapy is believed to be very important for optimizing management of treatment. However, few noninvasive strategies are currently available to monitor the therapeutic response in vivo. Ultrasonography has been used to detect apoptotic cell death in vivo, but a high-frequency transducer is needed. Fortunately, the capability of ultrasound contrast agents (UCAs) to exit the leaky vasculature of tumors enables ultrasound-targeted imaging of molecular events in response to cancer therapy. In this study, we prepared a novel nano-sized UCA, namely, Annexin V-conjugated nanobubbles (AV-NBs, 635.5 ±â€¯25.4 nm). In vitro studies revealed that AV-NBs were relatively stable and highly echogenic. Moreover, these AV-NBs could easily extravasate into the tumor vasculature and recognize the apoptotic cells with high specificity and affinity in tumors sensitive to chemotherapy. Ultrasound imaging results demonstrated that AV-NBs had higher echogenicity and significantly greater enhancement compared with the untargeted control NBs (P < 0.01) inside the tumors after chemotherapy. Taken together, this study provides a promising method to accurately evaluate therapeutic effects at the molecular level to support cancer management.

Assessment of intrahepatic blood flow by Doppler ultrasonography: relationship between the hepatic vein, portal vein, hepatic artery and portal pressure measured intraoperatively in patients with portal hypertension.

BACKGROUND: Abnormality of hepatic vein (HV) waveforms evaluated by Doppler ultrasonography has been widely studied in patients with chronic liver disease. We investigated the correlation between changes in HV waveforms and portal vein velocity (PVVel), the hepatic artery pulsatility index (HAPI), and also the extent of abnormal Doppler HV waveforms expressed as damping index (DI), severity of portal hypertension expressed as Child-Pugh scores and portal pressure (PP) measured directly from patients with portal hypertension (PHT) to evaluate the indicative value of abnormal HV waveforms and discuss the cause of abnormal HV waveform. METHODS: Sixty patients who had been diagnosed with PHT and accepted surgical therapy of portosystemic shunts were investigated. PP was measured intraoperatively. Thirty healthy volunteers with no history of chronic liver disease were enrolled as the control group. HV waveforms were categorized as triphasic, biphasic or monophasic. DI was compared as the quantitative indicator of abnormal HV waveforms. Another two Doppler parameters, PVVel and HAPI were also measured. These Doppler features were compared with PP, Child-Pugh scores and histological changes assessed by liver biopsy. RESULTS: In the patient group, the Doppler flow waveforms in the middle HV were triphasic in 31.6%, biphasic in 46.7%, and monophasic in 21.6% of subjects. These figures were 86.7%, 10.0%, and 3.3%, respectively, in healthy subjects. With the flattening of HV waveforms, the HAPI increased significantly (r = 00.438, p < 0.0001), whereas PVVel decreased significantly (r = -0.44, p <0.0001). Blood flow parameters, HAPI, PVVel and HV-waveform changes showed no significant correlations with Child-Pugh scores. The latter showed a significant correlation with PP (r = 0.589, p = 0.044). Changes of HV waveform and DI significantly correlated with PP (r = 0.579, r = 0.473, p <0.0001), and significant correlation between DI and Child-Pugh scores was observed (r = 0.411, p = 0.001). PP was significantly different with respect to nodule size (p < 0.05), but HV-waveform changes were not significantly correlated with pathological changes. CONCLUSION: In patients with PHT, a monophasic HV waveform indicates higher portal pressure. Furthermore, quantitative indicator DI can reflect both higher portal pressure and more severe liver dysfunction. Flattening of HV waveforms accompanied by an increase in the HAPI and decrease in PVVel support the hypothesis that histological changes reducing HV compliance be the cause of abnormality of Doppler HV waveforms from the hemodynamic angle.

High-resolution echocardiographic assessment of infarct size and cardiac function in mice with myocardial infarction.

BACKGROUND: The aim of this study was to develop a simple and reasonably precise echocardiographic method for the assessment of infarct size (IS) and cardiac dysfunction in mice after myocardial infarction. METHODS: In vivo experiments were performed in C57BL/6J wild-type mice (n = 18) before and 48 hours after left anterior descending coronary artery ligation. Endocardial length-based echocardiographic IS was validated with that by three different histologic measurements. Left ventricular function was evaluated. RESULTS: Excellent agreement was found between endocardial length-based echocardiographic measurement and angle-based histologic measurement of IS (r = 0.82, P < .001), and both methods strongly correlated with Tei index (r = 0.82, P < .001, and r = 0.74, P < .01) and fractional area change (r = -0.61, P < .05, and r = -0.81, P < .001). CONCLUSIONS: Endocardial length-based echocardiographic measurement proved to be a useful method for assessing myocardial IS and is applicable for biomedical and imaging research, and appears particularly promising in studies of left ventricular remodeling after myocardial infarction.

Noninvasive assessment of influence of resistant respiration on blood flow velocities across the cardiac valves in humans--a quantification study by echocardiography.

UNLABELLED: The aim of our study is to quantitatively investigate influence of the intrathoracic pressure change on the four cardiac valves' velocities and further verify a new proposal of the mechanism of respiratory influence on hemodynamics. METHODS: Thirty healthy volunteers with no cardiopulmonary diseases were included. The intrathoracic pressure changes were measured with self-designed device. The velocity across the four cardiac valves during spontaneous respiration and with the intrathoracic pressure change at -4, -8, and -12 mmHg, respectively, were recorded simultaneously with the electrocardiogram and respiratory curve. The respiratory variation indices (RVIs) were calculated. The average RVIs of mitral, aortic, tricuspid, and pulmonary valves were 12.54%, 13.19%; 6.23%, 8.27%; 20.27%, 24.36%; and 6.45%, 7.69% with intrathoracic pressure change at -8 mmHg and -12 mmHg, respectively. All the above parameters have a significant difference from those during spontaneous respiration (P < 0.01 or P < 0.001). We concluded that it might be the respiratory intrathoracic pressure change that causes the change of the velocity across the valves.