Diss. (sammanfattning) Umeå : Umeå universitet, 2005. / Härtill 5 uppsatser.

Thesis (M.Med.Sc.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 62-65). Also available in print.

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Hypertension and heart failure are intimately related with the incidence of heart failure among hypertensive subjects between 1% and 2% per year. Structural and functional myocardial abnormalities identified in hypertensive patients contribute to the progression of myocardial dysfunction. Systolic abnormalities in hypertension begin to develop in the early stages of the disease despite normal left ventricular (LV) ejection fraction (EF) and contribute to the progressive deterioration of LV systolic performance. However, these systolic abnormalities are initially not detectable by conventional echocardiographic methods. Speckle tracking echocardiography (STE) is a sensitive quantitative technique for assessing LV function. LV twist is an important contributing factor to the systolic function of the LV in health and disease and may be a better index of systolic function than ejection fraction (EF) in hypertensive patients (HTP). The remodelling process of the left ventricle in hypertension entails a complex interplay between myocyte hypertrophy and dysfunction, with qualitative changes in the extracellular matrix contributing to progressive dysfunction. Adverse LV remodeling in HTP is associated with an imbalance in collagen degradation and may contribute to the remodelling phenotype and systolic dysfunction in hypertension. Increased matrix metalloproteinase-1 (MMP1) levels contribute to development of LV dilatation and failure with higher levels of MMP1 in the myocardium of hypertensive patients with low EF than those with normal EF. Hypertension can cause systolic dysfunction as a consequence of adverse remodelling and LV hypertrophy, but given the multitude of factors involved in LV decompensation mediated by mechanical, neurohormonal and cytokine routes, the exact mechanisms that contribute to the adverse remodelling and EF deterioration are not fully elucidated. LV twist may be a contributing factor to systolic dysfunction independent of other factors, thus, a focus on abnormalities in the cardiac mechanics of twist in the left ventricle may be helpful in understanding the pathogenesis behind the transition from compensated to decompensated heart failure. Furthermore, the changes in the extracellular matrix may account for the varying morphology, EF and LV twist in HTP. The purpose of this thesis was to 1) determine LV twist in healthy adults of different age groups (n=127), 2) evaluate LV twist changes in African HTP with low (EF<50%) and preserved EF (EF ≥ 50%) (n=82) and 3) examine the relationship between LV twist and biomarkers of collagen degradation in HTP with preserved and low EF. Parasternal short-axis images of three consecutive end-expiratory cardiac cycles at LV basal and apical levels were obtained. Apical rotation (AR) and basal rotation (BR) during ejection and instantaneous LV peak systolic twist (net twist, defined as maximal value of instantaneous AR minus BR) were measured. 127 normal subjects were divided into four age groups: 20-29 (n=34); 30-39 (n=33); 40-49 (n=29); and 50-65 (n=31) years. LV twist and markers of collagen turnover (serum concentrations of matrix metalloproteinase -1 (MMP1), tissue inhibitor of MMP1 (TIMP1) and ratio of MMP1:TIMP1) were measured in 82 hypertensive patients, 41 with EF < 50% (HTLEF) and 41 with EF ≥ 50% (HTNEF). Rigid body rotation (RBR) was defined as AR and BR occurring in the same direction. Serum biomarkers were log transformed before analysis. LV twist increased with age in normal subjects. Multivariate linear regression analysis showed age as the main predictor of net LV twist (R2=0.82, P<0.0001) in normal subjects. Net LV twist was lower in HTLEF compared with HTNEF (3.34 + 1.10 vs. 11.70 + 0.67, p < 0.0001). Of 41 HTLEF patients, 28 (68%) had normal twist pattern while 13 (32%) exhibited RBR. The subgroup with RBR showed greater LV dysfunction (EF: 27.9±5.8% vs. 35±7.5%; p=0.005) and more spherical LV geometry (p=0.0009) compared with those who had normal pattern of twist. Log TIMP1, Log MMP1 and Log MMP1:TIMP1 ratio levels were higher in HTLEF compared with HTNEF (12.32 ± 0.25 vs. 11.81 ± 0.13, p<0.0001; 9.08 ± 0.32 vs. 8.00 ± 0.18, p<0.0001; -3.25 ± 0.30 vs. -3.81 ± 0.18, p<0.0001; respectively). There was an inverse correlation between Log MMP1:TIMP1 and net LV twist after adjusting for EF (r = -0.41, p <0.0001). This study established normative data and patterns for myocardial deformation (strain and LV twist) in a normal black-African adult population across different age groups and can be used as a baseline for future studies. Age was the major determinant of increased LV twist in a normal black population. LV twist may be a compensatory mechanism to preserve EF and maintain normal systolic function with advancing age and in hypertension. LV twist varies with the degree of remodeling and systolic function in hypertension. RBR represents a novel assessment of more severe LV remodeling and LV systolic dysfunction in hypertensive patients. Alterations in collagen turnover not only accompanies more adverse remodelling but also contributes to LV twist differences observed between HTLEF and HTNEF patients. The inverse relation between LV twist and loss of myocardial collagen scaffolding suggests that integrity of the extracellular matrix may play an important role in preservation of LV twist. These findings highlight the value of LV twist as a sensitive global parameter of LV systolic myocardial performance. Longitudinal studies assessing LV twist may provide significant value in clinical practice as an early marker for risk stratification in hypertensive patients who may benefit from aggressive medical therapy to prevent LV remodelling and heart failure.

Dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfillment of the requirements for the degree of the Master of Science in Medicine, Johannesburg, 2013 / Cardiac disease is a major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Accurate evaluation of cardiac function is therefore important but difficult with commonly used imaging modalities such as echocardiography being subject to variable load changes in haemodialysis.

Medical ultrasound imaging is widely used to diagnose cardiacdiseases. The recent availability of real time 3D ultrasound posesseveral interesting challenges and opportunities, and the work of thisthesis is devoted to both challenges and opportunities. One of the key benefits of ultrasound imaging is that its images arereal time. This has been challenged with the recent introduction of 3Dimages, where the number of ultrasound beams is squared compared totraditional 2D images. One common way to alleviate this is byreceiving several closely spaced ultrasound beams from each pulsetransmission, which increases acquisition speed but affects the imagequality. Specifically, B-mode images are irregularly sampled and losespatial shift invariance while a bias in the Doppler velocityestimates causes a discontinuity in the velocity estimates in colorflow images. We have found that these artifacts can be reducedsignificantly by interpolation of the beamformed data from overlappingbeams, with the limitation of requiring at least twice the number ofbeamformers. We have also found that valvular regurgitation is one of thecardiac diseases that can benefit greatly from quantification ofseverity using 3D ultrasound. We have devised a modality that useshigh pulse repetition frequency 3D Doppler to isolate thebackscattered signal power from the vena contracta of a regurgitantjet. This measure is calibrated with a narrow reference beam insidethe jet to estimate the cross-sectional area of the vena contracta. Wehave validated this method with computer simulations, with an in vitrostudy and finally in vivo with 27 patients who had mitralregurgitation. We found that the cross-sectional area and regurgitantvolume of the vena contracta could be quantified without bias as long as the orifice was sufficiently large for a calibration beam tofit inside it. The severity of smaller regurgitations will beoverestimated, but this does not pose a clinical problem, as thesepatients can easily be identified by standard 2D Doppler examination and donot typically need further quantification. Finally, we have developed a new, fast 3D ultrasound simulation methodthat can incorporate anisotropic scattering from cardiac muscle cells. This approach is three orders of magnitudefaster than the most commonly used simulation methods, making it wellsuited for the simulation of dynamic 3D images for development and testingof quantitative diagnostic methods such as 3D speckle tracking andvolumetric measurements.

Background: Preliminary observations suggest that aberrations in maternal central hemodynamics and uterine artery Doppler velocimetry reflect the severity of hypertensive disorders of pregnancy. In addition, the precise changes of cardiac output in normal pregnancy, particularly in the third trimester, have remained controversial. Aims and Objective: To measure concomitantly Doppler echocardiographic maternal central hemodynamics and uterine artery Doppler velocimetry and evaluate their association with adverse feto-neonatal outcome in hypertensive pregnant women. To evaluate cardiac output longitudinally in the latter half of pregnancy in normal healthy women. Design and Setting: Prospective study conducted at the Obstetric Unit, King Edward VIII Hospital, Durban, South Africa. Study sample: forty (40) pregnant hypertensives without any prior therapy and a further group of pre-eclamptic women (n=22) treated with stat dose sodium gardinal and alpha-methyldopa were studied. Results: i) A trend to a higher cardiac output was seen in the hypertensives compared to the normotensives. Hypertensive women were of larger stature; there was no difference in cardiac index. Fetal birthweight correlated poorly with cardiac index in pre-eclamptic women (r =0.21). A better correlation was seen with uterine artery resistance index (r = - 0.65) and systemic vascular resistance index (r = -0.49). Critical values for cardiac index and systemic vascular resistance index to predict poor adverse feto-neonatal outcome with good predictive values were not identified. ii) Pre-eclamptics treated with stat dose of sodium gardinal and/or methyldopa prior to echocardiography had a significantly lower systemic vascular resistance index and uterine artery resistance index compared to the untreated group. The lower systemic vascular resistance index in this treated cohort occurred from a combination of non-significant lower blood pressure and higher cardiac index. iii) Compared to normotensive women, untreated pre-eclamptics had a significantly lower heart rate (p< 0.001), a higher stroke index (p=0.018) and no difference in resultant cardiac index (p=0.452). iv) In gestational apoteinuric hypertensives presenting after 34 weeks gestation, maternal hemodynamics and uterine artery resistance index did not help define a higher risk group. v) In chronic hypertensives pregnancies, left ventricular hypertrophy correlated with severity of blood pressure. Higher risk chronic hypertensives were better selected by proteinuria than maternal central hemodynamics or uterine artery resistance index. vi) In normal pregnancy, maternal cardiac output peaked in early to mid third trimester and was maintained till term. Significant correlations were observed among maternal cardiac output, maternal body surface area and fetal birth weight. Discussion: i) This study shows that cardiac index and systemic vascular resistance index measured in the latter part of the second and third trimesters in hypertensive pregnant women were not associated with adverse fetal outcome. Large variations in cardiac index values were observed that restricted detection of satisfactory critical values for cardiac index and systemic vascular resistance index to predict adverse outcome. ii) An improved correlation of uterine artery resistance index with maternal hemodynamics and fetal birthweight in pre-eclampsia supports the hypothesis that poor placentation does not allow for a normal increase in uterine blood flow. iii) The poor correlation between uterine artery resistance index and maternal central hemodynamics, does not support the hypothesis that elevated cardiac output in hypertensive pregnancies (hyperdynamic disease model) occurs as a compensatory response to maintain adequate perfusion in a utero-placental bed with high resistance that did not decrease. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2004.

Increasingly, diagnosis of cardiac disease, relies on computer processing of images to aid decision making. In this thesis, we use echocardiography, which is the most widely used cardiac imaging modality to study the motion of the left ventricle. Currently, clinical reporting of echocardiography examinations is operator-dependent and largely qualitative. Commercially available software does not track the left ven- tricle. Also, it does not provide quantification of regional function. This thesis establishes a framework for the quantitative regional analysis of left ven- tricular function. The endocardial and epicardial contours are automatically tracked during the cardiac cycle. A quantitative measure of regional endocardial wall excur- sion and myocardial thickening, based on a 16-segment model of the heart, is then obtained based on these boundaries. The new tracking framework is based on Kalman filtering which makes a single pre- diction as to the position of the boundary on the next frame. We develop a mea- surement model for the endocardial border, the tissue/blood interface, and the epi- cardium, the tissue/tissue interface. Having tracked the endocardial and epicardial boundaries, we introduce an interpretational space which provides clinically mean- ingful regional quantitative measures of left ventricular function. We illustrate all the concepts on one example. We apply the ideas developed to stress echocardiography, in a small retrospective clinical test.