Motivation A close association exists between hypertension and arterial stiffness. Whether the increased arterial stiffness seen in hypertensives are due to structural or functional adaptations in the vasculature is uncertain. Hypertension is more common in blacks and they have an increased arterial stiffness and higer stroke prevalence than white populations. Arterial stiffening, or a loss of arterial distensibility, increases the risk for cardiovascular events, including stroke and heart failure, as it increases the afterload on the heart, as well as creating a higher pulsatile load on the microcirculation. The stiffness of the carotid artery is associated with cardiovascular events, like stroke, and all-cause mortality. Furthermore, carotid stiffness is independently associated with stroke, probably because stiffening of the carotid artery may lead to a higher pressure load on the brain. Inflammation, endothelial activation, dyslipidemia, hyperglycemia and health behaviours may also influence hypertension and arterial stiffness. Limited information is availiable on these associations in black South Africans. The high prevalence of hypertension and cardiovascular disease in blacks creates the need for effective prevention and intervention programs in South Africa. Aim We aimed to compare the characteristics of the carotid artery between 5-year sustained hypertensive and normotensive black participants. Furthermore, we aimed to determine whether blood pressure, conventional cardio-metabolic risk factors, markers of inflammation, endothelial activation and measures of health behaviours are related to these carotid characteristics. Methodology This sub-study forms part of the South African leg of the multi-national Prospective Urban and Rural Epidemiology (PURE) study. The participants of the PURE-SA study were from the North West Province of South Africa, and baseline data collection took place in 2005 (N=2010), while follow-up data was collected five years later, in 2010 (N=1288). HIV-free participants who were either hypertensive or normotensive (N=592) for the 5-year period, and who had complete datasets, were included in this sub-study. The study population thus consists of a group of 5-year sustained normotensive (n=241) and hypertensive (n=351) black participants. Anthropometric measurements included height, weight, waist circumference and the calculation of body mass index (BMI). We included several cardiovascular measurements, namely brachial systolic- and diastolic blood pressure, heart rate, central systolic blood pressure, central pulse pressure and the carotid dorsalis-pedis pulse wave velocity. Carotid characteristics included distensibility, intima media thickness, cross sectional wall area, maximum and minimum lumen diameter. Biochemical variables that were determined included HIV status, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, glycated haemoglobin (HbA1c), creatinine clearance, interleukin-6, C-reactive protein, intracellular adhesion-molecule-1 and vascular adhesion molecule-1. Health behaviours were quantified by measuring γ-glutamyltransferase and by self-reported alcohol, tobacco and anti-hypertensive, anti-inflammatory and lipid-lowering medication use. We compared the normotensive and hypertensive groups by using independent t-tests and chi-square tests. The carotid characteristics were plotted according to quartiles of central systolic blood pressure by making use of standard analyses of variance (ANOVA) and the analyses of co-variance (ANCOVA). Pearson correlations done in the normotensive and hypertensive Africans helped to determine covariates for the multiple regression models. We used forward stepwise multiple regression analyses with the carotid characteristics as dependent variables to determine independent associations between variables. Results and Conclusion The cardiovascular measures, including pulse wave velocity, were significantly higher in the hypertensive group (all p≤0.024). The lipid profile, markers of inflammation, endothelial activation and glycaemia, as well as health behaviours, did not differ between the hypertensives and normotensives after adjustments for age, sex, waist circumference, γ-glutamyltransferase, tobacco use and anti-hypertensive medication use. After similar adjustments, all carotid characteristics, except IMT, were significantly different between the groups (all p≤0.008). However, upon additional adjustment for cSBP, significance was lost. The stiffness and functional adaptation seen in this study are not explained by the classic cardio-metabolic risk factors, markers of endothelial activation or health behaviours of the participants. The differences that exist in terms of arterial stiffness between the normotensive and hypertensive groups may be explained by the increased distending pressure in the hypertensive group. Despite their hypertensive status, it seems that there are no structural adaptations in these hypertensive Africans. / MSc (Physiology), North-West University, Potchefstroom Campus, 2015

Motivation A close association exists between hypertension and arterial stiffness. Whether the increased arterial stiffness seen in hypertensives are due to structural or functional adaptations in the vasculature is uncertain. Hypertension is more common in blacks and they have an increased arterial stiffness and higer stroke prevalence than white populations. Arterial stiffening, or a loss of arterial distensibility, increases the risk for cardiovascular events, including stroke and heart failure, as it increases the afterload on the heart, as well as creating a higher pulsatile load on the microcirculation. The stiffness of the carotid artery is associated with cardiovascular events, like stroke, and all-cause mortality. Furthermore, carotid stiffness is independently associated with stroke, probably because stiffening of the carotid artery may lead to a higher pressure load on the brain. Inflammation, endothelial activation, dyslipidemia, hyperglycemia and health behaviours may also influence hypertension and arterial stiffness. Limited information is availiable on these associations in black South Africans. The high prevalence of hypertension and cardiovascular disease in blacks creates the need for effective prevention and intervention programs in South Africa. Aim We aimed to compare the characteristics of the carotid artery between 5-year sustained hypertensive and normotensive black participants. Furthermore, we aimed to determine whether blood pressure, conventional cardio-metabolic risk factors, markers of inflammation, endothelial activation and measures of health behaviours are related to these carotid characteristics. Methodology This sub-study forms part of the South African leg of the multi-national Prospective Urban and Rural Epidemiology (PURE) study. The participants of the PURE-SA study were from the North West Province of South Africa, and baseline data collection took place in 2005 (N=2010), while follow-up data was collected five years later, in 2010 (N=1288). HIV-free participants who were either hypertensive or normotensive (N=592) for the 5-year period, and who had complete datasets, were included in this sub-study. The study population thus consists of a group of 5-year sustained normotensive (n=241) and hypertensive (n=351) black participants. Anthropometric measurements included height, weight, waist circumference and the calculation of body mass index (BMI). We included several cardiovascular measurements, namely brachial systolic- and diastolic blood pressure, heart rate, central systolic blood pressure, central pulse pressure and the carotid dorsalis-pedis pulse wave velocity. Carotid characteristics included distensibility, intima media thickness, cross sectional wall area, maximum and minimum lumen diameter. Biochemical variables that were determined included HIV status, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, glycated haemoglobin (HbA1c), creatinine clearance, interleukin-6, C-reactive protein, intracellular adhesion-molecule-1 and vascular adhesion molecule-1. Health behaviours were quantified by measuring γ-glutamyltransferase and by self-reported alcohol, tobacco and anti-hypertensive, anti-inflammatory and lipid-lowering medication use. We compared the normotensive and hypertensive groups by using independent t-tests and chi-square tests. The carotid characteristics were plotted according to quartiles of central systolic blood pressure by making use of standard analyses of variance (ANOVA) and the analyses of co-variance (ANCOVA). Pearson correlations done in the normotensive and hypertensive Africans helped to determine covariates for the multiple regression models. We used forward stepwise multiple regression analyses with the carotid characteristics as dependent variables to determine independent associations between variables. Results and Conclusion The cardiovascular measures, including pulse wave velocity, were significantly higher in the hypertensive group (all p≤0.024). The lipid profile, markers of inflammation, endothelial activation and glycaemia, as well as health behaviours, did not differ between the hypertensives and normotensives after adjustments for age, sex, waist circumference, γ-glutamyltransferase, tobacco use and anti-hypertensive medication use. After similar adjustments, all carotid characteristics, except IMT, were significantly different between the groups (all p≤0.008). However, upon additional adjustment for cSBP, significance was lost. The stiffness and functional adaptation seen in this study are not explained by the classic cardio-metabolic risk factors, markers of endothelial activation or health behaviours of the participants. The differences that exist in terms of arterial stiffness between the normotensive and hypertensive groups may be explained by the increased distending pressure in the hypertensive group. Despite their hypertensive status, it seems that there are no structural adaptations in these hypertensive Africans. / MSc (Physiology), North-West University, Potchefstroom Campus, 2015

Pulmonary artery hypertension (PAH), which is diagnosed by an abnormal increase of blood pressure in the pulmonary artery, can be a severe disease, leading to heart failure. In recent years, medical imaging, such as echocardiography, magnetic resonance imaging (MRI), and computed tomography (CT), has been widely used due to its non-invasive property. Right pulmonary artery (RPA) wall distensibility derived from CT angiography was reported to serve as a reliabile marker for the diagnosis of PAH. This study presented a robust method for automatic segmentation of artery based on CT angiography. The algorithm can be divided into two steps: generation of initial contour and refinement of edge. In the first step, a series of original images at different cardiac phases were thresholded to retrieve appropriate intensity window of vessels, followed by the determination of initial contours by a series of morphological image processing on the binary images with two simple manual initializations. Initial contours without touching can be taken as the final results of segmentation, when others need further refinement of edge. In the second step, the center of vessel was automatically located by an ellipse fitting method and then the ray casting algorithm was applied to search for possible edge. Disconnected segments of edge will be linked to complete the vessel segmentation. Furthermore, cross-sectional areas of arteries at different cardiac phases can be measured and used to obtain distensibility. In this study, artery wall distensibility of patients and healthy subjects was evaluated on four vessels, including aorta, main pulmonary artery, right and left pulmonary artery. In addition, segmentation results of five subjects were compared with those obtained by manual selection to evaluate the reliability of the proposed method.

Aging is associated with increases in carotid arterial stiffness and this process appears to be accelerated in older adults with diabetes. It is known that older adults with higher levels of physical activity (PA) tend to have lower arterial stiffness values compared to their more sedentary counterparts. Women typically experience an increase in arterial stiffness and cardiovascular events after menopause compared to older men. It is currently unknown whether a greater degree of physical activity modulates vascular aging in individuals with diabetes, and whether sex differences exist. This study examined arterial stiffness estimated from carotid artery ultrasound images and blood pressure data available from the Canadian Longitudinal Study on Aging (CLSA) baseline data set in participants with non-Type 1 diabetes. Arterial stiffness was expressed as carotid artery distensibility, a measure of local arterial stiffness and calculated as the relative change in arterial diameter for a given change in pressure. PA was assessed via the Physical Activity Scale for the Elderly (PASE), a brief and easily scored 12-item survey used to assess usual PA in adults 65 years and older. This study evaluated the association between known cardiovascular disease risk factors/markers and carotid artery distensibility and examined the influence of PA on arterial stiffness. The influence of age and sex, while controlling for known cardiovascular disease risk factors and markers was examined in individuals with non-Type 1 diabetes. There was no main effect of PASE score on arterial distensibility before (P = 0.143) and after (P = 0.998) adjusting for known cardiovascular risk factors and markers, and there were no interactions between PASE and sex, or PASE and age. There was a main effect of age on arterial distensibility in both models (P=<0.001) and there was a main effect of sex on arterial distensibility in the final adjusted model only (P=0.040). These findings suggest that PASE is not predictive of arterial distensibility in older adults with non-Type 1 diabetes, and these results do not differ by age or sex. Follow-up analysis, using longitudinal models is required to further assess the influence of PA on vascular aging. / Thesis / Master of Science (MSc) / It is well-known that aging is associated with increases in arterial stiffness, which is the progressive impairment of the ability of the arteries to respond to changes in blood pressure and flow. Increased arterial stiffness is associated with the development of cardiovascular disease and appears to be accelerated in females and individuals with diabetes. Physical activity has been highlighted as a potential moderator of age-induced arterial stiffening. Healthy and physically active older adults typically display reduced arterial stiffening compared to their more sedentary counterparts, but the extent to which physical activity attenuates vascular stiffening in older adults with diabetes is unclear. Our results, from a cohort of approximately 2000 older Canadians with non-Type 1 diabetes, show that self-report physical activity level does not appear to be associated with arterial stiffness in this population, and these results do not differ by sex. Follow-up analysis should be conducted to assess the impact of physical activity over time on arterial stiffness in this population.

Enquanto há inúmeros trabalhos evidenciando a participação do território arterial na fisiopatologia da Hipertensão Arterial Sistêmica (HAS), pouco ainda se conhece da real participação do território venoso nessa doença. Estudos prévios demonstraram menor complacência venosa até mesmo em pacientes hipertensos limítrofe, e esta alteração não pode ser explicada como sendo apenas conseqüente a alteração do sistema simpático. Acrescidos a estas alterações, foi demonstrada disfunção endotelial no território venoso em pacientes com fatores de risco cardiovascular, incluindo HAS. Entretanto, ainda existem poucas informações sobre a correlação da disfunção endotelial venosa e/ou da capacitância e complacência venosas e seu impacto funcional na HAS. Neste protocolo foram avaliados 27 indivíduos do Grupo Controle (GC) (idade de 36,8±9,2 anos, 13 homens, IMC de 24,6±4,6 Kg/m2) e 31 pacientes do Grupo Hipertenso (GH) (idade de 38,2±10,5 anos, 15 homens e IMC de 26,1±3,1 Kg/m2). Curvas de pressão arterial (PA) foram obtidas de forma não invasiva com o Finometer®, durante 10 minutos de repouso na posição supina (basal) e durante 10minutos em manobra de modulação de volume (Tilt test). Por meio da análise das curvas, foram calculadas variáveis hemodinâmicas [PA sistólica e diastólica (PAS e PAD), freqüência cardíaca (FC), débito cardíaco (DC), índice cardíaco (CI), índice de volume sistólico (SVI) e índice de resistência vascular periférica (PRI)], além de ser realizada a análise espectral da FC (VFC) e da PAS (VPA). A capacitância e complacência venosas do antebraço foram aferidas por meio da pletismografia e a função endotelial venosa pela técnica da veia dorsal da mão (DHV), ambas avaliadas somente no momento basal. Resultados: O padrão hemodinâmico: o GH comparado com o GC apresentou maior PAS e PAD no momento basal (p<0,05). Em resposta ao Tilt test, houve: aumento de FC (p<0,05), diminuição da PAS (p<0,05), do DC (p<0,05), do CI (p<0,05) e do SVI (p<0,05) em ambos os grupos, de semelhante intensidade. Na avaliação da VFC no basal, não se detectou diferença entre os grupos com relação à FC, aos componentes normalizados da VFC (%LF, %HF) e na relação LF/HF (modulação autonômica). Em resposta ao Tilt test, em ambos os Grupos, houve aumento da FC (p<0,05) e da %LF (p<0,05), e queda da %HF (p<0,05), porém o GC apresentou respostas mais exacerbadas comparadas as do GH. Na avaliação da variabilidade da pressão arterial (VPA), observamos que todos os parâmetros foram semelhantes entre os grupos, tanto no basal quanto em reposta ao Tilt test, o mesmo ocorrendo na avaliação da sensibilidade do barorreflexo (ALFA LF). Com relação à capacitância venosa, o GH apresentou uma redução significativa (p<0,05) comparada ao GC nas pressões de oclusão de 30 e 40mmHg [4,8 (3,8-5,7) - 3,6 (2,8-4,6) vs 5,5 (4,8-7,3) - 4,7 (3,8-6,4), respectivamente]. A complacência venosa foi menor no GH. Considerando a função endotelial venosa, detectou-se uma menor venodilatação máxima em resposta a acetilcolina no GH [62,9 (38,3 79,9) vs 81,7 (65,3 99,1)], e similar venodilatação em resposta ao nitroprussiato de sódio, indicando a presença de disfunção endotelial venosa neste Grupo. Não foi possível evidenciar correlações entre diferentes parâmetros: complacência venosa e função endotelial venosa, DC, RVP e componente LF da PAS e nem entre função endotelial venosa com DC e RVP. Pode-se concluir que, na população de hipertensos estudada, há uma coexistência entre disfunção endotelial venosa e menor complacência venosa, porém não se evidenciaram correlações significativas entre estas variáveis, com os métodos utilizados no presente estudo / While there are numerous studies showing the involvement of the arteries in the pathophysiology of systemic arterial hypertension (AH), less is known about the role of the venous system in this disease. Previous studies have demonstrated lower venous compliance in established and borderline hypertensive patients, and this change can not be explained only by an increase in sympathetic activity. It is hypothesized that a lower venous compliance may have an impact on cardiac filling pressures and consequently on blood pressure levels. Furthermore, venous endothelial dysfunction, characterized by a decrease in venous dilation, was detected in patients with AH and with other cardiovascular risk factors. Therefore, we aimed to establish a correlation between venous endothelial dysfunction with venous compliance, and with venous compliance with different hemodynamic parameters. Casuistic and Methods: a total of 31 patients with stage 1 and 2 of AH (HG) (age of 38.2 ± 10.5 years, 15 men and BMI of 26.1 ± 3.1 kg/m2) and 27 normotensive subjects the control group (CG) (age 36.8 ± 9.2 years, 13 men, BMI 24.6 ± 4.6 kg/m2) were evaluated. Curves of blood pressure (BP) were obtained non-invasively with Finometer ® device, and were recorded for 10-minute in both supine (baseline) position and during tilt test maneuver. By analyzing the curves, hemodynamic variables [systolic and diastolic BP (SBP and DBP), heart rate (HR), cardiac output (CO), cardiac index (CI), stroke volume index (SVI) and index vascular resistance (IVS)], and spectral analysis of HR (HRV) and SBP (BPV) were performed. The venous capacitance and compliance of the forearm were measured by plethysmography and venous endothelial function by the technique of dorsal hand vein (DHV), both assessed only at baseline. Results: At baseline, the HG showed a different hemodynamic pattern compared to the CG, with higher SBP and DBP. In response to the tilt test, both groups presented a similar response: an increase in HR (p<0.05) and a decrease in SBP, CO, IC, and of SVI (p<0.05). In the assessment of HRV at baseline, there was no difference between groups for HR, %LF, %HF and LF/HF ratio. In response to Tilt test in both groups both groups showed an increase in HR (p<0.05) and LF% (p<0.05), and a decrease in HF% (p<0.05), but the CG had higher changes compared to HG. All parameters of blood pressure variability and baroreflex sensitivity (ALFA LF) were similar between groups. HG showed a significant reduction (p<0.05) in venous capacitance compared to GC at occlusion pressures of 30 and 40 mmHg [4.8 (3.8 to 5.7) - 3.6 (2, 8 to 4.6) vs 5.5 (4.8 to 7.3) - 4.7 (3.8 to 6.4), respectively]. Venous compliance was lower in HG, and also the venous endothelial function. It was possible to detect a smaller venodilation response to acetylcholine in the HC [62.9 (38.3 to 79.9) vs 81.7 (65.3 to 99.1)], and similar venodilation in response to sodium nitroprusside, indicating the presence of venous endothelial dysfunction in this group. There were no significant correlations between venous endothelial dysfunction with venous compliance, and with venous compliance with different hemodynamic parameters and autonomic parameters. In conclusion, in the hypertensive population studied it was demonstrated the coexistence of venous endothelial dysfunction and reduced venous compliance, but it was not possible to detect significant correlations between those variables with the methods used in the present study

Enquanto há inúmeros trabalhos evidenciando a participação do território arterial na fisiopatologia da Hipertensão Arterial Sistêmica (HAS), pouco ainda se conhece da real participação do território venoso nessa doença. Estudos prévios demonstraram menor complacência venosa até mesmo em pacientes hipertensos limítrofe, e esta alteração não pode ser explicada como sendo apenas conseqüente a alteração do sistema simpático. Acrescidos a estas alterações, foi demonstrada disfunção endotelial no território venoso em pacientes com fatores de risco cardiovascular, incluindo HAS. Entretanto, ainda existem poucas informações sobre a correlação da disfunção endotelial venosa e/ou da capacitância e complacência venosas e seu impacto funcional na HAS. Neste protocolo foram avaliados 27 indivíduos do Grupo Controle (GC) (idade de 36,8±9,2 anos, 13 homens, IMC de 24,6±4,6 Kg/m2) e 31 pacientes do Grupo Hipertenso (GH) (idade de 38,2±10,5 anos, 15 homens e IMC de 26,1±3,1 Kg/m2). Curvas de pressão arterial (PA) foram obtidas de forma não invasiva com o Finometer®, durante 10 minutos de repouso na posição supina (basal) e durante 10minutos em manobra de modulação de volume (Tilt test). Por meio da análise das curvas, foram calculadas variáveis hemodinâmicas [PA sistólica e diastólica (PAS e PAD), freqüência cardíaca (FC), débito cardíaco (DC), índice cardíaco (CI), índice de volume sistólico (SVI) e índice de resistência vascular periférica (PRI)], além de ser realizada a análise espectral da FC (VFC) e da PAS (VPA). A capacitância e complacência venosas do antebraço foram aferidas por meio da pletismografia e a função endotelial venosa pela técnica da veia dorsal da mão (DHV), ambas avaliadas somente no momento basal. Resultados: O padrão hemodinâmico: o GH comparado com o GC apresentou maior PAS e PAD no momento basal (p<0,05). Em resposta ao Tilt test, houve: aumento de FC (p<0,05), diminuição da PAS (p<0,05), do DC (p<0,05), do CI (p<0,05) e do SVI (p<0,05) em ambos os grupos, de semelhante intensidade. Na avaliação da VFC no basal, não se detectou diferença entre os grupos com relação à FC, aos componentes normalizados da VFC (%LF, %HF) e na relação LF/HF (modulação autonômica). Em resposta ao Tilt test, em ambos os Grupos, houve aumento da FC (p<0,05) e da %LF (p<0,05), e queda da %HF (p<0,05), porém o GC apresentou respostas mais exacerbadas comparadas as do GH. Na avaliação da variabilidade da pressão arterial (VPA), observamos que todos os parâmetros foram semelhantes entre os grupos, tanto no basal quanto em reposta ao Tilt test, o mesmo ocorrendo na avaliação da sensibilidade do barorreflexo (ALFA LF). Com relação à capacitância venosa, o GH apresentou uma redução significativa (p<0,05) comparada ao GC nas pressões de oclusão de 30 e 40mmHg [4,8 (3,8-5,7) - 3,6 (2,8-4,6) vs 5,5 (4,8-7,3) - 4,7 (3,8-6,4), respectivamente]. A complacência venosa foi menor no GH. Considerando a função endotelial venosa, detectou-se uma menor venodilatação máxima em resposta a acetilcolina no GH [62,9 (38,3 79,9) vs 81,7 (65,3 99,1)], e similar venodilatação em resposta ao nitroprussiato de sódio, indicando a presença de disfunção endotelial venosa neste Grupo. Não foi possível evidenciar correlações entre diferentes parâmetros: complacência venosa e função endotelial venosa, DC, RVP e componente LF da PAS e nem entre função endotelial venosa com DC e RVP. Pode-se concluir que, na população de hipertensos estudada, há uma coexistência entre disfunção endotelial venosa e menor complacência venosa, porém não se evidenciaram correlações significativas entre estas variáveis, com os métodos utilizados no presente estudo / While there are numerous studies showing the involvement of the arteries in the pathophysiology of systemic arterial hypertension (AH), less is known about the role of the venous system in this disease. Previous studies have demonstrated lower venous compliance in established and borderline hypertensive patients, and this change can not be explained only by an increase in sympathetic activity. It is hypothesized that a lower venous compliance may have an impact on cardiac filling pressures and consequently on blood pressure levels. Furthermore, venous endothelial dysfunction, characterized by a decrease in venous dilation, was detected in patients with AH and with other cardiovascular risk factors. Therefore, we aimed to establish a correlation between venous endothelial dysfunction with venous compliance, and with venous compliance with different hemodynamic parameters. Casuistic and Methods: a total of 31 patients with stage 1 and 2 of AH (HG) (age of 38.2 ± 10.5 years, 15 men and BMI of 26.1 ± 3.1 kg/m2) and 27 normotensive subjects the control group (CG) (age 36.8 ± 9.2 years, 13 men, BMI 24.6 ± 4.6 kg/m2) were evaluated. Curves of blood pressure (BP) were obtained non-invasively with Finometer ® device, and were recorded for 10-minute in both supine (baseline) position and during tilt test maneuver. By analyzing the curves, hemodynamic variables [systolic and diastolic BP (SBP and DBP), heart rate (HR), cardiac output (CO), cardiac index (CI), stroke volume index (SVI) and index vascular resistance (IVS)], and spectral analysis of HR (HRV) and SBP (BPV) were performed. The venous capacitance and compliance of the forearm were measured by plethysmography and venous endothelial function by the technique of dorsal hand vein (DHV), both assessed only at baseline. Results: At baseline, the HG showed a different hemodynamic pattern compared to the CG, with higher SBP and DBP. In response to the tilt test, both groups presented a similar response: an increase in HR (p<0.05) and a decrease in SBP, CO, IC, and of SVI (p<0.05). In the assessment of HRV at baseline, there was no difference between groups for HR, %LF, %HF and LF/HF ratio. In response to Tilt test in both groups both groups showed an increase in HR (p<0.05) and LF% (p<0.05), and a decrease in HF% (p<0.05), but the CG had higher changes compared to HG. All parameters of blood pressure variability and baroreflex sensitivity (ALFA LF) were similar between groups. HG showed a significant reduction (p<0.05) in venous capacitance compared to GC at occlusion pressures of 30 and 40 mmHg [4.8 (3.8 to 5.7) - 3.6 (2, 8 to 4.6) vs 5.5 (4.8 to 7.3) - 4.7 (3.8 to 6.4), respectively]. Venous compliance was lower in HG, and also the venous endothelial function. It was possible to detect a smaller venodilation response to acetylcholine in the HC [62.9 (38.3 to 79.9) vs 81.7 (65.3 to 99.1)], and similar venodilation in response to sodium nitroprusside, indicating the presence of venous endothelial dysfunction in this group. There were no significant correlations between venous endothelial dysfunction with venous compliance, and with venous compliance with different hemodynamic parameters and autonomic parameters. In conclusion, in the hypertensive population studied it was demonstrated the coexistence of venous endothelial dysfunction and reduced venous compliance, but it was not possible to detect significant correlations between those variables with the methods used in the present study

The present series of in vivo experiments in healthy subjects, were performed to investigate wall stiffness in peripheral vessels and how this modality adapts to iterative increments or sustained reductions in local intravascular pressures. Vascular stiffness was measured as changes in arterial and venous diameters, and in arterial flow, during graded increments in distending pressures in the vasculature of an arm or a lower leg. In addition, effects of intravascular pressure elevation on flow characteristics in veins, and on limb pain were elucidated. Arteries and veins were stiffer (i.e. pressure distension was less) in the lower leg than in the arm. The pressure-induced increase in arterial flow was substantially greater in the arm than in the lower leg, indicating a greater stiffness in the arterioles of the lower leg. Prolonged reduction of intravascular pressures in the lower body, induced by 5 wks of sustained horizontal bedrest (BR), decreased stiffness in the leg vasculature. BR increased pressure distension in the tibial artery threefold and in the tibial vein by 86 %. The pressure-induced increase in tibial artery flow was greater post bedrest, indicating reduced stiffness in the arterioles of the lower leg. Intermittent increases of intravascular pressures in one arm (pressure training; PT) during a 5-wk period decreased vascular stiffness. Pressure distension and pressure-induced flow in the brachial artery were reduced by about 50 % by PT. PT reduced pressure distension in arm veins by 30 to 50 %. High intravascular pressures changed venous flow to arterial-like pulsatile patterns, reflecting propagation of pulse waves from the arteries to the veins either via the capillary network or through arteriovenous anastomoses. High vascular pressures induced pain, which was aggravated by BR and attenuated by PT; the results suggest that the pain was predominantly caused by vascular overdistension. In conclusion, vascular wall stiffness constitutes a plastic modality that adapts to meet demands imposed by a change in the prevailing local intravascular pressure. That increased intravascular pressure leads to increased arteriolar wall stiffness supports the notion that local pressure load may serve as a “prime mover” in the development of vascular changes in hypertension. / medicine doktorsexamen QC 20101109

Cerebral palsy (CP) is a disability that impacts a person throughout their lifespan and may place adults with the condition at an increased risk of physical inactivity and cardiovascular disease. Cardiovascular structure and function in adults with CP has not been comprehensively investigated previously. In the current cross-sectional, observational study, endothelial function, carotid distensibility, and arterial stiffness were assessed using flow-mediated dilation (FMD), B-mode ultrasound, and pulse wave velocity (PWV), respectively, in forty adults with CP (age 33.7 ± 12.7 years). The study sample was separated based on whether subjects were community ambulant or community non-ambulant using the Gross Motor Function Classification System (GMFCS). Those in GMFCS I-II were labeled community ambulant (age 31.7 ± 10.4 years) while those in GMFCS III-V were community non-ambulant (age 34.8 ± 13.6 years). Resting arterial stiffness was examined through assessment of central and upper and lower limb peripheral PWV (cPWV, uPWV, lPWV). Carotid intima-media thickness (IMT), a measure of vascular structure, was also quantified using B-mode ultrasound images and a semi-automated edge detection software program. cPWV was calculated using the distance (carotid to femoral using the subtraction method) and time delay between the foot of the carotid waveform and the foot of the femoral waveform. uPWV was calculated from the carotid to radial artery distance (subtracting the distance from the carotid to sternal notch from the carotid to radial distance) and the time delay between the arrival of the foot of each corresponding waveform. lPWV was calculated from the femoral to posterior tibialis artery using the distance between each site and time delay between the arrival of the foot of each corresponding waveform. Physical activity (PA) levels were assessed using Actigraph accelerometry with cut points that had been previously determined in normal adults. Cardiometabolic markers of fasting serum interleukin-6, insulin, glucose, and a lipid panel were analyzed. The non-ambulant group had an increased uPWV (10.2 m/s ± 1.9) compared to the ambulant group (8.28 m/s ± 1.6) (p<0.01) despite no differences in cPWV or lPWV. There were no group differences (p>0.05) in absolute, relative or normalized FMD responses. Both groups also had similar values of carotid IMT and carotid distensibility. No group differences were found in any of the cardiometabolic or inflammatory markers. Moderate-to-vigorous PA (MVPA) levels were greater in the ambulant group (2.4 mins ± 2.1 per hour) compared to the non-ambulant group (0.3 mins ± 0.6 per hour) (p<0.01). Furthermore, sedentary time was greater in the non-ambulant group (57.8 mins ± 1.9 per hour) compared to the ambulant group (51.6 mins ± 4.7 per hour) (p<0.01). Despite differences in PA levels, MVPA was not a significant independent predictor of vascular or metabolic health in this cohort of adults with CP. However, GMFCS level was predictive of both uPWV and resting heart rate. Future research should include adults with CP who are older in age to gain further insight into the potential consequences of an activity-limited lifestyle (specifically in the non-ambulant group) on cardiovascular and metabolic health in this clinical population. / Thesis / Master of Science in Kinesiology

Perivascular adipose (PVAT) has been hypothesized to influence arterial health, where an excess can lead to pathogenesis of atherosclerosis and other arterial pathologies. A novel assessment of carotid PVAT is the use of carotid extra media thickness (EMT) ultrasonography. Currently, there is a lack of research to demonstrate the relationship between carotid EMT and existing measures of arterial health, notably, central pulse wave velocity, and carotid distensibility and intimal media thickness. In the current cross sectional study, 81 participants of younger recreationally active (ages 23.2 ± 2.5 years), younger sedentary (ages 26.4 ± 7.2 years), older healthy (ages 70.3 ± 5.4 years) and older adults with coronary artery disease (CAD) (ages 67.9 ± 8.7 years) were recruited. Resting measures of central arterial stiffness was examined through the assessment of aPWV, while measures of local carotid stiffness were examined through carotid distensibility. Aortic PWV was calculated using an accepted direct distance method (80% of carotid to femoral direct distance) and time difference between the feet of the carotid and femoral waveforms. Carotid intima-media thickness (IMT), a measure of the inner arterial walls, and carotid extra media thickness (EMT), a measure of carotid PVAT, were assessed through B-mode ultrasound images and a semi-automated edge tracking software. Carotid EMT, IMT, and aPWV were significantly greater in older adults than in younger adults (p < 0.05). No difference in carotid EMT was found between younger recreationally active (0.47 ± .08 mm) and sedentary adults (0.46 ± .06 mm). There were also no differences in carotid EMT between the older healthy (0.58 ± .06 mm) and older adults with CAD (0.54 ± 0.08 mm). Carotid EMT was also significantly correlated with age (r =0 .500), waist circumference (r = 0.521), aPWV (r =0.431), carotid distensibility (r = -0.364 and IMT (r = 0.404). Despite significant correlations, carotid EMT was not an independent predictor of aPWV, carotid distensibility and IMT. Because of the lack of predictive power in measures of arterial stiffness and carotid IMT, there is a potential that carotid EMT may be an independent vascular disease marker. Future investigations should involve carotid EMT in longitudinal studies to evaluate the potential marker for a more comprehensive cardiovascular risk assessment. / Thesis / Master of Science (MSc)

<p> Recent evidence suggests that isometric handgrip training improves resting arterial blood pressure (BP) in normotensive and hypertensive individuals, however the mechanisms remain elusive. The purposes of the current investigation were to replicate the finding that 8 weeks of isometric handgrip training (IHG) improve resting BP in persons medicated for hypertension, to determine if training could improve aortic stiffness and to examine the acute cardiovascular response to IHG. Seventeen participants were recruited and familiarized with the laboratory and techniques used. Training consisted of 8 weeks of thrice weekly IHG training sessions using a pre-programmed handgrip dynamometer (4, 2-minute contractions separated by 4 minutes rest). Measurements of resting ABP (assessed by automated oscillometry), aortic stiffness (assessed by simultaneous ultrasound and applanation tonometry), and the acute cardiovascular response (heart rate, blood pressure, rate-pressure product, and cardiac output) were made at baseline and following 8 weeks of IHG training.</p> <p> Following training, there were no differences observed in resting systolic or diastolic systolic blood pressure, resting heart rate or cardiac output. Furthermore, handgrip training did not improve aortic distensibility or reduce stiffness index. The acute responses of heart rate, blood pressure, rate pressure product and cardiac output were not altered with training. In response to an acute bout of IHG there were significant increases seen in heart rate (55±2 to 65±3 BPM, p<0.01), blood pressure (systolic: 137.2±3.7 to 157.1±7.3; diastolic: 77.8±3.4 to 92.2±4.8 mmHg, p<0.01) and rate-pressure product (7369.4±302.0 to 10159.0±666.6 beatsxmmHg/min). Thus isometric handgrip training is a safe modality which does not appear to alter the stiffness of the proximal aorta or generate a significant cardiovascular strain in the acute phase.</p> / Thesis / Master of Science (MSc)