Given the current obesity epidemic in tandem with the aging US population, it is imperative to identify methods for reducing cardiovascular disease (CVD) risk that will be efficacious for both sexes. Arterial stiffness (AS) is an independent risk factor for a first cardiovascular event that increases with advancing age and obesity. Previous studies have found that modest weight loss (WL) of 5 to 10 percent successfully reduces AS and other risk factors for CVD. However, it remains unclear whether WL via caloric restriction reduces AS similarly among sexes. We tested the hypothesis that WL via caloric restriction would reduce AS more in men than women because men accumulate more abdominal visceral fat (VF) and lose more with WL compared with women of similar age and adiposity. To test our hypothesis AS was assessed from measurements of pulse wave velocity and ultrasonography of the carotid artery (Ã -SI). Total body and VF were measured using dual energy x-ray absorptiometry and computed tomography scans, respectively. Subjects underwent a 12-week WL intervention. No baseline differences in AS were observed between sexes. However, men were heavier and demonstrated higher levels of VF while women were fatter and had higher levels of abdominal subcutaneous fat. Contrary to our hypothesis both sexes experienced similar decreases in AS with WL despite greater reductions in VF in men. Our findings suggest that VF loss is not the primary mechanism mediating reductions in AS with WL. Future studies are needed to determine the mechanisms of arterial destiffening with WL. / Master of Science

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No description available.

Introdução: A rigidez arterial é um fenômeno complexo caracterizado pela diminuição da complacência vascular frente aos estímulos fisiológicos e patológicos. Semelhantemente a outros fenótipos cardiovasculares, a etiologia da rigidez arterial é modulada por fatores ambientais e genéticos. Levando em consideração a moderada herdabilidade e a característica poligênica do presente fenótipo, torna-se interessante a investigação de marcadores genéticos referentes aos diferentes sistemas envolvidos no remodelamento vascular. Objetivo: Avaliar o impacto dos polimorfismos C242T da subunidade p22phox da NADPH oxidase, G1036C da TXNIP, C609T/T471C da APOE, G1355A da elastina, I/D da ECA e A855G da MMP-9 no fenótipo de rigidez arterial em uma população geral. Métodos: Participaram do estudo 1.663 indivíduos da população geral da cidade de Vitória-ES. O DNA foi extraído a partir de uma amostra de sangue venoso. Posteriormente foram realizadas as genotipagens para as variantes genéticas supracitadas. A rigidez arterial foi avaliada por meio do método da velocidade de onda de pulso (VOP). Resultados: Em relação à VOP, os polimorfismos C242T da subunidade p22phox da NADPH oxidase e G1036C da TXNIP foram signifcativamente associados. Os indivíduos portadores do genótipo TT do polimorfismo C242T da subunidade p22phox (CC+TC=9,8 m/s versus TT=10,1 m/s, p=0,02) e do alelo G do polimorfismo G1036C da TXNIP (CC=9,8 m/s versus CG+GG=10,0 m/s, p=0,03) apresentaram maiores valores da VOP. Entretanto os polimorfismos C609T/T471C da APOE (2=10,0 m/s, 3=9,8 m/s, 4=9,8 m/s, p=0,60), G1355A da elastina (AA=9,8 m/s, GA=9,9 m/s, GG=9,8 m/s, p=0,92), I/D da ECA (DD=9,8 m/s, DI=9,8 m/s, II=9,9 m/s, p=0,53) e A855G da MMP-9 (AA=9,8 m/s, GA=9,8 m/s, GG= 9,8 m/s, p=0,60) não demonstraram tal associação. Somente o genótipo TT do polimorfismo C242T da subunidade p22phox (OR=1,93, p=0,002) apresentou um risco significativamente aumentado para o fenótipo de rigidez arterial. Já os polimorfismos G1036C da TXNIP (OR=1,19, p=0,19), C609T/T471C da APOE (OR=1,14, p=0,33), G1355A da elastina (OR=0,81, p=0,28), I/D da ECA (OR=0,91, p=0,48) e A855G da MMP-9 (OR=1,01, p=0,95) não apresentaram risco. Conclusão: Os polimorfismos C242T da subunidade p22phox da NADPH oxidase e G1036C da TXNIP podem contribuir como moduladores genéticos no enrijecimento vascular / Introduction: Arterial stiffness is a complex phenomenon characterized by decreased vascular compliance during physiological and pathological stimuli. Similar to other cardiovascular phenotypes, arterial stiffness etiology is modulated by environmental and genetic factors. Considering the moderate heritability and its polygenic phenotype, genetic markers investigations related to different systems involved in vascular remodeling are interesting. Objectives: To assess the impact of the p22phox C242T, TXNIP G1036C, APOE C609T/T471C, elastin G1355A, ACE I/D and MMP-9 A855G polymorphisms on arterial stiffness phenotype in a general population. Methods: This study included 1,663 individuals of the general population from Vitória-ES. DNA was extracted from a venous blood sample and genotyping assays were performed for the genetic variants described above. Arterial stiffness was evaluated by pulse wave velocity (PWV). Results: Regarding PWV, p22phox C242T and TXNIP G1036C polymorphisms were significantly associated. Individuals carrying TT genotype of the p22phox C242T (CC + CT vs TT = 9.8 m/s = 10.1 m/s, p = 0.02) and individuals carrying G allele of the TXNIP G1036C polymorphisms (CG + CC = 9.8 m/s vs GG = 10.0 m/s, p = 0.03) had higher PWV values. However, APOE C609T/T471C (2=10.0 m/s, 3=9.8 m/s, 4=9.8 m/s, p=0.60), elastin G1355A (AA=9.8 m/s, GA=9.9 m/s, GG=9.8 m/s, p=0.92), ACE I/D (DD=9.8 m/s, DI=9.8 m/s, II=9.9 m/s, p=0.53) and MMP-9 A855G (AA=9.8 m/s, GA=9.8 m/s, GG= 9.8 m/s, p=0.60) polymorphisms did not present association. Only the TT genotype of the p22phox C242T polymorphism (OR = 1.93, p = 0.002) presented an increased risk for the arterial stiffness phenotype. Already TXNIP G1036C (OR=1.19, p=0.19), APOE C609T/T471C (OR=1.14, p=0.33), elastin G1355A (OR=0.81, p=0.28), ACE I/D (OR=0.91, p=0.48) and MMP-9 A855G (OR=1.01, p=0.95) polymorphisms did not present risk. Conclusion: The p22phox C242T and the TXNIP G1036C polymorphisms may contribute to genetic modulators in vascular stiffening

The prevalence of cardiovascular disease (CVD) among law enforcement officers (LEOs) is slightly higher than the general population. Furthermore, the prevalence of CVD doubles among LEOs following retirement compared to the general population. The measure of arterial stiffness serves as an independent risk factor that has prognostic value for future incidence of CVD. However, there is limited research on lifestyle, occupational, and demographic factors that may be associated with increased arterial stiffness in LEOs. Therefore, the purpose of this investigation was to compare the level of arterial stiffness among LEOs versus the general population and to identify lifestyle, occupational, and demographic predictors of arterial stiffness in LEOs. Seventy male career LEOs between the ages of 24 to 54 years from Kentucky and southwest Ohio participated in this study. LEOs completed a variety of questionnaires related to health/occupational histories, occupational stress, and diet. LEOs’ body composition (bioelectrical impedance), central and brachial blood pressures, and physical activity (triaxial accelerometers) were assessed. The dependent variable of arterial stiffness was measured by carotid-femoral pulse wave velocity (cfPWV). A variety of statistical techniques including 1 sample t-tests, Pearson product moment correlations, and multiple linear regression were utilized in study analyses, with a level of significance set at p < 0.05. Compared to the general population cfPWV was significantly lower among LEO’s under 30 years of age (mean difference = -0.6 m·s-1), but significantly higher among LEOs 50-55 years of age (mean difference = 1.1 m·s-1). Utilizing stepwise multiple linear regression, age, relative body fat, and diastolic blood pressure explained the most variance in LEO’s cfPWV (adj. R2 = 0.56, p < 0.001). The primary findings of this investigation demonstrate that arterial stiffness may progress more rapidly in LEOs compared to the general population and that LEOs should focus on maintaining appropriate levels of relative body fat and blood pressure to regulate arterial stiffness and risk of CVD.

<p>The aim of the work was to investigate the possibility to combine information from PPG and bio-acoustic technology to extract information that is related to the blood pressure. The measurements have been carried out with several different configurations. First the relation between arterial sounds and the PPG-signal was studied. After those measurements with both PPG and the bio- acoustic technique was concluded on people in different positions and after riding a bike. The goal was to vary the blood pressure. The conclusion that can be drawn in this report is that the bio-acoustic and the PPG-signal in peripheral arteries have the same source. That implies that arterial sounds are a product of turbulence when the pulse wave passes by. Further it can be assumed that it is the first heart sound that is represented in the arterial sounds. The time before and after the arterial sound in one heart cycle vary whit the blood pressure. There relationship seems also to vary with the bloodpressure but it vary differently under different conditions.</p>

Background Anthropometric measurements are useful in clinical practice since they are non-invasive and cheap. Previous studies suggest that sagittal abdominal diameter (SAD) may be a better measure of visceral fat depots. The aim of this study was to prospectively explore and compare how laboratory and anthropometric risk markers predicted subclinical organ damage in 255 patients, with type 2 diabetes, after four years. Methods Baseline investigations were performed in 2006 and were repeated at follow-up in 2010. Carotid intima-media thickness (IMT) was evaluated by ultrasonography and aortic pulse wave velocity (PWV) was measured with applanation tonometry over the carotid and femoral arteries at baseline and at follow-up in a cohort of subjects with type 2 diabetes aged 55–65 years old. Results There were significant correlations between apolipoprotein B (apoB) (r = 0.144, p = 0.03), C - reactive protein (CRP) (r = 0.172, p = 0.009) at baseline and IMT measured at follow-up. After adjustment for sex, age, treatment with statins and Hba1c, the associations remained statistically significant. HbA1c, total cholesterol or LDL-cholesterol did not correlate to IMT at follow-up. Baseline body mass index (BMI) (r = 0.130, p = 0.049), waist circumference (WC) (r = 0.147, p = 0.027) and sagittal Abdominal Diameter (SAD) (r = 0.184, p = 0.007) correlated to PWV at follow-up. Challenged with sex, SBP and HbA1c, the association between SAD, not WC nor BMI, and PWV remained statistically significant (p = 0.036). In a stepwise linear regression, entering both SAD and WC, the association between SAD and PWV was stronger than the association between WC and PWV. Conclusions We conclude that apoB and CRP, but not LDL-cholesterol predicted subclinical atherosclerosis. Furthermore, SAD was more independent in predicting arterial stiffness over time, compared with WC, in middle-aged men and women with type 2 diabetes. / <p>Funding Agencies|Medical Research Council of Southeast Sweden||Center for Medical Image Science and Visualization (CMIV)||Linkoping University||Futurum||King Gustaf V and Queen Victoria Freemason Foundation||GE Healthcare||Swedish Heart-Lung Foundation||Swedish Research Council Grant|12661|</p>

The aim of the work was to investigate the possibility to combine information from PPG and bio-acoustic technology to extract information that is related to the blood pressure. The measurements have been carried out with several different configurations. First the relation between arterial sounds and the PPG-signal was studied. After those measurements with both PPG and the bio- acoustic technique was concluded on people in different positions and after riding a bike. The goal was to vary the blood pressure. The conclusion that can be drawn in this report is that the bio-acoustic and the PPG-signal in peripheral arteries have the same source. That implies that arterial sounds are a product of turbulence when the pulse wave passes by. Further it can be assumed that it is the first heart sound that is represented in the arterial sounds. The time before and after the arterial sound in one heart cycle vary whit the blood pressure. There relationship seems also to vary with the bloodpressure but it vary differently under different conditions.

The purpose of this master thesis was to evaluate the estimation of pulse wave velocity (PWV) in the aorta using 4D flow MRI. PWV is the velocity of the pressure wave generated by the heart during systole and is a marker of arterial stiffness and a predictor of cardiovascular disease (CVD). PWV can in principle be estimated based on the time (travel-time) it takes for the pulse wave to travel a fixed distance (travel-distance), or based on the distance the pulse wave travels during a fixed time. In the commonly used time-to-travel-a-fixed-distance approach, planes are placed at two or more locations along the aorta. The travel-time is found by studying velocity waveforms at these pre-defined locations over time and thereby by estimating the time-difference for the pressure wave to reach each of these locations. In the distance-travelled-in-a-fixed-time approach, the pulse wave is located by studying at the velocity along the aorta at pre-defined instances in time. The travel-distance for the pulse wave between two instances in time is set as the difference in location of the pulse wave, where the location is identified as the location when the velocity has reached a predefined baseline. The specific aims of this thesis was to investigate the effect of using multiple locations as well as the effects of temporal and spatial resolution in the time-to-travel-a-fixed-distance approach, and to evaluate the possibility of using the distance-travelled-in-a-fixed-time approach. Additionally, the possibility of combining the two approaches was investigated. The study of using multiple locations revealed that more planes reduces the uncertainty of PWV estimation. Temporal resolution was found to have a major impact on PWV estimation, whereas spatial resolution had a more minor effect. A method for estimating PWV using 4D flow MRI using the distance-travelled-in-a-fixed-time approach was presented. Values obtained were compared favourably against previous findings and reference values, in the case of healthy young volunteers. The combination of the time-to-travel-a-fixed-distance and distance-travelled-in-a-fixed-time approaches appears feasible.

Introdução: A rigidez arterial é um fenômeno complexo caracterizado pela diminuição da complacência vascular frente aos estímulos fisiológicos e patológicos. Semelhantemente a outros fenótipos cardiovasculares, a etiologia da rigidez arterial é modulada por fatores ambientais e genéticos. Levando em consideração a moderada herdabilidade e a característica poligênica do presente fenótipo, torna-se interessante a investigação de marcadores genéticos referentes aos diferentes sistemas envolvidos no remodelamento vascular. Objetivo: Avaliar o impacto dos polimorfismos C242T da subunidade p22phox da NADPH oxidase, G1036C da TXNIP, C609T/T471C da APOE, G1355A da elastina, I/D da ECA e A855G da MMP-9 no fenótipo de rigidez arterial em uma população geral. Métodos: Participaram do estudo 1.663 indivíduos da população geral da cidade de Vitória-ES. O DNA foi extraído a partir de uma amostra de sangue venoso. Posteriormente foram realizadas as genotipagens para as variantes genéticas supracitadas. A rigidez arterial foi avaliada por meio do método da velocidade de onda de pulso (VOP). Resultados: Em relação à VOP, os polimorfismos C242T da subunidade p22phox da NADPH oxidase e G1036C da TXNIP foram signifcativamente associados. Os indivíduos portadores do genótipo TT do polimorfismo C242T da subunidade p22phox (CC+TC=9,8 m/s versus TT=10,1 m/s, p=0,02) e do alelo G do polimorfismo G1036C da TXNIP (CC=9,8 m/s versus CG+GG=10,0 m/s, p=0,03) apresentaram maiores valores da VOP. Entretanto os polimorfismos C609T/T471C da APOE (2=10,0 m/s, 3=9,8 m/s, 4=9,8 m/s, p=0,60), G1355A da elastina (AA=9,8 m/s, GA=9,9 m/s, GG=9,8 m/s, p=0,92), I/D da ECA (DD=9,8 m/s, DI=9,8 m/s, II=9,9 m/s, p=0,53) e A855G da MMP-9 (AA=9,8 m/s, GA=9,8 m/s, GG= 9,8 m/s, p=0,60) não demonstraram tal associação. Somente o genótipo TT do polimorfismo C242T da subunidade p22phox (OR=1,93, p=0,002) apresentou um risco significativamente aumentado para o fenótipo de rigidez arterial. Já os polimorfismos G1036C da TXNIP (OR=1,19, p=0,19), C609T/T471C da APOE (OR=1,14, p=0,33), G1355A da elastina (OR=0,81, p=0,28), I/D da ECA (OR=0,91, p=0,48) e A855G da MMP-9 (OR=1,01, p=0,95) não apresentaram risco. Conclusão: Os polimorfismos C242T da subunidade p22phox da NADPH oxidase e G1036C da TXNIP podem contribuir como moduladores genéticos no enrijecimento vascular / Introduction: Arterial stiffness is a complex phenomenon characterized by decreased vascular compliance during physiological and pathological stimuli. Similar to other cardiovascular phenotypes, arterial stiffness etiology is modulated by environmental and genetic factors. Considering the moderate heritability and its polygenic phenotype, genetic markers investigations related to different systems involved in vascular remodeling are interesting. Objectives: To assess the impact of the p22phox C242T, TXNIP G1036C, APOE C609T/T471C, elastin G1355A, ACE I/D and MMP-9 A855G polymorphisms on arterial stiffness phenotype in a general population. Methods: This study included 1,663 individuals of the general population from Vitória-ES. DNA was extracted from a venous blood sample and genotyping assays were performed for the genetic variants described above. Arterial stiffness was evaluated by pulse wave velocity (PWV). Results: Regarding PWV, p22phox C242T and TXNIP G1036C polymorphisms were significantly associated. Individuals carrying TT genotype of the p22phox C242T (CC + CT vs TT = 9.8 m/s = 10.1 m/s, p = 0.02) and individuals carrying G allele of the TXNIP G1036C polymorphisms (CG + CC = 9.8 m/s vs GG = 10.0 m/s, p = 0.03) had higher PWV values. However, APOE C609T/T471C (2=10.0 m/s, 3=9.8 m/s, 4=9.8 m/s, p=0.60), elastin G1355A (AA=9.8 m/s, GA=9.9 m/s, GG=9.8 m/s, p=0.92), ACE I/D (DD=9.8 m/s, DI=9.8 m/s, II=9.9 m/s, p=0.53) and MMP-9 A855G (AA=9.8 m/s, GA=9.8 m/s, GG= 9.8 m/s, p=0.60) polymorphisms did not present association. Only the TT genotype of the p22phox C242T polymorphism (OR = 1.93, p = 0.002) presented an increased risk for the arterial stiffness phenotype. Already TXNIP G1036C (OR=1.19, p=0.19), APOE C609T/T471C (OR=1.14, p=0.33), elastin G1355A (OR=0.81, p=0.28), ACE I/D (OR=0.91, p=0.48) and MMP-9 A855G (OR=1.01, p=0.95) polymorphisms did not present risk. Conclusion: The p22phox C242T and the TXNIP G1036C polymorphisms may contribute to genetic modulators in vascular stiffening