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1
Erqou, Sebhat. "Lipoprotein(a) and the risk of vascular disease." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/225182.
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Background: Lipoprotein(a) [Lp(a)] is composed of a low density-lipoprotein (LDL) particle and a glycoprotein molecule known as apolipoprotein(a) [apo(a)]. Apo(a) exists in several differently-sized isoforms and is responsible for the unique properties of Lp(a). Although Lp(a) has been known for the past 40 years its relationship with coronary heart disease (CHD) has not been characterized in sufficient detail. Whether Lp(a) causes CHD is not clear. Furthermore, the role of apo(a) isoform variation and other sources of Lp(a) heterogeneity (e.g., level of oxidized phospholipids) in Lp(a)-disease association has not been determined. Objectives: To characterize in detail the association of circulating Lp(a) levels with the risk CHD To assess the nature of Lp(a)-CHD association using an integrative genetic study To explore the role of Lp(a) heterogeneity in its association with CHD Data sources: 1. The Emerging Risk Factors Collaboration (ERFC) database (36 studies, 127,000 participants) 2. The European Prospective Investigation of Cancer – Norfolk (EPIC-Norfolk) study (2200CHD cases, 2200 controls) 3. The Pakistani Risk of Myocardial Infarction Study (PROMIS) (1800 MI cases and 1800 controls) 4. Systematic quantitative reviews of published epidemiological studies Results: ERFC data - Analyses of cross-sectional data on up to 127,000 participants (predominantly of European descent) demonstrated that Lp(a) is generally not strongly correlated with known CHD risk factors. Weakly positive correlations were observed with LDL-cholesterol, apolipoprotein B100 and fibrinogen. Levels were over 2-fold higher in Blacks compared to Whites. Analyses of available data on repeat measurements in 6600 participants demonstrated that Lp(a) values have very high long-term within-person consistency (regression dilution ratio ~ 0.9). Outcome data involved 9300 incident CHD events, 1900 ischaemic strokes and 8100 nonvascular deaths. The risk ratio for CHD per 1SD higher Lp(a) concentration, adjusted for age, sex, lipids and other conventional vascular risk factors, was 1.13 (95% CI, 1.09-1.18). The corresponding risk ratios for ischaemic stroke and nonvascular death were 1.10 (1.02 – 1.18) and 1.01 (0.98-1.05), respectively. Data were too limited to assess association in nonwhites. PROMIS data – the adjusted odds ratio for MI in South Asians was comparable to that of Europeans. EPIC-Norfolk genetic data - The odds ratio for CHD per 1-SD higher Lp(a) concentration, after adjustment for cardiovascular risk factors, was 1.37 (1.20-1.56). Tagging SNPs rs10455872 and rs11751605 (minor allele frequency: 8% and 18%, respectively) were associated with 207% (95% CI, 188 - 227%) and 38% (31 - 46%) higher Lp(a) concentrations per copy of minor allele, respectively. These SNPs accounted for 35% and 5% of the variation in circulating Lp(a) levels, respectively, and were associated with an odds ratio for CHD of 1.34 (1.14-1.58) and 1.17 (1.04-1.33), respectively. The observed SNP-CHD associations were consistent with expected odds ratios corresponding to the Lp(a) effect of the SNPs. Systematic reviews – meta-analysis of published data from 40 studies (11,300 cases, 47,000 controls) demonstrated that people with smaller apo(a) isoforms have about a 2-fold higher risk of CHD or ischemic stroke than those with larger isoforms. Meta-analysis of published data from 10 studies (1500 cases, 10,200 controls) showed that people in the top third of baseline distribution of oxidized LDL levels have a 1.8-fold higher risk of CHD than those in bottom third. EPIC-Norfolk biomarker data – Levels of oxidized phospholipids were strongly correlated with Lp(a) concentration (r = 0.7, p-value < 0.0001). One SD higher concentration of oxidized phospholipids was associated with an adjusted odds ratio for CHD of 1.31 (1.15-1.49). The risk ratio was no longer significant after adjustment for Lp(a) concentration (1.08; 95% CI, 0.91-1.29). Conclusion: Lp(a) concentration is specifically, continuously and independently associated with the risk of ischaemic vascular outcomes. Available evidence supports the causal role of the particle in CHD. Lp(a) appears to induce vascular damage through causal mechanisms that involve apo(a) isoforms and oxidized phospholipids. A comprehensive study of markers of Lp(a) heterogeneity should help to understand the full impact of Lp(a) on cardiovascular diseases. In addition, further study is needed in nonwhites to assess the relevance of the factor to vascular disease risk in these populations.
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McKinley, Michelle. "B-vitamin status and plasma homocysteine, a risk factor for vascular disease." Thesis, University of Ulster, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322421.
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Stevens, Kathryn K. "Phosphate as a cardiovascular risk factor : effects on vascular and endothelial function." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5301/.
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Chronic kidney disease (CKD) is prevalent affecting 8.5% of the population in the UK and it is associated with premature cardiovascular disease (CVD) and death. The association between CKD and accelerated CVD arises as a consequence of traditional and non-traditional cardiovascular (CV) risk factors, including serum phosphate. Currently, there is no therapeutic intervention which has been shown to effectively reverse the increased CV risk in CKD. Phosphate metabolism is disordered in CKD particularly in the advanced stages (CKD 4 and 5). Even at the upper limit of the normal reference range, serum phosphate has been shown to be associated with CV mortality and morbidity including left ventricular hypertrophy, vascular calcification (VC) and endothelial dysfunction (ED). These associations also extend to populations without CKD. Serum phosphate is an appealing CV risk factor because it can be modified by dietary and pharmacological therapies. However, there has been no study linking lowered phosphate with improved outcomes and whilst several small mechanistic studies have suggested a role of phosphate in VC, oxidative stress and more recently ED, the precise mechanism of action of phosphate as a CV risk factor remains elusive. Our lack of understanding of the mechanism of action of phosphate makes it difficult to ascertain how to best manage phosphate. The hypothesis of this thesis is that long term exposure to elevated phosphate is associated with endothelial and vascular dysfunction and it is this which contributes to the elevated CV risk seen in CKD. Endothelial and vascular dysfunction will be evident in individual cell lines and in blood vessels as well as in humans, who have been exposed to sustained oral phosphate. This hypothesis has been explored in a translational manner in three ways: 1. The function of resistance vessels from rats and from humans, with and without CKD, has been studied. Experiments were performed looking at endothelium dependent and independent relaxation of vessels exposed to either normal or high phosphate concentration medium. The anti-oxidant, ascorbic acid and zaprinast, a phosphodiesterase 5 inhibitor were studied in the rat vessels to assess if these additions altered the vessels’ relaxation response. 2. Cells were cultured in normal and high phosphate concentration medium from the outset to mimic the chronicity of the uraemic environment. The nitric oxide (NO) pathway was studied considering eNOS expression, VEGF and cGMP production, intracellular calcium concentration and NO production. Proliferation and cell growth pathways have also been studied. 3. A cross-over clinical trial was performed in 19 healthy volunteers, without CKD. Volunteers attended for three visits. Prior to each visit, they fasted for 12 hours and performed a 24 hour urine collection. Bloods were drawn and endothelial function was measured with flow mediated dilatation and vascular stiffness with pulse wave velocity and analysis. There was a baseline visit and then two further visits. Prior to visit two, volunteers were randomised to take phosphate supplementation or phosphate binding medication for two weeks, followed by a wash out period and then volunteers took the other tablet for two weeks, before attending for a final visit. In rat vessels, there was impaired endothelium dependent and independent relaxation in vessels exposed to high phosphate concentration medium. Vessels in high phosphate produced less basal NO and less cGMP. The impaired relaxation could be ameliorated with the addition of a phosphodiesterase 5 inhibitor. This suggests reversibility of the detrimental effects of phosphate. In human vessels from patients without CKD, there was similarly attenuated endothelium dependent and independent relaxation. In vessels from patients with CKD, there was impaired endothelium dependent relaxation but independent relaxation was preserved. The CKD vessels exposed to normal phosphate medium relaxed to the same degree as their counterparts from patients without CKD, again suggesting that the effects of phosphate may be reversible. These effects are independent of intracellular calcium concentration which was found to be similar in cells cultured in normal or high phosphate medium. There was evidence of disruption to the NO pathway with reduced eNOS expression in human and rat endothelial cells and reduced protein kinase G expression in vascular smooth muscle cells. NO measured by the Griess reaction was lower in cells cultured in high phosphate medium. NO has an inhibitory effect on growth and cells cultured in high phosphate proliferated more (measured with the MTT assay) and were bigger than cells cultured in normal phosphate medium. Gene expression studies showed alterations in growth genes and cell cycle regulators. ED was demonstrated in healthy volunteers exposed to sustained oral phosphate loading. This was independent of serum phosphate level which was unchanged. Urinary phosphate and fibroblast growth factor 23 level independently predicted ED and suggest that whilst the normal homeostatic mechanisms maintain serum phosphate within the normal reference range, total body phosphate was elevated and urinary phosphate excretion was a surrogate for this. These relationships are novel and have not been demonstrated previously. It has previously been difficult to separate the effects of phosphate from other effects of the uraemic environment, including acidosis. The studies in this thesis have achieved this and the results provide strong evidence of an association between phosphate and ED. There is also evidence that these effects may be reversible. In contrast to conventional thinking that the effects of phosphate, like VC, are largely irreversible, these studies suggest that there may be dynamic effects of phosphate. This may be explained by alterations in intracellular phosphate. These findings have important implications for patients with CKD because they provide a sound explanation for the increased CV risk seen with phosphate and advocate further study of phosphate lowering (and outcome) as a therapeutic strategy to reverse this elevated CV risk.
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Zagten, Maria Sophia Gerarda van. "Cerebral small-vessel disease vascular risk factor profiles, clinical manifestations, and disease progression in stroke /." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=6019.
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PIAZZA, FABRIZIO. "Biological markers of vascular damage in Alzheimer’s disease patients." Doctoral thesis, Università degli Studi di Milano Bicocca, 2008. http://hdl.handle.net/10281/33165.
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Alzheimer's disease (AD) represents the most common type of dementia, accounting for 50% of the total amount of cognitive impairment, while vascular dementia (VD) accounts for approximately 20% of the cases.
AD has traditionally been considered a neurodegenerative condition in which vascular dysfunction plays a marginal role. On the other hand, VD is thought to be caused by a subacute or chronic reduction in cerebral blood flow (CBF) leading to neuronal dysfunction and death. However, it is not clear if these two major causes of dementia also share pathogenetic mechanisms.
Many evidences point out a vascular pathogenetic involvement in its etiology. The recent finding that Abeta has also harmful effects on vessels indicates that vascular damage could be involved in the pathogenesis of AD, thus explaining how AD and VD are not always distinct entities but overlap by varying degrees.
Abeta peptide, which plays a central role in AD, not only exerts harmful effects on the vessel walls increasing the risk of silent hemorrhagic/ischemic strokes, but it also facilitates the ultrastructural degeneration of the vessels, reducing vessels’ diameters, cerebral blood flow and energetic metabolism. Conversely, vascular damage which results in hypoxia/ischemia, inflammation, microglia activation and oxidative stress, can influence APP processing, modulating the expression of enzymes responsible for Abeta production.
These mechanisms have been described in animal models, while few independent observations have been performed in humans.
Classical neuropathological markers of AD are: (i) deposits of amyloid β (Abeta) in brain tissue (neuritic plaques), as well as within the wall of cerebral blood vessels; (ii) microglia activation; (iii) dystrophic neuronal processes in proximity and within Abeta plaques; (iv) progressive loss of synapses and neurons; and (v) severe structural damage of cerebral blood vessels.
Nonetheless, many vascular risk factors have been also associated to AD, i.e. ApoE-e4 genotype, diabetes and hyperinsulinemia, high systolic blood pressure in midlife to late life and low diastolic blood pressure in late life, smoking, stroke, traumatic brain injury, elevated serum homocysteine (Hcy) levels, hypercholesterolemia and atherosclerosis. Furthermore, there are many evidences of peripheral haemostatic abnormalities, in particular platelets alterations, Von Willebrand Factor and Activated Factor VII, and increased level of thrombomodulin and E-selectin in AD, suggesting that an endothelial dysfunction may be involved in AD pathogenesis.
Based on these evidences, a possible hypothesis is that Abeta induces endothelial injury, thus promoting ischemic damage, which may in turn affect APP processing and Abeta production. This reciprocal interaction may provide an explanation to the pathogenetic link between these two conditions.
In this contest, elevated plasma levels of Homocysteine (Hcy), also know as Hyperhomocysteinemia (HHcy), is one of the strongest independent risk factors for vascular and cerebrovascular disorders and it has been associated to the risk of develop AD in elderly people. Recently, our group has published evidences of elevated plasma levels of Hcy in AD, correlated with folate deficiencies. Moreover, we have demonstrated that Post Methionine Load (PML) test is able to reveal twice as many HHcy AD subjects with respect to the fasting analysis, suggesting PML as useful test in detecting AD patients who may have the chance of an early folate treatment.
Since vascular lesions often coexist with Abeta deposits in AD, and aberrant Abeta deposition in the intima may be pathologically important, it is possible that this phenomena is not only the consequence of the AD-related aberrant APP processing but may represent the early trigger of Amyloid deposition, in response to the primary endothelial damage.
Moreover, after Abeta or hypoxia exposure, the endothelium undergoes changes which trigger the inflammatory response, as demonstrated in cerebral small vessel disease where there is histopathological evidence of endothelial cell activation. The increased vascular permeability is one of the features of endothelial cell activation, and it is thought that entry of serum proteins, such as coagulation and/or inflammatory mediators, into the vascular wall and perivascular neural parenchyma may sustain toxic effects.
Indeed the blood-brain barrier (BBB) microvasculature, plays a crucial role in the regulation of cerebral blood flow (CBF) and may also play a pivotal role in AD pathogenesis by regulating the entry into brain parenchyma of a plethora of circulating molecules and xenobiotics, also triggering inflammation and oxidative stress.
Cerebral endothelium could be of clinical relevance to investigate BBB permeability, indicating early endothelial perturbation as a consequence of hypoxia or Abeta deposition, events involved in inflammatory and oxidative cerebrovascular activity.
Indeed, it has been previously demonstrated that proinflammatory cytokines alter the expression and processing of Abeta precursor protein, and fibrillar Abeta itself in turn promotes the production of proinflammatory cytokines by microglial and monocytic cell lines.
Microglia is the major component of the intrinsic brain immune system and its pivotal role in cerebral inflammation-like responses could trigger and sustain neurodegenerative events.
However, clinical observations on the potential role of inflammation in AD have yielded inconsistent results. Whereas several community-based studies have linked antiinflammatory interventions to a lowered risk of developing AD, a randomized, placebo-controlled clinical trial failed to demonstrate a beneficial effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the progression of disease.
It is noteworthy that, in the brain, perivascular macrophages and microglia that participate in intraparenchymal inflammation are derived from circulating macrophages. Previous studies have reported higher CSF levels of TNF-alpha than serum levels in AD patients, strengthening the hypothesis of a pivotal role of BBB and microglia activity in the pathogenetic mechanisms of AD.
Activated microglia may also be involved in mechanisms of impaired glial glutamate uptake and reduced expression of glutamate transporters, or increased free radicals and nitric oxide synthesis in brain parenchyma.
Central nervous system is particularly exposed to free radical injury, given its high metal content, which can catalyze the formation of oxygen free radicals, and the relatively low content of antioxidant defenses. Indeed, several studies show markers of oxidative damage (lipid peroxidation, protein oxidation, DNA oxidation and glycosidation markers) in brain areas affected by neurodegenerative disorders.
Our group published several works demonstrating a link between oxidative stress and excitotoxicity in AD, and described peripheral markers of these mechanisms, that may be analyzed in patients as possible diagnostic and therapeutic tools.
On the other hand, hypoxia and stroke could influence Abeta processing, as demonstrated by the hypoxia-inducible factor1 alpha (HIF-1alpha) regulation of BACE promoter or increased production of Abeta after stroke, which may increase caspase 3 cleavage of the GGA3 protein carrier resulting in decreased degradation of BACE.
Studies of the effect of vascular risk factors on Abeta processing could help to elucidate whether vascular disease has only an additive effect on cognitive performance or it is also intrinsic to the pathogenesis of AD. We have recently analyzed some markers of vascular damage, in particular we have demonstrated that mean plasma levels of TF (Tissue Factor) and TFPI (TF Pathway Inhibitor) are both correlated with Hcy and they are significantly higher in AD and MCI patients than in healthy subjects (Piazza 2007).
Moreover, the measurement of immunologically defined "circulating endothelial cells" (CECs) has been used to assess vascular integrity and the amount of microparticles (MP) has been reported elevated in a number of conditions where vascular dysfunction, thrombosis and inflammation are relevant. However, the identification of relevant biological markers for the state of brain microvessels in demented patients is still lacking.
Such biomarkers, together with known risk factors common to AD and VD, can be used to better understand the involvement of cerebrovascular implications in the pathophysiology of dementia, with possible therapeutic interventions.
In conclusion, it is possible that the initial endothelial damage in AD brains can trigger Abeta deposits which, in turn, may fuel monocytes infiltration through damaged BBB and microglia activation. Abeta deposits and inflammation can lead to the production of superoxide radicals, exacerbating endothelial injury. Moreover, all these processes can support previous findings of the generalized peripheral and CNS oxidative stress that typically defines AD.
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Mansfield, Michael William. "The interaction of genetic and environmental vascular risk markers in patients with non-insulin-dependent diabetes mellitus and their first degree relatives." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388894.
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Goins, Laura K. "The Effect of DASH Dietary Adherence and Participant Characteristics on CVD Risk Factor Response to a DASH Dietary Intervention in Adolescents with Elevated Blood Pressure." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504871786313111.
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Mahlman, M. (Mari). "Genetic background and antenatal risk factors of bronchopulmonary dysplasia." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526219530.
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Abstract Advances over the past few decades in ante- and neonatal care have led to the survival of a growing number of premature infants of extremely low gestational age. However, the occurrence of serious diseases, particularly those affecting the most immature infants, remains high. Bronchopulmonary dysplasia (BPD), a chronic lung disease of premature infants, is one such disease. Our current understanding of the molecular pathogenesis of BPD is incomplete; consequently, there are few preventive and therapeutic options for BPD. Moreover, it is challenging to predict the risk of BPD. Previous studies of BPD in twins revealed that the heritability of BPD is quite high. However, the individual genes that predispose premature infants to BPD are largely unknown. The aim of this study was to identify and study genes associated with BPD in order to investigate its pathogenesis. An additional aim was to add to knowledge of the risk of BPD in newborn premature infants, with an emphasis on twins. A candidate gene study found no consistent association between common polymorphisms of vascular endothelial growth factor receptor 2 and BPD. A second candidate gene study noted an association between the gene encoding Kit ligand and BPD. A genome-wide association study found a suggestive association between a locus close to the gene encoding C-reactive protein (CRP) and BPD, and in subsequent analyses, plasma levels of CRP during the first week of life predicted BPD. Finally, a nationwide register study found that the risk of BPD was lower in twins than in singletons. The results of this study add to what is known of the genetics and pathogenesis of BPD. They also provide new data on the risk of BPD, which may be used to improve early identification of infants for whom the risk of developing BPD is highTiivistelmä Ennenaikaisen syntymän ja keskoslasten hoidon kehittymisen myötä yhä useammat huomattavan epäkypsinä syntyneet lapset jäävät henkiin. Samalla erityisesti juuri näitä lapsia uhkaavien sairauksien esiintyvyys on pysynyt korkeana. Bronkopulmonaalinen dysplasia (BPD, keskosen krooninen keuhkosairaus) on yksi näistä sairauksista. BPD:n molekyylitasoinen tautimekanismi on vielä osin tuntematon, eikä BPD:tä tehokkaasti estävää tai siitä parantavaa hoitoa ole. Myös BPD riskin arvioiminen vastasyntyneen keskoslapsen kohdalla on vaikeaa. BPD on huomattavan perinnöllinen tauti. BPD:lle altistavista geeneistä on kuitenkin vasta vähän tietoa. Tämän tutkimuksen tavoitteena oli lisätä tietoa BPD:n tautimekanismista tutkimalla BPD:lle altistavia geenejä. Lisäksi tutkimuksessa tarkasteltiin BPD:n esiintyvyyttä ja syntymää edeltäviä riskitekijöitä erityisesti kaksosten osalta. Ehdokasgeenitutkimuksessa verisuonten endoteelikasvutekijää koodaava geeni ei assosioitunut toistuvasti BPD:hen. Kit ligandia koodaava geeni sen sijaan assosioitui. Koko genomin assosiaatiotutkimuksessa C-reaktiivista proteiinia (CRP) koodaavan geenin lähistöltä löydettiin BPD:hen mahdollisesti assosioituva alue. Lisäksi ensimmäisen viikon CRP-arvojen osoitettiin ennakoivan myöhemmin kehittyvää BPD:tä. BPD-riskin todettiin olevan matalampi kaksi- kuin yksisikiöisistä raskauksista syntyneillä lapsilla. Tutkimuksen tulokset lisäävät tietoa BPD:n perinnöllisyydestä ja sitä kautta BPD:n tautimekanismista. Tutkimus toi myös uutta tietoa BPD:n riskitekijöistä parantaen vastasyntyneen keskoslapsen BPD-riskin arviota
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Howard, Dominic Peter James. "Extra-coronary arterial disease : incidence, projected future burden, risk factors and prevention." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:6ac90d2b-b919-45d4-abfd-2128efb31bc6.
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Vascular disease is the leading cause of death and disability worldwide. Incidence, risk factors, and outcome of coronary artery disease have been extensively studied, but there are fewer data on other forms of arterial disease, including carotid, aortic, visceral, and peripheral arterial disease. Although the burden of these diseases may be increasing due to the ageing population, we lack the most basic epidemiological data on which to base clinical decisions on individual patients (short and long-term prognosis); local service provision (current incidence and projected future burden); public health / screening initiatives (age and sex-specific incidence, risk factors, and outcome); and with which to assess current levels of primary prevention (pre-morbid risk factor control). Indeed, it is this lack of data, rather than a lack of treatments that is the greatest barrier to effective prevention. I have contributed to, cleaned, and analysed data from the Oxford Vascular Study, a prospective, population-based study (n=92,728) of all acute vascular events (2002-2012), and the Oxford Plaque Study, a carotid atherosclerosis biobank of over 1000 carotid plaques, in order to study these conditions. For acute aortic disease, I aimed to assess the risk factors associated with acute abdominal aortic aneurysms (AAA) and the population impact of the current UK AAA screening programme; and the incidence, risk factors, outcome, and projected future burden of acute aortic dissection. For acute peripheral arterial disease, I assessed the risk factors associated with premature onset and poor outcome, together with current levels of primary prevention. For symptomatic carotid artery disease, I studied the timing and benefits of surgical intervention in the current era; and went on to assess whether underlying carotid plaque morphology can be used to improve stroke risk stratification and help explain why ocular and cerebral stroke types have vast differences in future ipsilateral stroke risk. I found that compared with the current UK AAA screening strategy (one-off scan for men aged 65), screening of male smokers at 65 and all men at 75 would prevent nearly four-times as many deaths and three-times as many life-years lost with 21% fewer annual scans. I have also shown that incidence of acute aortic dissection is higher than previous estimates, a third of cases are out-of-hospital deaths, and uncontrolled hypertension is the most significant treatable risk factor for this condition. For acute peripheral arterial disease, the presence of multiple atherosclerotic risk factors are associated with premature onset, and severity of ischaemia, pre-morbid renal dysfunction, cardiac failure, and diabetes mellitus are predictive of future limb loss and survival. A significant proportion of acute peripheral events are AF-related in high risk patients who were not pre-morbidly anticoagulated despite having no contraindications and being at low risk of bleeding. Symptomatic carotid artery disease currently accounts for <10% of incident cerebrovascular events, and only 40% of these patients undergo surgical intervention. Due to improvements in medical therapy and on-going delays to intervention, little benefit is currently obtained from intervening in patients with <70% stenosis. Ipsilateral stroke risk is correlated with several carotid plaque features in a time-dependent manner, confirming the potential utility of plaque morphology in risk stratification. In addition, plaques from patients with cerebral events were significantly more unstable and inflammatory than from those with ocular events, helping explain differences in stroke risk between these groups. My findings advance the understanding of these conditions that form the backbone of modern vascular surgical practice, and I hope will improve prevention, clinical management, and outcome for patients with vascular disease.
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Cornett, Patricia F. "Risk Factors for Vascular Dementia." Thesis, University of North Texas, 2005. https://digital.library.unt.edu/ark:/67531/metadc4781/.
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Dementia is a devastating disorder that commonly affects people over the age of 65. Alzheimer's disease and vascular dementia are the most common forms of dementias. A number of studies have implicated cardiovascular risks as important factors in the development of dementia. These risks include high-risk behaviors such as smoking and risks related at least partially to health behaviors such as diet and exercise. This study examines a group of cardiovascular risk factors, as defined by the Framingham study, to ascertain if they are predictors of dementia. A retrospective chart review of 481consecutive patients seen in a geriatric medicine clinic produced a sample of 177 individuals diagnosed with dementia and 304 individuals without a dementia diagnosis. Relative risk ratio (RRR) results indicate that a history of hypertension (RRR= 1.80, p = .009) and a history of hypercholesterolemia (RRR = 1.85, p = .016) are significant predictors of Alzheimer's disease. A history of tobacco use (RRR = 2.18, p = .01) is a significant predictor of vascular dementia. Stepwise regression analyses indicate that hypercholesterolemia is an independent predictor of dementia (b = -.113, p = .009) and hypercholesterolemia (b = -.104, p = .018) and hypertension (b = -.094, p = .031) clustered together have an additive risk factor effect. These results are discussed in terms of the importance of specific health behaviors in the development and possible prevention of dementia.
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Leeson, Christopher Paul Maxted. "Early risk factors for later vascular disease." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624836.
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Seshadri, Swathi. "Retinal vascular function and cardiovascular risk factors." Thesis, Aston University, 2015. http://publications.aston.ac.uk/27347/.
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The current platform of conventional cardiovascular risk assessments tends to forsake the importance of endothelial function - a key biological mechanism by which cardiovascular risk factors exert their propensity for adverse vascular events. Moreover, the presence and severity of endothelial dysfunction in ‘low-risk’ individuals suggests considerable variability in pre-clinical risk that could potentially be detected well before the onset of disease. The aim of the present thesis was to investigate the presence and impact of retinal vascular dysfunction, as a barometer of endothelial function, in otherwise healthy individuals with one or more cardiovascular risk factors, but low to moderate cardiovascular risk. Systemic circulatory influences on retinal vascular function were also evaluated. The principle sections and findings of this work are: 1. Ageing effect on retinal vascular function • In low-risk individuals, there are age differences in retinal vascular function throughout the entire functional response curve for arteries and veins. Gender differences mainly affect the dilatory phase and are only present in young individuals. 2. Retinal vascular function in healthy individuals with a family history of cardiovascular disease • In low-risk individuals with a family history of cardiovascular disease, impairments in microvascular function at the retinal level correlate with established plasma markers for cardiovascular risk. 3. Ethnic differences in retinal vascular function • When compared to age-matched White Europeans, in low-risk middle-aged South Asians, there are impairments in retinal vascular function that correlate with established cardiovascular risk indicators. 4. Systemic circulatory influences on retinalµvascular function • Systemic antioxidant capacity (redox index) and plasma markers for cardiovascular risk (lipids) influence retinal microvascular function at both arterial and venous levels. 5. Retinal vascular function in individuals with obstructive sleep apnoea: a preliminarystudy • Patients with moderate to severe sleep apnoea exhibit attenuated retinal vascular function.
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VERTICCHIO, VERCELLIN ALICE CHANDRA. "VASCULAR RISK FACTORS AND GLAUCOMA OPTIC NEUROPATHY." Doctoral thesis, Università degli studi di Pavia, 2021. http://hdl.handle.net/11571/1434314.
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Kerr, Gillian. "Cerebrovascular diseases, vascular risk factors and socioeconomic status." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1892/.
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Cerebrovascular disease, has an enormous, and increasing, impact on global health. As well as causing clinical stroke, cerebrovascular disease is thought to be a major contributor to cognitive decline and dementia. Socioeconomic status (SES) is associated with risk of stroke. Those in the lowest SES group are estimated to be at twice the risk of stroke compared to those in the highest SES group. Those with low SES may also have a more severe stroke and a poorer outcome. It is imperative that the extent and mechanism of this association is clarified. This thesis aims to determine if the association between SES and stroke is explained by a greater prevalence of traditional vascular risk factors amongst those of low SES. It also explains the link with a novel risk factor, poor oral health. Lastly it addresses the long-term cognitive outcome in older people at risk of vascular disease. A systematic review and meta-analysis was undertaken to establish if vascular risk factors explain the association between SES and stroke incidence / post-stroke mortality. This demonstrated that lower SES was associated with an increased risk of stroke and that a greater burden of vascular risk factors in those with low SES explained about 50% of the additional risk of stroke. However this meta-analysis could not clarify what vascular risk factors are most critical. Low SES was also associated with increased mortality risk in those who have a stroke although study results were heterogeneous and this link was not readily explained by known vascular risk factors. A prospective study of 467 consecutive stroke and transient ischameic attack (TIA) patients from three Scottish hospitals was undertaken with the aim of establishing whether those with low SES carry higher levels of vascular risk factors, have a more severe stroke and have equal access to stroke care services and investigations. Stroke / TIA patients with low SES were younger and more likely to be current smokers but there was no association with other vascular risk factors /co-morbidity. Those who had lower SES had a more severe stroke. The lowest SES group were less likely to have neuroimaging or an electrocardiogram although differences were not significant on multivariate analysis. There was however equal access to stroke unit care. A secondary analysis of a prospective cohort study of 412 stroke patients was conducted. The aim was to explore oral health after acute stroke and assess if poor oral health explains the association between SES and stroke. Dry mouth amongst acute stroke patients was very common, however there was no association between oral health and low SES. There was an association of dry mouth with pre-stroke disability and Urinary Tract Infection. There was also a link with oral Candida glabrata colonisation, although the clinical relevance of this is uncertain. In the acute phase after stroke there was no convincing association of dry mouth with dysphagia or pneumonia. Therefore there was no association between SES and poor oral health as measured in this study but oral health may still be part of the explanation of the association between SES and acute stroke and this needs further investigation. Vascular disease is an important contributor to cognitive decline and dementia. Low SES may be associated with an increased risk of cognitive decline in later life and vascular disease may be a mediating factor. More effective prevention of vascular disease may slow cognitive decline and prevent dementia in later life, particularly in low SES groups. Lipid lowering with statins might be effective in preventing dementia but so far evidence from randomised control trials does not show benefit from statins in preventing cognitive decline and dementia. However the duration of follow-up in these trials was short and there may be benefit in the long-term. My aim was therefore to establish if long-term follow-up of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) study was feasible. I found that it was feasible to follow-up 300 elderly survivors from the Scottish arm of the PROSPER study and the methods could be extended to the whole group. As expected nearly half of the PROSPER participants were dead. Additionally a large proportion of traceable participants had significant cognitive impairment. Smoking cessation, control of blood pressure and management of other vascular risk factors should be made a priority in areas of low SES. Additionally further research is needed to fully clarify the association between SES and stroke incidence. Avenues for exploration might include the possibilities of poorer access to effective stroke care, reduced uptake of care and poorer oral health in lower SES groups. In addition public health campaigns regarding smoking cessation should be directed at lower SES groups. I have shown that a large scale follow-up of the PROSPER participants is feasible and may determine new and novel risk factors for dementia and assess the long-term effect of a period of treatment with pravastatin.
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Stanyer, Lee. "Beta-amyloid/plasma lipoprotein interactions : implications for vascular damage." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270774.
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Warsch, Jessica. "Subclinical Vascular Brain Damage, Vascular Risk Factors, and Depression in Successful Cognitive Aging." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/644.
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Currently, about one in every eight Americans is age 65 or older; by the year 2050, it will be one in five people. Given this graying of the population, research into successful aging is of increasing relevance. The question of how to precisely define successful aging, however, has not been completely answered. Likewise, the role of vascular risk factors, subclinical vascular brain damage, and other biopsychosocial characteristics in normal cognitive aging are not well understood. This Dissertation focused on the identification of some of the physiological, behavioral, and social risk factors that distinguish people able to maintain extraordinary health at an advanced age. Specifically, we aimed to create an ecologically valid definition of successful aging that incorporates both physical well-being and cognitive abilities, and to report the prevalence of successful cognitive aging in a population-based multi-ethnic cohort of older adults. We sought to describe how the prevalence varies by several sociodemographic and psychosocial determinants, and to investigate global vascular risk, depressive symptomatology, and MRI markers of subclinical vascular brain damage as correlates of successful cognitive aging. We observed the prevalence of successful cognitive aging to be 37% in the study sample (N=1,162) of a diverse racial/ethnic population in Northern Manhattan (NYC, NY). The prevalence decreased with increasing age; we did not observe any differences by racial/ethnic group, but did note a lower prevalence with lower socioeconomic status. Several social resources and self-reported quality of life were related to successful cognitive aging, and appeared more important than demographic variables alone. We found that the likelihood of successful cognitive aging decreases with increasing global vascular risk score, more severe depressive symptomatology, and greater white matter damage. The field of successful aging requires further study. Consideration of such biopsychosocial factors as socioeconomic status, social support, quality of life, and depressive symptoms alongside novel indicators of disease and disability including global vascular risk and white matter hyperintensity burden is essential. It may lead to a more robust definition of successful cognitive aging replete with opportunities to modify the aging process, as many of the factors investigated in this study are modifiable.
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Matas, Pericas Laia. "Risc cardiovascular en pacients que consulten a urgències d’un hospital general amb un accident vascular agut." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/405517.
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La malaltia cardiovascular suposa un problema de salut mundial amb gran morbimortalitat associada. L’arteriosclerosi, que la ocasiona, és una malaltia inflamatòria sistèmica en la que hi influencien diversos factors de risc cardiovasculars: edat, gènere, hipertensió arterial (HTA), dislipèmia, tabac, diabetis mellitus (DM), obesitat i malaltia renal crònica (MRC). Altres factors com la fibril·lació auricular (FA) i la malaltia vascular prèvia (MVP) hi influencien. En ocasions es produeixen canvis en la placa d’ateroma que condueixen a l’infart, sigui en territori coronari, cerebrovascular o arterial perifèric. El per què es desenvolupen en unes artèries o unes altres no és del tot conegut però els pacients tendeixen a repetir esdeveniments en el mateix territori.
La hipòtesi: Els factors de risc cardiovascular influencien d’una manera diferent que un accident vascular agut es presenti en un territori arterial o en un altre (Síndrome coronària aguda (SCA), accident cerebrovascular (AVC) o malaltia arterial perifèrica crítica (MAP)).
S’han descrit les característiques d’una població de 2993 pacients consecutius que han ingressat a urgències d’un hospital general per SCA, AVC o MAP durant tres anys comparant els tres motius d’ingrés. La població estudiada presenta una elevada prevalença de factors de risc clàssic, té menys dones i més edat que d’altres poblacions descrites a la literatura.
Els pacients estudiats presenten: 74.2 anys (62.9;81.4), 70.7% són homes, 75.6% HTA, 59% DLP, 20.2% DLP-aterogènica, 18.4% FA, 23% MRC, >35.7% MVP, DM en un 40%, i disglicèmia en 30.3%, diagnòstic de nou d’HTA en 7%. Determinar la HbA1C és una eina fàcil d’implementar i millora la detecció de nous casos de DM en pacients que ingressen per accident vascular agut. S’han diagnosticat 7.2% de DM de nou. Hi ha marge de millora en la prevenció secundària i el grau de control tant en SCA, AVC com en MAP. Destaca el menor ús de fàrmacs antihipertensius en el grup que ingressa per AVC. Un 6.6% dels pacients són èxitus durant l’ingrés, moren més els que ingressen per MAP i menys els SCA. Els factors que predisposen a reingressar per un nou accident vascular són: presència de MVP, MRC, DM i tabac. En canvi en els >75 anys aquests factors són: MVP i DM.
En la població estudiada la dislipèmia, l’obesitat l’exposició al tabac (fumadors i exfumadors) i la MRC són els factors que més pesen a l’hora de presentar un primer SCA en comptes d’AVC o MAP. L’edat avançada, la HTA i la FA són els factors que més influencien a l’hora de presentar un AVC en comptes de SCA o MAP. L’edat avançada i la DM són els factors que influencien més a l’hora de presentar una MAP en comptes d’un accident vascular agut en forma de SCA o AVC. En els pacients amb DM el pes dels altres factors de risc per a presentar un accident en un determinat territori en comptes d’un altre s’atenua, mantenint-se la HTA i FA com a factors de major pes per patir un primer AVC respecte SCA i MAP.Cardiovascular disease (CVD) represents a global health problem with high morbidity and mortality. Atherosclerosis, the cause of CVD, is a systemic inflammatory disease that is influenced by traditional cardiovascular risk factors: age, gender, high blood pressure (HBP), dyslipidaemia (DLP), smoking, diabetes mellitus (DM), obesity and chronic kidney disease ( CKD), as Atrial fibrillation (AF) and prior vascular disease (PVD) are also contributing factors to CVD. Changes in the atherosclerotic plaque can lead to an acute vascular event in different territories: acute coronary syndrome (ACS), cerebrovascular (stroke) or peripheral arterial critical limb disease (PAD). The development of a clinical atherosclerotic event in one arterial vascular territory is not fully understood, but patients tend to repeat events in the same territory. This thesis shows that an association between cardiovascular risk factors and the probability of developing an atherosclerotic event in a particular territory can be made. The study group consists on 2993 patients that were admitted consecutively in the emergency room due to an acute vascular event, ACS, CVA or PAD during a 3 years period. Demographic data, CVR factors, previous events (PVD), previous treatments, in hospital readmission and mortality during the study period were collected from the medical record in a data base. The study also included the evaluation lipid and glycaemic control (HvA1c) and renal function by blood samples analysis. The study compared the collected data for the three events. The analysis of data shows that the population included in this study had a high prevalence of classical CV risk factors, there were less proportion of women and first events appeared in older ages than other populations described in the literature. The characteristics of the studied group were: 74.2 years old [62.9; 81.4], 70.7% men, 75.6% HBP, 59% DLP 20.2% DLP-atherogenic, 18.4% FA, 23% MRC,> 35.7% PVD DM 40%, preDM in 30.3% and 7% of patients have been diagnosed of of new onset hypertension. HbA1C helped detecting 7.2% of new onset DM, showing that HbA1c study should be included for all patients diagnosed for an accute vascular event . The study shows that the secondary prevention for the vascular events included needs to be improved. In particular, we detected a lesser use of antihypertensive drugs in the patients admitted due to a first stroke even if they represented higher proportion of HBP. In our series there was 6.6% inhospital mortality. Mortality rate tended to be higher in patients admitted by PAD than by SCA. Predisposing readmission risk factors were: presence of PVD, CKD, DM and tobacco. However in the> 75 years these factors were: PVD and DM. Factors that have a positive influence on presenting ACS instead of the other two vascular accidents were: DLP, obesity, tobacco exposure (smokers and ex-smokers) and CKD. In the cerebrovascular territory predisposing factors are: the elderly, HBP and AF. Older age and DM are factors that influence in presenting PAD instead of an ACV or ACS. In DM patients the influence of other risk factors is attenuated when having the first acute vascular event. HBP and AF mantain their influence in suffering a first stroke in population with DM.
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Rönnemaa, Elina. "Predictors of Dementia : Insulin, Fatty Acids and Vascular Risk Factors." Doctoral thesis, Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-164528.
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Identification of modifiable risk factors for Alzheimer’s disease (AD) is crucial in order to diminish suffering from this devastating disease. The aim of this thesis was to investigate if different aspects of glucose metabolism, insulin, fatty-acid composition or other vascular risk factors predict the future development of AD and dementia. This thesis is based on the Uppsala Longitudinal Study of Adult Men (ULSAM) cohort, which started in 1970. A total of 2322 men at age 50 were examined with focus on vascular risk factors. The cohort was re-examined at ages 60, 71, 77, 82 and 88. Incident diagnoses of AD, vascular dementia, other dementias and cognitive impairment were assessed in 2005–2010. The risk of AD was increased in subjects with lower early insulin response measured with both an intravenous glucose tolerance test at 50 years and an oral glucose tolerance test at 71 years of age. The presence of vascular risk factors such as hypertension, obesity, hypercholesterolemia and smoking increased the risk of future vascular dementia but not of AD. Furthermore, saturated fatty acids at midlife were inversely associated with risk of AD. No evidence of a protective effect of omega-3 fatty acids against dementia was found. The susceptibility allele, APOE ε4, was the strongest individual risk factor. APOE ε4 carriers with vascular risk factors had the greatest risk of developing dementia. Low insulin response was a risk factor for AD mainly in APOE ε4 non-carriers. Disturbances in insulin and glucose metabolism, vascular risk factors and fatty acids are linked differentially to the pathogenesis of AD and vascular dementia. These observations should be considered when future clinical approaches are planned to prevent and postpone the onset of dementia.ULSAM
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Howard, Kellee. "The relationship between vascular risk factors and vascular cognitive impairment, a secondary analysis of a dataset." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0033/MQ66626.pdf.
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Al-Shoumer, Kamal Abdul Aziz Sulaiman. "Studies on intermediary metabolism and vascular risk factors in hypopituitary patients." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289334.
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Satuè, Gracia Eva María. "Epidemiología de la enfermedad cerebrovascular isquémica en mayores de 60 años del área de Tarragona: datos del estudio CAPAMIS." Doctoral thesis, Universitat Rovira i Virgili, 2019. http://hdl.handle.net/10803/667076.
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Antecedents. L'ictus és una important causa de mortalitat però també va en augment el nombre de persones que sobreviuen després de patir-lo. El seu abordatge i seguiment constitueixen una prioritat en política sanitària. Aquest estudi aporta dades rigoroses i actualitzades, incloent incidències en subgrups de població específics, del nostre territori que permetran un millor coneixement i maneig de la malaltia.
Material i mètodes. Estudi de cohorts de base poblacional. Va incloure 27.204 pacients ≥ 60 anys de la comarca del tarragonès, seguits durant 36 mesos. A partir de registres de l’estació clínica atenció primària (e-cap), es van recollir variables demogràfiques, factors de risc i comorbiditats a l'inici. Es van revisar informes d'alta hospitalària amb diagnòstic d'ictus isquèmic i es van calcular taxes d'incidència (per 100.000 persones-any), globals i per subgrups de pacients, i índexs de letalitat. Mitjançant model de regressió de Cox es va estimar l'associació entre característiques basals i temps fins a primer esdeveniment.
Resultats. La incidència global va ser de 435 / 100.000 persones-any. Es van associar de manera significativa i independent a major risc d'ictus isquèmic: ictus previ, fibril·lació auricular, cardiopatia isquèmica, tabaquisme actiu, diabetis i edat. L'índex de letalitat va ser de 13,1% i va augmentar amb l'edat, arribant al 21% en el grup de 80 o més anys.
Discussió. La incidència i letalitat d'ictus isquèmic en el nostre territori es poden considerar mitjanes respecte a Espanya i baixes respecte al conjunt d'Europa. Cal destacar l'antecedent de malaltia arterioscleròtica (principalment ictus previ) i la fibril·lació auricular com els principals factors de risc en aquest grup d'edat.Antecedentes. El ictus es una importante causa de mortalidad pero también va en aumento el número de personas que sobreviven tras sufrirlo. Su abordaje y seguimiento constituyen una prioridad en política sanitaria. Este estudio aporta datos rigurosos y actualizados, incluyendo incidencias en subgrupos de población específicos, de nuestro territorio que permitirán un mejor conocimiento y manejo de la enfermedad. Material y métodos. Estudio de cohortes de base poblacional. Incluyó 27.204 pacientes ≥ 60 años de la comarca del tarragonés, seguidos durante 36 meses. A partir de registros de estación clínica atención primaria (e-cap), se recogieron variables demográficas, factores de riesgo y comorbilidades al inicio. Se revisaron informes de alta hospitalaria con diagnóstico de ictus isquémico y se calcularon tasas de incidencia (por 100.000 personas-año), globales y por subgrupos de pacientes, e índices de letalidad. Mediante modelo de regresión de Cox se estimó la asociación entre características basales y tiempo hasta primer evento Resultados. La incidencia global fue de 435/100.000 personas-año. Se asociaron de manera significativa e independiente a mayor riesgo de ictus isquémico: ictus previo, fibrilación auricular, cardiopatía isquémica, tabaquismo activo, diabetes y edad. El índice de letalidad fue de 13,1% y aumentó con la edad, alcanzando el 21% en el grupo de 80 ó más años. Discusión. La incidencia y letalidad de ictus isquémico en nuestro territorio se pueden considerar medias respecto a España y bajas respecto al conjunto de Europa. Cabe destacar el antecedente de enfermedad arteriosclerótica (principalmente ictus previo) y la fibrilación auricular como los principales factores de riesgo en este grupo de edad.
Background. Stroke is an important cause of mortality and the number of stroke survivors is also increasing. Their approach and follow-up are a priority in health policy. This study provides rigorous and up-to-date data, including incidences in specific population subgroups, of our territory that will allow a better knowledge and management of the disease. Methods. Population based cohort study. It included 27,204 patients ≥ 60 years of the region of Tarragona, followed during 36 months. Demographic variables, risk factors and basal comorbidities were registered from primary care computerized clinical records (e-cap). Hospital discharge reports with ischemic stroke diagnosis were reviewed; global and by subgroups of patients incidence rates (per 100,000 persons-year) were calculated, as well as lethality rates. The association between basal characteristics and time to first event was estimated using Cox regression models. Results. The overall incidence was 435 / 100,000 persons-year. Basal conditions significantly and independently associated with an increased risk of ischemic stroke were: previous stroke, atrial fibrillation, ischemic heart disease, active smoking, diabetes and age. The case-fatality rate was 13.1% and increased with age, reaching 21% in the group of 80 or more years. Discussion. The incidence and lethality of ischemic stroke in our territory can be considered medium referred to Spain and low referred to the whole of Europe. The history of arteriosclerotic disease (especially previous stroke) and atrial fibrillation are the main risk factors in this age group.
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Pathansali, Rohan. "The role of megakaryocytes and platelets in vascular risk factors and vascular disease and the effects of treatment." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412571.
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Sigvant, Birgitta. "Epidemiological aspects of peripheral arterial disease." Stockholm : Department of Molecular Medicine and Surgery, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-670-5/.
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Reitz, Christiane. "Genetic and vascular risk factors for cognitive decline and cerebral small-vessel disease." [S.l.] : [The Author], 2006. http://hdl.handle.net/1765/13309.
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Webb, A. T. "Vascular disease in renal replacement therapy and its relation to underlying risk factors." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398457.
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Inthawong, Rungkarn. "Assessing the impact of reducing risk factors for cardio-vascular disease in Thailand." Thesis, Sheffield Hallam University, 2015. http://shura.shu.ac.uk/20833/.
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Cardiovascular disease (CVD) is a global health problem and there has been an epidemiological transition of CVD from high income countries to low-middle income countries. In the case of Thailand, the prevalence of heart disease and stroke is increasing. In order to reduce the risk of CVD, the Ministry of Public Health in Thailand has implemented a number of primary CVD prevention strategies within the last decade. These strategies are being specifically implemented to address the future potential economic burden of increasing CVD. However, the economic impact of reducing multiple risk factors, at a population level in Thailand, in terms of health care costs is unclear. In order to plan for investment in public health interventions within finite resources, it is imperative that decision makers have sufficient information to identify the target populations and risk reduction strategies, and to assess the impact of these strategies on the population. This study aims to estimate the future prevalence of CVD in Thailand over the next 5-10 years and the potential economic and health benefits of strategies to reduce the population risk factors during this period. The mathematic CVD cost-offset model has been developed in this study in 7 stages. 1) Descriptive analysis of the CVD risk profile data from the 4th National Health Examination Survey (NHESIV) 2008-2009 data set in order to explore the association of CVD risk factors in Thailand. 2) Calculate the probability of future CVD event which applies the CVD risk prediction equation. 3) Estimate of the number of future CVD events. 4) Validation of the estimated number of annual CVD event with the actual CVD hospitalisation event in Thailand. 5) Calculate the cost of hospital admission due to CVD from the Universal Coverage Health Care Scheme (UC) data in 2009. 6) Estimate the burden of CVD in terms of the DALYs. 7) Estimate the impact of reducingCVD risk factors in different scenarios. The study outcomes being the number of hospitalisation cost savings, number of premature death savings, DALY savings and health care cost savings. The outcomes will also account for the uncertainty analysis. As indicated above, no studies currently exist that focus specifically on the mathematic model for estimating the future situation of CVD in Thailand. Therefore, this study represents an original contribution to that knowledge. The findings of this study will contribute to health policy by providing specific new knowledge and information regarding Thai CVD risk factors and the impact of the risk reduction which will assist health policy makers in the planning and future investment in prevention programs for CVD in Thailand. Moreover, it is expected that the finding from this research will establish a CVD prediction model for Thailand, and one which may be applicable and compatible to the Asia and Pacific regions.
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Israelsson, Larsen Hanna. "Comorbidity and vascular risk factors associated with idiopathic normal pressure hydrocephalus : the INPH-CRasH Study." Doctoral thesis, Umeå universitet, Institutionen för farmakologi och klinisk neurovetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120175.
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Idiopathic normal pressure hydrocephalus (INPH) is a dementia treatable by insertion of a cerebrospinal fluid shunt. It has been suggested that INPH has similar pathophysiological mechanisms as cerebrovascular disease, but the vascular risk factor (VRF) profile of INPH patients has not been assessed using a modern epidemiological approach. The cognitive symptoms of INPH resemble the symptoms of depression, but the prevalence of depression among INPH patients is unknown. In addition, few studies investigate the impact of shunting on the quality of life (QoL), and no study has investigated the impact of comorbidity on QoL in INPH patients. The objective of this dissertation was to present the VRF profile of INPH and to investigate the hypothesis that INPH may be a subgroup of vascular dementia. Additional objectives were to assess the prevalence of depression in INPH patients and to investigate the impact of shunting and comorbidities on QoL in INPH. In the first cohort, the prevalence of possible INPH was assessed through clinical and radiological examinations in patients with a transient ischemic attack (TIA), consecutively admitted to the same hospital during 2006-2008. In the second cohort, VRFs, vascular disease and QoL were analysed in INPH patients consecutively shunted 2008-2010 in five out of six neurosurgical centres in Sweden. Patients remaining after inclusion (n=176, within the age-span 60-85 years and not having dementia) were compared to population-based age- and gender-matched controls (n=368, same inclusion criteria as for the INPH patients). Assessed VRFs were: hypertension, diabetes, obesity, hyperlipidemia, psychosocial factors (stress and depression), smoking, alcohol intake, physical activity and, dietary pattern. Cardiovascular, cerebrovascular and peripheral vascular disease as well as QoL were also assessed. Parameters were assessed through questionnaires, clinical examinations, measurements, ECG and, blood samples. In the first cohort, 4% of the TIA patients had clinically and radiologically verified INPH. In the second cohort, VRFs were overrepresented among the INPH patients compared with the controls. The VRFs independently associated with INPH were: hyperlipidemia (Odds ratio (OR): 2.4, 95%CI: 1.4-4.0), diabetes (OR: 2.2, 95%CI: 1.2-3.9), obesity (OR: 5.4, 95%CI: 2.5-11.8) and, psychosocial factors (OR: 5.3, 95%CI: 3.2-8.9). When adding the VRFs that were overrepresented in INPH, although not independently (physical inactivity and hypertension), these six VRFs accounted for 24% of the INPH cases in the elderly population (population attributable risk %: 24). Depression was overrepresented in shunted INPH patients compared to the controls (46% vs. 13%, p<0.001) and the main predictor for low QoL was a coexisting depression (p<0.001). In conclusion, the results of the INPH-CRasH study are consistent with a vascular pathophysiological component of INPH and indicate that INPH may be subgroup of vascular dementia. In clinical care and research, a complete risk factor analysis as well as screening for depression and a measurement for quality of life should be included in the work-up of INPH patients. The effect of targeted interventions against modifiable VRFs and anti-depressant treatment in INPH patients should be evaluated.Idiopatisk normaltryckshydrocefalus (INPH, från engelskans ”idiopathic normal pressure hydrocephalus”) är en neurokirurgiskt behandlingsbar demens. Behandlingen är att operera in en shunt som dränerar cerebrospinalvätska från ventriklarna. Det har föreslagits att INPH skulle kunna orsakas av liknande patofysiologiska mekanismer som vid cerebrovaskulär sjukdom, men den vaskulära riskfaktorprofilen hos INPH-patienter har aldrig undersökts i en modern epidemiologisk studie. De kognitiva symtomen vid INPH påminner om symtomen vid depression, men prevalensen av depression hos INPH-patienter är okänd. Få studier undersöker hur shuntning påverkar livskvalitet och ingen studie har undersökt hur komorbiditet påverkar livskvaliteten vid INPH. Syftet med den här avhandlingen var att undersöka den vaskulära riskfaktorprofilen hos INPH-patienter samt att utforska hypotesen att INPH skulle kunna vara en undergrupp till vaskulär demens. Ytterligare ett syfte med avhandlingen var att undersöka hur många INPH-patienter som har depression samt undersöka hur shunting och komorbiditet påverkar livskvalitet vid INPH. I den första kohorten undersöktes kliniska och radiologiska fynd som tydde på INPH hos de patienter som blivit diagnostiserade med en TIA (från engelskans: transient ischemic attack) 2006-2008 på Norrlands Universitetssjukhus i Umeå. I den andra kohorten undersöktes konsekutivt shuntade INPH-patienter 2008-2010 från fem av sex neurokirurgiska kliniker i Sverige. De patienter som inkluderades i studien (n=176, ålder: 60-85 år, ej dementa) jämfördes med köns- och åldersmatchade kontroller från normalpopulationen (n=368, samma inklusionskriterier som för INPH-patienterna). De riskfaktorer som undersöktes var: hypertension, hyperlipidemi, diabetes, fetma, psykosociala faktorer (stress och depression), rökning, alkohol, fysisk aktivitet och diet. Även kardiovaskulära och cerebrovaskulära sjukdomar undersöktes, liksom perifer vaskulär sjukdom samt livskvalitet. Datainsamling skedde genom frågeformulär, kliniska undersökningar, mätningar, EKG och blodprov. I den första kohorten hade 4% av TIA-patienterna kliniskt och radiologiskt verifierad INPH. I den andra kohorten var vaskulära riskfaktorer överrepresenterade hos INPH-patienterna jämfört med iv normalpopulationen. Hyperlipidemi (OR: 2.4, 95%CI: 1.4-4.0), diabetes (OR: 2.2, 95%CI: 1.2-3.9), fetma (OR: 5.4, 95%CI: 2.5-11.8) och psykosociala faktorer (OR: 5.3, 95%CI: 3.2-8.9) var associerade med INPH oberoende av kön, ålder och de andra riskfaktorerna. Hypertension och fysisk inaktivitet var också associerade med INPH, dock inte oberoende av övriga riskfaktorer. Sammanlagd PAR% (från engelskans: population attributable risk %) för de här sex riskfaktorerna var 24%. INPH-patienterna hade depression i högre utsträckning än kontrollerna (46% vs. 13%, p<0.001), och depression var den viktigaste prediktorn för låg livskvalitet. Resultaten tyder på att vaskulär sjukdom och vaskulära riskfaktorer är involverade i den patofysiologiska mekanismen vid INPH. INPH kan vara en undergrupp till vaskulär demens. En fullständig riskfaktoranalys och screening för depression bör ingå i den preoperativa utvärderingen såväl som i forskning på INPH-patienter, och ett mått på livskvalitet bör införas. Effekten av riktade insatser mot såväl vaskulära riskfaktorer som depression vid INPH bör utvärderas.
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Félix, Joana Filipa Cancela. "Influência dos factores de risco vascular no desempenho cognitivo." Master's thesis, Universidade de Évora, 2009. http://hdl.handle.net/10174/19014.
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O objetivo deste estudo consiste em verificar até que ponto os sujeitos com fatores de risco vascular acentuados apresentam alterações no seu desempenho cognitivo, na ausência de lesão vascular conhecida. Para tal, os défices apresentados por estes foram comparados com sujeitos que se encontram na fase pós-aguda do AVC (Acidente Vascular Cerebral) e sujeitos do grupo de controlo. Os défices cognitivos foram avaliados através de uma bateria de testes neuro psicológicos estandardizados, nos quais se avaliou a atenção, memória e funções executivas. Os resultados parecem confirmar a existência de um défice significativo nos sujeitos com fatores de risco em relação ao grupo de controlo, no que diz respeito à memória verbal e visual a curto-prazo e capacidade de aprendizagem. Assim, com base nos resultados podemos inferir a possibilidade de que os fatores de risco, por si só, podem causar determinado tipo de défice cognitivo. / ABSTRACT: The aim of this study is to determine the extent to which individuals with vascular risk factors have pronounced changes in their cognitive performance, in the absence of known vascular injury. For this purpose, the deficits presented by these subjects were compared to those who are in the post-acute stage of the Stroke and subjects in the control group. Cognitive deficits were assessed using a battery of standardized neuro¬ psychological tests, in which it was assessed attention, memory and executive functions. The results seem to confirm the existence of a significant deficit in subjects with risk factors in relation to the control group in what regards to short-term verbal and visual memory and learning ability. Therefore, based on the results we may imply the possibility that risk factors by themselves can cause certain types of cognitive impairment.
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Dynan, Kevin B. "A study of recently proposed cardiovascular risk factors in Alzheimer's disease and vascular dementia." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322645.
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Kemp, Merlisa Claudia. "Ultrasound investigation of risk factors for extracranial vascular pathology in patients with multiple sclerosis." Thesis, Cape Peninsula University of Technology, 2019. http://hdl.handle.net/20.500.11838/3078.
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Thesis (Doctor of Radiography (Ultrasound))--Cape Peninsula University of Technology, 2019Introduction: Cerebral hypoperfusion and impaired cerebral venous drainage are reported to be risk factors for multiple sclerosis (MS). Furthermore, lifestyle and biochemistry have significant effects on the brain and vascular system. This study investigates, with vascular ultrasound, the risk factors for extracranial vascular disease in patients with MS. Methods: Grey-scale imaging, Colour and Spectral Doppler analysis of the carotid arteries and internal jugular veins were performed on a cohort of 50 female participants (25 MS patients and 25 age-matched controls). The major neck vessels were sonographically interrogated to determine patency, carotid intima media thickness (cIMT), carotid artery cross-sectional diameters (CSD), internal jugular vein (IJV) cross-sectional area (CSA), stenosis, occlusions and abnormal blood flow patterns. Both cohorts underwent blood tests, genetic tests and a lifestyle assessment. The MS participants had a neurological assessment to determine MS disability status (Expanded Disability Status Scale, EDSS). Results: Statistically significant associations (p-value <0.05) were found between the extracranial vascular ultrasound variables and biochemical markers (s-iron, s-transferrin, %Tf saturation, ferritin, haemoglobin, vitamin B12, s-folate, homocysteine, CRP, 25-OH vitamin D, total cholesterol, HDL and triglycerides), lifestyle factors, genetic factors (HLA DRB1*1501 allele) and MS disability in both cohorts. The carotid artery blood flow parameters were negatively associated with MS disability, whereas the cIMT was positively associated with MS disability. Physical activity was positively associated with carotid artery blood flow velocities and passive smoking was found to have a negative association in the MS cohort of participants. Passive smokers also demonstrated a larger IJV CSA in comparison to non-smokers in both cohorts. In addition, drinking 1-13 units of alcohol/week was positively associated with carotid blood flow velocities in MS participants. Conclusion: Several significant positive and negative associations between extracranial vascular ultrasound variables and genetic, lifestyle, biochemical and vascular factors as well as MS disability were demonstrated in this study. The new MS findings that unfolded in this study include significant associations between: 1) the carotid vessel diameters and biochemical and lifestyle parameters as well as the presence of the HLA DRB1*1501 allele; 2) IJV CSA in MS and biochemical and lifestyle parameters, specifically passive smoking; 3) MS disability and carotid artery blood flow velocities; and 4) carotid artery blood flow parameters and biochemical markers. Further studies are therefore needed to establish the clinical relevance of these new findings.
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Mumaw, Matthew A. "The Role of Frontal Lobe White Matter Integrity and Executive Functioning in Predicting Adaptive Functioning in Alzheimer's Disease." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/psych_diss/102.
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Alzheimer’s disease (AD) is the most common form of dementia and is characterized by a gradual deterioration of the patients’ ability to independently perform day to day activities. Researchers have discovered significant changes in neuroanatomy, cognition and behavior that are related to the disease process of AD and researchers continue to uncover new variables, such as the presence of vascular risk factors, which may further increase our ability to understand and characterize the disease. The purpose of this study is to identify the neuroanatomical, cognitive and behavioral variables that best predict impairment of instrumental activities of daily living in individuals with probable AD.
Reduced white matter integrity in the dorsolateral prefrontal cortex as well as the presence of vascular risk factors significantly predicted impairments in activities of daily living (ADLs). Executive functioning skills, typically described as frontal lobe system behaviors, were positively associated with ADLs. Further, executive functions fully mediated the relationship between frontal lobe white matter integrity and ADLs. A better understanding of the variables responsible for diminished ADLs in AD will allow researchers and clinicians to better target prevention and intervention strategies and ultimately help individuals with AD to maintain their independence for a longer duration.
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McCullagh, C. D. "An investigation of inflammatory and vascular genetic risk factors for stroke and dementia following stroke." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403191.
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Al-Janabi, Omar M. "CEREBROVASCULAR RISK FACTORS, ARTERIOLAR SCLEROSIS, AND COGNITIVE DECLINE IN THE KENTUCKY APPALACHIAN “STROKE-BELT”." UKnowledge, 2016. http://uknowledge.uky.edu/medsci_etds/5.
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The relationship between cerebrovascular disease (CVD) risk factors and cognitive impairment or dementia has been widely studied with significant variability in findings between groups. We hypothesized that chronic small vessel injury in the form of arteriolar sclerosis, measured quantitatively using MRI to measure total white matter hyperintensity (WMH) volumes, would identify specific association of CVD risk factors and patterns of cognitive decline, associated with mild cognitive impairment of the cerebrovascular type, that represent the core features of vascular cognitive impairment in our cohort.
A Cross-sectional analysis of clinical and quantitative MRI data on 114 subjects with normal cognitive function (n=52) and mild cognitive impairment (MCI; n=62) was performed. Quantitative total WMH volumes were examined in relation to potentially causative CVD risk factors and resultant test scores across cognitive domains using linear regression models adjusted for age, gender, and education.
Among CVD risk factors analyzed, age (p< 0.001), education (p= 0.003), hypertension (p= 0.012), and hyperlipidemia (p= 0.008) demonstrated the strongest associations with WMH volumes. Conversely, diabetes, smoking, history of heart attacks, atrial fibrillation, and history of stroke that have shown associations with CVD pathology on imaging in other studies were not statistically associated with increased WMH in this cohort. WMH volumes were associated with decrease performance on the Trial Making Test type A & B and long delayed free recall on the California Verbal Learning Test.
Our findings suggest similarities and yet differences in comparison to other studies. Hypertension and hyperlipidemia appear to represent common shared risks across geographically disparate groups. Our findings, like others, suggest CVD pathology impact processing speed and executive function and provide further evidence for CVD effects on short-term memory in those at risk for cognitive decline and the future development of dementia in our cohort.
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Silva, Magnolia Moreira da. "Associação entre fatores de risco cardiovasculares e demência vascular definitiva." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/7/7139/tde-05112018-151715/.
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Introdução: Estudos prévios analisaram a associação entre fatores de risco cardiovascular (FRCV) associados ao diagnóstico de demência vascular (DV) provável ou possível. No entanto, não foram encontrados estudos que analisassem a associação entre FRCV e a ocorrência de DV definitiva. Dessa maneira, ainda permanece obscura a associação entre os FRCV e a ocorrência de DV definitiva, ou seja, aquela diagnosticada por meio do exame neuropatológico, no qual se apresenta como padrão ouro. Objetivo: Avaliar a associação entre os FRCV e a ocorrência de DV definitiva, pura e mista. Método: Por meio de um estudo transversal foram analisados 707 casos pertencentes à casuística do Banco de Encéfalos Humanos do Grupo de Estudos em Envelhecimento (BEHGEEC) da FMUSP, que respeitaram os critérios de inclusão. A existência de fatores de risco cardiovascular em vida (Hipertensão Arterial, Diabetes Mellitus, Dislipidemia, Tabagismo, Etilismo, Obesidade e Sedentarismo), reportada por um informante com convivido minimamente semanal durante a autópsia, foi associada ao diagnóstico neuropatológico de demência vascular emitido por um neuropatologista. Modelos de regressão logística (sem e com ajuste para sexo, idade e raça) foram construídos para testar a associação entre os FRCV e o diagnóstico de DV, DV pura e DV mista. Foi testada a capacidade preditiva dos fatores que se mostraram preditores de DV por meio da Curva ROC. Resultados: O sedentarismo foi um preditor independente de DV (OR 1,943; IC95% 1,198 3,151; p= 0,007) e DV pura (OR 3,148; IC95% 1,428 6,941;p= 0,004). A HAS foi um preditor independente de DV mista (OR 2,240; IC95% 1,216 4,126; p= 0.01). O sedentarismo não apresentou boa capacidade preditiva para a DV e DV Pura (AUC = 0,380 e 0,337, respectivamente), assim como a HAS para a DV Mista (AUC = 0,459). Conclusões: Dentre os FRCV o sedentarismo e a HAS foram os que se associaram a um aumento no risco de DV.Introduction: Previous studies have analyzed the association between cardiovascular risk factors (CVRF) associated with the diagnosis (probable or possible) of vascular dementia (VaD). However, there are no studies that have analyzed the association between CVRF and the occurrence of definitive VaD. The association between CVRF and the occurrence of definite VaD, neuropathologically defined and considered as gold-standard, remains obscure. Objectives: To evaluate the association between CVRF and the occurrence of definitive VaD, pure and mixed. Methods: This is a cross-sectional study which evaluated 707 cases belonging to the Bain Bank of the Brazilian Aging Brain Study Group (BBBABSG) of FMUSP, respecting the inclusion criteria. The history of existence of cardiovascular risk factors in life (hypertension, diabetes mellitus, dyslipidemia, smoking, alcoholism, obesity, and sedentarism) reported by a knowledgeable next-of-kin, with at least weekly contact with the deceased, was associated with the neuropathological diagnosis of vascular dementia reported by a neuropathologist after the autopsy exam. Logistic regression models (with and without adjustment for sex, age and race) were tested to show the association between CVRF and the diagnosis of VaD, pure Vad and mixed VaD. It was also tested the predictive capacity of the factors that proved to be predictors of VaD through the ROC Curve. Results: Sedentary lifestyle was an independent predictor of VaD (OR 1,943, CI 95% 1,198 - 3,151, p = 0.007) and of Pure VaD (OR 3,148, 95% CI, 1.428 - 6.941, p = 0.004). Hypertension was an independent predictor of Mixed VaD (OR 2,240, 95% CI 1,216 - 4,126, p = 0.01). Sedentary lifestyle did not present good predictive capacity for VaD and Pure VaD (AUC = 0.380 and 0.337, respectively), as Hypertension for Mixed DV did not either (AUC = 0.459). Conclusions: Among the CVRF, sedentarism and hypertension were those associated with an increase VaD risk.
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Achmat, Ghaleelullah. "Coronary artery disease risk factors among fire-fighters in the Western Cape Province." University of the Western Cape, 2017. http://hdl.handle.net/11394/6294.
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Magister Sport, Recreation and Exercise Science - MSRESThe work demands involved in fire-fighting place significant stress on the cardiovascular system. Cardiovascular disease is the leading cause of on-duty death among fire fighters and is a major cause of morbidity. This study investigated the prevalence of coronary artery disease risk factors among career fire fighters in the Western Cape.
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Florvall, Gösta, Samar Basu, Johanna Helmersson, and Anders Larsson. "Microalbuminuria, blood pressure and cardiovascular risk factors in elderly males." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6151.
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Objective - To correlate blood pressure and inflammatory markers with urine albumin analysed with a point-of-care testing (POCT) instrument, nephelometric determination of albumin and creatinine related urine albumin in elderly males.
Methods and Results - The study population consisted of 103 diabetic and 603 nondiabetic males (age 77 years) in a cross-sectional study in central Sweden. We analyzed urine albumin with a HemoCue® Urine Albumin POCT instrument and a ProSpec® nephelometer and creatinine related urine albumin. There were strong correlation between both systolic and diastolic blood pressure and all three urine albumin methods (p<0.0001). There were also significant correlations between the different urine albumin measurements and SAA, hsCRP and IL-6.
Conclusions - Hypertension has a strong impact on hyperfiltration in diabetic and nondiabetic elderly males.
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Harbaoui, Brahim. "Rigidité Vasculaire en cardiologie interventionnelle." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1265/document.
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Le vieillissement vasculaire est un phénomène inéluctable. Il s'accompagne de modifications structurelles et fonctionnelles du système cardio-vasculaire constituant la rigidité vasculaire. Ce processus dégénératif affecte essentiellement la matrice extra cellulaire des artères élastiques. La perte de l'élasticité du système vasculaire va impacter la fonction ventriculaire gauche et la perfusion cardiaque, rénale et cérébrale par des mécanismes différents. La rigidité vasculaire est un puissant marqueur de risque cardio-vasculaire. Cette notion est peu répandue dans le domaine de la cardiologie interventionnelle alors qu'elle pourrait avoir des implications pronostiques et thérapeutiques importantes. Nous nous sommes intéressés à deux domaines de la cardiologie interventionnelle, pour lesquels la rigidité vasculaire pourrait ouvrir de nouvelles voies de recherche, la maladie coronaire et le traitement interventionnel du rétrécissement aortique. Concernant la maladie coronaire il existe un besoin de mieux comprendre la physiopathologie de la microcirculation et de l'ischémie myocardique. La survenue des accidents coronaires aigus reste également incomplètement comprise. Nous avons abordé la problématique par une approche épidémiologique en étudiant l'impact pronostique de la rigidité vasculaire sur la mortalité liée aux coronaropathies dans une cohorte de 1034 patients hypertendus avec 30 années de suivi. La rigidité vasculaire a été appréciée par la pression pulsée et un score d'athérosclérose de l'aorte abdominale. Un lien très fort a été mis en évidence entre la rigidité vasculaire et la survenue d'infarctus du myocarde. Nous avons ensuite développé un moyen d'étudier la rigidité vasculaire localement au niveau des artères coronaires. Nous avons mis au point une technique de mesure de la vitesse de l'onde de pouls coronaire. Cette technique repose sur l'utilisation d'un guide de pression ntra-coronaire et un algorithme breveté du traitement de signal. Nous sommes parvenus à mesurer une vitesse de l'onde de pouls sur 71 artères coronaires chez 49 patients. Nous avons observé une vitesse de l'onde de pouls plus lente témoignant d'artères plus compliantes chez les patients présentant un infarctus du myocarde en comparaison aux patients présentant un angor stable. Nous avons également constaté une augmentation de la vitesse de l'onde de pouls après implantation d'un stent endocoronaire témoignant d'une rigidification attendue de l'artère coronaire. Ces travaux pourraient ouvrir une nouvelle voie de recherche dans la compréhension de l'ischémie myocardique et de la survenue de l'accident coronaire aigu à savoir l'interaction rigidité vasculaire globale et rigidité locale coronaire. Concernant le traitement interventionnel du rétrécissement aortique, de nouveaux facteurs prédictifs du bénéfice de l'intervention sont nécessaires chez des patients souvent âgés et fragiles. Nous nous sommes intéressés à l'étude du volume de calcifications de l'aorte, reflet de la rigidité vasculaire. Ce paramètre a été mesuré par scanner chez des patients traités par remplacement valvulaire aortique par voie percutanée appelé TAVI pour transcatheter aortic valve implantation. Nous avons d'abord montré que le volume de calcifications de l'aorte ascendante était un puissant marqueur de risque indépendant de mortalité cardiaque et d'insuffisance cardiaque sur une série de 127 patients consécutifs traités par TAVI, avec un suivi médian de 907 jours. Ce travail a ensuite été complété en étudiant le volume de calcifications de l'aorte totale sur une série de 164 patients. Le volume de calcifications de l'aorte complète était prédicteur de mortalité totale et cardiaque. De plus, chaque segment d'aorte pris séparément (aorte ascendante, descendante et abdominale) prédisait la mortalité cardiaque. Enfin, seul le volume de calcifications du segment ascendant était prédicteur d'insuffisance cardiaque [etc…]Vascular aging is an inevitable phenomenon. It is accompanied by structural and functional modifications of the cardiovascular system mainly referred to as vascular stiffening. This degenerative process essentially affects the extracellular matrix of the elastic arteries. The loss of elasticity of the vascular tree affects left ventricular function as well as cardiac, renal and cerebral perfusions involving different mechanisms. Vascular stiffness is a powerful risk marker of cardiovascular disease. However, most interventional cardiologists are not familiar with this concept while it may have both important prognostic and therapeutic implications. We tackled two areas of interventional cardiology, where vascular stiffness may open new fields of research; coronary artery disease and interventional treatment of aortic stenosis namely, transcatheter aortic valve implantation (TAVI). With regards to coronary artery disease there is a need to better understand the pathophysiology of microcirculation and myocardial ischemia. Moreover, the occurrence of acute coronary events is also incompletely understood. Our first approach was epidemiological. We studied the prognostic impact of vascular stiffness on coronary artery disease mortality in a cohort of 1034 hypertensive patients after 30 years of follow-up. Vascular stiffness was assessed both by pulse pressure and by a score related to atherosclerosis of the abdominal aorta. A strong link was found between vascular stiffness and the occurrence of myocardial infarction and coronary artery disease related deaths. We then developed a way to study the local vascular stiffness at coronary artery level by measuring coronary pulse wave velocity. This technique relies on the use of an intracoronary pressure wire and a patented signal processing algorithm. We measured a coronary pulse wave velocity on 71 coronary arteries in 49 patients. Interestingly, patients with acute coronary syndromes had a lower coronary pulse wave velocity (which means more compliant arteries) when compared to patients with stable coronary artery disease. After an endocoronary stent implantation we noticed an increase of coronary pulse wave velocity in line with an expected stiffening. This work opens a new avenue of research regarding coronary perfusion physiology and plaque complications by studying the interaction of regional vascular stiffness and local coronary stiffness. Regarding TAVI, a procedure that often concerns elderly and frail patients, new factors predicting the benefit of the intervention are needed. We studied aortic calcifications as a surrogate of vascular stiffness. This parameter was measured by CT scan before TAVI. We first showed in 127 consecutive patients with a median follow-up of 907 days that ascending aorta calcifications were a powerful risk marker of cardiac mortality and heart failure after TAVI. This study was then completed by studying the volume of the whole aorta in 164 patients. The volume of calcifications of the whole aorta was a predictor of both all-cause and cardiac mortality. In addition, each segment of aorta taken separately (ascending, descending and abdominal aorta) predicted cardiac mortality. Finally, only ascending aorta calcifications predicted heart failure. These results support the hypothesis that ascending aorta calcifications are a marker of vascular stiffness and contribute to the left ventricular afterload. Moreover the volume of the whole aorta could mirror the global atherosclerosis burden of the patient. This easily measurable parameter could thus represent a new risk stratification tool in patients treated with TAVI. This work on vascular stiffness opens a new field of research in several areas of interventional cardiology. Regarding coronary artery disease, coronary pulse wave velocity could represent a way to better understand coronary perfusion, microcirculation, ischemia and the occurrence of coronary plaque rupture [etc...]
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Ponte, Márquez Paola Helena. "Grado de control de los factores de riesgo cardiovascular al año de haber sufrido un accidente vascular agudo, en pacientes atendidos en un hospital de 3er nivel." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/669878.
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Se trata de un estudio observacional de tipo transversal con una muestra de 276 pacientes (p) afectos de enfermedad vascular con una edad media de 59.26 años y en seguimiento por medicina especializada o primaria para control de los FRCV, que habían ingresado el año previo por padecer un evento vascular agudo. El evento vascular que motivó el ingreso fue un síndrome coronario agudo (SCA) en el 57.95% de los casos, un accidente cerebrovascular (ACV) en el 35.87% de los casos y una enfermedad vascular periférica (EVP) en el 6.16% de los pacientes. En relación con la prevalencia de los FRCV al año del evento, el 69.93% presentaba dislipemia (DLP), el 65.58% tenía hipertensión arterial (HTA), el 43.48% de los pacientes había estado expuesto al tabaco, el 41.67% refería hábitos sedentarios, el 31.88% de los pacientes presentaba diabetes mellitus (DM) y el 30.80% obesidad.
El grado de control de cada FRCV al año del evento vascular fue el siguiente: el 68% de los pacientes con DM presentaba una hemoglobina glicosilada (Hb A1c) ≤ 7%, el 56% presentó una PA en objetivo obtenida durante los 3 periodos del registro de la MAPA, el 25% tenía niveles de colesterol total (CT) ≤ 150mg/dL y colesterol de baja densidad (c-LDL) ≤ 70 mg/dL y el 71% de presentó un índice de masa corporal (IMC) < 30Kg/m2. Además, el 15% mostró una adecuada adherencia a la dieta mediterránea y el 12% llevó a cabo niveles de actividad física recomendados. Sin embargo, el control integral de todos los FRCV sólo se consiguió en el 11% de los casos. Los pacientes con antecedente de enfermedad cardiovascular (ECV) previa (el 38% del total) presentaron peor control de los FRCV (sólo un 10%), mayor comorbilidad y menor supervivencia estimada en 10 años. Cuarenta y un pacientes (15%) presentó un reingreso hospitalario por un nuevo evento vascular tras los 12 meses posteriores al evento inicial que motivó el ingreso en el estudio. En ellos se observó mayor media de estancia hospitalaria (10.51 días), mayor prevalencia de enfermedad renal crónica (ERC), mejor control del perfil lipídico y un porcentaje superior del control integral de los FRCV en la población no diabética (del 17%). Con relación a los factores emergentes, niveles superiores de lipoproteína A [Lp(a) > 300mg/L] se asoció con el SCA [OR = 1.78(0.49), IC 95% 1.04 - 3.05, p-valor = 0.04], y con reingresos hospitalarios por causa vascular [OR = 3.29(1.25), IC 95% 1.56 -6.29, p-valor = 0.002].This is a cross-sectional observational study with a sample of 276 patients(p) affected of vascular disease and with a specialised or primary medicine follow-up for CVRF controlling. They were hospitalised the previous year in a 3rd level hospital due to an acute vascular event. The average age is 59,26 years. In 57.95% of cases, the vascular event that caused the hospitalisation was an acute coronary syndrome (ACS), in 35.87% of cases cerebrovascular accident (CVA) and Peripheral Vascular Disease (PVD) in 6.16% of patients. 69.93% had dyslipidemia (DLP), 65.58% had Arterial hypertension (HTN), 43.48% of patients had been exposed to tobacco, 41.67% reported sedentary lifestyle, 31.88% of patients had diabetes mellitus (DM) and 30.80% obesity one year after the event with reference of the CVRF prevalence. Higher smoking prevalence and obesity were highlighted in male patients (< 0.001 p-value.) HTN was diagnosed in 26 new patients, 18 DLP patients, 18 patients with obesity and eight patients with DM. The level of control of each CVRF one year after the vascular event was as follows: 68% of patients with DM showed a glycohemoglobin (HbA1C) ≤ 7%, 56% had a BP in target obtained during the 3 submitted periods of ABPM, 25% had levels of total cholesterol (TC) ≤ 150mg/dL and low-density cholesterol (c-LDL) ≤ 70 mg/dL and 71% showed < 30Kg/m2 Body Mass Index (BMI.) Besides, 15% had a correct adherence to the Mediterranean Diet, and 12% performed recommended physical activity levels. Despite this, the comprehensive control of all CVRF only was achieved in 11% of cases. Patients with previous cardiovascular disease (CVD) history (38% of total) reported a worse control of the CVRF (only 10%), greater comorbidity and less estimated survival in 10 years. Forty-one patients (15%) reported hospital readmissions due to a new vascular event after the next 12 months after the initial event that caused the study recruitment. A greater average of inpatient stay (10.51 days) was observed in these patients, higher prevalence of Chronic Kidney Disease (CKD), better control of lipidic profile and a larger percentage of comprehensive control of CVRF in the non-diabetic population (17%). Corresponding to rising factors, higher levels of lipoprotein A [Lp(a) > 300mg/L] were related to the ACS [OR = 1.78(0.49), IC 95% 1.04 - 3.05, p-value = 0.04] and with hospital readmissions caused by vascular [OR = 3.29(1.25), IC 95% 1.56 -6.29, p-value = 0.002.]
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Silver, Annemarie E. "Vascular endothelial expression of atherogenic and anti-atherogenic proteins in humans: Relations to cardiovascular disease risk factors." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/cr/colorado/fullcit?p3190370.
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Zrelak, Patricia Ann. "The relationship of vitamin E to cognition, white matter hyperintensities and vascular risk factors in elderly Latinos /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.
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Thesis (Ph.D.)--University of California, Davis, 2003.Degree granted in Epidemiology. Dissertation completed in 2002; degree granted in 2003. Also available via the World Wide Web. (Restricted to UC campuses)
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Patrier, Laure. "Stratification du risque cardio-vasculaire en insuffisance rénale chronique : place des biomarqueurs émergents." Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20227.
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L'insuffisance rénale chronique (IRC) demeure un problème de santé publique du fait de l'augmentation de sa prévalence. Malgré l'amélioration de la prise en charge, le taux de mortalité reste plus élevé comparé à la population générale. Parmi les causes de décès, les maladies cardiovasculaires, d'origine multifactorielle (élargissement et hypertrophie des artères, athérosclérose, calcifications vasculaires et valvulaires) sont au premier plan. A côté des facteurs de risque classiques, des facteurs non traditionnels, liés aux perturbations métaboliques de l'IRC, ont été mis en évidence, comme l'inflammation, la malnutrition, le stress oxydant, les anomalies du métabolisme minéralo-osseux. La meilleure connaissance de la physiopathologie de la vasculopathie de l'IRC permet d'émerger de nouveaux biomarqueurs pour stratifier le risque cardiovasculaire chez l'IRC.OBJECTIFS-METHODOLOGIE GENERALE : Nous avons réalisé une approche biochimique pour explorer trois composantes du risque cardiovasculaire chez l'IRC : stress oxydant, perturbations qualitatives des HDL (high-density lipoprotein) et métabolisme minéralo-osseux.RESULTATS : Dans une première publication la production d'anion superoxyde a été évaluée, via une méthode de chemoluminescence, en fonction du stade de l'IRC. Alors que la surproduction de formes réactives de l'oxygène est bien connue au stade 5d et peut être liée à la procédure dialytique, il existe peu de données aux stades précoces. Notre étude a porté sur 136 patients IRC non dialysés des stades 1à 5. Les résultats montrent que la production de FRO est assurée aux stades 4 et 5. Un bas débit de filtration glomérulaire (MDRD<30ml/min/1.73m2), l'inflammation (fibrinogène >3.7g/l) et des taux anormaux d' HDL (<1.42mM et >1.75mM) apparaissent comme les principaux déterminants du stress oxydant chez l'IRC non dialysé.Alors que dans la population générale, un taux bas de HDL est reconnu comme un facteur de risque important, nous avons montré (publication 1) que des taux anormaux de HDL, bas comme hauts, étaient indépendamment associés au stress oxydant chez les sujets IRC. Dans une deuxième publication, nous avons précisé la composition des HDL en se basant sur d'éventuelles modifications qualitatives des protéines associées à la structure des lipoprotéines. Une étude protéomique a été réalisée chez 7 patients hémodialysés versus 7 sujets sains. Nous avons retrouvé 40 protéines exprimées différemment sur les 122 identifiées, dont l'apoCII, l'apoCIII qui sont significativement augmentées et la transferrine abaissée. Ces protéines interviennent dans de nombreuses fonctions comme la réponse inflammatoire, l'activation du complément, la régulation de l'oxydation des lipoprotéines, l'homéostasie des cations.Dans une troisième publication, l'épuration du FGF23, phosphatonine impliquée dans les anomalies du métabolisme minéralo-osseux, été étudiée chez l'hémodialysé chronique en fonction de la techniques de dialyse (hémodialyse (HD) high flux versus hémodiafiltration on line (OL-HDF)). Notre étude a porté sur 53 patients dans le groupe HD et 32 patients dans le groupe OL-HDF. Dans les deux groupes le taux de FGF23 en post-dialyse est significativement plus bas qu'en pré-dialyse. Cependant, le taux de réduction, la clairance et le KT/V du FGF23 sont significativement plus bas dans le groupe OL-HDF.CONCLUSION-PERSPECTIVES : Chez l'IRC, avec l'appariation de facteurs de risque non traditionnels, de nouveaux biomarqueurs ont émergés dans la stratification du risque cardio-vasculaire. Ces biomarqueurs peuvent devenir des bioacteurs et représenter de nouvelles cibles d'action et de prévention de l'atteinte cardio-vasculaire chez l'IRC. La complexité des mécanismes physiopathologiques impliqués, nous incite à proposer des approches multimarqueurs. Actuellement des études biocliniques se poursuivent en mettant en place des cohortes régionales de patients aux stades 1 à 5 et de patients incidents en dialyseBACKGROUND: Chronic kidney disease (CKD) is a public health problem because of its increasing prevalence. Despite care improvements, the mortality rate remains higher compared to general population. Among causes of death, cardiovascular diseases with multifactorial origins (enlargement and hypertrophy of arteries, atherosclerosis, vascular and valvular calcifications) are in the foreground. Besides the traditional risk factors, non-traditional factors associated with metabolic disorders in CKD were bring out, such as inflammation, malnutrition, oxidative stress, mineral and bone disorder. A better knowledge of vasculopathy physiopathology in CKD allows the emergence of new biomarkers to stratify cardiovascular risk in CKD.AIMS-METHODOLOGY: We performed a biochemical approach to explore three components of cardiovascular risk in CKD: oxidative stress, qualitative alterations of HDL (high-density lipoprotein) and mineral and bone disorder.RESULTS: In a first publication, the superoxide anion production, according to the stage of CKD, was assessed using a chemiluminescence method. While the overproduction of reactive oxygen species is well known at the 5d stage of CKD and may be related to the dialysis procedure, there are few data in the early stages. Our study included 136 non-dialysis patients at stages 1 to 5 of CKD. Results showed an enhanced superoxide production at the pre-dialysis phase, stages 4 and 5 of CKD. Reduced glomerular filtration rate (MDRD <30 ml / min / 1.73m2), inflammation (fibrinogène≥3.7g / l) and abnormal levels of HDL (<1.42mM and ≥1.75mM) appears as main determinants of oxidative stress in non-dialysis CKD patients.While in general population, a low HDL rate is recognized as an important risk factor, we showed (publication 1) that abnormal levels of HDL, low as high, were independently associated with oxidative stress in CKD subjects. In a second publication, we have defined the HDL composition based on qualitative changes in the structure of proteins associated with lipoproteins. A proteomic study was performed in 7 patients on hemodialysis versus 7 healthy subjects. We found 40 proteins differently expressed on the 122 identified, including apoCII, apoCIII which are significantly increased and transferrin lowered. These proteins are involved in many functions such as inflammatory response, complement activation, regulation of lipoprotein oxidation and homeostasis cations. In a third publication, the removal of FGF23, phosphatonin involved in mineral and bone metabolism, was studied in chronic hemodialysis according to the dialysis techniques (high flux hemodialysis (HD) versus on line hemodiafiltration (OL- HDF)). Our study included 53 patients in the HD group and 32 patients in the OL-HDF group. In both groups the rate of FGF23 in post-dialysis was significantly lower than in pre-dialysis. However, rate of reduction, clearance and KT / V of FGF23 were significantly lower in the OL-HDF group.CONCLUSION-PROSPECTS: In the IRC, with the appearance of non traditional risk-factors, new biomarkers have emerged in the stratification of cardiovascular risk. These biomarkers can become bioactors and represent novel targets of action and prevention in the cardiovascular disease in CKD. The complexity of the involved physiopatholological mechanisms, leads us to propose multimarkers approaches. Currently bioclinical studies continue with the constitution of regional cohorts of patients at stages 1 to 5 of CKD and incident dialysis
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Boxtel, Martinus Petrus Johannes van van. "Physical health, vascular risk factors, and age-related cognitive decline studies into physical determinants of normal cognitive aging /." Maastricht : Maastricht : Neuropsych Publishers ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5812.
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Rubies, Espinalt Cira. "Estudi de l'exercici fisic intens i la sindrome de l'apnea del son com a factors de risc emergents per a patologia cardiovascular. Caracterització en models animals." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/461299.
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L'exercici físic de molt elevada intensitat i la síndrome d'apnea obstructiva del son (SAOS) són dues causes emergents de patologia cardiovascular que poden promoure canvis maladaptatius a nivell vascular i cardíac. Aquests canvis podrien ser la base de l'increment del risc de malaltia ateroscleròtica i de fibril·lació auricular (FA) en individus amb aquestes condicions. Un dels punts centrals de la present tesi és l'anàlisi del remodelat cardiovascular associat a la pràctica d'exercici físic a dosis molt elevades i l'exploració dels possibles mecanismes fisiopatològics associats. Amb aquesta finalitat es va utilitzar un model animal de rata corredora en cinta rodant en la qual es van comparar els canvis provocats per diferents dosis d'activitat física (intensa i moderada). S'ha demostrat que l'exercici d'alta intensitat, contràriament a l'exercici moderat, promou un remodelat advers de la paret de l'aorta amb un increment de fibrosi acompanyat d'una reducció de les seves propietats elàstiques. Alhora s'ha observat un remodelat estructural patològic de l'artèria caròtida i dels vasos intramiocàrdics associat a l'exercici intens. Les diferents dosis d'exercici s'associen a patrons característics d'expressió de miARNs en la paret aòrtica que podrien constituir un mecanisme regulador important. A més, s'ha confirmat que l'exercici d'alta intensitat en el nostre model animal promou la fibrogènesi auricular. El sildenafil ha previngut el desenvolupament de fibrosi únicament en la cavitat esquerra auricular, suggerint una possible acció directa sobre el miocardi. El TGF-β sembla jugar un paper clau en l'efecte protector del sildenafil. D'altra banda, la SAOS té una sèrie d’efectes (hipòxia i hipercàpnia intermitent, pressió intratoràcica que es torna molt negativa i microdespertars) que a llarg termini poden promoure l'aparició de complicacions cardiovasculars. El model crònic descrit en aquesta tesi és un model no invasiu que es pot aplicar a l'exploració de diferents conseqüències de la SAOS: la hipòxia i hipercàpnia intermitent i els esforços respiratoris. El model de SAOS ha promogut una dilatació de l'aorta i un engruiximent de la seva paret. A nivell fisiopatològic, s'ha demostrat la importància de l'estrès oxidatiu i de l'activació del sistema RAA en la promoció del remodelat vascular. Els resultats suggereixen que el tractament amb cèl·lules mare mesenquimals (CMMs) podria resultar beneficiós, atenuant el remodelat vascular induït per la SAOS. A més, la SAOS ha promogut el desenvolupament de fibrosi auricular promoguda per una acció proinflamatòria i per una reducció en la degradació del col·lagen en la qual la MMP-2 hi juga un paper principal. Les CMMs poden tenir un paper potencial en la prevenció del remodelat fibròtic auricular possiblement a través d'un mecanisme antiinflamatori.High intensity resistance training and obstructive sleep apnea (OSA) are emerging risk factors for cardiovascular disease that may promote maladaptative changes in the vessels and the heart. These changes could lead to an increased risk of atherosclerotic burden and atrial fibrillation (AF), affecting individuals under such conductions. One of the main goal of this doctoral thesis is the analysis of the cardiovascular remodelling associated with very-high doses of exercise and its physiopathology. A rat model subjected to aerobic treadmill training is used to compared the changes induced by different exercise doses (very-high and moderate). We demonstrated that intense exercise, unlike moderate exercise, promote an adverse aortic wall remodelling with fibrosis and decreased elastic proprieties. Also, intense exercise induce pathologic structural remodeling of the carotid artery and intramyocardial vessels. Exercise-dose- dependent miRNA profile expression in the aorta may regulate this response. Moreover, our study supported that intense exercise induce atrial fibrogenesis. Sildenafil specifically prevented the increase of fibrosis in the left atria, suggesting a direct action within the myocardium. TGF-β likely contributes to this protective effect. OSA is characterized by intermittent hypoxia and hypercapnia, negative intratoracic pressures and arousals, that may ultimately induce cardiovascular complications. Here, we use a chronic non-invasive OSA rat model involving both thoracic pressure swings and intermittent hypoxia and hypercapnia to explore its cardiovascular consequences. In our model, OSA promote aortic dilatation and increase wall thickness. We demonstrate that increased oxidative stress and RAAS upregulation likely mediate these effects. Results suggest that mesenchymal stem cells (MSC ) infusions could prevent OSA-induced aortic remodeling. Moreover, OSA promoted an increase in atrial fibrosis, which can be mediated in part by the systemic and local inflammation and by decreased collagen-degradation, possibly due to a MMP-2 downregulation. MSC might potentially prevent the atrial profibrotic remodelling induced by OSA by blunting the inflammatory response and normalizing MMP-2 synthesis.
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Chen, Xiaohua Psychiatry Faculty of Medicine UNSW. "Vascular risk factors and brain structure in healthy middle-aged adults: a series of studies using high resolution MRI." Awarded by:University of New South Wales. Psychiatry, 2007. http://handle.unsw.edu.au/1959.4/31545.
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A number of chronic disease and behavioural factors are recognised to increase the risk of cardiovascular and cerebrovascular diseases. These putative ???vascular??? risk factors have increasingly been recognised to increase the risk of cognitive impairment in the absence of clinically manifest ischemic events. Their relationship to structural brain changes has received limited attention. In this dissertation, I used high resolution magnetic resonance image (MRI) to examine two structural features of the brain, regional gray matter (GM) volumes and silent lacunar infarcts, and determined their association with vascular risk factors. I related these to cognitive function in both cross-sectional and longitudinal studies. The work was based on the data of three waves in two healthy cohorts drawn from the PATH Through Life Study, which is a population-based longitudinal study of ageing comprising 3 cohorts aged 20-24, 40-44, and 60-64 years, with about 2500 participants in each cohort. Random subsamples of Wave 1 of the cohort aged 60-64 years (N = 478) and Wave 2 of the 40+ cohort (aged 44-48 years) (N = 411) were examined cross-sectionally for the MRI sub-study. The MRI cohort aged 60-64 years was re-examined 4 years later in Wave 2. These studies showed that vascular risk factors are associated with lower regional GM volumes and this association varies at different ages. In adults aged 44-48 years, individual risk factors did not show a significant relationship with GM volumes, but the Framingham risk score was associated with less GM volumes in a number of brain regions, suggesting an additive effect of the risk factors. In the 60+ cohort, hypertension was independently associated with less regional GM volumes in bilateral medial frontal, right superior frontal, left superior temporal and precentral gyri. The same cohort, when examined in Wave 2, showed the negative association of hypertension with gray matter volumes to be more widespread. These associations were observed in men but not in women in either wave. Sex dimorphism was observed in the younger cohort as well, with greater GM volumes in temporal and occipital cortices, midbrain and cerebellum in men, while less GM volumes in cingulate and parietal cortices in comparison with women. Lacunar infarcts were present in 7.8 % of the 60+ cohort, and asymptomatic new lacunar lesions developed in 0.4 % per year in this group. The prevalence of lacunar infarcts was correlated with hypertension and a steeper decline in mental speed. These series of studies indicate the relationship of vascular risk factors with changes in brain structure and cognitive function in healthy middle-aged adults. It is suggested that modifying these vascular risk factors may protect the brain from silent lesions and cognitive impairment, and that intervention should begin early in life to have a major impact.
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Mateus, Sónia Matilde Fonseca. "Acidente vascular cerebral: fatores de risco, exames imagiológicos e repercussões económicas." Doctoral thesis, Universidade de Évora, 2015. http://hdl.handle.net/10174/16842.
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Os acidentes vasculares cerebrais são a primeira causa de mortalidade em Portugal. É uma patologia com vários fatores de risco e mecanismos etiopatogénicos, cujo diagnóstico é possível através de exames complementares de diagnóstico. O diagnóstico, tratamento e reabilitação acarreta muitos custos a nível socioeconómico, sendo importante perceber quais os fatores mais frequentes, onde deve incidir a pesquisa, tratamento e também quais os exames que fornecem informação mais completa e rápida, contribuindo para a formação de um modelo de auxílio à tomada de decisão e obtenção de bons resultados no combate e resposta da doença, otimizando custos. Realizou-se um estudo retrospetivo, descritivo, correlacional com um grupo de 3209 indivíduos que realizaram triplex scan carotídeo e um segundo grupo com 1657 indivíduos sem acidente vascular cerebral.
Antecedentes familiares de doenças cérebro e cardiovasculares, hipertensão arterial, tabagismo, doenças cardíacas embólicas e a dislipidémia em simultâneo com fibrilhação auricular são fatores que revelaram maior influência na probabilidade de ter acidente vascular cerebral de qualquer tipo.
Os indivíduos têm maior probabilidade de morte mais jovens se tiverem acidente vascular cerebral ou fatores de risco como história de tabagismo ou diabetes mellitus. A idade é o fator com maior influência no aumento do risco de morte instantânea após evento.
Ressonância magnética crâneo-encefálica e o triplex scan cervical foram os exames que apresentaram maior sensibilidade na deteção de lesão intra e extracraneana, respetivamente.
Combinando técnicas de análise de decisão em contexto de incerteza e decisão multicritério, analisaram-se várias estratégias de realização do triplex scan cervical e angio ressonância levando em conta o custo e o benefício esperados. Esta análise permitiu identificar três estratégias eficientes (em ordem crescente de custos e benefícios): não realizar nenhum dos exames; realizar apenas o triplex scan cervical; realizar primeiro o triplex scan cervical e, se este for negativo, realizar a angio ressonância; Stroke: risk factors, imagiologic exams and economic repercussions.
Abstract:
Stroke is the first cause of mortality in Portugal. This disease has several vascular risk factors and etiopathogenic mechanisms, whose diagnosis is possible through the aid of various diagnostic exams. The diagnosis, treatment and rehabilitation entails substantial social and economic costs. Therefore, it is important to understand which are the most frequent risk factors, that should be emphasized in research and treatment, and also to understand which exams provide a more complete and rapid information, contributing to the development of a decision making model so as to achieve good results in combating the disease while optimizing costs. For this we conducted a retrospective, descriptive and correlational study, with a group of 3209 subjects who underwent carotid triplex scan and a second group of 1657 subjects without stroke.
Family history of cerebrovascular and cardiovascular diseases, hypertension, smoking, embolic heart disease and dyslipidemia simultaneously with atrial fibrillation are factors that revealed greater influence on the probability of having stroke of any kind.
Individuals with stroke or risk factors such as smoking history or diabetes mellitus are more likely to have younger death. Age was the most influential factor in risk increase of instant death after stroke.
The skull-brain and cervical triplex scan were the tests that showed higher sensitivity in the detection of intra and extracreana injury, respectively.
Combining decision analysis techniques in the context of uncertainty and multi-criteria decision making, we analized various strategies for implementing the cervical triplex scan and angiography resonance taking into account their cost and expected benefit. This analysis identified three efficient strategies (in order of increasing costs and benefits): not conduct any examinations; perform only the cervical triplex scan; first perform cervical triplex scan and, if this is negative, perform resonance angiography.
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van, Rooijen Marianne. "Effects of combined oral contraceptives on hemostasis and biochemical risk indicators for venous thromboembolism and atherothrombosis /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-089-3/.
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Mamadu, Hadii M., Timir Paul, Liang Wang, Sreenivas P. Veeranki, Hemang B. Panchal, Arsham Alamian, Pooja Subedi, and Mattew Budoff. "Association Between Multiple Modifiable Risk Factors of Cardiovascular Disease and Hypertension in Rural Appalachia. Arteriosclerosis, Thrombosis and Vascular Biology (ATVB)/Peripheral Vascular Disease (PVD) 2016 Scientific Sessions." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/1394.
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Alves, Cabratosa Lia. "Factors associats a la incidència de fibril·lació auricular i estudi de l'associació del tractament amb estatines amb la incidència d'aquesta arítmia en població hipertensa sense antecedents de malaltia isquèmica vascular." Doctoral thesis, Universitat de Girona, 2016. http://hdl.handle.net/10803/666808.
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Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and implies a huge social, medical, and economical burden. Analyses of AF risk factors in certain groups of population would allow tailored preventative recommendations.
We sought to analyse a) AF risk factors in hypertensive patients; b) the association of diabetes with AF; c) effectiveness of statin treatment initiation to prevent AF.
Three retrospective cohorts were designed using the Information System for Research Development in Primary Care.
Risk factors of AF were fitted into a prediction model built with variables commonly used in primary care.
Diabetes presented a modest association with AF.
The net benefit from the use of statines could be considered in the highest risk group examined, in which the association of statins with AF incidence was at the limit of statistical significanceLa fibril·lació auricular (FA) és l’arítmia més freqüent en la pràctica clínica i representa una important càrrega mèdica, social i económica. L’anàlisi del risc de FA en certs grups poblacionals permetria individualitzar les recomanacions preventives segons les característiques de cada pacient. Ens vam proposar d’analitzar els factors de risc de FA en pacients hipertensos; l'associació de la diabetes amb la FA; i l'efectivitat del tractament amb estatines en la prevenció de FA. Es dissenyaren tres cohorts retrospectives amb les dades del Sistema d’Informació pel Desenvolupament de la Investigació a l’Atenció Primària. Els factors de risc de FA s’integrarenen un model de predicció composat de variables d’ús habitual a l’atenció primària. La diabetis presentà una associació modesta amb la FA. En el grup de més alt risc es podria considerar el benefici net del tractament amb estatines, ja que l’associació d’aquest amb la FA quedà al límit de la significació estadística
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Rodrigues, Sara. "Avaliação da rigidez arterial e da resistência vascular periférica em pacientes recém-diagnosticados com síndrome metabólica." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-24102016-115125/.
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Além das alterações autonômicas, a síndrome metabólica (SMet) causa disfunção vascular relacionada a eventos cardiovasculares e morte. Considerando que a resistência à insulina é associada à hiperativação simpática, testamos a hipótese de que a presença da glicemia de jejum alterada (GLI) é a principal causa das alterações estruturais e funcionais em grandes e pequenos vasos, via aumento do tônus simpático nesses pacientes. Foram avaliados pacientes com SMet recém diagnosticados (ATP-III) e não medicados, divididos em: glicemia de jejum alterada >=100mg/dL (SMet+GLI, n=35; 50±1 anos) e glicemia normal < 100mg/dL (SMet-GLI, n=24, 46 ± 1). Um grupo de indivíduos saudáveis foi estudado como controle (CS, n=17, 50±1 anos). Foram medidas rigidez arterial (velocidade de onda de pulso, VOP), atividade nervosa simpática muscular (ANSM, microneurografia) fluxo sanguíneo muscular (FSM, pletismografia), pressão arterial média (PAM, oscilométrico), resistência vascular periférica (RVP=PAM/FSM) e dimetilarginina assimétrica (ADMA). SMet+GLI apresentou maior VOP que SMet-GLI e CS (8,0[7,2-8,6], 7,3[6,9-7,9] e 6,9[6,6-7,2]m/s, respectivamente, P=0,001), não havendo diferença entre SMet-GLI e CS. Além disso, SMet+GLI foi similar ao SMet-GLI mas teve maior RVP que CS (P=0,008), não havendo diferença entre SMet-GLI e CS. Adicionalmente, SMet+GLI teve maior ANSM que SMet-GLI e CS; enquanto SMet-GLI teve maior ANSM que CS (31+-1; 26+-1; 19+-1 disparos /min, P < 0,001). ADMA foi similar entre os grupos (0,62 [0,56-0,71], 0,67 [0,59-0,92] e 0,60 [0,54-1,43] umol/L). Dentre os fatores de risco da SMet, GLI foi preditor do aumento da ANSM. ANSM foi associada à VOP (R=0.39; P=0,002) e à RVP (R=0,30, P=0,034). Em conclusão, a hiperativação simpática, que está aumentada na presença da glicemia alterada, é o mecanismo básico que pode explicar, pelo menos em parte, o aumento na VOP e na RVP. GLI parece ser o principal fator de risco no prejuízo da função e estrutura vascular nos pacientes com SMetBesides autonomic alterations, metabolic syndrome (MetS) causes vascular dysfunction related to cardiovascular events and death. Since insulin resistance is associated with sympathetic hyperactivation, we tested the hypothesis that the presence of impaired fasting glucose (IFG) is the main cause of structural and functional changes of large and small vessels via elevated sympathetic tonus in these patients. We evaluated never treated, newly diagnosed MetS (ATP-III) patients divided into: impaired fasting glucose >100mg/dL (MetS+IFG, n=35; 50±1 y) and normal fasting glucose <100mg/dL (MetS-IFG, n=24, 46±1 y). A healthy control group was also studied (C, n=17, 50±1 y). We measured the arterial stiffness (pulse wave velocity, PWV), muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), mean blood pressure (MBP, oscillometric), peripheral vascular resistance (PVR=MBP/FBF) and asymmetric dimethylarginine (ADMA). MetS+IFG had higher PWV than MetS-IFG and C (8.0[7.2-8.6], 7.3[6.9-7.9] and 6.9[6.6-7.2]m/s, respectively, P=0.001), whereas SMet-GLI was similar to CS. Moreover, MetS+IFG was similar to MetS-IFG, but had higher PVR than C (P=0.008) and SMet-GLI was similar to CS. In addition, MetS+IFG had higher MSNA than MetS-IFG and C; whereas MetS-IFG had higher MSNA than C (31 +- 1; 26+- 1; 19+-1 bursts/min, P < 0.001). ADMA were similar among groups (0.62 [0.56-0.71] vs 0.67 [0.59-0.92] and 0.60 [0.54-1.43] umol/L). Among MetS risk factors, IFG was predictor of increased MSNA. Further, MSNA was associated with PWV (R=0.39; P=0.002) and PVR (R=0.30, P=0.034). In conclusion, sympathetic hyperactivation, which is enhanced in the presence of high blood glucose, is the basic mechanism that could explain, at least in part, the increase in PWV and PVR. IFG appears to be the main risk factor in the vascular function and structure damage in MetS patients
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Johansson, Mimmi, and Charlott Ekholm. "Postoperativa sårinfektioner efter kärlkirurgiska ingrepp med inguinal inscision." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-200804.
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Syftet för denna studie var att studera förekomsten av postoperativa sårinfektioner hos patienter som genomgått kärloperation med inguinal incision under åren 2008 till och med mars månad 2013. Undersöka skillnader gällande riskfaktorer inom studerad patientgrupp för förekomst av postoperativ sårinfektion samt studera om patienter som utfört endovaskulär metod under samma vårdtillfälle oftare drabbades av postoperativ sårinfektion än de patienter som inte genomgått endovaskulär metod under samma vårdtillfälle. Metoden som användes var granskning av patientjournaler efter utifrån studien utvalda specifika operationskoder. Granskningen av de 54 patientjournalerna skedde med hjälp av egenmodifierad tidigare använd granskningsmall. Studieresultatet visar att förekomsten av postoperativa sårinfektioner hos den studerade patientgruppen uppgår till 22,2 %. Skillnader mellan infektion och utförd endovaskulär metod kunde ses men inte påvisas med statistisk signifikans. Studien visade också att kvinnor oftare än män drabbas av postoperativ sårinfektion. Slutsatsen är att ungefär var femte patient i studien, som genomgått denna typ av kirurgi, ådrog sig en postoperativ sårinfektion och att många av dessa ledde till en kostsam postoperativ sårbehandling med Vacuum assisted closure, (VAC).The purpose of this study was to investigate the incidence of postoperative wound infections in patients undergoing vascular surgery with inguinal incision in the years 2008 until March 2013. Examining differences in the risk factors in the studied group of patients occurrence of postoperative wound infection and to study whether patients who performed endovascular method during the same hospitalization more often suffered postoperative wound infection than patients who did not undergo endovascular method during the same hospitalization. The method used was the examination of patient records for the study, based on selected specific audit template. Study results show that the incidence of postoperative wound infections in the studied patient population amounts to 22,2 %. Differences between infection and performed endovascular method could be seen but not detected with statistical significance. The study also showed that women more often than men suffer from postoperative wound infection. The conclusion is that approximately one in five patients in the study who have undergone this type of surgery, suffered a postoperative wound infection and that many of these led to a costly postoperative wound Vacuum Assisted Closure (VAC).