Relevant bibliographies by topics / Vascular risk factor

Academic literature on the topic 'Vascular risk factor'

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Published: 9 March 2023
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Journal articles on the topic "Vascular risk factor"

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HR Rao, Gundu. "Coronavirus Disease: An Additional Risk Factor for Acute Vascular Events." Diabetes & Obesity International Journal 6, no. 4 (2021): 1–8. http://dx.doi.org/10.23880/doij-16000250.

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Unprecedented spread of a killer coronavirus from Wuhan, China, has caused a catastrophic public health and economic crisis worldwide. Since its initial discovery in late 2019, the virus has spread to all the countries, infected 237 million individuals, and caused death of 4.8 million individuals. No country was prepared to face such a devastating infectious disease pandemic. Global Pharma industries responded rapidly to the call of ‘Operation Warp Speed’ and developed effective vaccines, faster than at any other time in our history. Despite the availability of safe and effective vaccines, large sections of global population, do not have access to these COVID-vaccines. Coronavirus which is highly contagious is transmitted by the respiratory particles and enters the cell by interacting with the angiotensin-converting enzyme-11- receptor (ACE2), which is present on a variety of cells in the human body. Since ACE2 receptors are abundantly expressed on vascular endothelium, upon entry, this virus replicates and spreads to all the vital organs of the body, which are served by the vasculature. Several studies have reported that the severity of the coronavirus disease increases in individuals with underlying health conditions such as hypertension, excess weight, obesity, diabetes, and vascular diseases. These metabolic diseases have increased in the last four decades to epidemic proportions. Individuals with metabolic diseases are at risk for severe coronavirus disease. In view of these observations, those ‘at risk’ population, should take extra precaution from getting infected with this virus. If infected, all attempts should be made to neutralize the virus, reduce the viral load, or initiate appropriate therapies, -to prevent known clinical complications associated with coronavirus disease.
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MIRSHAHI, F., M. VASSE, L. VINCENT, V. TROCHON, J. POURTAU, J. P. VANNIER, H. LI, J. SORIA, and C. SORIA. "Fibrinogen: A Vascular Risk Factor, Why?" Annals of the New York Academy of Sciences 936, no. 1 (January 25, 2006): 621–24. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03550.x.

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Millichap, J. Gordon. "Headache as Risk Factor for Vascular Disease." Pediatric Neurology Briefs 24, no. 5 (May 1, 2010): 37. http://dx.doi.org/10.15844/pedneurbriefs-24-5-6.

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Cwinup, G., and A. N. Elias. "Insulin as Risk Factor for Vascular Disease." Diabetes Care 13, no. 5 (May 1, 1990): 543–45. http://dx.doi.org/10.2337/diacare.13.5.543b.

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Sirtori, C. R., M. Mancini, and R. Paoletti. "Consensus: Hypertriglyceridaemia as a vascular risk factor." European Heart Journal 11, suppl H (January 2, 1990): 44–48. http://dx.doi.org/10.1093/eurheartj/11.suppl_h.44.

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O'Brien, John P. "A New Risk Factor in Vascular Disease." International Journal of Dermatology 26, no. 6 (July 1987): 345–48. http://dx.doi.org/10.1111/j.1365-4362.1987.tb00554.x.

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Gordon, Phyllis, and Patty Flanagan. "Smoking: A risk factor for vascular disease." Journal of Vascular Nursing 34, no. 3 (September 2016): 79–86. http://dx.doi.org/10.1016/j.jvn.2016.04.001.

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Román, Gustavo C. "Vascular Dementia Prevention: A Risk Factor Analysis." Cerebrovascular Diseases 20, no. 2 (2005): 91–100. http://dx.doi.org/10.1159/000089361.

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Neves, Mario Fritsch, and Ernesto L. Schiffrin. "Aldosterone: A risk factor for vascular disease." Current Hypertension Reports 5, no. 1 (January 2003): 59–65. http://dx.doi.org/10.1007/s11906-003-0012-2.

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Pase, Matthew P., Kendra Davis-Plourde, Jayandra J. Himali, Claudia L. Satizabal, Hugo Aparicio, Sudha Seshadri, Alexa S. Beiser, and Charles DeCarli. "Vascular risk at younger ages most strongly associates with current and future brain volume." Neurology 91, no. 16 (September 19, 2018): e1479-e1486. http://dx.doi.org/10.1212/wnl.0000000000006360.

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ObjectiveGiven the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan.MethodsWe studied participants from the community-based prospective Framingham Heart Study. Overall vascular risk factor burden was calculated according to the Framingham Stroke Risk Profile, a validated algorithm that predicts stroke risk. Brain volume was estimated by MRI. We used cross-sectional data to examine how the strength of association between vascular risk factor burden and brain volume changed across each age decade from age 45–54 years through to 85–94 years (N = 2,887). Second, we leveraged up to 40 years of longitudinal data to determine how the strength of association between vascular risk factor burden and brain volume changed when vascular risk factors were examined at progressively earlier ages (N = 7,868).ResultsIn both cross-sectional and longitudinal analyses, higher vascular risk factor burden was associated with lower brain volume across each age decade. In the cross-sectional analysis, the strength of this association decreased with each decade of advancing age (p for trend < 0.0001). In longitudinal analysis, the strength of association between vascular risk factor burden and brain volume was stronger when vascular risk factors were measured at younger ages. For example, vascular risk factor burden was most strongly associated with lower brain volume in later life when vascular risk factors were measured at age 45 years.ConclusionVascular risk factors at younger ages appear to have detrimental effects on current and future brain volume.
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Dissertations / Theses on the topic "Vascular risk factor"

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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 high
Tiivistelmä 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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Books on the topic "Vascular risk factor"

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Boers, G. H. J. Homocysttinuria: A risk factor of premature vascular disease. Dortrecht: Foris Publications, 1986.

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McKinley, Michelle. B-Vitamin status and plasma homocysteine: A risk factor for vascular disease. [S.l: The Author], 1999.

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Tousoulis, Dimitris. Risk factors and vascular endothelium. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Jacobsen, Sarah R. Vascular dementia: Risk factors, diagnosis, and treatment. Hauppauge, N.Y: Nova Science, 2011.

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Román, Gustavo C. Managing vascular dementia: Concepts, issues, and management. London: Science Press, 2003.

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Andris, Kazmers, ed. Cardiac risk assessment before vascular surgery. Armonk, NY: Futura Pub. Co., 1994.

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M, Drance Stephen, ed. Vascular risk factors and neuroprotection in glaucoma: Update 1996. Amsterdam: Kugler Publications, 1997.

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Boers, G. H. J. Homocystinuria: A Risk Factor of Premature Vascular Disease. de Gruyter GmbH, Walter, 1986.

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Stewart, Robert. Vascular and mixed dementias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0034.

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Vascular disease is the most important environmental risk factor for dementia but this research area has been hampered by inadequate outcome definitions – in particular, a diagnostic system that attempts to separate overlapping and probably interacting pathologies. There is now substantial evidence that the well-recognised risk factors for cardiovascular disease and stroke are also risk factors for dementia, including Alzheimer’s disease. However, these risk factors frequently act over several decades, meaning that the chances of definitive randomised controlled trial evidence for risk-modifying interventions are slim. This should not obscure the wide opportunity for delaying or preventing dementia through risk factor control and uncontroversial healthy lifestyles. Care should also be taken that comorbid cerebrovascular disease is not considered as excluding a diagnosis of Alzheimer’s disease, particularly now that this determines treatment eligibility.
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Fromm, Annette. Vascular aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0004.

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Vascular aetiology of young ischaemic stroke covers a broad spectrum of causes. It includes the risk factor-mediated causes considered more common among the elderly on one hand, and a large number of rather rare disorders and conditions typical for younger ages on the other hand. This chapter is focused on atherosclerotic aetiology and comorbidity, small vessel disease and arterial dissection, which account for a majority of young ischaemic strokes worldwide, are treatable, and need to be considered as overall or contributing causes early during investigation. Specific and rare causes of young ischaemic stroke will be presented elsewhere.
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Book chapters on the topic "Vascular risk factor"

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de Man, Frits H. A. F., Mariëtte J. V. Hoffer, Augustinus H. M. Smelt, Jan A. Gevers Leuven, and Arnoud van der Laarse. "Is Hypertriglyceridemia always a Risk Factor?" In Vascular Medicine, 133–60. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-009-0037-0_9.

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Brasier, Allan R., Adrian Recinos, and Mohsen S. Eledrisi. "Vascular Inflammation as a Cardiovascular Risk Factor." In Principles of Molecular Cardiology, 577–604. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1007/978-1-59259-878-6_32.

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Duell, P. Barton, and M. René Malinow. "Homocysteine as a Risk Factor for Coronary Artery Disease." In Homocysteine and Vascular Disease, 173–202. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2_11.

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Abou-Zamzam, Ahmed M., Gregory L. Moneta, John M. Porter, and Lloyd M. Taylor. "Homocysteine as a Risk Factor for Peripheral Vascular Disease." In Homocysteine and Vascular Disease, 135–49. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2_9.

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Perry, Ivan J. "Homocysteine as a Risk Factor for Cerebrovascular Disease and Stroke." In Homocysteine and Vascular Disease, 151–72. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2_10.

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Verhoef, Petra. "Homocysteine as a Risk Factor for Cardiovascular Disease in Women." In Homocysteine and Vascular Disease, 217–38. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2_13.

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Pande, Reena L., and Mark A. Creager. "Risk Factor Management of Atherosclerotic Peripheral Vascular Disease." In Handbook of Endovascular Peripheral Interventions, 175–92. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0839-0_10.

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Egan, Brent M., and Konrad T. Stepniakowski. "Evidence Linking Fatty Fat Acids, the Risk Factor Cluster, and Vascular Pathophysiology." In Endocrinology of the Vasculature, 157–72. Totowa, NJ: Humana Press, 1996. http://dx.doi.org/10.1007/978-1-4612-0231-8_12.

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Pola, P., P. Tondi, M. Serricchio, and R. Pola. "Role of Fibrinogen as a Vascular Risk Factor in Atherogenesis and Thrombogenesis." In Textbook of Angiology, 419–26. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4612-1190-7_33.

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Gerstein, Hertzel C. "The Plasma Glucose Level - A Continuous Risk Factor for Vascular Disease in Both Diabetic and Non-Diabetic People." In Diabetes and Cardiovascular Disease, 35–39. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1321-6_6.

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Conference papers on the topic "Vascular risk factor"

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Khachatryan, K. V. "DUST LOAD AS PROBABLE CARDIOVASCULAR RISK FACTOR." In The 4th «OCCUPATION and HEALTH» International Youth Forum (OHIYF-2022). FSBSI «IRIOH», 2022. http://dx.doi.org/10.31089/978-5-6042929-6-9-2022-1-185-189.

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Introduction: The impact of harmful occupational factors has adverse effect to human body functional state due to regulatory mechanisms tension, which contributes to occupational diseases and premature aging development. The goal of the work: dust professions workers comparative assessment of cardiovascular risk indicators and elastic properties of vascular wall. Methods: First group included workers exposed to industrial aerosols during work (17 people), second group included workers working out of contact with industrial aerosol (15 people). The groups were comparable by age (53.0±1.43 and 54.7±2.41 years, respectively (p > 0.05). Vascular wall arterial stiffness were assessed by volumetric sphygmography, electrical impedance parameters, indicators of carbohydrate, lipid and nitrogen metabolism, cardiovascular risk assessment carried out by SCORE scale. Results: Working with dust factor, under lower levels of body mass index and lipid spectrum indices, higher indicators of vascular wall stiffness and pulse wave propagation velocity were noted compared to workers without contact with industrial aerosols. Stiffness indicators showed positive relationship with age, urea levels, high-density lipoproteins. Indicators of lipid metabolism (total cholesterol, triglycerides and low-density lipoproteins) showed positive relationship with fat mass level and negative relationship with musculoskeletal mass proportion and specific basal metabolism. Conclusions: There is reason to assume that dust load is probably significant cardiovascular risk factor and may be comparable in importance to traditional risk factors.
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Kozhevnikova, Olga, Leyla Namazova-Baranova, Eka Abashidze, Vlad Lebedev, Elena Antonova, Olga Logacheva, Anna Batyrova, and Irina Shirokova. "P153 Height≥85 percentile with increased body mass index (BMI) is risk factor for cardio-vascular diseases height≥85 percentile with increased body mass index (BMI) is risk factor for cardio-vascular diseases." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.241.

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Zhang, Qi, David A. Steinman, and Morton H. Friedman. "Prediction of Disturbed Flow by Factor Analysis of Carotid Bifurcation Geometry." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204798.

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Hemodynamics plays an important role in the development and progression of carotid artery atherosclerotic lesions. Certain aspects of vascular geometry, which mediates local hemodynamics, might be risk factors that increase a vessel’s atherosusceptibility [1]. To further evaluate this “geometric risk factor” hypothesis, the relationship between geometric features and hemodynamic quantities thought to typify “disturbed flow” was recently investigated [2]. Fourteen intercorrelated geometric features were initially extracted from MR images of 50 carotid bifurcations, and multivariate regression based on an a priori selection of a subset of four of these geometric features was used to identify two that were predictors of disturbed hemodynamics. Here, this work is extended to simultaneously analyze the combined role of all geometric variables using factor analysis.
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Wang, Yuan-Hung, Chia-Chang Wu, Kuan-Chou Chen, Hsin-An Chen, Ming-Te Huang, Chih-Hsiung Wu, and Hung-Yi Chiou. "Abstract 4837: Joint effect of arsenic exposure and vascular endothelial growth factor polymorphisms on urothelial carcinoma risk." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4837.

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Sozzi, G., FM Re, R. Berretta, G. Lo Balbo, V. Giallombardo, VA Capozzi, N. Ceresi, G. Scambia, and V. Chiantera. "EP626 Lymph vascular space invasion, an independent risk factor of sentinel node mapping failure in endometrial cancer, the sentifail study: a multicentric prospective analysis." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.683.

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Cruz, Mariana Portella Lopes, João Gustavo dos Anjos Morais Oliveira, Gabriela Sarno Brandão, Ana Flávia Paiva Bandeira Assis, Isaac Rêgo Purificação, Leonardo Mattos Santos, Matheus Almeida Ribeiro da Cunha, Isabella Trindade Lopes Alves, and Raimundo Nonato Ribeiro Fernandes. "Influence of atherosclerosis on intracranial aneurysm rupture: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.391.

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Background: Aneurysms have their wall more susceptible to rupture. It is postulated whether the presence of atherosclerotic plaque can influence this, protecting or not. Objective: This review aims to investigate atherosclerosis (AT) as a potential risk factor for rupture of intracranial aneurysms. Design and Setting: this is a literature review, produced in Bahiana School of Medicine and Public Health. Methods: The evaluated studies were obtained in published between 2011 and 2021, using the MeSH terms with following search: ((“atherosclerosis” OR “atherogenesis” OR “atheroscleroses” OR “Vascular Disease”)) AND ((“intracranial aneurysm” OR “brain aneurysm” OR “brain aneurysms” OR “cerebral aneurysm” OR “cerebral aneurysms”)) AND ((“ruptured” OR “rupture” OR “subarachnoid hemorrhage”)). Those that did not correspond the purpose of this review were excluded. Results: 13 of the 103 articles found, were selected. In 03 retrospective cohorts, AT was not a risk factor associated with aneurysm rupture, but a protective factor. In the control case, AT did not obtain statistical significance, but hypercholesterolemia was considered a protective factor. In the postmortem, atheromatous plaque was found only in a one patient who had subarachnoid hemorrhage. The other studies were inconclusive on the subject. Conclusions: Atherosclerosis cannot yet be said as a risk factor for aneurysm rupture due to literary insufficiency. In this way, new research is needed to ensure the evidence.
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Toloui, Mostafa, Mark Marshall, Pierce Vatterott, Peter Zhang, Ryan Lahm, Thomas Lulic, and Megan Harris. "Numerical Modeling of Vascular Stresses During Lead Extraction: Subclavian vs. Femoral." In 2020 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/dmd2020-9003.

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Abstract Transvenous lead extraction is a critical and growing technique used to treat patients with chronically implanted pacemakers and defibrillators. This procedure is commonly executed via the subclavian vein or the femoral vein. Some physicians’ experiences indicate that the femoral approach results in fewer vascular tears. This study is aimed to present a physics-based comparative assessment of intravenous mechanical stresses for chronic lead management between the two approaches. Finite Element (FE) modeling is employed to quantify the vascular stress distributions. A full 3-D model including veins, heart, fibrotic scar regions and the lead was created to simulate the different lead extraction methods. Results: (1) highest stresses are generally in the vicinity of SVC lead attachments; (2) femoral approach results in a ∼uniform distribution of stress over the scar while the subclavian approach leads to patches of concentrated high stress; (3) 2–3 times higher maximum vascular stress during subclavian; (4) insignificant maximum stress at the apex for both; (5) inverse variation of stress levels with: (i) branch-to-scar distance for SVC method; and (ii)vein wall thickness in both methods. (6) lower stress levels for scars with longer attachment lengths. The importance and effectiveness of mechanical stress analysis in risk analysis for chronic lead management is illustrated. Overall, the localized intravascular wall stress is meaningfully higher for subclavian vs. femoral extraction with same SVC shear force. This may help explain the higher rate of SVC tears when extracting from the left subclavian approach. The individual anatomy (e.g. vascular angles) is a key factor in the resulting stress and this understanding may be critical when choosing an extraction approach and future lead design.
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Bielawiec, M., J. Kloczko, M. Wojtukiewicz, and M. Borowska. "PROTEIN C AND AT III IN ESSENTIAL HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644257.

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Since hypertension is generally accepted as a risk factor for atherosclerosis and, on the other hand, alterations in haemostasis were reported in the disease, we focused our interest on two plasma inhibitors-protein C and antithrombin III, which play critical roles in the regulation of blood clotting process. We studied 19 patients with newly diagnosed essential hypertension at ist and 2ncl degreeof the disease (acc.to WHO criteria). Protein C antigen level was measured by means of ELISA Protein C test (Boehringer Mannheim GmbH).AT III and Factor VIII R:Ag concentrations were measured by rocket immunoelectrophoresis acc.to Laurell using monospecific antisera (Behringwerke AG, Marburg). In comparison with healthy subjects the patients with essential hypertension revealed statistically significant decrease in protein C antigen level (79 t 21% vs 101 ± 16; p≺0.01) and substantially increased F. VIII R: Ag values (174 ± 72% vs 103 ± 33%; p p≺0.01). No significant correlation was found between F. VIII R:Ag and protein C level. The patients had also elevation of AT III concentration ofno statistical significance. Since F. VIII R:Ag is produced and released by endothelial cells its elevated level in patients with hypertension may reflect injuryto the vascular wall. Decreased levels of protein C probably due to its increased consumption observed in the patients may contribute to imbalance in the haemostatic system and promote vascular complications.
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Nasim, S., BA Sousa, RA Dent, and KI Pritchard. "Abstract P6-12-01: A Meta Analysis of Risk of Cardiovascular Events in Patients with Metastatic Breast Cancer (MBC) Treated with Anti Vascular Endothelial Growth Factor (VEGF) Therapy — Bevacizumab." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p6-12-01.

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Agianniotis, Aristotelis, Nikos Stergiopulos, Raymond P. Vito, Tarek Shazly, and Alexander Rachev. "A Theoretical Simulation of Maladaptive Remodeling in Response to Hypertension." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14462.

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Hypertension is a key risk factor for many adverse cardiovascular events. The sustained increase in pressure causes arterial remodeling, which results in long-term changes in the geometrical dimensions and mechanical properties of the vascular tissue. The remodeling response in experimental animal models of hypertension is often described according to the structurally determined change in lumen diameter. Depending on whether the process resulted in a decrease or increase in the diameter, remodeling is termed inward or outward, while depending on the increase, no change, or decrease in the amount of material, remodeling is hypertrophic, eutrophic, or hypotrophic [1]. Due to the multi-factorial and complex nature of remodeling, it is exceedingly difficult to evaluate the relative importance of any one factor in isolation. Predictive mathematical models based on continuum mechanics are powerful tools for studying the mechanical and remodeling response of blood vessels. So far, most theoretical studies addressed adaptive remodeling in response to sustained hypertension. An adaptive response manifests as preservation of the normotensive deformed diameter, change in residual strains and axial stretch ratio, and thickening of the arterial wall, such that the tensile wall stress and flow-induced shear stress remain at baseline values. Maladaptive remodeling could result from a variety of dysfunctional biological processes, and is characterized by the incomplete restoration of the baseline mechanical environment. This study is devoted to a theoretical simulation of some modes of maladaptive remodeling and aims to evaluate the relative importance of certain geometrical and mechanical factors in the remodeling response to hypertension.
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Reports on the topic "Vascular risk factor"

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Goodwin, Simon. IMPROVE-Stroke: IMproving the PRevention Of Vascular Events after Stroke or TIA – a randomised controlled pilot trial of nurse independent prescriber-led care pathway-based risk factor management. National Institute for Health and Care Research (NIHR), March 2022. http://dx.doi.org/10.3310/nihropenres.1115183.1.

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Kanner, Joseph, Mark Richards, Ron Kohen, and Reed Jess. Improvement of quality and nutritional value of muscle foods. United States Department of Agriculture, December 2008. http://dx.doi.org/10.32747/2008.7591735.bard.

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Food is an essential to our existence but under certain conditions it could become the origin to the accumulative health damages. Technological processes as heating, chopping, mincing, grounding, promote the lipid oxidation process in muscle tissues and meat foodstuffs. Lipid oxidation occurred rapidly in turkey muscle, intermediate in duck, and slowest in chicken during frozen storage. Depletion of tocopherol during frozen storage was more rapid in turkey and duck compared to chicken. These processes developed from lipid peroxides produce many cytotoxic compounds including malondialdehyde (MDA). The muscle tissue is further oxidized in stomach conditions producing additional cytotoxic compounds. Oxidized lipids that are formed during digestion of a meal possess the potential to promote reactions that incur vascular diseases. A grape seed extract (1% of the meat weight) and butylated hydroxytoluene (0.2% of the lipid weight) were each effective at preventing formation of lipid oxidation products for 3 hours during co-incubation with cooked turkey meat in simulated gastric fluid (SGF). Polyphenols in the human diet, as an integral part of the meal prevent the generation and absorption of cytotoxic compounds and the destruction of essential nutrients, eg. antioxidants vitamins during the meal. Polyphenols act as antioxidants in the gastrointestinal tract; they scavenge free radicals and may interact with reactive carbonyls, enzymes and proteins. These all reactions results in decreasing the absorption of reactive carbonyls and possible other cytotoxic compounds into the plasma. Consumptions of diet high in fat and red meat are contributory risk factors partly due to an increase production of cytotoxic oxidized lipid products eg. MDA. However, the simultaneously consumption of polyphenols rich foods reduce these factors. Locating the biological site of action of polyphenols in the in the gastrointestinal tract may explain the paradox between the protective effect of a highly polyphenols rich diet and the low bioavailability of these molecules in human plasma. It may also explain the "French paradox" and the beneficial effect of Mediterranean and Japanese diets, in which food products with high antioxidants content such as polyphenols are consumed during the meal.
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FEDOTKINA, S. A., O. V. MUZALEVA, and E. V. KHUGAEVA. RETROSPECTIVE ANALYSIS OF THE USE OF TELEMEDICINE TECHNOLOGIES FOR THE PREVENTION, DIAGNOSIS AND TREATMENT OF HYPERTENSION. Science and Innovation Center Publishing House, 2021. http://dx.doi.org/10.12731/978-0-615-67320-2-4-22.

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Introduction. The economic losses associated with disability due to diseases of the circulatory system, as well as the costs of providing medical care to patients suffering from heart and vascular diseases, are increasing annually. The state preventive measures currently being carried out are of a delayed nature. The results of the medical examination of the population of the Russian Federation in recent years (2015-2019) indicate that the incidence of cardiovascular diseases, including hypertension, is at a fairly high level. In the middle of the last century, the Concept of risk factors for the development of chronic non-communicable diseases were formulated, in the structure of which cardiovascular diseases, including arterial hypertension, occupies one of the primary positions. The concept is based on the results of promising epidemiological studies, and, at present, is a methodological basis for planning and organizing primary prevention of cardiovascular diseases. The purpose of the study. Based on the analysis of literary sources (including foreign ones) containing experience in the use of telemedicine technologies, to assess their significance for the prevention, diagnosis and treatment of hypertension, as well as forecasting improvements in the quality of medical care when adapting to the use of clinical recommendations. Materials and methods. The article provides an analytical review of the use of modern telemedicine technologies in the prevention of hypertension. The results of the study and their discussion. The analysis of literary sources has shown that in the context of the progress of information and telecommunication technologies in the healthcare system, a fundamentally new direction has appeared in the organization and provision of medical care to the population - telemedicine, which will ensure the modern level of prevention, detection and treatment of chronic non-communicable diseases, and also determines positive medical, social and economic performance indicators. To date, updates in the legislative framework of the Russian Federation are aimed at ensuring that medical care with the use of telemedicine technologies is more widespread, taking into account the standards of medical care and clinical recommendations. Conclusion. Based on a review of literature sources, it has been established that the modern solution to the problem of improving the quality of medical care for patients, including those with hypertension, diseases is medical care using telemedicine technologies that prove their medical, social and economic effectiveness.
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