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Journal articles on the topic 'Vascular risk factor'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Howard, Kellee A., Susan A. Kirkland, Patrick R. Montgomery, David Hogan, Howard Feldman, Sandra E. Black, and Kenneth Rockwood. "Vascular risk factor and vascular cognitive impairment: What is the relationship?" Neurobiology of Aging 21 (May 2000): 170. http://dx.doi.org/10.1016/s0197-4580(00)82105-3.

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12

Milosevic-Tosic, Mirjana, and Jela Borota. "Hyperhomocysteinemia: Risk factor for development of occlusive vascular diseases." Medical review 55, no. 9-10 (2002): 385–91. http://dx.doi.org/10.2298/mpns0210385m.

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Introduction Occlusive vascular diseases take the first places on lists of diseases in general population today. In spite of this, all risk factors which contribute to development of these diseases are not yet known. Recent studies have shown that homocysteine plays a critical role in it and is established as a new risk factor. What is homocysteine? Homocysteine is a sulfur containing amino acid formed in the metabolism of methionine. Reference values of homocysteine in circulation and different forms in plasma are described. Hyperhomocysteinemia - a risk factor Homocysteine was associated with atherosclerosis and occlusive vascular disease in 1960s for the first time. Since then, many studies - prospective and retrospective, have confirmed the role of hyperhomocysteinemia as a risk factor in 42% of patients with cerebrovascular disease, 28% with peripheral vascular and 30% with coronary artery disease. The Physician's Health Study, a prospective study in which 15.000 male physicians took part, revealed that increase in homocysteine concentration of 1.7 ?mol/l above normal values was associated by threefold higher risk for myocardial infarction. The risk for carotid artery stenosis also increases with elevation of homocysteine concentration. Hyperhomocysteinemia is associated with poor prognosis in patients with angiographically established coronary disease. Stroke, venous thromboembolism, and atherosclerosis in chronic renal failure are some of the complications of hyperhomocysteinemia. Causes of hyperhomocysteinemia Hyperhomocysteinemia has numerous genetic and nongenetic etiologic factors. Cystationine synthase deficiency, methylentetrahydrofolate reductase deficiency and defects in the synthesis of cobalamin cofactors are genetically determined. Nutritional factors such as B12, folate or B6 vitamin deficiency, cofactors in homocysteine metabolism, lead to hyperhomocysteinemia. Mechanisms of homocysteine action Atherogenic propensity of homocysteine is related to endothelial dysfunction, blood thrombocyte aggregation changes in factors of coagulation. Oxidative stress is involved, but the exact mechanism is still unknown. Conclusion Hyperhomocysteinemia is established as an important risk factor for occlusive vascular diseases. Reduction in homocysteine concentration can be achieved by supplementation of B-group vitamins, cofactors in homocysteine metabolism. Is it going to be effective in reducing cardiovascular risks remains to be seen.

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13

Lijnen, H. R. "Obesity and vascular risk." Hämostaseologie 29, no. 01 (2009): 44–45. http://dx.doi.org/10.1055/s-0037-1616938.

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SummaryObesity is a common disorder and a known risk factor for vascular thrombotic complications. Development of obesity is associated with extensive modifications in adipose tissue involving adipogenesis, angiogenesis and extracellular matrix proteolysis. Studies using a nutritionally induced obesity model in transgenic mice support a role of the fibrinolytic (plasminogen/plasmin) and matrix metalloproteinase (MMP) systems in these processes. Venous or arterial thrombosis models in obese mice confirm a prothrombotic risk associated with obesity.

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14

Auer, J., R. Berent, and B. Eber. "Homocysteine: a novel risk factor in vascular disease." Coronary Health Care 5, no. 2 (May 2001): 89–99. http://dx.doi.org/10.1054/chec.2001.0121.

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15

Chambers, John C., Michael D. I. Seddon, Sapna Shah, and Jaspal S. Kooner. "Homocysteine—a novel risk factor for vascular disease." Journal of the Royal Society of Medicine 94, no. 1 (January 2001): 10–13. http://dx.doi.org/10.1177/014107680109400103.

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16

Reeves, Katherine W., Roberta B. Ness, Roslyn A. Stone, Joel L. Weissfeld, Victor G. Vogel, Robert W. Powers, Francesmary Modugno, and Jane A. Cauley. "Vascular endothelial growth factor and breast cancer risk." Cancer Causes & Control 20, no. 3 (November 6, 2008): 375–86. http://dx.doi.org/10.1007/s10552-008-9252-4.

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17

Clarke, Robert, Leslie Daly, Killian Robinson, Eileen Naughten, Seamus Cahalane, Brian Fowler, and Ian Graham. "Hyperhomocysteinemia: An Independent Risk Factor for Vascular Disease." New England Journal of Medicine 324, no. 17 (April 25, 1991): 1149–55. http://dx.doi.org/10.1056/nejm199104253241701.

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18

Majors, Alana, L. Allen Ehrhart, and Ewa H. Pezacka. "Homocysteine as a Risk Factor for Vascular Disease." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 10 (October 1997): 2074–81. http://dx.doi.org/10.1161/01.atv.17.10.2074.

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19

Bader, Alexandra P., Claudia P. Barone, and Matthew R. Smeds. "Risk Factor Modification Behaviors of Practicing Vascular Surgeons." Annals of Vascular Surgery 41 (May 2017): 16–17. http://dx.doi.org/10.1016/j.avsg.2017.03.138.

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Bader, Alexandra P., Claudia P. Barone, and Matthew R. Smeds. "Risk Factor Modification Behaviors of Practicing Vascular Surgeons." Annals of Vascular Surgery 46 (January 2018): 90–96. http://dx.doi.org/10.1016/j.avsg.2017.05.010.

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21

Weiss, Hilge, and Hoffmann. "Mild hyperhomocysteinemia: risk factor or just risk predictor for cardiovascular diseases?" Vasa 33, no. 4 (November 1, 2004): 191–203. http://dx.doi.org/10.1024/0301-1526.33.4.191.

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Elevated plasma levels of homocysteine (hyperhomocysteinemia) are increasingly recognized as a potential risk for atherothrombotic vascular diseases by numerous epidemiological and clinical studies. There are increasing experimental data that indicate mechanisms by which homocysteine may alter the vasculature in a way that predisposes to atherosclerotic vascular disease. A key event in the vascular pathobiology of hyperhomocysteinemia seems to involve the induction of endothelial dysfunction due to a reduction of the endogenous antiatherothrombotic molecular nitric oxide. Elevated homocysteine levels can be efficiently and safely reduced in most of hyperhomocysteinemic patients by supplementation of folic acid and cobalamin. This reduction is associated with an improvement in endothelial function and other surrogate markers of atherothrombosis, like carotid plaque area and the rate of abnormal stress electrocardiograms. Whether or not this translates into clinical benefits, is still under investigation. The first clinical study on homocysteine-lowering vitamin supplementation in patients that had undergone coronary intervention showed a benefitial effect on the rate on restenosis and the need for revascularization which translated into a reduction of major coronary events. In contrast, in three larger scaled secondary intervention trials in patients with stable coronary disease or post non-disabling stroke, vitamin supplementation had no effect on future vascular events although baseline homocysteine levels were significantly associated with a worse prognosis. Until the results of more clinical trials are available, the clinical relevant question whether or not homocysteine is just a risk predictor or a modifiable risk factor can not definitely be answered.

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22

Israelsson, Hanna, Bo Carlberg, Carsten Wikkelsö, Katarina Laurell, Babar Kahlon, Göran Leijon, Anders Eklund, and Jan Malm. "Vascular risk factors in INPH." Neurology 88, no. 6 (January 6, 2017): 577–85. http://dx.doi.org/10.1212/wnl.0000000000003583.

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Objective:To assess the complete vascular risk factor (VRF) profile of idiopathic normal pressure hydrocephalus (INPH) using a large sample of representative patients with INPH and population-based controls to determine the extent to which vascular disease influences INPH pathophysiology.Methods:All patients with INPH who underwent shunting in Sweden in 2008–2010 were compared to age- and sex-matched population-based controls. Inclusion criteria were age 60–85 years and no dementia. The 10 most important VRFs and cerebrovascular and peripheral vascular disease were prospectively assessed using blood samples, clinical examinations, and standardized questionnaires. Assessed VRFs were hypertension, hyperlipidemia, diabetes, obesity, psychosocial factors, smoking habits, diet, alcohol intake, cardiac disease, and physical activity.Results:In total, 176 patients with INPH and 368 controls participated. Multivariable logistic regression analysis indicated that hyperlipidemia (odds ratio [OR] 2.380; 95% confidence interval [CI] 1.434–3.950), diabetes (OR 2.169; 95% CI 1.195–3.938), obesity (OR 5.428; 95% CI 2.502–11.772), and psychosocial factors (OR 5.343; 95% CI 3.219–8.868) were independently associated with INPH. Hypertension, physical inactivity, and cerebrovascular and peripheral vascular disease were also overrepresented in INPH. Moderate alcohol intake and physical activity were overrepresented among the controls. The population-attributable risk percentage was 24%.Conclusions:Our findings confirm that patients with INPH have more VRFs and lack the protective factors present in the general population. Almost 25% of cases of INPH may be explained by VRFs. This suggests that INPH may be a subtype of vascular dementia. Targeted interventions against modifiable VRFs are likely to have beneficial effects on INPH.

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Chauhan, Nagendra Singh. "To Evaluate Serum Uric Acid as a Risk Factor For Micro- Vascular Complications of Diabetes Mellitus." Academia Journal of Medicine 2, no. 1 (July 10, 2019): 12–14. http://dx.doi.org/10.21276/ajm.2019.2.1.4.

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24

Wiesmann, Maximilian, Amanda J. Kiliaan, and Jurgen AHR Claassen. "Vascular Aspects of Cognitive Impairment and Dementia." Journal of Cerebral Blood Flow & Metabolism 33, no. 11 (September 11, 2013): 1696–706. http://dx.doi.org/10.1038/jcbfm.2013.159.

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Hypertension and stroke are highly prevalent risk factors for cognitive impairment and dementia. Alzheimer's disease (AD) and vascular dementia (VaD) are the most common forms of dementia, and both conditions are preceded by a stage of cognitive impairment. Stroke is a major risk factor for the development of vascular cognitive impairment (VCI) and VaD; however, stroke may also predispose to AD. Hypertension is a major risk factor for stroke, thus linking hypertension to VCI and VaD, but hypertension is also an important risk factor for AD. Reducing these two major, but modifiable, risk factors—hypertension and stroke—could be a successful strategy for reducing the public health burden of cognitive impairment and dementia. Intake of long-chain omega-3 polyunsaturated fatty acids (LC-n3-FA) and the manipulation of factors involved in the renin-angiotensin system (e.g. angiotensin II or angiotensin-converting enzyme) have been shown to reduce the risk of developing hypertension and stroke, thereby reducing dementia risk. This paper will review the research conducted on the relationship between hypertension, stroke, and dementia and also on the impact of LC-n3-FA or antihypertensive treatments on risk factors for VCI, VaD, and AD.

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Hisatome, Ichiro, Peili Li, Fikri Taufiq, Nani Maharani, Masanari Kuwabara, Haruaki Ninomiya, and Udin Bahrudin. "Hyperuricemia as a Risk Factor for Cardiovascular Diseases." Journal of Biomedicine and Translational Research 6, no. 3 (December 23, 2020): 101–9. http://dx.doi.org/10.14710/jbtr.v6i3.9383.

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Serum uric acid level above 7 mg/dl is defined as hyperuricemia, which gives rise to the monosodium urate (MSU), causing gout and urolithiasis. Hyperuricemia is an independent risk factor as well as a marker for hypertension, heart failure, atherosclerosis, atrial fibrillation, and chronic kidney disease. MSU crystals, soluble uric acid (UA), or oxidative stress derived from xanthine oxidoreductase (XOR) might be plausible explanations for the association of cardio-renovascular diseases with hyperuricemia. In macrophages, MSU activates the Nod-like receptor family, pyrin domain containing 3(NLRP3) inflammasome, and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1β and IL-18 secretion. Soluble UA accumulates intracellularly through UA transporters (UAT) in vascular and atrial myocytes, causing endothelial dysfunction ad atrial electrical remodeling. XOR generates reactive oxygen species (ROS) that lead to cardiovascular diseases. Since it remains unclear whether asymptomatic hyperuricemia could be a risk factor for cardiovascular and kidney diseases, European and American guidelines do not recommend pharmacological treatment for asymptomatic patients with cardio-renovascular diseases. The Japanese guideline, on the contrary, recommends pharmacological treatment for hyperuricemia with CKD to protect renal function, and it attaches importance of the cardio-renal interaction for the treatment of asymptomatic hyperuricemia patients with hypertension and heart failure.

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Khan, Naqab, Najma Bibi, Zahid Rasul Niazi, Kifayatullah Shah, Syed Azhar Sherazi, and Samiullah Khan. "ENDOTHELIAL DYSFUNCTION: A CARDIOVASCULAR RISK FACTOR." Gomal Journal of Medical Sciences 16, no. 1 (March 31, 2018): 27–30. http://dx.doi.org/10.46903/gjms/16.01.1813.

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Endothelium is one of the largest organ by area and consist of at least one trillion endothelial cells having more than 100 gram weight and covering more than 3000 square meters area in an adult human body. Endothelium interacts with most of the body systems and is implicated in end organ diseases particularly the cardiovascular. The endothelium maintains vascular tone by precisely regulating the vasodilatation and vasoconstriction while effectively providing the adequate supply of blood to the target organs. Factors that affect the endothelium and subsequently cardiovascular system include hypertension, smoking, obesity, hyperglycemia, hyperlipidemia, poor dietary habits and physical inactivity. Endothelial dysfunction is strongly associated with cardiovascular risk factors such as atherosclerosis, elevated level of low density lipoprotein oxidation, cytokine elaboration, up regulation of adhesion molecules, increased cell permeability, platelet aggregation as well as proliferation and migration of vascular smooth muscles. Endothelial dysfunction is a pathophysiological term used to indicate diminished production of nitric oxide and an imbalance in endothelial derived contraction and relaxation.

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Strauss, Shira A., Daniel Kobewka, and Evgeniya Vishnyakova. "Optimizing Risk Factor Management and Referral Patterns to the Vascular Risk Factor Clinic for Vascular Surgery Patients: A Quality Improvement Initiative." Journal of Vascular Surgery 72, no. 1 (July 2020): e249. http://dx.doi.org/10.1016/j.jvs.2020.04.413.

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Válková, Andrea, and Petr Hubka. "Covid-19 as a possible risk factor of intrauterine fetal death." Česká gynekologie 86, no. 6 (December 21, 2021): 410–13. http://dx.doi.org/10.48095/cccg2021410.

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Objective: To summarize information about possible effects of covid-19 on intrauterine fetal death and present three cases of intrauterine fetal death in women with recent covid-19 infection. Methods: Review of available information about pregnancy with covid-19 and comparison with own observation of cases during spring 2021. Conclusion: Covid-19 influences risk of intrauterine fetal death, preeclampsia/eclampsia or HELLP syndrome. Coagulation changes and drop of platelets is considered as one of the causes of intrauterine fetaldeath due to fetal vascular malperfusion. Key words: covid-19 – intrauterine fetal death – obstetrics

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29

Asselbergs, F. W., R. A. de Boer, G. F. H. Diercks, B. Langeveld, R. A. Tio, P. E. de Jong, D. J. van Veldhuisen, and W. H. van Gilst. "Vascular endothelial growth factor: the link between cardiovascular risk factors and microalbuminuria?" International Journal of Cardiology 93, no. 2-3 (February 2004): 211–15. http://dx.doi.org/10.1016/j.ijcard.2003.04.001.

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ŠTUDENTOVÁ, HANA, JARMILA INDRÁKOVÁ, PAVLA PETROVÁ, MILAN KAMÍNEK, HANA KALÁBOVÁ, VLASTISLAV ŠRÁMEK, TOMÁŠ ADAM, and BOHUSLAV MELICHAR. "Risk factors of atherosclerosis during systemic therapy targeting vascular endothelial growth factor." Oncology Letters 11, no. 2 (December 9, 2015): 939–44. http://dx.doi.org/10.3892/ol.2015.4017.

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Magdy, Ahmed M., Khaled N. Abd-El Razik, Hisham S. Hamza, Wael T. Elgarf, and Waleed S. Abd-Elgaber. "Vascular endothelial growth factor gene polymorphism as a risk factor of endometriosis." Evidence Based Womenʼs Health Journal 4, no. 2 (May 2014): 92–95. http://dx.doi.org/10.1097/01.ebx.0000440892.99947.19.

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Levi, N., J. Skov Jensen, J. Prag, J. Eiberg, J. Jørgensen, and T. V. Schroeder. "Vascular graft infections with Mycoplasma: an overlooked risk factor?" International Journal of Risk and Safety in Medicine 7, no. 3 (1995): 235–38. http://dx.doi.org/10.3233/jrs-1995-7310.

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Pandey, Pratima, and Sunil Pradhan. "Homocysteine: A Possible Modifiable Risk Factor in Vascular Dementia." Annals of Neurosciences 13, no. 1 (January 1, 2006): 12–17. http://dx.doi.org/10.5214/ans.0972.7531.2006.130103.

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Perkins, Bruce A., and Vera Bril. "Early Vascular Risk Factor Modification in Type 1 Diabetes." New England Journal of Medicine 352, no. 4 (January 27, 2005): 408–9. http://dx.doi.org/10.1056/nejme048340.

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35

Druzhilov, M. A. Druzhilov, and T. Yu Kuznetsova Kuznetsova. "Visceral Obesity as Risk Factor of Early Vascular Aging." Kardiologiia 2_2016 (February 27, 2016): 52–56. http://dx.doi.org/10.18565/cardio.2016.2.52-56.

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Finsterer, Josef, Astrid Dossenbach-Glaninger, Walter Krugluger, Claudia Stöllberger, and Piere Hopmeier. "Risk-Factor Profile in Severe, Generalized, Obliterating Vascular Disease." Southern Medical Journal 97, no. 1 (January 2004): 87–92. http://dx.doi.org/10.1097/01.smj.0000050688.18400.0c.

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Bondar', I. A., and V. V. Klimontov. "Hyperhomocysteinemia: a risk factor for vascular complications of diabetes." Problems of Endocrinology 50, no. 2 (April 15, 2004): 24–29. http://dx.doi.org/10.14341/probl11390.

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Vascular complications are a leading cause of reduced quality and longer life of patients with diabetes mellitus (DM). The mechanisms of development of these complications are not fully disclosed. It is known that in not all cases the occurrence and progression of diabetic angiopathies can be explained by traditional risk factors, such as hyperglycemia, arterial hypertension, smoking or dyslipidemia. Therefore, the search for the missing links in the pathogenesis of angiopathy remains an extremely urgent task.

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GRAHAM, IAN M., LESLIE E. DALY, HELGA M. REFSUM, KILLIAN ROBINSON, LARS E. BRATTSTR??M, PER M. UELAND, ROBERTO J. PALMA-REIS, et al. "Plasma Homocysteine as a Risk Factor for Vascular Disease." Survey of Anesthesiology 42, no. 4 (August 1998): 243. http://dx.doi.org/10.1097/00132586-199808000-00060.

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Seshadri, Sudha, and Philip A. Wolf. "Homocysteine and the brain: vascular risk factor or neurotoxin?" Lancet Neurology 2, no. 1 (January 2003): 11. http://dx.doi.org/10.1016/s1474-4422(03)00258-8.

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Widmann, Mark D., and Bauer E. Sumpio. "Lipoprotein (a): A Risk Factor for Peripheral Vascular Disease." Annals of Vascular Surgery 7, no. 5 (September 1993): 446–51. http://dx.doi.org/10.1007/bf02002128.

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41

Sheen, S. S., H. J. Kim, D. Singh, S. C. Hwang, K. J. Park, S. V. Ahn, E. Lee, et al. "Airflow limitation as a risk factor for vascular stiffness." International Journal of Tuberculosis and Lung Disease 24, no. 6 (June 1, 2020): 577–84. http://dx.doi.org/10.5588/ijtld.19.0457.

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BACKGROUND: Cardiovascular disease is one of the main causes of mortality in patients with chronic obstructive pulmonary disease (COPD), and atherosclerosis is a cause of cardiac comorbidities in COPD. However, it is not clear whether airflow limitation is associated with atherosclerosis irrespective of smoking.OBJECTIVE: To investigate whether airflow limitation is independently associated with vascular stiffness.METHODS: We enrolled 18 893 participants (male 70.5%; mean age 47.5 ± 9.8 years; never smokers 44.2%) who underwent spirometry and brachial-ankle pulse wave velocity (baPWV) as part of a standard health examination at Ajou University Hospital, Suwon, South Korea, from January 2010 to December 2015.We defined vascular peripheral atherosclerosis as baPWV ≥ 1400 cm/s and airflow limitation as pre-bronchodilator ratio of forced expiratory volume in 1 sec (FEV1) to forced vital capacity (FVC) <70%.RESULTS: Mean baPWV was higher in subjects with airflow limitation (1477.6 ± 331.7 cm/sec, n = 638) than in those without airflow limitation (1344.1 ± 231.8 cm/sec, n = 18255, P < 0.001). In multivariate logistic regression analysis, the following were independent predictors associated with peripheral atherosclerosis (P < 0.05): age, male sex, fasting serum glucose, mean blood pressure, serum leukocyte count, serum low density lipoprotein level and FEV1.CONCLUSION: Airflow limitation was an independent predictor of vascular stiffness irrespective of smoking history, which suggests that airflow limitation is linked with atherosclerosis.

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Valentine, R. J. "Lipoprotein(a): A New Risk Factor for Vascular Disease." Perspectives in Vascular Surgery and Endovascular Therapy 5, no. 2 (January 1, 1992): 84–99. http://dx.doi.org/10.1177/153100359200500209.

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43

Schurgers, Leon J. "VASCULAR CALCIFICATION: FROM INNOCENT BYSTANDER TO CULPRIT RISK FACTOR." Artery Research 20, no. C (2017): 45. http://dx.doi.org/10.1016/j.artres.2017.10.007.

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Kalman, Peter G., Jane Irvine, and Paul Ritvo. "How Do Vascular Surgeons Perceive Atherosclerotic Risk Factor Management?" Annals of Vascular Surgery 14, no. 6 (November 2000): 652–58. http://dx.doi.org/10.1007/s100169910116.

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Bo, S., S. Valpreda, G. Menato, C. Bardelli, C. Botto, R. Gambino, C. Rabbia, et al. "Should we consider gestational diabetes a vascular risk factor?" Atherosclerosis 194, no. 2 (October 2007): e72-e79. http://dx.doi.org/10.1016/j.atherosclerosis.2006.09.017.

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Graham, Ian M. "Plasma Homocysteine as a Risk Factor for Vascular Disease." JAMA 277, no. 22 (June 11, 1997): 1775. http://dx.doi.org/10.1001/jama.1997.03540460039030.

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Williams, Katherine, Brandon Schneider, Paul Lajos, Michael Marin, and Peter Faries. "Supply and demand: Will we have enough vascular surgeons by 2030?" Vascular 24, no. 4 (July 9, 2016): 414–20. http://dx.doi.org/10.1177/1708538115596652.

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Abstract:

The increase in prevalence of certain cardiovascular risk factors increases susceptibility to vascular disease, which may create demand for surgical intervention. In our study, data collected by the American Association of Medical Colleges Physician Specialty Databook of 2012, the United States Census Bureau, and other nationwide organizations were referenced to calculate future changes in vascular surgeon supply and prevalence of people at risk for vascular disease. In 2010, there were 2853 active vascular surgeons. By 2040, the workforce is expected to linearly rise to 3573. There will be an exponential rise in people with cardiovascular risk factors. Adding to concern, in 2030, an estimated 3333 vascular surgeons will be available for 180,000,000 people with at least one risk factor for peripheral arterial disease. The paucity of properly trained surgeons entering the workforce needs to be addressed before this shortage becomes a larger burden on healthcare providers and governmental spending.

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Song, Juhyun, Won Taek Lee, Kyung Ah Park, and Jong Eun Lee. "Association between Risk Factors for Vascular Dementia and Adiponectin." BioMed Research International 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/261672.

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Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.

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EROL, Gökhan, Barış DURGUN, İsmail SELÇUK, Gökhan ÖZKAN, Murat KADAN, Kubilay KARABACAK, Mehmet Emin İNCE, Suat DOĞANCI, Vedat YILDIRIM, and Ufuk DEMİRKILIÇ. "Vitamın D Deficiency: Can be a Risk Factor for Atherosclerostic Vascular Diseases?" Damar Cerrahi Dergisi 25, no. 1 (2016): 6–10. http://dx.doi.org/10.9739/uvcd.2016-51735.

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Krsteska, Roza. "Risk factors for dementia of the Alzheimer and vascular type." Medical review 62, no. 5-6 (2009): 201–6. http://dx.doi.org/10.2298/mpns0906201k.

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The current study was aimed at examining the risk factors in 30 patients with Alzheimer's dementia and 30 patients with vascular dementia. The reports of the caregivers and the medical documentation were used to estimate the risk factors. The condition for the patients to enter this study was the age above 60 years. The results showed that the average age in the patients with dementia of the Alzheimer type was statistically significantly higher than in the patients with vascular dementia (p<0.0043), which is the confirmation that the most potential risk factor for Alzheimer's disease is aging, and for vascular dementia it is an additional factor. The incomplete education is more common in patients with Alzheimer's disease than in the group with vascular dementia and the difference had statistical significance (p=0.0199). The patients with vascular dementia have higher rate of heart disease (p=0.0002), hypertension (p=0.0005) and diabetes mellitus (p=0.0228) than in the group with Alzheimer's disease with a statistically significant difference. In regard to marital status, head injury and smoking, the difference had no significance in either groups.

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