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Vascular Risk (vascular + risk)

Distribution by Scientific Domains

Medical Sciences	100%

Terms modified by Vascular Risk

vascular risk factor

Selected Abstracts

Highlights of Papers in Clinical Investigations Section: Vascular Risk and Cognitive Impairment in an Older, British, African-Caribbean Population

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 3 2001
R Steward
In this study, 278 adults age 55 to 75 who were born in a Caribbean nation were interviewed and examined for cardiovascular risk factors and their association with cognitive impairment. Marked differences were found between groups with low and normal/high levels of education in the strength of associations between measures of vascular risk and cognitive impairment. However, physical activity was negatively associated with cognitive impairment. Physical exercise may be an important public health strategy in reducing the burden of cognitive impairment. [source]

The metabolic syndrome in type 2 diabetes: When does it matter?

DIABETES OBESITY & METABOLISM, Issue 6 2006
J. Wong
Aims:, Young adults with type 2 diabetes (T2Dm) present the clinician with the problem of when to start therapies for the primary prevention of vascular disease and how to identify those at most vascular risk. We examine whether the metabolic syndrome (MetS) can be a useful clinical tool to stratify vascular risk in this context. Methods:, Data were collected from 5928 subjects with T2Dm, and subjects were categorized as having MetS by World Health Organization criteria (body mass index criteria modified for Asians using >23 kg/m2). The prevalence of macrovascular disease was examined by MetS status and age. Results:, The overall MetS prevalence was 72.3%. MetS was associated with an increased prevalence of ischaemic heart disease (IHD) (17.2% MetS vs. 11.6% no MetS, p < 0.0001), coronary artery bypass graft (7.6 vs. 4.7%, p < 0.0003), peripheral vascular disease (PVD) (4.7 vs. 3.7%, p = 0.08) and stroke (6 vs. 3.9%, p = 0.002) across all age groups. MetS subjects had an IHD prevalence equivalent to that seen in subjects who were one decade older without MetS. The most significant impact of MetS was for the age group of 40,49 years with much lesser impact seen with progressively increasing age [odds ratio (OR) = 2.1 for IHD in MetS compared with no MetS at age 40,50 years, p < 0.05; falling progressively to OR = 1.5 at age >70 years, p > 0.05]. Similar trends were seen for coronary artery by-pass graft (CABG) and PVD. There was a strong relationship between the number of MetS risk factors and IHD prevalence (r = 0.99, p = 0.0001). Conclusions:, These data suggest that MetS is particularly useful in stratifying vascular risk in younger T2Dm patients and in those with a high number of MetS components. For patients with MetS, especially those with a full house of MetS risk factors, commencing risk-lowering interventions 10 years earlier than their MetS-free counterparts could be considered. [source]

Assessing vascular risk in people with Type 1 diabetes: implications for the effectiveness of statin therapy

DIABETIC MEDICINE, Issue 6 2007
J. A. McKnight
First page of article [source]

Ankle,branch index and HIV: the role of antiretrovirals

HIV MEDICINE, Issue 1 2009
J Olalla
Objective To study the relationship between antiretroviral (ARV) treatment and abnormal ankle,branch index (ABI) and to compare the risk factors for altered ABI. Methods Patients coming to the office from April 2007 until July 2007 were offered the chance to take part in the study. ABI was obtained by the standard technique. Those ,0.9 or ,1.3 were considered altered ABI. Clinical reports were reviewed to examine traditional vascular risk factors, coinfection with hepatitis C virus and/or hepatitis B virus, tobacco use, highly active antiretroviral therapy use and its components and length of use of each ARV drug. Results ABI was measured in 147 patients, 82.3% males. Thirty-three patients (22.45%) had an altered ABI, and it was related to CD4 cell nadir, dyslipidaemia and protease inhibitor (PI) use. When logistic regression was carried out, only dyslipidaemia (OR 2.68, CI 95%: 1.06,6.91) and PI use (OR 2.79, CI 95%: 1.15,6.54) remained in the model. Conclusions Altered ABI is associated with PI use independently of dyslipidaemia. Probably, it marks patients with high vascular risk not identified with traditional scales. [source]

Avandamet: combined metformin,rosiglitazone treatment for insulin resistance in type 2 diabetes

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2004
C.J. Bailey
Summary Insulin resistance is a major endocrinopathy underlying the development of hyperglycaemia and cardiovascular disease in type 2 diabetes. Metformin (a biguanide) and rosiglitazone (a thiazolidinedione) counter insulin resistance, acting by different cellular mechanisms. The two agents can be used in combination to achieve additive glucose-lowering efficacy in the treatment of type 2 diabetes, without stimulating insulin secretion and without causing hypoglycaemia. Both agents also reduce a range of atherothrombotic factors and markers, indicating a lower cardiovascular risk. Early intervention with metformin is already known to reduce myocardial infarction and increase survival in overweight type 2 patients. Recently, a single-tablet combination of metformin and rosiglitazone, Avandamet, has become available. Avandamet is suitable for type 2 diabetic patients who are inadequately controlled by monotherapy with metformin or rosiglitazone. Patients already receiving separate tablets of metformin and rosiglitazone may switch to the single-tablet combination for convenience. Also, early introduction of the combination before maximal titration of one agent can reduce side effects. Use of Avandamet requires attention to the precautions for both metformin and rosiglitazone, especially renal, cardiac and hepatic competence. In summary, Avandamet is a single-tablet metformin,rosiglitazone combination that doubly targets insulin resistance as therapy for hyperglycaemia and vascular risk in type 2 diabetes. [source]

Highlights of Papers in Clinical Investigations Section: Vascular Risk and Cognitive Impairment in an Older, British, African-Caribbean Population

Point/Counterpoint: The Role of Carotid Ultrasound

PREVENTIVE CARDIOLOGY, Issue 2 2005
Point: Uses Of Carotid Plaque Measurement As A Predictor Of Cardiovascular Events
Vascular prevention is most cost-effective in high-risk patients, but secondary prevention misses many opportunities. The high-risk strategy-identifying patients with high levels of risk factors-is problematic because traditional risk factors predict only half of vascular events. In multiple regression, traditional risk factors explained only half of carotid atherosclerosis. New strategies are being explored, such as electron-beam computerized tomographic measurement of coronary calcification, to identify high-risk patients. Carotid plaque is a powerful tool for identifying and managing high-risk vascular patients, as it explains twice as much of unexplained vascular risk as coronary calcium by electron beam computerized tomography, and it has significant advantages compared with intimal-medial thickness. After adjustment for risk factors, patients in the highest quartile of baseline plaque area have 3.5 times the risk of stroke, death, or myocardial infarction compared with those in the lowest quartile. Those with regression or stable plaque have half the risk of those with progression after adjustment for the same panel of risk factors. The therapeutic target is plaque regression or stabilization, not just control of traditional risk factors. Trying to treat arteries without measuring plaque is like trying to treat hypertension without measuring the pressure, or hyperlipidemia without measuring the lipids. [source]

Effects of antiepileptic drugs on lipids, homocysteine, and C-reactive protein,

ANNALS OF NEUROLOGY, Issue 4 2009
Scott Mintzer MD
Objective The widely prescribed anticonvulsants phenytoin and carbamazepine are potent inducers of cytochrome P450 enzymes, which are involved in cholesterol synthesis. We sought to determine whether these drugs have an effect on cholesterol and other serological markers of vascular risk. Methods We recruited 34 epilepsy patients taking carbamazepine or phenytoin in monotherapy whose physicians had elected to change treatment to one of the noninducing anticonvulsants lamotrigine or levetiracetam. Fasting blood samples were obtained both before and 6 weeks after the switch to measure serum lipid fractions, lipoprotein(a), C-reactive protein, and homocysteine. A comparator group of 16 healthy subjects underwent the same serial studies. Results In the epilepsy patients, switch from either phenytoin or carbamazepine produced significant declines in total cholesterol (,24.8mg/dl), atherogenic (non,high-density lipoprotein) cholesterol (,19.9mg/dl), triglycerides (,47.1mg/dl) (all p < 0.0001), and C-reactive protein (,31.4%; p = 0.027). Patients who stopped taking carbamazepine also had a 31.2% decline in lipoprotein(a) level (p = 0.0004), whereas those taken off phenytoin had a decrease in homocysteine level (,1.7,mol/L; p = 0.005). All of these changes were significant when compared with those seen in healthy subjects (p < 0.05). Results were similar whether patients were switched to lamotrigine or levetiracetam. Interpretation Switching epilepsy patients from the enzyme-inducers carbamazepine or phenytoin to the noninducing drugs levetiracetam or lamotrigine produces rapid and clinically significant amelioration in several serological markers of vascular risk. These findings suggest that phenytoin and carbamazepine may substantially increase the risk for cardiovascular and cerebrovascular disease. Ann Neurol 2009;65:448,456 [source]

Growth hormone deficiency and vascular risk

CLINICAL ENDOCRINOLOGY, Issue 1 2002
Roland W. McCallum
Summary The importance of growth hormone deficiency (GHD) in adult life has become more apparent over the last decade. As well as a distinct clinical syndrome there is a significant excess risk of cardiovascular disease. Although it is difficult to ascertain what part is played by the original pituitary disorder and the concomitant replacement hormonal therapies, there is clear evidence that GHD is associated with known cardiovascular risk factors such as body shape, lipid profile, insulin resistance, blood pressure, vessel wall morphology and haemostatic factors. Novel means of assessing vascular risk such as pulse wave velocity and flow-mediated dilatation can also estimate the risk without invasive procedures. The role of possible mediators of endothelial function such as nitric oxide and free radicals is being investigated further. Replacement of GH in GH-deficient patients leads to many effects on the above indices, some but not all of which are associated with reduced vascular risk. Long-term follow-up studies of morbidity and mortality are required for an accurate assessment of the beneficial effects of therapy. [source]