14/06/2010
EPIDEMIOLOGY
Differences in atherosclerosis according to area level socioeconomic deprivation: cross sectional, population based study.
Deans KA, Bezlyak V, Ford I, Batty GD, Burns H, Cavanagh J, de Groot E, McGinty A, Millar K, Shiels PG, Tannahill C, Velupillai YN, Sattar N, Packard CJ.
Department of Vascular Biochemistry, Glasgow Royal Infirmary, Glasgow G31 2ER. kevindeans@nhs.net
Abstract
OBJECTIVES: To examine the relation between area level social deprivation and ultrasound markers of atherosclerosis (common carotid intima-media thickness and plaque score), and to determine whether any differences can be explained by "classic" (currently recognised) or "emerging" (novel) cardiovascular risk factors. DESIGN: Cross sectional, population based study. SETTING: NHS Greater Glasgow Health Board area. PARTICIPANTS: 666 participants were selected on the basis of how their area ranked in the Scottish Index of Multiple Deprivation 2004. Approximately equal numbers of participants from the most deprived areas and the least deprived areas were included, as well as equal numbers of men and women and equal numbers of participants from each age group studied (35-44, 45-54, and 55-64 years). MAIN OUTCOME MEASURES: Carotid intima-media thickness and plaque score, as detected by ultrasound. RESULTS: The mean age and sex adjusted intima-media thickness was significantly higher in participants from the most deprived areas than in those from the least deprived areas (0.70 mm (standard deviation (SD) 0.16 mm) v 0.68 mm (SD 0.12 mm); P=0.015). On subgroup analysis, however, this difference was only apparent in the highest age tertile in men (56.3-66.5 years). The difference in unadjusted mean plaque score between participants from the most deprived and those from the least deprived areas was more striking than the difference in intima-media thickness (least deprived 1.0 (SD 1.5) v most deprived 1.7 (SD 2.0); P<0.0001). In addition, a significant difference in plaque score was apparent in the two highest age tertiles in men (46.8-56.2 years and 56.3-66.5 years; P=0.0073 and P<0.001) and the highest age tertile in women (56.3-66.5 years; P<0.001). The difference in intima-media thickness between most deprived and least deprived males remained significant after adjustment for classic risk factors, emerging risk factors, and individual level markers of socioeconomic status (P=0.010). Adjustment for classic risk factors and emerging cardiovascular risk factors, either alone or in combination, did not abolish the deprivation based difference in plaque presence (as a binary measure; adjusted odds ratio of 1.73, 95% confidence interval 1.07 to 2.82). However, adjustment for classic risk factors and individual level markers of early life socioeconomic status abolished the difference in plaque presence between the most deprived and the least deprived individuals (adjusted odds ratio 0.94, 95% CI 0.54 to 1.65; P=0.84). CONCLUSIONS: Deprivation is associated with increased carotid plaque score and intima-media thickness. The association of deprivation with atherosclerosis is multifactorial and not adequately explained by classic or emerging risk factors.
SEE FULL ARTICLE
13/06/2010
PREVENTION
PREVENTION
Try to follow these tips to prevent atherosclerosis:
Quit smoking. Smoking accelerates the development of atherosclerosis, which often leads to coronary heart disease. Women who smoke are two to six times as likely to suffer a heart attack as nonsmoking women, and the risk increases with the number of cigarettes smoked per day. The good news is that quitting dramatically cuts your risk, even during the first year, no matter what your age.
Lower your blood pressure. Even slightly high blood pressure levels can double your risk for heart disease. Normal blood pressure is less than 120/80 mm/Hg, according to the National Heart, Lung and Blood Institute. High blood pressure, or "hypertension," is a blood pressure reading of 140/90 mm/Hg or higher. Between 120/80 mm/Hg and 139/89 mmHg is considered prehypertension.
High blood pressure also increases your chance of stroke, congestive heart failure and kidney disease. High blood pressure can be treated successfully with medication. Commonly prescribed drugs include diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, beta blockers and calcium channel blockers (CCBs).
If your blood pressure is not too high, you may be able to control it entirely through weight loss (if you are overweight), regular physical activity and cutting down on alcohol as well as salt and sodium. Sodium is an ingredient in salt that is found in many packaged foods, carbonated beverages, baking soda and some antacids.
Get regular exercise and lose weight. Regular physical activity is defined as 30 minutes of moderate-intensity physical activity, such as brisk walking, on most and preferably all days of the week, or 20 minutes of vigorous exercise, such as running, at least three days a week.
Control your blood sugar if you have diabetes. Diabetes is typically diagnosed by a fasting glucose (sugar) over 126. Patients with diabetes should be treated to prevent complications from cardiovascular disease; treatment typically consists of a combination of lifestyle changes and medications. Your goal hemoglobin A1C with treatment should be less than seven percent. Those with diabetes who also have good sugar control are much less likely to develop cardiovascular complications than those with poor sugar control.
Those individuals with a fasting glucose (sugar) of 100-126 may be considered pre-diabetes or glucose intolerant. This is often associated with metabolic syndrome and individuals with glucose intolerance are at high risk for developing true diabetes within the next couple years. Weight loss, healthy diet, and exercise are important to improve blood sugar levels and prevent the onset of diabetes.
Lower your LDL-cholesterol level. Today, about a quarter of all American women have blood cholesterol levels high enough to pose a serious risk for atherosclerosis and heart disease. More than half of the women over age 55 need to lower their blood LDL cholesterol.
Keep triglycerides in check. The lipoprotein profile that determines your cholesterol levels also measures another fatty substance called triglyceride. Produced in the liver, triglycerides are made up of saturated, polyunsaturated and monounsaturated fats. The optimal target triglyceride level for individuals without heart disease or heart disease-related risk factors is less than 150 mg/dL, with 100 mg/dL being an ideal level.
For most people, cutting back on foods high in saturated fat and cholesterol will lower both total and LDL cholesterol. Regular physical activity and weight loss if you're overweight also reduces blood cholesterol levels. Losing extra weight, quitting smoking and becoming more physically active may also help boost HDL cholesterol levels.
Reduce your homocysteine level. Homocysteine is an amino acid normally found in the body. Recent studies suggest that high blood levels of this substance may increase the risk of heart disease, stroke, and reduced blood flow to the hands and feet. It is believed that high levels of homocysteine may damage the arteries, making blood more likely to clot and/or making blood vessels less flexible.
Homocysteine levels are affected by three vitamins—afolic acid and vitamins B6 and B12. Women who consume less than the recommended daily amounts of these vitamins are more likely to have higher homocysteine levels. Recommended daily amounts are 400 micrograms of folic acid, two mg of B6, and 2.4 mcg of B12.
Good sources of folic acid include citrus fruits; tomatoes; dark green, leafy vegetables; whole-grain and fortified-grain products (whole wheat bread and oatmeal, for example) and beans and lentils. Foods high in B6 include beef, poultry, fish, fruits, vegetables and grain products. Major sources of B12 are beef, poultry, fish, milk and other dairy products.
SEE WEB SITE
SLIDE PRESENTATION
Check out this SlideShare Presentation:
Atherosclerosis
View more presentations from chaoticboi.
CASE REPORT
Intravascular ultrasound of symptomatic intracranial stenosis demonstrates atherosclerotic plaque with intraplaque hemorrhage: a case report.
.
Meyers PM, Schumacher HC, Gray WA, Fifi J, Gaudet JG, Heyer EJ, Chong JY.
.
Department of Radiology, Columbia University, College of Physicians & Surgeons, Neurological Institute of New York, New York, New York 10032, USA. pmm2002@columbia.edu
.
Abstract
.
BACKGROUND: Intracranial artery stenosis is assumed to represent atherosclerotic plaque. Catheter cerebral arteriography shows that intracranial stenosis may progress, regress, or remain unchanged. It is counterintuitive that atherosclerotic plaque should spontaneously regress, raising questions about the composition of intracranial stenoses. Little is known about this disease entity in vivo. We provide the first demonstration of in vivo atherosclerotic plaque with intraplaque hemorrhage using intravascular ultrasound (IVUS). CASE DESCRIPTION: A 35-year-old man with multiple vascular risk factors presented with recurrent stroke failing medical therapy. Imaging demonstrated left internal carotid artery occlusion, severe intracranial right internal carotid artery stenosis, and cerebral perfusion failure. Cerebral arteriography with IVUS confirmed 85% stenosis of the petrous right carotid artery due to atherosclerotic plaque with intraplaque hemorrhage. Intracranial stent-supported angioplasty was performed with IRB approval. The patient recovered without complication. CONCLUSIONS: This case supports the premise that symptomatic intracranial stenosis can be caused by atherosclerotic plaque complicated by intraplaque hemorrhage similar to coronary artery plaque. IVUS provides additional characteristics that define intracranial atherosclerosis and high-risk features. To our knowledge, this is the first report of stroke due to unstable atherosclerotic plaque with intraplaque hemorrhage in vivo.
.
Suscribirse a:
Entradas (Atom)