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Atherosclerosis

NIH - What Is Atherosclerosis? “Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, and pelvis. As a result, different diseases may develop based on which arteries are affected. • Coronary artery disease (CAD). This is when plaque builds up in the coronary arteries. These arteries supply oxygen-rich blood to your heart. When blood flow to your heart is reduced or blocked, it can lead to chest pain and heart attack. CAD also is called heart disease, and it's the leading cause of death in the United States. • Carotid (ka-ROT-id) artery disease. This happens when plaque builds up in the carotid arteries. These arteries supply oxygen-rich blood to your brain. When blood flow to your brain is reduced or blocked, it can lead to stroke. • Peripheral arterial disease (PAD). This occurs when plaque builds up in the major arteries that supply oxygen-rich blood to the legs, arms, and pelvis. When blood flow to these parts of your body is reduced or blocked, it can lead to numbness, pain, and sometimes dangerous infections. “

NIH - Medical Encyclopedia: Atherosclerosis "Atherosclerosis is a condition in which fatty material is deposited along the walls of arteries. This fatty material thickens, hardens, and may eventually block the arteries."

NHS – Atherosclerosis “Arteriosclerosis is a major risk factor for many different conditions that involve the flow of blood. Collectively, these conditions are known as cardiovascular disease (CVD). Examples of CVD include: • deep vein thrombosis (DVT) - blood clots in the legs, • peripheral arterial disease - a condition where the supply of blood to your legs is blocked, causing muscle pain, • heart disease, • strokes, and • heart attacks. … Arteriosclerosis does not usually produce any symptoms until your blood circulation becomes restricted, or blocked. Your symptoms will then depend on where the blockage occurs. Blockage in the limbs A blockage in the arteries of your limbs (in most cases, it is your legs) is known as peripheral arterial disease. The main symptom of peripheral arterial disease is pain and/or cramping in your legs when you are walking. The pain can range from mild to severe. … Blockage near the heart If the artery that supplies your heart with blood (the coronary artery) becomes blocked, you may experience a heart attack. … Blockage near the brain If the artery that supplies your brain with blood (the carotid artery) gets blocked, you may experience a stroke. … As well as an arterial blockage causing a stroke, it can also cause a related condition, known as a transient ischaemic attack (TIA). A TIA is where the supply of blood to the brain is temporarily interrupted, causing a sort of 'mini-stroke'. The symptoms of a TIA are the same as for a stroke, but they only last from between a few minutes to a few hours before completely disappearing. However, you should never ignore a TIA because it is a serious warning sign that there is a problem with the blood supply to your brain.”

Highlighted Articles

Tiny Air Pollution Particles Hurt Heart: Study: The Smallest Air Pollutants May Increase Atherosclerosis More Than Bigger Particles (2008) “The tiniest air pollution particles may be particularly bad for heart health. A new study links ultrafine particulates from traffic to worse atherosclerosis (hardening of the arteries) in mice. Ultrafine particulates "may constitute a significant cardiovascular risk factor," write Jesus Araujo, MD, PhD, of the University of California at Los Angeles (UCLA), and colleagues.“

Air Pollution, High-Fat Diet Cause Atherosclerosis in Laboratory Mice "The study showed that the combination of fine particle pollution and high-fat diet can promote the development of atherosclerosis, and may explain why people who live in highly polluted areas have a higher risk of heart disease."

Visit InfoMedSearch's Home Page for all InfoMedLinks Cardiovascular Topics: Atherosclerosis, Atrial Fibrillation, Coronary Artery Disease, Cholesterol - Lipids, General Cardiovascular, Heart Failure, Hypertension, Myocardial Infarction (Heart Attack), Peripheral Artery Disease, and Stroke.

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Atherosclerosis

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Atherosclerosis

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Bacterial signatures in atherosclerotic lesions represent human commensals and pathogens. (Atherosclerosis. 2008)

Inflammation and Plaque Vulnerability. (Cardiovasc Drugs Ther. 2008) “Development of a thrombus at the site of an atherosclerotic plaque initiates abrupt arterial occlusion and is the proximate event responsible for the vast majority of acute ischemic syndromes. In nearly 75% of cases thrombus overlies a disrupted or ruptured plaque whereas the remainder of the thrombi overly an intact plaque with superficial endothelial erosion. Over the past several years, it has been recognized that plaque composition rather than plaque size or stenosis severity is important for plaque rupture and subsequent thrombosis. Ruptured plaques, and by inference, plaques prone to rupture, tend to be large in size with associated expansive arterial remodeling, thin fibrous cap with a thick or large necrotic lipid core with immuno-inflammatory cell infiltration in fibrous cap and adventitia and increased plaque neovascularity and intraplaque hemorrhage. The size of the necrotic lipid core and extent and location of plaque inflammation appear to be key factors in determining plaque instability. Inflammation and immune cell activation appears to play a key role in the loss of collagen in the fibrous cap, a prelude to fibrous cap rupture, through release of collagen degrading enzymes.”

Interrelation of saturated fat, trans fat, alcohol intake, and subclinical atherosclerosis. (Am J Clin Nutr. 2008) "CONCLUSION: Higher habitual intakes of saturated and trans fats are independently associated with increased subclinical atherosclerosis, and alcohol intake may attenuate the relation between saturated fat and subclinical atherosclerosis."

Progression of Symptomatic Intracranial Large Artery Atherosclerosis Is Associated With a Proinflammatory State and Impaired Fibrinolysis. (Stroke. 2008)

Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects. (Ageing Res Rev. 2008) “Zinc deficiency has been suggested as an environmental risk factor for AT. With advancing age, the incidence of zinc deficiency increases for several reasons. Among them, dietary intake, malabsorption and genetic background of inflammatory markers may be involved. A crucial contribution may also be played by increased oxidative stress which may lead to the appearance of dysfunctional proteins, including metallothioneins (MT) that are in turn involved in zinc homeostasis. The detection of candidate genes related to inflammation and promoting AT and their reciprocal influence/interaction with zinc status might allow earlier appropriate dietary interventions in genetically susceptible subjects.”

The relation of exposure to shift work with atherosclerosis and myocardial infarction in a general population. (Atherosclerosis. 2008)

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