. Introduction
Behc¸et’s disease is a systemic vasculitis of unknown origin, characterized by recurrent oral and genital ulcers, uveitis, vas-cular manifestations and other multisystem affections [1,2]. Vasculitis causes endothelial destruction and thrombosis [3]. Inflammatory thrombosis is well-known in BD [4]. It has been recognized that vascular endothelial dysfunction occurs in BD and plays a substantial role in the vascular lesions. The path-ogenic mechanism is uncertain [5].
There are several identified vascular endothelial growth factor (VEGF) family members: VEGF (VEGF-A), VEGF-B, VEGF-C, VEGF-D and placenta growth factor which are key regulators of physiological and pathological vasculogene-sis, angiogenesis, lymphangiogenesis, hematopoiesis and vascu-lar permeability. VEGF is essential for angiogenesis and inflammation that are pathophysiologic factors of BD [6]. Vascular endothelial growth factor (VEGF) is a potent cytokine that modulates angiogenesis and vasculogenesis by acting as an essential mitogen for vascular endothelial cells [7]. It is an important factor in the progression of atherosclerosis [8].
Common carotid intima-media thickness is an endothelial cell dysfunction parameter that may be associated with athero-sclerosis [9]. Its thickness is a known good predictor of cardio-vascular accidents in the general population [10] and has been reported in the patients with different rheumatic diseases as a strong predictor of cardiovascular events [11]. The
6. Atherosclerosis, pp.1157. is a form of arteriosclerosis in which thickening and hardening of the vessel are caused by the accumulation of lipid-laden macrophages w/I the arterial wall, which leads to the formation of a lesion called a plaque. It is not a single disease but rather a pathologic process that can affect vascular syustemns throughtout the body, resulting in ischemic syndromes that can vary widely in their severity and clinical manisfestations. It is the leading contributor to coronary artery and cerebrocascular disease. Athrosclerosis is an inflammatory disease, the lesions progress from endothelial injury and dysfunction
Cardiovascular diseases are diseases which involve the heart or blood vessels, they are in fact the leading causes of death and disability in the world. Cardiovascular diseases include coronary artery disease, or ischaemic heart disease (heart attack), cerebrovascular disease (stroke) and diseases of the aorta and arteries including hypertension and peripheral vascular disease (Mendis, Puska, & Norrving, 2011). They are all due to a disease known as atherosclerosis which affects arteries (George, & Johnson, 2010). There are also other cardiovascular disease that are not related to atherosclerosis, for instance, congenital heart disease caused by abnormal structures of the heart existing at birth, rheumatic heart disease due to Type II hypersensitivity reaction following streptococcal bacteria infection, cardiomyopathies (disorders of the heart muscle) and cardiac arrhythmias (disorders of electrical conduction system of the heart). Among all the cardiovascular diseases, coronary artery disease and cerebrovascular disease are the first two major contributors to global mortality (Mendis, Puska, & Norrving, 2011).
Cardiovascular disease is the disease that influences the veins which incorporate veins, corridors and vessels and the heart, overall this framework is known as the cardiovascular system. This disease is confounded for the coronary illness and comprises of plentiful issues joined with a natural methodology known as atherosclerosis; when substances develop in the dividers of the conduits. Under the cardiovascular disease flag, there are coronary diseases which influence the corridors, hear musicality issues, known as arrhythmias lastly the cogenital heart defects. The World Health Organization group cardiovascular disease into inherent coronary illness, cerebrovascular disease, coronary infection, rheumatic coronary illness, peripheral arterial disease and the profound vein thrombosis and pulmonary embolism.
The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.
Stiffening of the artery has also been shown to have a high correlation with atherosclerosis [76].
With the increased consumption of fast-food and poor lifestyle choices, we have become an increasingly obese nation. For this reason, diseases such as cardiovascular disease have been on the rise. Cardiovascular disease is the combined term for a number of diseases concerning the heart and the blood vessels. Many of these life threatening diseases are related to a condition called atherosclerosis. The condition creates plaque build-up on the walls of the blood vessels. The plaque effects the flow of blood making it harder and can lead to blood clots which stops the flow of blood altogether. The two main effects to this are heart attacks and strokes however, other types of cardiovascular disease includes complete heart failure, arrhythmia
disease in which abnormal cells divide without control and can invade tissues nearby. Cancer can also spread to other parts of the body through the blood and lymph systems. The National cancer Institute and the World Health Organization (WHO) report that in 2012, there were 14 million new cancer cases and 8.2 million cancer related deaths. The number of new cases is expected to rise by about 70% over the next two decades. WHO also reports that in 2012 the most common cause of cancer death was lung cancer with 1.59 million deaths. The two main types of lung cancer are Small cell lung cancer (SCLC) and Non-small cell lung cancer (NSCLC). NSCLC makes up about 85% to 90% of lung cancers. Treatments for NSCLC can include surgery, radiation therapy, chemotherapy, immunotherapy and targeted therapies. One example of targeted therapy is angiogenesis therapy. Angiogenesis is the formation of blood vessels. Tumors need a blood supply to grow beyond a certain size and will give off a chemical signals to stimulate angiogenesis. One method of preventing this is to find ways to block tumor angiogenesis. This can be done through angiogenesis therapy, which is also called antiangiogenic agents. Angiogenesis is unique in fighting cancer because it focuses on blood vessels rather than tumor cells. Because angiogenesis is unique, arguments can be made for and against this type of treatment. This goal of this paper is to provide pros and cons for angiogenesis therapy.
Peripheral vascular disease (PVD) is a type of circulatory disorder that affects blood vessels in areas other than the heart or brain. Blood vessels that carry blood from the heart to the legs are most commonly affected. Blood vessels in the arms, kidneys, and stomach are also commonly affected. PVD is sometimes called peripheral arterial disease (PAD).
One source of great mortality and morbidity in Europe and North America is the cardiovascular disease, Atherosclerosis. It is recognized as a chronic inflammatory disease of the intermediate and large arteries characterized by the thickening of the arterial wall and is the primary cause of coronary and cerebrovascular heart disease (Wilson, 2005). It accounts for 4.35 million deaths in Europe and 35% death in the UK each year. Mortality rate are generally higher in men than pre-menopausal woman. Past the menopause, a woman’s risk is similar to a man’s (George and Johnston, 2010). Clinical trials have confirmed that lipid accumulation, endothelial dysfunction, cell proliferation, inflammation matrix alteration and foam cell formation are
Arteriosclerosis is the buildup of fats, cholesterol, and other substances that cause arterial walls to become less elastic and more narrow. Arteriosclerosis often has no symptoms, but if the buildup of plaques becomes severe enough, a blood clot could be triggered causing a heart attack or stroke.
Narrowing and hardening of the artery walls causing buildup of fatty tissues (plaque), cholesterol and other substances, which may restrict blood flow is referred to as atherosclerosis. Having restriction of blood flow develops damage to a patients’ organs and also increases the risk of heart attacks, blood clots, and strokes overtime (WebMD, 2015). It is said to be the most common form of arteriosclerosis that forms small patches and arterial spasms. The plaque also known as atheroma, builds up and may cause the blood clots to burst. Atherosclerosis is considered to be a heart condition, but may also affect arteries in any part of the body and could be prevented and treated (Mayo Clinic, 2015).
An atherothrombotic event result in infiltration of the vessel wall caused by high levels of fibrongen, increased blood viscosity, increased platelet aggregation and thrombus formation. A pivotal role is played by inflammation in all phases of atherosclerosis. There are several characteristics of atherosclerotic plaques including the expression of cellular adhesion molecules (CAM), blunted vascular reactivity, and a prothrombotic state. Recent studies suggest that in atherosclerotic plaques PPAR- gamma (Peroxisome proliferator activated receptor gamma) is highly expressed and dugs that mimic PPAR gamma may have inhibitory effects on inflammatory process resulting in improvement of endothelial dysfunction and can modify major transcription factor
Cardiovascular disease is the most common cause of mortality and morbidity and is accounted for almost 1 out of 5 deaths in the world. Atherosclerosis is a chronic heart disease that causes most of the vascular deaths. The fat deposition in arterial walls progressively develop into atheroma leading to restriction in blood circulation thus increasing risk of local thrombosis. Local thrombosis often forms the base that leads to partial or total obstruction of the artery. At the time of birth, the probability of a cardiovascular disease is 47%. The impact of Atherosclerosis on morbidity and mortality and its economic implications created a necessity for new treatments and prevention strategies. It
Epidemiologic information demonstrates that rheumatoid joint pain is an autonomous danger element for cardiovascular illness. Epicardial fat tissue is a novel cardio-metabolic danger element. Our point was to assess epicardial fat thickness (EFT) utilizing echocardiography as a part of patients with rheumatoid joint inflammation contrasted with sound control subjects. Furthermore, we examined relationship between epicardial fat thickness and clinical and echocardiographic parameters in patients with rheumatoid joint
Peripheral vascular disease is divided into subcategories of functional and organic. “Functional PVD does not involve physical problems in the blood vessels. It causes incidental or short-term symptoms. These are usually spasms that occur erratically. Organic PVD involves changes in blood vessel structure. This type of PVD causes inflammation, tissue damage, and blockages” (Giorgi 2015). The number one leading cause of peripheral vascular disease is atherosclerosis. “This is a gradual process in which a fatty material builds up inside the arteries” (emedicinehealth 2015). Other contributing factors to PVD include smoking, inactivity, diabetes, obesity, high blood cholesterol, hypertension, emboli from another location, inflammation of blood vessels, injury to blood vessels, and stress. (Giorgi 2015)