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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis is a systemic disease of the vessel wall that mainly affects medium- and large-sized arteries, and accounts for 50% of all deaths in western countries. Imaging of atheromatous plaques has traditionally centered on assessing the degree of luminal narrowing. More recently it has become clear that it is of the utmost importance to identify the vulnerable atherosclerotic plaques responsible for the majority of life-threatening syndromes. Molecular imaging using nuclear medicine techniques such as single-photon emission computed tomography (SPECT) and positron emission tomography (PET), has the potential to characterize the activity of atheromas. In the present review we summarize the results of radionuclide imaging in the detection of vulnerable atherosclerotic lesions.
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PMID:Molecular imaging of atheroslerotic plaque with nuclear medicine techniques. 1857 69

Atherosclerosis is a systemic disease that is responsible for most cardiovascular events and stroke. Epidemiologic studies and intervention trials based on the incidence of acute vascular disease end points require years of follow-up, the participation of large populations, or both. As a consequence, such studies consume considerable time and financial resources. The use of surrogate markers, therefore, is of paramount relevance because it allows researchers to have reliable data in less time and from reduced populations. Intima-media thickness (IMT) measured by B-mode ultrasound is the most studied surrogate marker and has been validated by official medical agencies. In this article, we review the most important technical considerations related to its measurement and highlight issues that should be systematically addressed in IMT-related studies. In summary, the use of IMT as an end point in clinical studies is of great value, but several technical limitations might jeopardize its interpretation.
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PMID:Carotid intima-media thickness measurements: techniques and clinical relevance. 1870 87

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are associated with increased mortality, largely as a consequence of cardiovascular disease. Increased cardiovascular morbidity and mortality in patients with RA and SLE cannot be entirely explained by traditional risk factors, suggesting that the systemic inflammation that characterizes these diseases may accelerate atherosclerosis. We used carotid ultrasonography to investigate the prevalence and correlates to preclinical atherosclerosis in patients with RA and SLE. Because atherosclerosis is a systemic disease, assessment of carotid plaque by ultrasonography provides a robust, direct measure of systemic atherosclerosis. We observed a substantially increased prevalence of carotid plaque in RA and SLE patients compared with age- and sex-matched controls, which remained after adjustment for traditional risk factors. The presence of carotid atherosclerosis was associated with disease duration in both RA and SLE and damage in SLE. These data support the hypothesis that inflammation associated with RA and SLE contributes to accelerated atherosclerosis and argue that RA and SLE disease activity should be more aggressively managed.
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PMID:Subclinical atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus. 1892 67

Migraine is a common disorder in which changes in cortical excitability, neuroinflammation and dysfunction of the vascular wall contribute to its pathophysiology. Repeated attacks of migraine over prolonged periods result in inflammatory arteriopathy of the cranial vessels. Several studies indicate that migraine is associated with special pattern of inflammatory markers and some adverse vascular risk factors including: increased levels of CRP, ILs, TNF-alpha and adhesion molecules which are markers of systemic inflammation, oxidative stress and thrombosis, increased body weight, high blood pressure, hypercholesterolemia, impaired insulin sensitivity, high homocysteine levels, stroke and coronary heart disease. Such comorbidities are not explained by bias but indicate possible shared underlying pathogenic mechanisms. Recent studies have shown involvement of cranial as well as peripheral vascular dysfunction with migraine indicating that migraine may be a local manifestation of a systemic disease rather than a primary brain phenomenon. The associated inflammatory process of migraine together with the associated adverse medical comorbidities exposes patients to endothelial vascular wall injury which further increases migraine susceptibility and progression as well as increases the risk for atherogenesis. The knowledge that migraine is a risk for vascular diseases raises important clinical implications, recommendations and future perspectives in migraine treatment and prevention.
Atherosclerosis 2009 Jul
PMID:The vascular risk associations with migraine: relation to migraine susceptibility and progression. 1905 16

Multiple risk factors have been associated with progression of atherosclerosis. To identify the individual patient who is at risk for disruption of a vulnerable plaque, leading to a cardiovascular event, remains a major challenge. Current screening methods, based on traditional risk factors, do not allow risk stratification on an individual level. The discovery of new biomarkers would aid in identifying specific patient groups at risk for adverse cardiovascular events due to atherosclerotic disease progression. The current definition of the vulnerable plaque, e.g. atheromatous inflammatory plaque with a thin fibrous cap, has been based on cross-sectional post-mortem studies. The predictive value of these histological characteristics of the vulnerable plaque is likely to be low, because they are also frequently observed at multiple locations in symptomatic and asymptomatic patients. The Athero-express study follows a new concept to search for the atherosclerotic patient who may suffer from adverse events. In this study, we investigate the predictive value of local plaque composition for adverse events in other vascular territories, regarding the plaque as a concentrated expression of this systemic disease. First results from this longitudinal biobank study show that the local plaque hides strong predictive value for cardiovascular events elsewhere in the vascular tree. Longitudinal biobank studies will facilitate the identification of novel local plaque markers. The search for the plaque protein signature that is predictive for adverse events might enable patient stratification that will allow individualized tailor made medicine and subsequently guide the choice for therapeutic interventions.
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PMID:Biobanks and the search for predictive biomarkers of local and systemic outcome in atherosclerotic disease. 1913 88

Atherosclerosis, a systemic disease, remains one of the leading causes of morbidity and mortality in the world. Our improved understanding of the molecular mechanisms underlying atherosclerotic lesion progression and sudden transformation into unstable plaques, indicate complex interactions of lipid metabolism, inflammatory processes and genetic predisposition. Currently, novel imaging approaches to visualize the process of atherosclerosis, particularly at the molecular level, are actively being developed. Important targets include inflammatory and endothelial cells, as well as apoptosis and angiogenesis. The next decade should solidify the role of targeted molecular imaging in all aspects of cardiovascular medicine.
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PMID:Emergence of targeted molecular imaging in atherosclerotic cardiovascular disease. 1921 Feb 15

Coronary heart disease is mainly caused by atherosclerosis, which is a multifactorial and systemic disease. Lipid metabolism disorder and chronic inflammation are two well accepted mechanisms leading to atherosclerosis. The key initiating process in athrogenesis is lipid retention in subendothelium. Inflammatory activity plays an important role in the whole pathogenesis of atherosclerosis. Recent investigations have demonstrated that rapamycin reduces lipid retention by increasing adipose-tissue lipase activity and decreasing lipoprotein lipase activity. Rapamycin also reduce intracellular lipid accumulation in smooth muscle cells and macrophages. Since rapamycin is a definite immunosuppressive agent, and inflammatory process has been involved in atherosclerosis, the compound would have effect on the progression of atherosclerosis through reducing inflammatory activity. Moreover, rapamycin would protect plaque from rupture by selectively clearing macrophages without affecting vascular smooth muscle cells. Even some in vivo studies demonstrate that rapamycin can notably inhibit the development of atherosclerosis. Rapamycin, especially its analog, everolimus, is a non-toxic, well-tolerated drug suitable for long term use. Clinical experiments demonstrate that everolimus can reduce graft vasculopathy in heart transplant patients. Therefore, we propose that everolimus administered systemically is a promising medical therapy to attenuate atherosclerosis and prevent further adverse events. In addition, rapamycin is a selective and effective mammalian target of rapamycin (mTOR) inhibitor. mTOR acts as a hub for cell metabolism, cell growth and cell survival. Based on previous evidences, we hypotheses that mTOR signaling pathway could play a significant role in the pathogenesis of atherosclerosis.
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PMID:Everolimus, a promising medical therapy for coronary heart disease? 1937 41

Atherothrombosis is a systemic disease that can manifest as involvement of distinct vascular territories; those most frequently leading to diagnosis being coronary, cerebrovascular and peripheral arterial vascular territories. Atheromatosis of the aorta or its branches can be asymptomatic or manifest clinically in the form of mesenteric ischemia or ischemic nephropathy. Atherothrombosis therefore involves distinct medical specialities and healthcare levels such as cardiology, neurology, nephrology, endocrinology, vascular surgery, internal medicine, and primary care. Simultaneous involvement of more than one vascular territory, whether symptomatic or asymptomatic, requires a global, multidisciplinary and coordinated approach. Additionally, medical intervention should not be limited to treatment of the acute accident as prevention, both primary and secondary, is a key factor in the management of this disease. It is here that specialties with an overall view such as internal medicine or primary care are especially well placed to play a fundamental and coordinating role. This multidisciplinary intervention involves not only physicians but also other health professionals such as dieticians, physical exercise specialists and, especially, nurses, who should play a key role in controlling risk factors, in health education and in monitoring treatment adherence.
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PMID:[Multidisciplinary approach to atherothrombotic disease]. 1963 38

Osteoporosis is a systemic disease that is associated with increased morbidity, mortality and health care costs. Whereas osteoclasts and osteoblasts are the main regulators of bone homeostasis, recent studies underscore a key role for the immune system, particularly via activation-induced T lymphocyte production of receptor activator of NFkappaB ligand (RANKL). Well-documented as a mediator of T lymphocyte/dendritic cell interactions, RANKL also stimulates the maturation and activation of bone-resorbing osteoclasts. Given that lipid oxidation products mediate inflammatory and metabolic disorders such as osteoporosis and atherosclerosis, and since oxidized lipids affect several T lymphocyte functions, we hypothesized that RANKL production might also be subject to modulation by oxidized lipids. Here, we show that short term exposure of both unstimulated and activated human T lymphocytes to minimally oxidized low density lipoprotein (LDL), but not native LDL, significantly enhances RANKL production and promotes expression of the lectin-like oxidized LDL receptor-1 (LOX-1). The effect, which is also observed with 8-iso-Prostaglandin E2, an inflammatory isoprostane produced by lipid peroxidation, is mediated via the NFkappaB pathway, and involves increased RANKL mRNA expression. The link between oxidized lipids and T lymphocytes is further reinforced by analysis of hyperlipidemic mice, in which bone loss is associated with increased RANKL mRNA in T lymphocytes and elevated RANKL serum levels. Our results suggest a novel pathway by which T lymphocytes contribute to bone changes, namely, via oxidized lipid enhancement of RANKL production. These findings may help elucidate clinical associations between cardiovascular disease and decreased bone mass, and may also lead to new immune-based approaches to osteoporosis.
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PMID:Oxidized lipids enhance RANKL production by T lymphocytes: implications for lipid-induced bone loss. 1969 88

Atherosclerotic plaques are a feature of abdominal aortic aneurysms (AAAs). Atherosclerosis and AAA appear to share similar risk factors. These observations have led to the conclusion that AAAs are a consequence of advanced atherosclerosis.This review explores current theories regarding the pathogenesis of AAA and their implications for treatment.A systematic literature search was conducted using the search terms abdominal aortic aneurysm, atherosclerosis, pathogenesis, and systemic disease. Articles were categorized according to the association of AAAs with atherosclerosis, arteriomegaly, peripheral aneurysm, systemic expression, genetics, autoimmunity, oxidative stress, and systemic disease. Twenty-nine articles reporting changes in the systemic vasculature associated with AAA and 12 articles examining the shared risk factor hypothesis were identified.There is insufficient evidence to confirm that AAAs are the result of advanced atherosclerosis. The bulk of evidence points to AAA disease being a systemic disease of the vasculature, with a predetermined genetic susceptibility leading to a phenotype governed by environmental factors.
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PMID:Review of current theories for abdominal aortic aneurysm pathogenesis. 1976 4


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