Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Age-related changes in liver function are important because they may promote susceptibility to adverse drug reactions, neurotoxicity, atherosclerosis, and other important diseases in older people. Age-related changes in the rat hepatic sinusoidal endothelium, termed pseudocapillarization, have been described recently and these may contribute to hepatic impairment. The present study has examined surgical and post-mortem specimens with immunohistochemistry and transmission electron microscopy to determine whether pseudocapillarization also occurs in older humans. The age of the subject, independent of systemic disease or hepatic pathology in surgical and post-mortem samples of human liver, was associated with increased peri-sinusoidal expression of von Willebrand's factor, collagen I, collagen IV, and staining with Masson's trichrome. Electron microscopy revealed significant age-related thickening of the sinusoidal endothelium (young 165 +/- 17 nm, middle age 222 +/- 11 nm, older 289 +/- 9 nm, p < 0.001) with loss of fenestrations (young 7.7 +/- 0.7 per 10 micro m, middle age 3.6 +/- 0.5 per 10 micro m, older 1.5 +/- 0.4 per 10 micro m, p < 0.001), and age-related deposition of basal lamina and collagen. In conclusion, ageing in humans is associated with morphological changes in the sinusoidal endothelium and space of Disse which are presumptively related to the ageing process and potentially represent an important link between the ageing process and disease susceptibility.
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PMID:Age-related pseudocapillarization of the human liver. 1269 49

The role of diagnostic imaging in the study of atherosclerosis of carotid and intracranial vessels is analyzed, after the illustration of the main characteristics of the disease. Atherosclerosis should be considered a systemic disease, however it tends to be segmental. The commonest sites are the coronary artery, the superficial femoral artery, the subrenal aorta and the carotid arteries at the level of the bifurcation. Traditionally, the percentage of intraluminal stenosis has represented the standard measurement of the severity of atheromatosis. However, the grade of stenosis is not the only sign predictive of clinical complications. The most vulnerable plaques show predominant core necrosis or hemorrhage, separated from the vascular lumen by a thin unstable fibrous cap. The two major aspects of lesions at high risk of rupture are the presence of a large soft core and the status of the fibrous cap that can be intact, ruptured or infiltrated by inflammatory cells. Imaging procedures should be addressed to the identification of these pathologic conditions predisposing to the embolic-thrombotic complication. However, additional information on blood flow dynamics, vascular collateral compensation and brain perfusion is useful for decision-making about the therapeutic approach. This is the reason why in diagnostic imaging of atheromatosis, digital angiography should be combined with color Doppler-US, CT and MRI.
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PMID:Atherosclerosis of carotid and intracranial arteries. 1269 80

Atherosclerosis is a systemic disease that can ultimately lead to ischaemia and infarction in the heart, brain and peripheral vasculature. According to the "response to injury" hypothesis, endothelial dysfunction is the early event that allows penetration of lipids and inflammatory cells into the arterial wall, contributing to the development of the atherosclerotic lesion. Endothelial dysfunction is causally related to a variety of risk factors for atherosclerosis, including hyperlipidaemia and hypertension. Agents that restore endothelial function and NO bioavailability have beneficial anti-atherogenic activities and can improve cardiovascular outcomes; this has been observed with angiotensin-converting enzyme (ACE) inhibitors, statins and certain dihydropyridine-type calcium channel blockers (CCBs). In the Prospective Randomised Evaluation of the Vascular Effects of Norvasc Trial (PREVENT), the CCB amlodipine provided significant clinical benefits compared with placebo, including a marked reduction in cardiovascular morbidity and a reduction in the progression of carotid atherosclerosis. As these beneficial effects of amlodipine have not been observed with other dihydropyridine-type CCBs, it has been proposed that this agent has distinct anti-atherosclerotic properties related to its strong lipophilicity and membrane location. Experimental support for this hypothesis has been obtained from various in vitro and in vivo models of atherosclerosis. These findings support a broader therapeutic role for third-generation dihydropyridine-type CCBs in the treatment of atherosclerosis.
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PMID:Atheroprotective effects of long-acting dihydropyridine-type calcium channel blockers: evidence from clinical trials and basic scientific research. 1274 May 51

Atherosclerosis is a systemic disease affecting the circulatory system throughout the body. Thus, patients with atherosclerosis of the carotid arteries are not only at risk of stroke but also of other manifestations of the disease, i.e. vascular death, myocardial infarction etc. So far, intervention trials evaluating the effect of treatment of this patient group, i.e. by surgical removal of the carotid lesion, has focussed on degree of stenosis of the lesion. However, many other factors may be of importance: local factors of the lesion (morphology, degree of stenosis), hemodynamic factors (collateral compensation) and systemic factors (clinical symptoms, accompanying diseases, risk factor control). Recent findings suggest that plaque morphology (composition and structure) may be of greater importance than the degree of stenosis and it may be speculated if current indications for carotid endarterectomy are optimal.
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PMID:The natural history of patients with carotid stenosis. 1367 80

Atherosclerosis is currently considered to be an inflammatory and thus a systemic disease affecting multiple arterial beds. Recent advances in intravascular imaging have shown multiple sites of atherosclerotic changes in coronary arterial wall. Traditionally, angiography has been used to detect and characterize atherosclerotic plaque in coronary arteries, but recently it has been found that plaques that are not significantly stenotic on angiography cause acute myocardial infarction. As a result, newer imaging and diagnostic modalities are required to predict which of the atherosclerotic plaque are prone to rupture and hence distinguish "stable" and "vulnerable" plaques. Intravascular ultrasound can identify multiple plaques that are not seen on coronary angiography. Thermography has shown much promise and is based on the concept that the inflammatory plaques are associated with increased temperature and can also identify "vulnerable patients." Of all these newer modalities, magnetic resonance imaging has shown the most promise in identification and characterization of vulnerable plaques. In this article, we review the newer coronary artery imaging modalities and discuss the limitations of traditional coronary angiography.
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PMID:Imaging of the vulnerable plaque: new modalities. 1463 65

Oral bacteria inhabit biofilms, which are firm clusters adhering in layers to surfaces and are not easily eliminated by immune responses and are resistant to antimicrobial agents. Dental plaque is one such biofilm. In the past 10 years, subgingival plaque bacteria forming biofilms have been increasingly reported to be involved in systemic diseases. A close relationship between microbial infections and vascular disease has also been reported in the past two decades. The present review discusses the significance of the ecologic characteristics of biofilms formed by periodontopathic bacteria in order to further clarify the associations between periodontal disease and systemic disease. We focus on the relationships between periodontal disease-associated bacteria forming biofilms and vascular diseases including atherosclerosis and carotid coronary stenotic artery disease, and we discuss the direct and indirect effects on vascular diseases of lipopolysaccharides as well as heat shock proteins produced by periodontopathic bacteria.
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PMID:Involvement of periodontopathic biofilm in vascular diseases. 1499 87

While atherosclerosis has traditionally been divided into three types of disease, coronary artery or coronary heart disease (CHD), cerebrovascular disease, and peripheral vascular or peripheral arterial disease (PAD), it is now clear that atherosclerosis is a systemic disease caused by the same pathologic processes regardless of the vascular bed involved. The burden of disease is enormous both in the US and around the world with 61,800,000 Americans affected with one or more types of CVD, responsible for 958,775 deaths annually at a cost of approximately US 329.2 billion dollars annually. Despite trends of decreasing cardiovascular mortality, the global burden of cardiovascular disease is expected to rise, with CHD and stroke becoming the first and fourth most common causes of mortality and morbidity globally. Atherosclerosis is a multibed process with a substantial portion of patients afflicted with disease in more than one bed, although often assymptomatic. Now that there are multiple therapies available to modify and treat atherosclerosis and atherosclerotic risk factors, identification and treatment of these patients are important since their leading cause of death is from co-existing cardiovascular disease.
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PMID:Multi-bed vascular disease and atherothrombosis: scope of the problem. 1527 88

Atherosclerosis is a chronic systemic disease of the vasculature with an inflammatory component. It accounts for the majority of cardiovascular morbidity and mortality in industrialized countries and its incidence is increasing in developing countries. The impairment of vascular endothelial cell function in atherosclerosis and in conditions associated with increased cardiovascular risk is an important determinant of disease progression. The reduction of endothelium-dependent relaxation in the coronary and systemic circulation in atherosclerosis is in part due to decreased bioavailability of nitric oxide and increased release of oxygen-derived free radicals. Atherosclerosis also increases the formation of vasoconstrictors and growth factors, adhesion of leukocytes, thrombosis, inflammation, cell proliferation, as well as increases in vascular tone. Here we review mechanisms and therapeutic approaches to improve endothelial pathways in atherosclerosis. Restoration of NO bioactivity through pharmacological inhibition of the renin-angiotensin system, statin therapy, or endothelin receptor blockade, ameliorates vascular function in experimental hypercholesterolemia, hypertension and heart failure. These treatments also have therapeutic benefit for patients at risk or with overt atherosclerosis, to reduce vascular and myocardial complications of this disease.
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PMID:Endothelial therapy of atherosclerosis and its risk factors. 1532 Aug 38

Atherosclerosis is a systemic disease that affects most major arteries of the body and is the most common cause of premature death in the western world. It develops slowly and often asymptomatically, so that for many patients its first manifestation is sudden cardiac death, stroke, or myocardial infarction. The current gold standard for imaging atherosclerosis is x-ray angiography. However, recent advances in understanding of the pathobiology of atherosclerosis have highlighted the inadequacies of this technique and the need for better imaging approaches. The purpose of this article is to briefly outline the biology of atherosclerosis and to review the techniques available to image it, concentrating specifically on those that detect metabolic or inflammatory changes within the atherosclerotic plaque.
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PMID:Molecular and metabolic imaging of atherosclerosis. 1553 61

Most acute coronary syndromes result from the rupture or erosion of high-risk plaques. Clinical imaging studies have shown that atherosclerotic plaque formation and rupture are widespread processes that are often asymptomatic. The rationale for atherosclerosis imaging is the in-vivo identification of high-risk lesions, which may subsequently lead to prevention of future cardiovascular events. Although intravascular ultrasound (IVUS) imaging studies demonstrated that echolucent appearance of the plaque and expansive (positive) remodelling are associated with unstable clinical presentation, these characteristics were not adequate for accurate plaque characterisation. Recent technical developments in ultrasound equipment and analytical methods, utilising several characteristics of the digitised ultrasound signal with radiofrequency analysis and elastography, promise accurate tissue characterisation. Other imaging modalities, including optical coherence tomography, also contribute to a more precise characterisation of the composition of atherosclerotic plaques. A non-imaging approach is the focal assessment of temperature differences using sensitive intravascular thermography catheters, presumably reflecting focal inflammatory changes of vulnerable lesions. Although the histological characteristics of the atheroma are critically important in the sequence of events leading to acute coronary syndromes, the clinical relevance of identifying these characteristics is not yet clear. There is increasing evidence that identifying and treating individual culprit lesions may not be enough to prevent the ischaemic cardiac events in most patients, because the acute coronary syndrome is not a disease of a single site or a few discrete segments, but rather a systemic disease that involves the entire coronary tree. In addition to detection and quantitation of early coronary atherosclerosis and disease activity, accurate and reproducible methods could help to identify high-risk patients and allow serial monitoring during various therapeutic interventions. Serial IVUS imaging makes it possible to visualise the vessel wall that harbours the atheroma at different time points. Typically, serial IVUS allows the assessment of the percentage change in atheroma volume, with considerable statistical power to detect small changes. Using this methodology, aggressive lipid lowering by a high-dose statin agent has been shown to stop the progression of atherosclerosis, and a new mutant high-density lipoprotein complex was found to be effective in regressing atheroma burden. Although intravascular ultrasound is very accurate for quantification of atheroma burden, widespread application and accurate and reproducible non-invasive imaging modalities are needed for large-scale risk assessment algorithms. Cardiovascular computed tomography is at the forefront of the non-invasive imaging modalities. Future prospective imaging studies will be necessary to identify focal or systemic characteristics of high-risk lesions and to demonstrate the relationship between plaque burden, biochemical markers and clinical events.
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PMID:Atherosclerosis imaging: intravascular ultrasound. 1576 87


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