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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A model of atherogenesis is described in which it is proposed that a state of relative impairment of intravascular fibrinolytic function is the primary defect which makes possible both the initiation and the continued progression of arterial plaques. The key mechanism by which impaired fibrinolysis is atherogenic centers on the unique disruptive effect which fibrin has on the contiguous endothelium of the vascular intimal surface. From this perspective, in areas of spontaneous endothelial injury, impaired fibrinolysis maintains and promotes the gradual enlargement of the area of injury by causing persistently increased intimal permeability and by allowing enhanced fibrin and platelet deposition. This hypothesis thus represents a modification of the response-to-injury hypothesis in which the emphasis has been shifted from the initial endothelial injury to a state of interference with the normal process of healing endothelial injuries. Consistent with this viewpoint, it is noted that all positive risk factors for vascular disease are associated with impairment of fibrinolytic function and, conversely, negative cardiac risk factors enhance fibrinolysis. It is further proposed that one or more prostaglandins, or closely related metabolites, represent the mediators of primary physiologic importance with regard to in vivo regulation of fibrinolysis. By this hypothesis, adequate dietary intake of essential fatty acids, as well as maintenance of unimpaired eicosanoid metabolism, become centrally important in both preventing and reversing arteriosclerosis. This two-tiered model can be used to organize and potentially explain the interrelationship between diverse and apparently divergent sets of epidemiological data which previous models have been unable to accommodate.
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PMID:Endothelium, fibrinolysis, cardiac risk factors, and prostaglandins: a unified model of atherogenesis. 853 44

We evaluated the usefulness of dipyridamole-thallium imaging for the detection of ischaemic heart disease in 257 patients with atherosclerotic vascular disease (80 patients with arteriosclerosis obliterans, 81 patients with aneurysm of the abdominal aorta, 60 patients with aneurysm of the thoracic aorta and 36 patients with dissecting aortic aneurysm). Clinical evidence of ischaemic heart disease was found in 69 of 257 (27%) patients, including 32 patients with arteriosclerosis obliterans, 23 with aneurysm of the abdominal aorta, 9 with aneurysm of the thoracic aorta and 5 with dissecting aortic aneurysm. Dipyridamole-thallium imaging identified myocardial ischaemia in 49 of 69 (71%) patients with clinical evidence of ischaemic heart disease. Dipyridamole-thallium imaging showed positive results in 67 of 81 (83%) patients with aneurysm of the abdominal aorta. In patients with no clinical evidence of ischaemic heart disease, the results of dipyridamole-thallium imaging were positive in 39 of 188 (21%) patients. Dipyridamole-thallium imaging was positive in 90 of the 257 (35%) patients as a whole. When we combined the patients with positive dipyridamole-thallium imaging with those with negative dipyridamole-thallium imaging but who had clinical evidence of ischaemic heart disease, 42% of all patients had evidence of ischaemic heart disease. Our findings suggest that atherosclerotic vascular disease is strongly associated with ischaemic heart disease and that dipyridamole-thallium imaging is useful for the detection of ischaemic heart disease.
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PMID:Usefulness of dipyridamole-thallium imaging in 257 patients with atherosclerotic vascular disease. 857 Jan 11

We studied the frequency, severity, and clinical correlations of cerebral amyloid angiopathy (CAA) in 117 CERAD subjects with autopsy-confirmed AD. Eighty-three percent showed at least a mild degree of amyloid angiopathy. Thirty of 117 brains (25.6%) showed moderate to severe CAA affecting the cerebral vessels in one or more cortical regions. These brains also showed a significantly higher frequency of hemorrhages or ischemic lesions than those of subjects with little or no amyloid angiopathy (43.3% versus 23.0%; odds ratio = 2.6, 95% CI = 1.1 to 6.2) High CAA scores also correlated with the presence of cerebral arteriosclerosis and with older age at onset of dementia. Our findings suggest that factors contributing to non-AD-related vascular pathology (e.g., atherosclerosis) may play a role in amyloid deposition in cerebral vessels in AD.
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PMID:Cerebral amyloid angiopathy in the brains of patients with Alzheimer's disease: the CERAD experience, Part XV. 864 54

Over a period of 5 years 81 vascular complications after 15,460 catheterizations of the femoral artery for diagnostic (n = 11,883) or therapeutic (n = 3577) procedures were registered. The following complications were observed in declining frequency: 1. False aneurysm (n = 65), 2. arterial occlusion (dissection, embolia, thrombosis) (n = 8), 3. vascular lesion causing profuse bleeding (n = 7), 4. AV-fistula (n = 1). The total complication rate was 0.52%. The complication rate was significantly higher in therapeutical procedures (1,03%) than in diagnostic investigations (0.37%). Pseudoaneurysms were complicated by thrombosis of the femoral vein (n = 3), lymphatic fistula (n = 3) and deep wound infection (n = 9); secondary complication rate 18.5%. Risk factors for local vascular complications are old age, female gender, high grade arteriosclerosis at the puncture site, overweight, manifest arterial hypertension and medication with cumarin, acetylsalicylic acid or heparin. Further complicating factors are connected with technical risks such as duration of the procedure. French size of the catheter, the catheter sheath and multiple punctures. Vascular repair was performed by simple angiography in most cases, but in 14.8% more extensive surgical procedures were required. In patients with signs of occlusive vascular disease the external iliac artery was replaced by a PTFE-vascular access graft in 4 cases and an arterioplasty of the deep femoral artery was performed in 2 patients. 36% of the operations were undertaken as emergencies. Reintervention was necessary for a postoperative bleeding complication in 1 case (surgical complication rate 1.2%). A female patient suffering from aortic valve stenosis died during emergency operation due to massive retroperitoneal hemorrhage after cardiac catheterization (mortality rate 1.2%). Over a median follow-up period of 37 months no late complications of the intervention were recorded, nor recurrences of peripheral arterial occlusive disease.
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PMID:[Local vascular complications after iatrogenic femoral artery puncture]. 867 63

The normal functional state of the vasculature and the events leading to the development of significant arterial disease involve the interaction of important vasoactive substances, which play important modulating or initiating roles in the development of hypertension and arteriosclerosis. Three endothelins have now been identified, of which ET-1 is the best characterized. ET-1 is produced by epithelial, mesangial, neuronal and glial, and liver cells, and is the most potent vasoconstrictor yet found. Each endothelin is derived from a different gene on separate chromosomes, and each binds to at least 2 types of receptor. The plasma half-life of ET-1 is about 7 min, and this provides a rapid mechanism for adjusting vascular resistance or blood pressure. The actions of endothelin are mediated through several pathways of postreceptor signaling, including activation of the mitogen-activated protein kinase cascade, which give rise to its growth-stimulating properties. Secretion of ET-1 from cultured endothelial cells is stimulated by a wide range of substances, and is inhibited by some prostaglandins. Endothelin in turn stimulates secretion of nitric oxide, arginine vasopressin and atrial natriuretic peptide, and participates in the hormonal control of salt and water balance. Hypoxia and ischemia augment ET-1 secretion, as does insulin, and this could play a role in the accelerated vascular disease of diabetes. ET-1 also causes bronchoconstriction and has been implicated in the development of acute asthma, primary pulmonary hypertension and pulmonary fibrosis. Its role in hypertension is still debatable, though most of the manifestations of congestive heart failure can theoretically be explained by the actions of ET-1. Endothelin also has extensive renovascular and parenchymal effects in the kidney. It is hoped that a fuller understanding of the role of endothelins in normal or pathologic vasculature will lead to effective therapy based on antagonism or augmentation of specific functions.
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PMID:Endothelins as cardiovascular peptides. 873 84

The negative role of smoking on circulation is widespread knowledge and it has been rated as a vascular risk factor. This paper evaluates the influence of smoking on the arterial supply to the erectile tissue, establishing the flow speed parameters in cavernous arteries with eco-doppler both at rest and after intracavernous PgE1 injection. Four groups were studied: non-smokers, without arterial disease and with arterial disease of non-smoking etiology; smokers with vascular disease, and another group where smoking was the only verified etiological factor. No significant differences were detected in flow speed parameters at rest among smokers and non smokers both in individuals with preserved erectile potency or with erectile dysfunction. Following drug therapy, impotent smokers showed the worse erectile response. With regard to flow speed parameters, although the differences were not significant, it can be seen that smokers, whether potent or not, show less differential speed, flow time, and acceleration, exhibiting a certain degree of arterial rigidity. That flow speed parameters, in cases with erectile dysfunction, can be superposed in individuals with arterial-origin impotence and those where smoking is the sole risk factor, indicates that this is a factor which causes erectile dysfunction due to vascular damage, as severe as any other caused by other factors such as arteriosclerosis, diabetes, or hypertension.
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PMID:[Assessment of tobacco impact on penile vascularization with echo-Doppler and intracavernous injection]. 880 98

A sufficient understanding of the risk factor and the natural history of arteriosclerosis obliterans, ASO, is essential for selecting the optimal treatment for this condition. Hypercholesterolemia, hypertension and cigarette smoking have been identified as independent major risk factors of ASO, and diabetics, obesity, hypertrigriceridemia, low HDL-cholesterol level, aging, gender, etc, as minor factors. The patients with ASO often have multiple risk factors, synergistically accelerating the disease progression. Recent objective studies on natural history of claudicants have demonstrated a more morbid prognosis, especially in the patients with disabling claudication, than that outlined by previous historical studies. Mortality rates for ASO patients in long-term follow-up have revealed to be significantly higher than those observed in control groups. The causes of death are mostly arteriosclerotic vascular disease, particularly coronary artery and cerebrovascular diseases, which indicate the significance of the systemic evaluation in treating patients with ASO.
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PMID:[Risk factor, natural history and prognosis of the patients with arteriosclerosis obliterans]. 880 7

Plasma/serum beta-hexosaminidase (Hex) activity is known to be increased in chronic alcoholism, liver disorders, pregnancy and diabetes mellitus. Hex activity also shows an association with risk factors for vascular disease and heredity for arteriosclerosis. There are several isoenzymes of Hex. Using an enzyme immunoassay for Hex isoenzymes (Hex A and Hex B) we studied possible determinants of Hex isoenzymes and their relation to vascular disease in randomly invited (n = 244) 35-95-year-old men and women. In both sexes there were significant age-related increases in Hex activities and men exhibited higher activity of both isoenzymes. Both Hex isoenzymes correlated with age, systolic blood pressure, serum triglycerides and liver enzymes, whereas Hex A was distinguished from Hex B by its stronger correlation with blood glucose. In multiple linear regression analysis Hex A was explained to 20.7% by blood glucose, age, serum aspartate aminotransferase and glutamyl transpeptidase. Hex B was explained to 14% by age, serum glutamyl transpeptidase and serum triglycerides. There was no significant increase in Hex isoenzymes in subjects with hypertension, diabetes mellitus or myocardial disease, nor did current smokers exhibit any increase of these enzymes compared to non-smokers. The main conclusion in that liver function, as reflected by the level of liver enzymes and glucose metabolism, is the major determinant for Hex isoenzymes in plasma.
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PMID:beta-Hexosaminidase isoenzymes A and B in middle-aged and elderly subjects: determinants of plasma levels and relation to vascular disease. 888 76

Chronic exposure to low levels of environmentally derived arsenite are associated with vascular diseases, such as arteriosclerosis. However, the cellular and molecular mechanisms for vascular disease in response to arsenic are not known. These studies investigated the hypothesis that nonlethal levels of arsenic increase intracellular oxidant levels, promote nuclear translocation of trans-acting factors, and are mitogenic. Incubation of second passage vascular endothelial cells with less than 5 microM arsenite for 4 h increased incorporation of [3H]thymidine into genomic DNA, while higher concentrations failed to stimulate or inhibit DNA synthesis. Within 1 h following addition of noncytotoxic concentrations of arsenite, oxidants accumulated and thiol status increased. During this time period, there was increased nuclear retention of NF-kappa B binding proteins and nuclear translocation of NF-kappa B also occurred in response to 100 microM H2O2. Supershift analysis demonstrated that p65/p50 heterodimers accounted for the majority of proteins binding consensus kappa B sequences in cells treated with arsenite or oxidants. The antioxidants, N-acetylcysteine or dimethylfumaric acid, increased intracellular thiol status and prevented both oxidant formation and translocation of NF-kappa B binding proteins in response to arsenite. These data suggest that arsenite initiates vascular dysfunction by activating oxidant-sensitive endothelial cell signaling.
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PMID:Arsenic induces oxidant stress and NF-kappa B activation in cultured aortic endothelial cells. 890 24

A unique peripheral vascular disorder called 'blackfoot disease' is endemic in a limited area on the south-west coast of Taiwan. Clinically, the signs and symptoms of blackfoot disease (BFD) are similar to those of arteriosclerosis and Buerger's disease. A destruction of vascular endothelial cells (ECs) takes place at an early stage in the affected limbs. Currently, the cause of BFD is believed to be artesian drinking water containing a high concentration of arsenic and/or humic substances, although the mechanism of EC destruction is not entirely understood. The purpose of the present study was to examine the factors related to EC damage in BFD. Thus, we investigated the effects of purified IgG collected from patients with BFD (BFD-IgG) and from normal controls (N-IgG) on cultured EC. We found that: (1) EC binding activity of BFD-IgG was significantly higher than that of N-IgG; (2) BFD-IgG, at a concentration higher than 100 microg/ml but not N-IgG, induced concentration-dependent EC cytotoxicity; (3) BFD-IgG at a concentration of 100 microg/ml stimulated neither the release of von Willebrand factor nor the expression of intercellular adhesion molecule-1 by EC. Fluorescent video microscopic examination revealed an increase in transcapillary and interstitial diffusion of nailfold capillary loops in clinically normal fingers of BFD patients. These findings strongly suggested that immunological mechanisms played a significant role in the pathogenesis of BFD. We propose that only persons who produce the IgG anti-endothelial cell antibody are potential victims of BFD.
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PMID:In vitro cytotoxicity of IgG antibodies on vascular endothelial cells from patients with endemic peripheral vascular disease in Taiwan. 956 46


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