Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind study comparing halofenate, a new lipid-lowering investigation drug, with an established drug, clofibrate, was conducted on 33 clinic patients with Type II hyperlipoproteinemia for a period of 48-96 weeks. All but 10 patients had some type of symptomatic major vascular disease. With respect to serum cholesterol levels, a comparable proportion (56-59%) of patients in each group responded to the respective treatment but the magnitude of lowering was substantially less for the halofenate responders (12% mean decrease versus 25%). Type IIa patients in both groups were more likely than Type IIb patients to have a favorable cholesterol-lowering response. Weight gain of 5% or greater was prejudicial to cholesterol lowering. In the case of serum triglycerides, the proportion of patients responding to clofibrate treatment was somewhat greater (87% versus 57% for halofenate) but the mean magnitude of lowering (27-34%) was comparable for responders in the two groups. Weight gain did not influence appreciably the triglyceride-lowering effect. Elevated concentrations of triglyceride (Type IIb) in the control period favored a triglyceride lowering response by clofibrate but was only a moderate influence on the response to halofenate.
Atherosclerosis 1976 Sep
PMID:Halofenate in the treatment of type II hyperlipoproteinemia. Double blind comparison with clofibrate. 78 22

Inbred Carworth Farms Nelson (CFN) congenitally hyperlipidemic rats had significantly shorter coagulation and prothrombin times and higher levels of coagulation factors, II, V, VII, VIII, and X than did controls. Conversely, congenitally hypolipidemic rats of the same strain had significantly longer coagulation and prothrombin times and lower levels of factors II, V, VII, X and XII and of blood platelets than did controls. A loop-shaped polyethylene cannula was inserted into the aorta to assess the potential for thrombosis. The hyperlipidemic group obstructed this significantly faster and the hypolipidemic group slower than did the controls. Normal CFN rats made hypertensive by unilateral renal artery clip developed hypertension together with significantly elevated serum cholesterol and factor VII and X levels. Rhesus monkeys with diet-induced hyperlipidemia showed shorter prothrombin times and higher factor X levels than did controls on normal diet. By selective breeding, two groups of squirrel monkeys were obtained. Both groups had similar serum cholesterol levels on a normal diet but one group (hyperresponders) showed higher serum cholesterol levels on a cholesterol-containing diet than did the other (hyporesponder) group. Both groups showed significantly elevated levels of factors II, V, VII, IX and X on a cholesterol-containing diet. There was good correlation between the levels of many coagulation factors and serum cholesterol in both rats and monkeys. If thrombosis is important in the genesis of atherosclerosis, these findings could indicate that elevation of plasma lipids may play a role, via the coagulation pathway, in the production of human vascular disease.
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PMID:Hyperlipidemia, hypercoagulability, and accelerated thrombosis: studies in congenitally hyperlipidemic rats and in rats and monkeys with induced hyperlipidemia. 81 75

Hypertension is associated with an increased incidence of generalized vascular disease. Antihypertensive drug therapy, while decreasing overall mortality due to cerebral hemorrhage, myocardial hypertrophy or renal failure, paradoxically does not appear to reduce the incidence of coronary atherosclerosis. This study investigates whether the drugs, as a possible side effect, may have an adverse influence on the development of atherosclerotic plaques. Groups of rabbits were fed an atherogenic diet containing 1% cholesterol for 12 weeks. Two commonly used antihypertensive agents (methyldopa and chlorthalidone) were added to the diet of some groups at levels of 100 mg and 10 mg per day respectively. No significant increase in total atherosclerotic plaque area was produced by either of the drugs tested singly or in combination. Plasma renin levels were only mildly elevated and in this experimental system there was no correlation between renin activity and atherosclerotic plaque intensity. There is thus no evidence from this study that antihypertensive drugs have any adverse effects on atherosclerotic plaque formation. While the ineffectiveness of these drugs against coronary atherosclerosis may indicate that normalization of pressure cannot arrest changes already initiated, it also supports the possibility that association of atherosclerosis with hypertension may be symptomatic of a common underlying defect not correlated by normalizing blood pressure.
Atherosclerosis 1977 Jan
PMID:Anti-inflammatory agents in experimental atherosclerosis. Part 2. Failure of antihypertensive drugs to exacerbate atherosclerotic plaque formation. 83 50

A group of 78 patients with severe hypercholesterolemia (-X = 464 mg/dl) and symptoms of vascular disease of the heart, the extremities, or the brain, started a beta-pyridylcarbinol treatment with an average daily dosage of 1.2 g in 1964. In 1976 we could re-examine 12 patients, still on the same therapy. No myocardial infarction has occurred in this group since 1973, only 2 patients have had more attacks of angina pectoris that 1964. In contrast patients discontinuing therapy or replacing beta-pyridylcarbinol by other hypolipidemic drugs had a higher mortality.
Atherosclerosis 1977 Apr
PMID:The treatment of hypercholesterolemia with beta-pyridylcarbinol. Part 5. Report on 16 cases with severe hypercholesterolemia treated for 12 years. 85 28

A case of gallbladder infarction, occurring in a 34-year old man with severe hypertension is described, with uneventful recovery following cholecystectomy. In the absence of other obvious etiologic factors, the gallbladder infarction is presumed to be directly related to hypertensive vascular disease. Infarction of the gallbladder is rare; a few cases associated with hypertension have been previously reported. Other types of vascular disease including embolization, thrombosis complicating atherosclerosis and celiac angiography, polyarteritis nodosa, occlusion following torsion and cystic vein thrombosis have been reported to cause gallbladder infarction.
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PMID:Infarction of the gallbladder: a complication of hypertension. Case report. 86 44

Measurements of aortic length and circumference in 336 post-mortem specimens confirm earlier, neglected observations on the progressive increase in aortic size which occurs with advancing years. The increase is not related to atherosclerosis , or to hypertension and seems to be part of a true ageing process. The value of measurement of aortic size in body age determination merits exploration by forensic pathologists. Aortic calcification is found in raised and complicated atherosclerotic plaques and its prevalence and severity closely follows the accepted pattern of plaque severity, occurring earlier and more severely in men, in the abdominal aorta and in patients with overt vascular disease in other territories such as patients with cardiac infarcts. No association was found between the amount of calcification and the presence of hypertension, diabetes or neoplasia.
Atherosclerosis 1977 Aug
PMID:Aortic size and aortic calcification. A necropsy Study. 88

Biomicroscopic examination of the bulbar conjunctival vessels regularly discloses degenerative microangiopathy in patients with overt arteriosclerotic cerebral vascular disease. Examination of a group of normotensive nondiabetic adults aged 21 to 39 years disclosed similar but less severe changes in 56 per cent of the men and 26 per cent of the women. The incidence was higher (88 per cent of the men and 45 per cent of the women) in those with a strong family history of early death from arteriosclerotic disease. There was no consistent correlation between the severity of the microangiopathy and the values for hematocrit, cholesterol, triglycerides or blood pressure. Conjunctival microangiopathy, like atherosclerosis of larger vessels, starts in the second and third decades and advances with age. We suggest that microangiopathic changes in the conjunctival vessels may provide the first readily detectable evidence of degenerative vascular disease.
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PMID:Conjunctival microangiopathy. An early sign of degenerative vascular disease? 88 44

Hyaluronate (HA), heparan sulfate (HS), dermatan sulfate (DS) and isomeric chondroitin sulfates (CS) were measured in vascular walls of 9-10 months old normal and hypophysectomized female beagles treated with sex hormones. Following hypophysectomy the animals were maintained for 8 weeks without any hormonal replacement therapy and then they were exposed for 3 weeks to parenteral treatment with sex hormones. One group received twice weekly 25 mg testosterone, another group was given the same amount of progesterone, and a third group received on day 1 and day 14, estrogens in 2 injections, consisting of a mixture of 10 mg short-acting estradiol-17-phenylpropionate and 2.5 mg long-acting estradiol benzoate. After 11 weeks all animals were sacrificed, coronary arteries and aortas were immediately removed and the latter were divided into three segments: arch, thoracic and abdominal. Removal of the pituitary led to a reduction of the HA content in the aortic arch and thoracic segment, but coronary arteries and abdominal aorta were not affected. The main consequence of hypophysectomy both in the entire aorta and in coronary arteries was a sharp reduction of the sulfated glycosaminoglycan (GAG) content. All three hormones produced a modest rise in the HS content of coronary arteries. A more definite response was seen in the thoracic aorta where each of the three hormones raised the low DS content to normal levels. Concerning the effect of sex hromones on aortic GAG other than DS, TESTOSTERONE RAISED THE CS content towards normal in thoracic and abdominal segments, while estrogen by doubling the normal HA concentration was particularly potent in the abdominal aorta. It is conceivable that the different sensitivity of various segments of aorta and coronary arteries to sex (and other) hormones in terms of regulating GAG metabolism may prove to be of relevance to the uneven distribution of lesions in degenerative vascular disease.
Atherosclerosis 1977 Jun
PMID:The effect of sex hormones on glycosaminoglycan content of canine aorta and coronary arteries. 90 20

A case of partially occluding post-traumatic thrombosis of the internal carotid artery and secondary embolism of the middle cerebral artery is reported. The patient was treated with Thrombolysin with coincident resolution of clinical symptoms and signs and clearing of the lesions on arteriography. This may have been fortuitous. The subject of traumatic carotid artery thrombosis is reviewed in detail, and its pathophysiology is discussed, especially in relation to facts known about occlusive vascular disease secondary to atherosclerosis and related embolic phenomena. Suggestions are made concerning the treatment of this condition, especially with regard to developing rational criteria for opening vascular beds through evaluation of collateral cerebral blood flow. The uses of microvascular surgical techniques and thrombolytic therapy are considered.
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PMID:Non-penetrating trauma to the carotid artery with secondary thrombosis and embolism: treatment by thrombolysin. 90 3

In clinical investigation on ehnanced platelet aggregation the changes of the various tests with time after blood sampling must be considered. The photometric PAT III for the evaluation of spontaneous aggregation showed enhanced aggregation in a high percentage of patients with vascular disease, and prospective data obtained so far make it likely that enhanced aggregation is a risk factor for thrombosis. More prospective studies are necessary to prove whether continuously enhanced spontaneous platelet aggregation is indicating progressive atherosclerosis.
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PMID:Photometric platelet aggregation test III: a new tool for the detection of enhancet platelet aggregation. 92 34


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