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

1. The results of the Veterans Administration Co-operative Study have been extended by the subsequent clinical trials, which included patients of both sexes and with less vascular disease. The later studies confirm the effectiveness of treatment in preventing most complications except myocardial infarction and sudden death. Furthermore, the lower diastolic blood pressure in which treatment has been shown to have a significant beneficial effect has been lowered from 105 mmHg as indicated by the Veterans Study to 100 mmHg as shown by the much larger Australian trial. The possibility of reducing the incidence of sudden death and fatal myocardial infarction has been suggested by other recent control trials using beta-adrenoreceptor-blocking drugs, an approach that needs further exploration. 2. A number of interesting and useful new drugs have appeared which include tienilic acid, minoxidil, saralasin and captopril, and in addition recent controlled trials have re-emphasized the effectiveness of the old drug, reserpine, when combined with a diuretic. The art of treatment of hypertension therefore appears to be in a healthy state and we should expect more advances in the future.
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PMID:Treatment of hypertension: state of the art in 1979. 4 33

Two thrombolytic agents are mainly used in patients: streptokinase (SK) and urokinase (UK). UK from human origin is an endopeptidase which is able to convert plasminogen into plasmin. UK is only secreted by the kidney and is only found in urine which is presently the only source of extraction. Studies in man have shown that UK produces a highly reproducible state of enhanced plasma thrombolytic activity with a high fibrinolysis/fibrnogenolysis ratio and a lack of toxicity and antigenicity. The half life in Animal is short as well as the duration of fibrinolytic activity in Man. In clinical experience, positive results have been reported in pulminary embolism while the issues in myocardial infarction are controversial. Suggestive results have been registered in deep vein thrombosis, in ophthalmologic field and in desobstruction of arterio-venious shunts. No evident benefit has been noted in cerebral vascular disease. Up to now, UK has been very well tolerated.
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PMID:[Urokinase. Biochemical therapeutical and therapeutical data (author's transl)]. 6 58

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.
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PMID:Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta. 14 28

The chemical composition of ultracentrifugal fractions of VLDL (d less than 1006), LDL (d 1006-1063) and HDL (d less than 1063) has been studied in males affected by atherosclerosis of different vascular beds. Thirty-seven subjects affected by post-infarction cardiopathy (M.I.) showed significantly higher values of total-C, VLDL-C and LDL-C when compared to 52 controls. Twenty-three patients affected by non-occlusive ischaemic heart disease (I.H.D.) showed higher values than controls of total-C, VLCL-C, LDL-C, total TG, VLDL-TG, and GDL-TG. Twenty-three patients with atherosclerosis of the inferior limbs (P.A.) were characterized by increased levels of total-TG, VLDL-TG, VLDL-C, HDL-C. A group of patients who had suffered a stroke from cerebro-vascular disease (C.V.D.) did not show any significant difference from controls. In the M.I. group, 56% of the patients had a high level of C-VLDL. Patients with I.H.D. were characterized mostly by an increase in C-LDL, Patients with P.A. showed the highest values of total -TG, VLDL-TG and LDL-TG. Some of the observed differences are probably due to different metabolic backgrounds. Some other differences may be due to variations in dietary habits after heart infarction. Patients with levels of plasma cholesterol and triglyceride beyond the 90th percentile of the normal group showed many abnormalities in the chemical composition of their lipoproteins. It is noteworthy that increased amounts of cholesterol may collect in lipoprotein classes different from LDL while increased amounts of triglyceride may collect in classes different from VLDL.
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PMID:Chemical composition of ultracentrifugal fractions in different patterns of human atheroslcerosis. 18 83

The thrombotic process, basic mechanisms of action of antiplatelet drugs, and clinical trials with platelet inhibitors are reviewed. The role of prostaglandins in platelet reactions and the mechanisms of aspirin's, dipyridamole's and sulfinpyrazone's inhibition of platelet function are discussed. Clinical studies of the use of these three drugs, alone or in combination with each other or with anticoagulants, for the treatment of thrombotic disorders associated with valvular heart disease, prosthetic heart valves, cerebral vascular disease (e.g., transient ischemic attacks), coronary artery diseases (including myocardial infarction), peripheral vascular disease, renal disease and renal allograft rejection are reviewed and evaluated. Clinical evidence suggests that antiplatelet drugs are useful in preventing thromboembolism associated with coronary and cerebral vascular disorders. In peripheral vascular and renal diseases and in renal allografts, their benefits have not been proved. Further controlled clinical studies of the preventive use of these drugs for arterial thrombosis are needed.
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PMID:Antiplatelet drugs in arterial thrombosis: a review. 36 14

This report extends an earlier analysis of a case-control study of the relationship of oral contraception (OC) to thrombosis in 104 idiopathic cases, 357 other thrombosis cases (excluding cerebrovascular), and 1302 matched controls which described a 7-fold increase in risk for OC users in the idiopathic series and a 2-fold increase for the whole series. This report analyzes factors which predispose or precipitate thrombosis related to risk with OC use. In the initial study, the control patients had not been matched with the cases for the presence or absence of 6 factors (history of thrombosis, of vascular disease, of central vascular disorders, of blood abnormalities, of metabolic disease, and of surgery or trauma) thought to predispose or precipitate thrombosis. In this report, 2 methods of analysis (matched set and logistic regression) gave closely similar results. Where the case series consisted of idiopathic cases, the revised estimate of relative risk was reduced form 7.2 to 4.7 by these procedures; for predisposed cases, it increased from 1.2-2.2. Variation in relative risk was examined for 4 separate diagnostic categories: venous thrombosis alone, pulmonary embolism alone, venous thrombosis and pulmonary embolism together, and myocardial infarction. Overall, the relative risk estimates were greater than unity for each thrombosis category for both predisposed and nonpredisposed cases. The relative risk was not found to vary significantly according to age or smoking status.
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PMID:Increased risk of thrombosis due to oral contraceptives: a further report. 46 73

We investigated the relation in women of various factors to risk of myocardial infarction, subarachnoid hemorrhage, other strokes, and venous thromboembolism. Smoking significantly increased risk of all four diseases, whereas oral contraceptive use was associated with an increase only in risk of subarachnoid hemorrhage and venous thromboembolism. Use of noncontraceptive estrogens was not associated with increased risk of any of these diseases. Hypertension, hypercholesterolemia, obesity, gallbladder disease, and nondrinking of alcohol were all associated with increased risk of myocardial infarction, whereas only hypertension and hypercholesterolemia were associated with increased risk of other strokes. Cigarette smoking was overwhelmingly the most important risk factor for vascular disease in women. Smoking should be considered a contraindication to oral contraceptive use, or at the very least, women wishing to use oral contraceptives should be strongly urged not to smoke.
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PMID:Risk of vascular disease in women. Smoking, oral contraceptives, noncontraceptive estrogens, and other factors. 47 67

The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.
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PMID:Degenerative vascular disease and myocardial infarction in mice with lupus-like syndrome. 47 7

A prospective study of mortality in 3,113 diabetics was carried out in Edinburgh over a period of eight years; 1,272 patients (41 %) died. Death rates for females equalled those for males and, in relation to the general population, there was a considerable excess mortality which was greater for females. Statistical analysis indicated that the important mortality risk-factors are age, duration of diabetes of greater than ten years and treatment. The risk of oral therapy or insulin were approximately equally greater than that of diet therapy and probably reflected severity of disease. Using international coding for diagnosis, 27 % of deaths were classified as directly due to diabetes and 49 % to vascular disease. Reclassifying the terminal cause of death left only 26 patients (2 %) recorded with diabetes as the direct cause of death. Three hundred and thirty five males (66 %) and 561 females (73 %) died of vascular disease. There was a predominance of myocardial infarction in males and cerebrovascular disease in females. These percentages were a little lower when post-mortem information was available. These results provide additional evidence that diabetes reduces life expectancy by inducing premature vascular disease and that the effect is greater in women than in men.
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PMID:Diabetic mortality in Edinburgh. 47 85


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