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

Physical conditioning appears to protect against the development of vascular disease. Although physical training often evokes favorable alterations in established cardiovascular risk factors, such as plasma lipids and lipoproteins, the metabolic sequelae of regular exercise that mediate a reduction in the risk of cardiovascular disease remain incompletely understood. Studies in recent years have shown physical training to have beneficial effects on blood coagulation and fibrinolytic activity. On general the data support the concept that blood clotting is potentiated by exercise. Mechanisms involved are an increased release of thromboplastine of tissue, increased coagulation with lactate accumulation during exercise, increased concentrations of plasma proteins owing to hemoconcentration, increased concentrations of specific clotting factors, e.g., Factor VIII and fibrinogen, and an alteration in platelet count and platelet function. The acceleration in coagulation is less in the well-exercised individual. There is evidence that an epinephrine mediated mechanism is responsible for the difference between individuals who have a lot of exercise and those who do not. Fibrinolytic activity seems to increase with exercise in a linear relationship with the heart rate during physical activity. An enhancement of the plasma fibrinolytic activity, stimulated experimentally by thrombotic stress such as venous occlusion, could be an important mechanism in the beneficial effect of habitual physical exercise on the risk of cardiovascular disease.
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PMID:[Modification of blood coagulation and fibrinolysis through physical activity]. 637 75

Since the realization that hypertension was a risk factor for cardiovascular disease, methods of lowering elevated blood pressure have been developed. The main goal of antihypertensive treatment is to prevent or to arrest cardiovascular damage. Based on the successes and failures encountered for over 30 years or more of therapeutic experience in hypertension, several treatment goals have been established. Previously, it was claimed that the advantages of lowering blood pressure were not dependent on the antihypertensive drug used. Now, this is being questioned. For instance, fatigue is often observed in hypertensive patients treated with drugs that reduce cardiac output and limit peripheral blood flow. Is it therefore more rational to reduce blood pressure by returning increased vascular resistance to normal? Since antihypertensive therapy is life-long, we are becoming increasingly aware of the long-term effects (both beneficial and adverse) of antihypertensive drugs. The metabolic changes caused by current antihypertensive drugs are now being studied in detail. The potassium-depleting action of diuretics is well-known, and the significance of such an effect is being re-examined. The effects of various antihypertensive agents on serum lipids are relatively recent observations, the clinical importance of which is worthy of wider discussion and investigation. The abolition or reduction of all vascular complications of hypertension is the goal for which current antihypertensive treatment has most often failed. Whereas prevention of cerebrovascular accidents, renal failure, and heart failure has indeed been successfully achieved, coronary complications (the most frequent adjunct of hypertension) have been little influenced by antihypertensive therapy. Is this because coronary heart disease may be simply an associated disease, rather than a consequence of hypertension? Or is this because the beneficial action of the most widely used antihypertensive drugs on vascular disease is largely counteracted by unfavorable metabolic effects? These and similar questions have to be debated and resolved before we can define treatment goals more precisely and develop the most appropriate means to achieve them.
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PMID:Treatment goals in hypertension. 670 59

Of 100 patients consecutively admitted to a rehabilitation hospital, 25 were cognitively impaired. On two brief tests of intellectual function, they scored below the criteria selected by the originators of those tests for clinically significant mental impairment. Nineteen of the 25 had vascular disease of the heart, brain, or peripheral vessels; two had cardiac valvular disease; three had head trauma; and one was mentally retarded. Mental impairment appears to be relatively common among the hospitalized elderly who do not carry the primary diagnosis of "dementia" or "organic brain syndrome." It appears to be particularly common among those with cardiovascular disease, even without frank stroke. Brief mental status examinations should be part of the routine evaluation of such patients.
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PMID:Underdiagnosis of cognitive impairment in a rehabilitation setting. 671 58

Cerebral blood flow was measured by the 133Xenon washout method in 44 cognitively intact subjects. Regression analysis of cerebral blood flow with age was performed on data from 33 subjects without arteriosclerotic cardiovascular disease, hypertension, or chronic obstructive pulmonary disease, factors which have been previously shown to lower cerebral blood flow. Changes with normal aging were significant in the left and right hemispheres with bilateral changes in temporal, parietal, and occipital regions. An additional group of 11 cognitively intact subjects with arteriosclerotic cardiovascular disease but no accompanying dementing disease had lower mean flow values at each detector position than did age- and sex-matched controls, although the differences did not always reach statistical significance. Decreased flows in temporal regions seem to be a concomitant of normal aging, and are not related to the presence of vascular disease.
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PMID:Regional decline of cerebral blood flow with age in cognitively intact subjects. 673 81

Cholesterol esterification, cholesteryl ester transfer between lipoproteins, and cholesterol transport between lipoproteins and cultured cells have been measured in the plasma of 22 patients with primary hyperlipidemia and 10 normolipidemic subjects. In hyperbetalipoproteinemia, increase in plasma low density lipoprotein levels was associated with a reduction of cholesteryl ester transfer rates, and with a reversal of the normal direction of sterol transport between fibroblasts and their plasma culture medium. Instead of net transport from cells to medium there was a net uptake of sterol from plasma by the cells, despite a level of plasma lecithin/cholesterol acyltransferase activity that was within the normal range. In dysbetalipoproteinemia, esterification rates were increased above normal levels, but cholesteryl ester transfer was reduced and the direction of sterol transport between the cells and plasma medium was reversed, as in the hyperbetalipoproteinemic group. In hypertriglyceridemia, those subjects with cardiovascular disease showed a metabolic pattern similar to the hyperbetalipoproteinemic group. The subjects in this group without symptoms of cardiovascular disease showed a normal direction of sterol transport, normal or raised rates of cholesteryl ester transfer between lipoproteins, and an increased rate of sterol esterification in plasma that decreased towards normal levels as plasma triglyceride levels decreased. Despite their quite distinct metabolic patterns there was no consistent difference between the two hypertriglyceridemic groups in triglyceride or cholesterol levels, very low density lipoprotein composition, or electrophoretic or isoelectric focussing patterns. All hypertriglyceridemic subjects with documented cardiovascular disease showed reversed cell-plasma sterol transport and all subjects without such disease showed a normal direction of cell-plasma sterol transport. The results of this study indicate major and reproducible abnormalities in plasma cholesterol metabolism in several groups of subjects with genetically distinct hyperlipidemias, who are at risk for atherosclerotic vascular disease. The possible predictive value of sterol metabolic measurements in the analysis of cardiovascular disease is discussed.
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PMID:Cholesterol net transport, esterification, and transfer in human hyperlipidemic plasma. 682 17

The mortality of 1564 Busselton subjects has been studied from 1966-79 to determine whether risk factors for cardiovascular disease (CVD) and coronary heart disease (CHD) showed any change in emphasis compared with the Framingham Population Study of 20 yr previously. The Busselton analysis used subjects free of probable and suspect coronary heart disease at onset. In men aged 40-59, systolic blood pressure (SBP), forced expiratory volume (FEV), and serum cholesterol levels were significant independent determining variables for CVD mortality and cholesterol for CHD mortality, with SBP being related to CVD in men aged 60-74 yr. In women, there were few indicators of future vascular risk with no significant determining variable for CVD and CHD in 40-59 yr olds, but blood glucose and FEV were significant risk factors for CVD in women aged 60-74 yr. Cholesterol was unrelated to mortality in women but showed negative relationship with cancer in 60-74 yr old men. In total mortality, smoking in men and women, and obesity in women were significant risk factors; 1 hr serum insulin had a negative relationship in men aged 40-59 yr, and a stronger positive relationship in men aged 60-74 yr, but this may have been due to the close negative association of the variable with body size (i.e. height). More studies are required to ascertain whether glucose and insulin have an aetiological role in vascular disease.
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PMID:Multiple regression analysis of risk factors for cardiovascular disease and cancer mortality in Busselton, Western Australia--13-year study. 685 63

Nonarteriosclerotic (virgin) and arteriosclerotic (breeder) rats were made diabetic with alloxan. Animals were treated with constantly adjusted doses of insulin, occasionally adjusted doses, or no treatment. The obese breeder rats lost weight; the lean virgin rats gained weight. All of the animals were autopsied 5 months post-alloxan. Blood pressure increased in virgin rats; the pre-existent mildly elevated blood pressure of arteriosclerotic breeder rats decreased. Glucosuria was effectively reduced in animals accorded good control; blood glucose was not effectively controlled. Circulating nonesterified fatty acids and triglycerides were more effectively normalised by insulin therapy. The diabetes was accompanied by adrenal hypertrophy, thymus gland involution, and increased circulating corticosterone. Virgin rats (68%) developed arterial disease when made alloxan-diabetic; treatment with insulin completely prevented arterial disease. Breeder rats with pre-existent arteriosclerosis showing worsening of their cardiovascular disease; when made severely diabetic those provided with good control of their diabetes were protected against exacerbation of their vascular disease.
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PMID:Good versus moderate regulation of alloxan-induced diabetes in arteriosclerotic and nonarteriosclerotic rats. 699 26

Throughout our professional lifetimes, we are conditioned by the need to choose; among careers, among treatments for our patients, among health habits and lifestyles. After detailing the extent to which a choice-making orientation has dominated our lives, our society, our health system, our science, this paper describes areas in which it is crucial that choices not be made. These include the choice between basic and applied research, between targeted and investigator-initiated research, between prevention and treatment of cardiovascular disease, and between the need to know (research on mechanisms of disease) and the need to take action (intervention in the individual and the community to control disease). In each of these areas, a decision to emphasize either alternative at the expense of the other is undesirable and defeats the basic goals of understanding and controlling heart and vascular disease. In discussing these sets of alternatives, the three major cardiovascular risk factors are discussed: cigarette smoking, high blood pressure and diet. Examples are chosen from research investigations on risk, intervention, treatment, prevention and community control.
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PMID:Lewis A. Conner Memorial Lecture. Choices that must not be made. 709 57

Nitric oxide (NO), derived from the vascular endothelium and other cells of the cardiovascular system, has important roles in physiological regulation of blood flow and may have pathophysiological functions in cardiovascular disease. The mechanisms involved in NO-induced vasodilatation and cytotoxicity are briefly reviewed in the context of inflammatory reactions and cardiovascular function. Although NO can hyperpolarize vascular smooth muscle, activation of the endothelium can induce hyperpolarization and vasodilatation by other means. Endogenous inhibitors of NO generated by leucocytes may compromise blood flow distribution after ischaemia and reperfusion injury. Chronic heart failure is associated simultaneously with impairment of endothelium-dependent vasodilatation and with excess production of NO via the inducible NO synthase (iNOS), although it is unclear whether the latter ameliorates or exacerbates ventricular dysfunction. Excess NO production is also one of the earliest signs of transplant rejection, and suppression of iNOS expression by immunosuppressant drugs such as cyclosporin A might be one means by which these drugs protect allografts. Disturbances in the activity of NOS isoforms in the artery wall also accompany the development of atherosclerosis, providing conditions propitious for vasospasm and thrombosis. Reversing the NO defects with therapeutic agents, including angiotensin converting enzyme (ACE) inhibitors, offers promise in protecting against some manifestations of vascular disease.
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PMID:Endogenous nitric oxide in cardiovascular disease and transplantation. 754 30

The eosinophil count and concentrations of eosinophil cationic protein (ECP) were measured in bronchoalveolar lavage fluid (BALF) from patients with idiopathic pulmonary fibrosis (IPF), pulmonary fibrosis associated with a collagen vascular disorder (PF-CVD), sarcoidosis, and healthy controls. The patients with IPF and PF-CVD showed significant increased eosinophil count and ECP levels in BALF compared with the controls. When the patients with IPF and PF-CVD were subclassified into chronic stable, progressive, and acute progressive subgroups in accordance with the observed progression of pulmonary dysfunction during the preceding 3- to 6-month period, those in the acute progressive subgroup showed significantly elevated recovered eosinophil count and ECP level, as well as recovered lymphocyte count and total protein, albumin, and type III procollagen aminoterminal peptide-related antigens (pIIIp) in BALF, compared with either of the other two subgroups. Multivariate stepwise logistic regression analysis revealed that, among these variables, only ECP and pIIIp significantly contributed to discrimination among the three subgroups differing in disease activity. These findings suggest that eosinophils are involved in the inflammatory process in pulmonary fibrosis and that the released ECP and other cytotoxic eosinophil products may contribute to the lung injury and development of fibrosis.
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PMID:Eosinophil activation in patients with pulmonary fibrosis. 760 90


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