Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although first suggested at the turn of the 20th century, there is a renewed interest in the infectious theory of atherosclerosis. Studies done in many laboratories around the world over the past several years have shown an association between markers of inflammation and coronary atherosclerosis with an exacerbation of the inflammatory process during acute myocardial ischemia, particularly in the early stages of reperfusion. It is also being recognized that the traditional risk factors, such as smoking, dyslipidemia, hypertension and diabetes mellitus, do not explain the presence of coronary atherosclerosis in a large proportion of patients. We believe that in certain genetically susceptible people, infection with very common organisms, such as Chlamydia pneumoniae or cytomegalovirus, may lead to a localized infection and a chronic inflammatory reaction. Persistence of infection may relate to the degree of inflammation and severity of atherosclerosis. Early trials with appropriate antibiotic agents in some patients with a recent history of acute myocardial infarction have led to very salutary results. If patients with an infectious basis of atherosclerosis can be identified, a therapy directed at eradication of the offending organism may be appropriate.
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PMID:Interactive role of infection, inflammation and traditional risk factors in atherosclerosis and coronary artery disease. 980 69

Platelet activation, impairment of fibrinolysis and dyslipidemia are important factors in the pathogenesis and progression of ischemic heart disease. Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1). The present study was performed in 57 patients with ischemic heart disease (IHD), divided into groups depending on coexistent hyperlipoproteinemia (HLP) and aspirin treatment. The control group included 21 healthy individuals, matched for age and sex. Parameters of hemostasis (SPA, PF4, PAI-1) and concentration of lipid fractions (TC, TG, LDL, HDL) were measured in plasma. Increased PF4 levels were found in all groups with IHD, irrespective of hyperlipoproteinemia or aspirin treatment. Enhanced SPA and higher PAI-1 were limited to group IHD-HLP without aspirin. Highest PAI-1 activities were observed after stimulation of platelets in vitro. In conclusion, patients with IHD and hyperlipoproteinemia presented most pronounced platelet activation and impairment of fibrinolysis. Aspirin had a beneficial effect on these changes. Lower activities of PAI-1, in patients treated with aspirin, can be ascribed to its reduced release from platelets. Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.
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PMID:[Evaluation of platelet function and tissue plasminogen activator activity in ischemic heart disease depending on concurrence with hyperlipoproteinemia and aspirin therapy]. 964 79

Most probably the decennia of the 1990s will be called the 'statin decennia' in the history of coronary heart disease prevention. Statins are effective, both in primary and secondary prevention of coronary heart disease, in middle-aged and older (< 76 years) men and women, in both diabetics and non-diabetics with coronary heart disease. Statins used in secondary prevention of coronary heart disease significantly reduce the risk of stroke. They also reduce daily attacks of myocardial ischemia. Pathogenetic pathways leading to 'biological plausibilities' of the statins favourable effects are multiple, which explains their rapid (less than 1 year) influence on coronary events. Until the results from new event trials become available, fibrates have very few indications as first line drug therapy in dyslipidemia. They should be considered in combined therapy with statins. The scientific evidence with statins is overwhelming and the question is no longer 'who should we treat?' but 'who can society afford to treat?'. Health economics are indeed pivotal in the use of statins and public health authorities have to find answers according to their resources or innovative strategies, including new aspects in dietary advice (the 'Mediterranean diet'?).
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PMID:Primary and secondary prevention of coronary artery disease: a follow-up on clinical controlled trials. 986 91

Cross-sectional studies suggest that an increased urinary albumin excretion rate is associated with cardiovascular disease, dyslipidemia, and hypertension. The purpose of this study was to analyze prospectively whether the urinary albumin-to -creatinine (A/C) ratio can independently predict ischemic heart disease (IHD) in a population-based cohort. In 1983, urinary albumin and creatinine levels were measured, along with the conventional atherosclerotic risk factors, in 2085 consecutive participants without IHD, renal disease, urinary tract infection, or diabetes mellitus. The participants were followed up until death, emigration, or December 31, 1993. IHD was defined as a hospital discharge diagnosis or cause of death including the diagnoses ICD-8 and 410 to 414. Seventy-nine individuals developed IHD during the 21 130 person-years of follow-up. They were characterized by a preponderance of males and higher age, body mass index, blood pressure, lipoproteins, and proportion of current smokers. Microalbuminuria was defined as an A/C ratio) >90 percentile (>0.65 mg/mmol). When adjusted for other risk factors, the relative risk of IHD associated with microalbuminuria was 2.3 (95% CI, 1.3 to 3.9, P=0.002), and the 10-year disease-free survival decreased from 97% to 91% (P<0.0001) when microalbuminuria was present. An interaction between microalbuminuria and smoking was observed, and the presence of microalbuminuria more than doubled the predictive effect of the conventional atherosclerotic risk factors for development of IHD. It is concluded that microalbuminuria is not only an independent predictor of IHD but also substantially increases the risk associated with other established risk factors.
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PMID:Urinary albumin excretion. An independent predictor of ischemic heart disease. 1044 83

The recent decrease of cardiovascular mortality in the USA is less pronounced than it has been in the preceding three decades. Elsewhere, cardiovascular mortality decreased and in some countries it increased. Cerebrovascular disease and ischemic heart disease were responsible for 21% of deaths recorded by the World Health Organization in 1990 and 1997, of which hypertension was estimated to be directly responsible for half of these deaths. Apart from blood pressure (BP) elevation, essential hypertension is frequently associated with factors that increase the risk of poor cardiovascular outcomes: insulin resistance/dyslipidemia, elevated angiotensin and norepinephrine, a tendency for hypercoagulability, platelet overactivity, tachycardia, vulnerability to arrhythmias, vascular hypertrophy, endothelial dysfunction, and left ventricular hypertrophy. Excess activation of the renin-angiotensin system, independent of BP elevation, contributes to these abnormalities. To achieve better results in the future, focus must be shifted from BP lowering to recognition of specific effects of drugs on these diverse pathophysiologic aspects of hypertension. The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial, which is evaluating the effect of valsartan (Diovan((R))) vs. amlodipine, is a milestone in the effort to test whether newer compounds offer a better reduction of the cardiovascular consequences of hypertension, as well as good BP control. The hypothesis is that valsartan by antagonizing the negative effects of angiotensin on smooth muscle cell growth, endothelial function, sympathetic overactivity, and coagulation, may have for the same degree of BP lowering, better protective effects than the leading calcium antagonist amlodipine.
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PMID:Long-term potential of angiotensin receptor blockade for cardiovascular protection in hypertension: the VALUE trial. Valsartan Antihypertensive Long-term Use Evaluation. 1044 89

Obesity results from excessive accumulation of fats in adipose tissue and constitutes one of the essential sources of increased incidence of some diseases harassing the highly industrialized and urbanized societies. Obesity-related metabolic disorders may be associated with the risk of circulatory diseases. The mechanism causing that obesity enhances the incidence of the metabolic disorders have not been explained to the full extent. Hyperinsulinaemia is one of effects of obesity and of the associated presence of excessive blood fatty acid levels. Overloading of the organism with fatty acids changes the function pancreatic beta cells. Insulin resistance and hyperglycaemia caused by high peripheral fatty acid levels trigger increased insulin secretion. Hyperinsulinaemia affects hepatic metabolism so as to make it hyperanabolic. Liver increases triacylglycerol and cholesterol synthesis and raises the rate of very low density lipoproteins (VLDL) secretion to the blood. Increased VLDL concentration contributes to increased LDL and is associated with reduced HDL cholesterol concentrations. Atherogenic dyslipidemia in obese people results, to a large extent, from increased VLDL secretion. Data collected heretofore point to an undoubtedly essential role of the adipose tissue in the pathogenesis of metabolic disorders in obese people. There are many causes of disturbed adipose tissue function which result in high blood fatty acid levels, excessive fat accumulation in other tissues and organs, or both. Another factor which may aggravate the metabolic disorders is the diet. It is worth noting that genetic determinants may cause that some individuals reveal a specified set of factors increasing the risk of ischaemic heart disease.
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PMID:Ischaemic heart disease as an effect of obesity-related metabolic disturbances. 1049 42

There has been considerable interest in the possibility that prenatal events could influence the adult life. Adults who were small at birth have been reported to have higher blood pressure and increased risk of death from ischaemic heart disease, although there are some contradictory results. The aim of the present study was to determine the association between size at birth and later risk factors (hypertension, hyperinsulinism, hyperglycaemia and dyslipidaemia) in prepubertal children. The authors examined 205 children (121 boys, 84 girls) at the age of 6-10. They compared children born full term with normal weight, height and head circumference (1st group), the children born full term with birthweight, height and head circumference less than 10th centile (2nd group), children born full term with birthweight less than 10th centile and with normal length and head circumference (3rd group) and children who were preterm at birth (4th group). The age of children at the time of investigation was comparable in the four groups. Weight and height of the children in the 2nd group were significantly lower than in the 1st and 4th groups (2nd group vs 4th group: p < 0.01; 2nd group vs 1st group: p < 0.001). Dyslipidaemia was found 21% in the 1st group, 17% in the 2nd group, 16% in the 3rd group and 28% in prematures. The mean of the systolic and diastolic blood pressures were similar in the four groups. Hypertension was 12.5% in the 1st and 3rd groups, 5.6% in the 2nd group and 8.9% among prematures. According to the results cardiovascular risk factors can not be proved among children at the age of 6-10 who were born with low birthweight. Further studies are required to determine whether which stage of pregnancy might influence birthweight and later risk factors.
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PMID:[Role of intrauterine growth in later cardiovascular risk factors in children 6-10 years of age]. 1062 97

Elderly diabetic patients were followed up prospectively for 4 years to see the effects of blood pressure and dyslipidemia on the development of diabetic micro- and macroangiopathies. We studied 84 elderly diabetic patients whom we divided into four groups according to the association of above complications: (1) diabetes alone group (DM), (2) hypertensive diabetic group (DM + HT), (3) hyperlipidemic diabetic group (DM + HL), and (4) hypertensive and hyperlipidemic diabetic group (DM + HTL). The treatment of diabetes was different among the groups. Glycemic control such as fasting blood glucose and HbA1c did not change between groups or through the follow-up years. As a matter of course, blood pressure of DM was lower and triglyceride of HTL was higher than in other groups. Microangiopathies such as retinopathy, nephropathy, and neuropathy and macroangiopathies such as ischemic heart disease (IHD), cerebral vascular disease (CVD), and arteriosclerosis obliterans were evaluated by using a grading scale according to the severity. The grade of microangiopathies in DM + HT increased gradually during the follow-up years and the grade of IHD and CVD in DM + HTL was relatively higher than in the other groups. Our findings support the general principle of control of hypertension and hyperlipidemia for the prevention of diabetic microangiopathy and macroangiopathy in the elderly diabetic patients.
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PMID:Follow-up of elderly diabetics with or without hypertension and hyperlipidemia. 1090 22

Treatment of high blood pressure (BP) has not produced the expected reduction in risk of ischemic heart disease (IHD). Subjects with high BP often have the metabolic syndrome X, an aggregation of abnormalities in glucose and lipid metabolism. We tested the hypothesis that the BP level would be less predictive of risk of IHD in those with high triglycerides (TG) and low HDL cholesterol (HDL-C), the characteristic dyslipidemia in the metabolic syndrome than in those without. Baseline measurements of fasting lipids, systolic BP (SBP), diastolic BP (DBP), and other risk factors were obtained in 2906 men, age 53 to 74 years, free of overt cardiovascular disease. High TG/low HDL-C was defined as TG >1.59 mmol/L and HDL-C <1.18 mmol/L. Within an 8-year period, 229 men developed IHD. In men with high TG/low HDL-C, the incidence of IHD according to SBP (<120, 120 to 140, >140 mm Hg) was 12.5%, 12.9%, and 10.0% (P=NS), respectively, and according to DBP, the incidence of IHD was (<75, 75 to 90, >90 mm Hg) 13.7%, 10.6%, and 13.7% (P=NS), respectively. The corresponding figures for other men were 5.2%, 8. 0%, and 9.7% for SBP (P<0.001), and 6.1%, 7.5%, and 9.9% for DBP (P<0.03). In conclusion, the BP level did not predict the risk of IHD in those with high TG/low HDL-C. This finding may explain the reason lowering BP has not produced the expected reduction in IHD.
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PMID:High triglycerides and low HDL cholesterol and blood pressure and risk of ischemic heart disease. 1094 82

Thyroid hormones influence all major metabolic pathways. Their most obvious and well-known action is an increase in basal energy expenditure obtained acting on protein, carbohydrate and lipid metabolism. With specific regard to lipid metabolism, thyroid hormones affect synthesis, mobilization and degradation of lipids, although degradation is influenced more than synthesis. The main and best-known effects on lipid metabolism include: (a) enhanced utilization of lipid substrates; (b) increase in the synthesis and mobilization of triglycerides stored in adipose tissue; (c) increase in the concentration of non-esterified fatty acids (NEFA); and (d) increase of lipoprotein-lipase activity. While severe hypothyroidism is usually associated with an increased serum concentration of total cholesterol and atherogenic lipoproteins, the occurrence of acute myocardial infarction (AMI) in hypothyroid patients is not frequent. However, hypothyroid patients appear to have an increased incidence of residual myocardial ischemia following AMI. Even in subclinical hypothyroidism, which is characterized by raised serum TSH levels with normal serum thyroid hormone concentrations, mild hyperlipidemia is present and may contribute to an increased risk of atherogenesis. Prudent substitution therapy with L-thyroxine is indicated in patients with both overt and subclinical hypothyroidism, with or without angina, to counteract the cardiovascular risk resulting from hyper-dyslipidemia.
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PMID:Thyroid and lipid metabolism. 1099 23


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