Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-physical activity levels are associated with reduced risk of symptomatic coronary artery disease (CAD). However, there are a number of reports of exercise-related sudden death and myocardial infarction in aerobically trained athletes. This study compared the prevalence of exercise-induced silent myocardial ischemia on maximum graded exercise tests with tomographic thallium scintigraphy in 70 master male athletes (63 +/- 6 years, mean +/- SD) (maximum aerobic capacity, VO2max >40 ml/kg/min) and in 85 healthy untrained men (61 +/- 7 years) with no history of CAD. The prevalence of silent ischemia (exercise-induced ST-segment depression on electrocardiogram and perfusion abnormalities on thallium scintigraphy) was similar in athletes and untrained men; 16% of the athletes (11 of 70) had silent ischemia compared with 21% of the untrained men (chi-square = 0.81, p = 0.36). No athletes had hyperlipidemia, systemic hypertension, or diabetes mellitus. However, the apolipoprotein E4 allele was present in 9 of the 11 athletes with silent ischemia compared with 2 of 32 athletes with normal exercise tests (chi-square = 24, p = 0.0001). These results suggest that older male athletes with the apolipoprotein E4 allele are at increased risk for the development of exercise-induced silent ischemia.
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PMID:Exercise-induced silent myocardial ischemia in master athletes. 946 64

Sudden cardiac death is the leading cause of death in industrialized countries. It is most frequently due to ventricular tachyarrhythmias occurring in the presence of coronary heart disease, but mechanisms linking sudden death to coronary atherosclerosis are still unclear. In autopsy studies of sudden death patients, the incidence of acute thrombotic coronary occlusions has varied between 4 and 74%. In over 600 consecutive patients with implantable cardioverter-defibrillators, we observed that appropriate shocks for electrogram-verified ventricular tachyarrhythmias was only very rarely followed by signs of acute myocardial infarction (< 3% of cases), not supporting the coronary occlusion theory of fatal arrhythmias. Cellular hypertrophy compensating for cell loss due to ischemia, intraventricular hypertension, cardiomyopathy, and myocarditis might play a role in arrhythmogenesis as evidenced by the fact that experimental induction and regression of hypertrophy are paralleled by changes in the inducibility of ventricular tachyarrhythmias. Atherogenic hyperlipidemias are associated with a systemic inflammatory response manifested by leukocytosis (lymphocytosis) and complex upregulations of proinflammatory-prothrombotic mediators, such as platelet-activating factor, cytokines, and hemostasis factors. The diurnal regulation of these mediators parallels circadian rhythms of coronary morbidity and mortality. Some upregulated mediators have been shown to exert direct arrhythmogenic effects. The potential contribution of hyperlipidemia-associated inflammatory factors to arrhythmogenesis is important, because it opens new molecular targets for antiarrhythmic drug design.
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PMID:Sudden cardiac death: still more questions than answers. 947 68

The role of hemostatic variables (which promote hemostatic plugs and thrombi) and rheological variables (which affect blood flow) in the pathogenesis of vascular diseases (ischemic heart disease, stroke, and peripheral arterial disease) is reviewed, with emphasis on epidemiological studies. Rheological variables are consistently associated with both prevalent and incident cardiovascular disease. These associations are only partly explained by conventional risk factors. The predictive value of plasma viscosity for cardiovascular events is partly explained by fibrinogen, and partly by lipoproteins. The associations of whole blood viscosity with cardiovascular disease are partly explained by plasma viscosity and partly by hematocrit. White cell count, but not platelet count, predicts ischemic heart disease events. Cigarette smokers have higher levels of rheological variables than non-smokers, these increases are partly or wholly reversible in ex-smokers. Lipoprotein reduction by pravastatin lowers plasma and whole-blood viscosity, which may be one mechanism through which lipid lowering produces an early reduction in cardiovascular events. Data from the Edinburgh Artery Study suggest that viscosity is related both to the extent of atherosclerosis, and to ischemia in the presence of a given degree of atherosclerotic stenoses. Among hemostatic variables, fibrinogen, factor VIII: vWF complex, tpA antigen, and fibrin D-dimer are associated with both prevalent and incident cardiovascular disease. Again, these associations are only partly explained by conventional risk factors They suggest that endothelial disturbance and increased fibrin turnover may play roles in cardiovascular disease. Hemostatic and rheological variables are therefore associated with both prevalent and incident cardiovascular disease, and may be mechanisms through which risk factors such as smoking, hyperlipidemia and infections (including oral infections) promote vascular events.
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PMID:Etiopathogenesis of cardiovascular disease: hemostasis, thrombosis, and vascular medicine. 972 96

Oligo-elements such as zinc (Zn), selenium (Se) and copper (Cu) have a significant influence on the function of the immune system. Various immunological and inflammatory changes are known to occur in patients undergoing cardiopulmonary bypass. The aim of this study was to evaluate changes in serum oligo-elements levels during and following cardiopulmonary bypass. The serum levels of Zn, Se and Cu were determined in 67 consecutive patients, with coronary artery disease admitted for coronary artery bypass grafting. Blood samples for oligo-elements, analysis were withdrawn into metal-free tubes just prior to the start of cardiopulmonary bypass; at 30, 60 and 90 min into cardiopulmonary bypass; following weaning from cardiopulmonary bypass; 30 min after termination of cardiopulmonary bypass; at 24 h; and on the 5th postoperative day. Trace elements analyses were performed using atomic absorption spectrophotometry. Interleukin 6 and 8, as well as serum albumin, creatine phosphokinase, lactate dehydrogenase and creatine phosphokinase-MB fractions were also analyzed. The mean age was 63 +/- 9 years and 91% (61) were men. The mean preoperative left ventricular function was 52 +/- 12%, Canadian Cardiovascular Society (CCS) angina class was 3.7 +/- 0.5 and 30% (20) of the operations were re-do's. All patients had normothermic cardiopulmonary bypass. Mean cardiopulmonary bypass-time was 85 +/- 31 min. One patient was lost for the recovery sampling (hospital mortality, 1.5%). Nine patients had a postoperative cardiac index < 2.0 liter/min per m2, which required pharmacological support and additional intra-aortic balloon pump in two of them. Other postoperative complications were few. There was a rapid depletion of S-selenium and S-Zn levels, which were halved at 30 min after cardiopulmonary bypass and remained low throughout the study period. The Cu/Zn ratio increased significantly at the start of cardiopulmonary bypass, which indicated an inflammatory reaction and was not normalized until the 5th postoperative day. Length of ischemia time, presence of diabetes. hypertension and hyperlipidemia did not influence the results, while a prolonged cardiopulmonary bypass-time > 120 min resulted in a higher Cu/Zn ratio than observed for shorter cardiopulmonary bypass-times. This indicates a more profound inflammatory response. Inflammatory parameters responded in the same manner as described earlier by others. These data indicate that severe loss of various oligo elements occur in patients undergoing coronary artery bypass grafting and suggests that a supplementary administration of zinc and perhaps also selenium could be appropriate during cardiopulmonary bypass.
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PMID:Inflammatory response and oligo-element alterations following cardiopulmonary bypass in patients undergoing coronary artery bypass grafting. 972 21

The phospholipid class of plasmalogens is ubiquitously found in considerable amounts as a constituent of mammalian cell membranes and of plasma lipoproteins. Plasmalogens are more susceptible to oxidative reactions compared to their fatty acid ester analogues, due to the reactivity of their enolether function. Studies on plasmalogen-deficient cell lines lead to the proposal that these ether lipids serve as endogenous antioxidants. No clear conclusions regarding the antioxidative effects of plasmalogens could be drawn from studies in patients of different ages with peroxisomal deficiency disorders. A defective peroxisomal plasmalogen synthesis is not necessarily associated with other defects in the metabolism of peroxisomes, as has been established in a cell line recently. In different mammalian tissues a decrease of plasmalogens with age was described. Moreover, an accumulation of plasmalogen oxidation products was measured in brain of old cattle compared to young ones. In pathologic conditions associated with oxidative stress like in spinal cord ischemia and reperfusion, plasmalogen levels varied inversely according to the oxidative burden. Oxidation products of plasmalogens increased with time of ischemia in infarcted porcine heart tissue. Enrichment of lipoproteins with plasmalogens increased their oxidative resistance, which was diminished in the case of LDL particles in patients with coronary arteriosclerosis. In red cell membranes plasmalogens were reduced with donor age and in hyperlipidemia. Under lipid lowering therapy with lovastatin an increase was observed, indicating a possible antioxidative impact of this treatment. Taken together, there is good evidence that plasmalogens are effective as endogenous antioxidants. However, more experimental approaches not confounded by other lipolytic processes are needed to establish this role of plasmalogens.
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PMID:The biological significance of plasmalogens in defense against oxidative damage. 976 17

INSUFFICIENT PROGRESS: The treatment of hyperlipidemia leads to a reduced risk of coronary disease. This has been displayed notably since clinical trials have used statins. However, despite these treatments, a risk of coronary ischemia remains, which is not insignificant. There are several causes of this persistent risk which need to be analyzed. THE QUALITATIVE ASPECT OF LOW DENSITY LIPOPROTEINS: LDL are heterogeneous. This is displayed by a distribution of sizes varying from one subject to another. The predominance of small LDL is frequently found in coronary subjects detected during prospective or retrospective studies. The atherogenicity of small LDL can be explained by their physico-chemical characteristics. A remarkable fact is the predominance of small LDL in subjects with a mixed hyperlipidemia presenting a high risk of atherosclerosis. THE EFFECTS OF HYPOLIPIDEMIANTS: Statins greatly decrease LDL-cholesterol without changing LDL distribution according to size. Conversely, fibrates noticeably modify LDL distribution, reducing the percentage of small LDL. A PROPOSAL FOR THE TREATMENT OF SUBJECTS SUFFERING FROM MIXED HYPERLIPIDEMIA: If the concentration of LDL (reflected by LDL-cholesterol) and LDL distribution are two risk factors of atherosclerosis, hypolipidemic treatment should aim to act upon these two parameters, but no commercialized hypolipidemiant is effective enough as fas as they are both concerned. Therefore the combination of two hypolipidemiants, a statin and a fibrate, each having a predominant effect on one of the two factors, could be particularly effective in reducing coronary risk. This therapeutic association is effective on classic lipid parameters, does not entail more side effects than a monotherapy, and is not precluded by the RMO when there is a high vascular risk, which is often the case in mixed hyperlipidemia.
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PMID:[Is combined statin and fibrate therapy indicated in the management of mixed hyperlipidemia?]. 976 13

The incidence of atherosclerosis of the heart transplant in long term survivors is 38% at 5 years. In the present work, myocardial perfusion 201Tl-SPET was assessed as a non-invasive diagnostic method for the detection of postransplant coronary artery disease, as well as its efficiency with regard to other techniques. Twenty patients, aged (47 +/- 9) years old, who underwent heart transplantation at least 3 years earlier, were studied by 201Tl-SPET. Qualitative and quantitative analysis of the images were performed. It was found ischemia in 6 patients, 4 of them asymptomatics. In 5 of the 6 positive cases by SPET coronary stenosis was found by angiography. Kappa coefficient and percent of agreement were k = 0. 76 and Pe = 90%, respectively. There were no relationships among rejection crisis, sepsis by cytomegalovirus and coronary artery disease detected by using 201Tl-SPET (p > 0.05). The most relevant risk factors in the sample were hypertension and hyperlipidemia. Two patients died because of coronary artery disease. It was confirmed by necropsy findings. These results suggest that thallium-201 myocardial perfusion tomography could be useful to detect coronary artery disease in the transplanted heart.
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PMID:[Myocardial perfusion SPET in the detection of coronary artery disease in orthotopic heart transplantation]. 987 29

Seventy-four patients with diabetes were taken on both stress and rest 99m-Tc-MIBI SPECT imaging: 44 patients (59.5%) were found having myocardial ischemic disorders, including 28 cases of myocardial ischemia, 7 cases of myocardial infarction and 9 cases of both conditions. 113 segments were involved and 46% were located in the posterior and inferior walls, indicating that the right coronary artery is most susceptive to ischemia. Diabetic patients complicated hypertension and/or hyperlipidemia were at higher risk of either early occurrence of coronary disease. 99mTc-MIBI SPECT imaging is helpful in early diagnosis and therefore is significant in directing.
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PMID:[99mTc-MIBI myocardial perfusion imaging in patients with diabetes]. 1007 95

This study was designed to establish a hyperlipidemic diet (significant increase in the cholesterol and triglycerides blood levels, but without atherogenic changes in heart muscle and coronary vessels) and to investigate the influence of experimental hyperlipidemia on the effects of ischemic preconditioning (PC) of rat-isolated papillary muscle on the time course of contractility during simulated ischemia and reperfusion and responsiveness to phenylephrine under such a condition. The animals were divided in four experimental groups: standard diet-fed control group (SD), SD underwent ischemic preconditioning (SD-PC), hyperlipidemic diet-fed group (HLD) and HLD underOFFt PC (HLD-PC). Force of contraction (Fc), velocity of contraction (+dF/dt), and velocity of relaxation (-dF/dt) were measured. HLD preparations were more sensitive to ischemia then SD ones. PC, performed by 5-min perfusion with no-substrate solution gassing with 95% N2/5% CO2 in the presence of fast electrical stimulation, and 10 min of reperfusion with normal solution and rate of stimulation, significantly increased the resistance of isolated cardiac tissues to simulated ischemia in SD-PC group, but not in HLD-PC group. Negative inotropic action of phenylephrine occured in SD group of preparations after simulated-ischemia/reperfusion period was also prevented by PC. Therefore, we conclude that experimental hyperlipidemia significantly influenced the function of rat heart muscle including the higher sensitivity to ischemia and different reaction to the same PC procedure.
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PMID:Experimental hyperlipidemia prevents the protective effect of ischemic preconditioning on the contractility and responsiveness to phenylephrine of rat-isolated stunned papillary muscle. 1048 Jun 53

Long-term prognosis in kidney transplant recipients depends on multiple factors. The purpose of this study was to quantify the influence of hyperuricemia and hyperglycemia (elements of the so-called 'syndrome X', i.e., a combination of metabolic disorders like hyperuricemia, diabetes mellitus, hyperlipidemia, and hypertension) on organ function in 350 kidney transplant recipients who had received 375 kidney transplants up to 1990 and in whom sex, age of recipient and donor, nephrologic disease, duration of dialysis, human leukocyte antigen (HLA) classification, and duration of transplant ischemia had been well matched. We found the influence of hyperuricemia on graft survival to be statistically significant (p < or = 0.05), while a statistically significant correlation between hyperglycemia and graft survival could not be detected in the present study. The transplant survival rates 2, 4, and 5 yr post-kidney-transplantation were 96.7, 80.7, and 78.7 in normogylcemic patients vs. 96.9, 85, and 82.7% in hyperglycemic ( > 100 mg,dL) kidney transplant recipients (p > 0.05). Transplant survival in hyperuricemic patients (male, > 8 mg dL; female, > 6.2 mg/dL) 2, 4, and 5 yr post-transplantation was significantly reduced (92.2, 70.6, and 68.8% vs. 98.1, 85.6, and 83.3%), as compared to normouricemic recipients. A combined presence of both hyperuricemia and hyperglycemia probably influencing the prognosis post-kidney-transplantation failed to reach the level of statistical significance. We found a significant correlation between age of recipients and plasma glucose (p < or = 0.01) and between serum uric acid concentrations and diuretic therapy (p < or = 0.05) and gender (p < or = 0.(5). In conclusion, hyperuricemia after kidney transplantation seems to reduce graft survival, whereas an influence of the carbohydrate metabolism has to be denied.
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PMID:Influence of hyperglycemia and hyperuricemia on long-term transplant survival in kidney transplant recipients. 1051 17


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