ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Atherosclerotic macrovascular disease is the leading cause of both morbidity and mortality in non-insulin dependent diabetes mellitus. Endothelial dysfunction is a key, early and potentially reversible event in pathogenesis of atherosclerosis. Its occurrence in non-insulin dependent diabetes mellitus is well supported by both in-vitro and in-vivo studies. Non-insulin dependent diabetes mellitus results in diverse abnormalities of lipid and lipoprotein metabolism, in particular hypertriglyceridaemia, low levels of high density lipoprotein and abnormalities of post-prandial lipaemia. A variety of studies demonstrate the presence of enhanced oxidative stress in noninsulin dependent diabetes mellitus, with recent data implying an association between oxidative stress, post-prandial lipaemia and endothelial dysfunction in non-diabetic subjects. In this article based on in-vitro and human studies, we develop the hypothesis that endothelial dysfunction in non-insulin dependent diabetes mellitus is the consequence of the diabetic dyslipidaemia, in particular post-prandial lipaemia, and of oxidative stress on the action of nitric oxide. The practical applications of this theory provide potential therapeutic options which may reduce the risk of vascular disease in noninsulin dependent diabetes mellitus.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The current report is a quantitative review of the relationship between lipoprotein lipase gene variants and cardiovascular disease based on published population-based studies. Sixteen studies, representing 17 630 individuals, report allelic distribution for lipoprotein lipase gene variants among patients and control individuals. Patient outcomes included clinical cardiovascular disease events, documented coronary disease based on angiography, or intimal media thickening by B-mode ultrasonography. Mantel-Haenszel stratified analysis was used to compute a summary odds ratio and 95% confidence intervals for the association between rare allele in the lipoprotein lipase gene and disease status. Because of potential differing effects associated with different lipoprotein lipase variants, each lipoprotein lipase mutant allele was considered separately. The lipoprotein lipase D9N/—93G to T allele has a summary odds ratio of 2.03 (95% confidence interval 1.30–3.18), indicating a twofold increase in risk of coronary disease for carriers with this allelic variant. The summary odds ratio for the relationship of the rare lipoprotein lipase G188E variant with cardiovascular disease is 5.25 (95% confidence interval 1.54–24.29). The lipoprotein lipase N291S allele is associated with a marginal increase in cardiovascular disease (summary odds ratio 1.25, 95% confidence interval 0.99–1.60,P=0.07). However, there is stronger evidence for a positive association in certain populations. The summary odds ratio for lipoprotein lipase S447X allele is 0.81 (95% confidence interval 0.65–1.0), which indicates a cardioprotective effect of this lipoprotein lipase gene variant. Thus, lipoprotein lipase gene variants are associated with differential susceptibility to cardiovascular disease.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The efficacy and safety of the therapeutic tool which directly removes LDL particles from circulation (LDL apheresis) has already been established for cholesterol-lowering in patients with refractory hypercholesterolemia, such as homozygous familial hypercholesterolemia. Several angiographic studies have demonstrated that regular LDL apheresis therapy had favorable effects on the progression of coronary atherosclerosis. Recently, two clinical reports described excellent long-term follow-up results for patients with coronary artery disease who had been treated with LDL apheresis using dextran sulfate cellulose columns plus adjunctive cholesterollowering drug therapy. In addition, there is increasing evidence that LDL apheresis is effective for the prevention of extracoronary atherosclerotic disease, and it is also reported to have the potential to improve microvascular disorders. Since the mechanisms of clinical improvement caused by LDL apheresis extend beyond simple and drastic reduction of LDL cholesterol, further investigation based on recent vascular biological evidence is needed.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The published studies of the association of the angiotensinconverting enzyme (ACE) genotype with cardiovascular disease have used many different diagnostic criteria for cardiovascular disease and have drawn their samples from different patient groups and different populations. This review examines the association of the ACE DD genotype with cardiovascular disease risk in studies grouped by their case criterion, the geographical region of the population samples, and by the cardiovascular risk level of the patient sample. In studies where the underlying odds ratios are determined to be homogeneous, the overall odds ratios for myocardial infarction and coronary artery disease with regard to the ACE DD genotype are estimated using the Mantel-Haenszel method.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Elevated plasma total homocysteine is an independent risk factor for atherosclerotic vascular disease. Risk rises continuously across the spectrum of homocysteine concentrations and may become appreciable at levels greater than 10 μmol/1. A compelling case can be made for screening all individuals with atherosclerotic disease or at high risk. A reasonable, but unproven, goal for treatment is a plasma total homocysteine concentration less than 10 μmol/1. Folic acid is the mainstay of treatment, but vitamins B12and B6may have added benefit in selected patients. The results of ongoing randomized placebo-controlled trials will not be available for several years, but will help determine whether homocysteine lowering reduces the risk of cardiovascular disease.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

A large amount of research continues to be conducted on the mechanisms of hormone replacement therapy (HRT) effects, and the first of the large clinical trials published its results during the past year. In addition to the well known effects on LDL-cholesterol, HDL-cholesterol, and triglycerides, recent studies confirmed that estrogen with or without a progestin lowers lipoprotein (a) concentrations in women (but not in men). In men, estrogen appears to have a similar effect on other lipids and lipoproteins and on plasminogen activator inhibitor-1 as in women. A comparison of estrogen with simvastatin indicated that simvastatin is better at lowering LDL-cholesterol while estrogen is better at raising HDL-cholesterol; when given in combination the additional effects were modest. Estrogen and simvastatin had similar beneficial effects on endothelial function. The estrogen effect on endothelial function may be blocked by medroxyprogesterone, but the data are inconsistent. These studies of intermediate outcomes were put in perspective by the results of a landmark secondary prevention trial of coronary heart disease (CHD). This randomized placebo-controlled trial (Heart and Estrogen/Progestin Replacement Study) of conjugated equine estrogens plus medroxyprogesterone failed to show the anticipated reduction in CHD, and at the same time the threefold increase in venous thromboembolism confirmed that HRT is procoagulant. Therefore, it is still not known whether HRT is a viable option for the prevention of CHD. The preliminary data on selective estrogen receptor modulators are not overly promising, but a definitive trial to test whether raloxrifene will reduce CHD is ongoing.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Evidence supports the position that the chronic atherothrombotic process is intimately associated with what has classically been called ‘inflammation'. Proteins that are part of the acute phase response (e.g. fibrinogen, C-reactive protein) are sensitive markers of low-level inflammation, and in population studies, inflammation marker levels at the upper end of the healthy reference range are associated with the presence of subclinical atherothrombotic disease (e.g. carotid wall thickness) and, prospectively, with future cardiovascular disease events. While there are plausible mechanisms for most of these markers, it remains to be demonstrated whether the markers actually participate in cardiovascular disease, or simply reflect the underlying disease process. This point is important, since marker-specific interventions might be useful if the former position is correct. Recent work suggests that inflammation markers may represent different aspects of the atherothrombotic process at different points in the natural history of the disease. This has implications for the interpretation of marker levels and the timing of the future events that they predict.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

In patients with excessive venous thrombosis, genetic defects predisposing to thrombosis can be found in 60–80%. Increased plasma levels of coagulation proteins such as fibrinogen and plasminogen activator inhibitor-1 (PAI-1) are associated with an increased risk of myocardial infarction. However, despite the presence of polymorphisms that regulate plasma levels of factor VIII, PAI-1, and fibrinogen the association between common polymorphisms of these coagulation protein and ischemic cardiac disease remains ambiguous. Up to 10% of the population have defects that predispose them to excessive venous thrombosis. In spite of the essential role of thrombosis in coronary ischemic syndrome, no convincing evidence has implicated the two most common venous hypercoagulable states in ischemic heart disease. Pathogenic polymorphisms in the platelet fibrinogen and collagen receptors remain an area of intense research interest. Finally, it has been shown that lipoproteins can act as mediators of coagulation processes.

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0957-9672    

出版商:OVID    

年代:1999

数据来源: OVID