Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine whether impaired glucose regulation, defined according to the new American Diabetes Association (ADA) criteria, is associated with early signs of carotid atherosclerosis. We examined 310 clinically healthy women from southern Italy, aged 30 to 69 years, recruited for a prospective study, currently ongoing, on the etiology of cardiovascular disease and cancer in the female population (Progetto Atena). All subjects underwent cardiovascular risk factor assessment and high resolution B-mode ultrasound to measure intima-media thickness (IMT) of common carotid arteries and carotid bifurcations. At the time of our survey, fasting glucose levels > or = 7.0 mmol/L had already been found in 7 women, 17 participants were diagnosed on that occasion as having new diabetes, 38 had impaired fasting glucose (IFG), and the remaining 248 presented normal fasting glucose values (NFG). Diabetic women showed a worse cardiovascular risk profile, with higher values of triglycerides, body mass index, and diastolic blood pressure than either normoglycemic or IFG subjects. The frequency of atherosclerotic plaques (IMT > 1.2 mm) increased as glucose homeostasis worsened. In multivariate logistic regression analyses, only diabetes mellitus was associated with a significantly increased risk of carotid atherosclerosis (odds ratio [OR], 11.5; 95% confidence interval [CI], 1.4 to 92.7). Our findings suggest a definite association between diabetes mellitus, as defined by the new ADA diagnostic criteria and early carotid structural changes. Furthermore, the condition of IFG does not seem to identify subjects at significantly increased atherosclerotic risk.
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PMID:Association of impaired glucose homeostasis with preclinical carotid atherosclerosis in women: Impact of the new American Diabetes Association criteria. 1178 72

The endothelium can greatly influence vascular tone and structure. The main endothelium-derived factor is nitric oxide (NO), which is not only a potent vasodilator but also inhibits platelet aggregation, smooth muscle cell proliferation, monocyte adhesion and adhesion molecule expression, thus protecting the vessel wall against the development of atherosclerosis and thrombosis. In human hypertension, endothelial dysfunction has been documented in peripheral and coronary macro- and microcirculation and in renal circulation. The mechanism responsible for endothelial alteration in essential hypertensive patients appears to be the activation of an alternative pathway involving cyclooxygenase, which reduces NO availability through production of oxidative stress. In the presence of impaired NO availability a hyperpolarizing factor seems to act as a compensatory pathway to sustain endothelium-dependent relaxation. This compensatory pathway can be further depressed by the simultaneous presence of essential hypertension and hyperhomocysteinaemia, another cardiovascular risk factor causing endothelial dysfunction. Finally, reduced NO availability can increase the biological activity of endothelin-1 because, while in healthy conditions the vasoconstrictor effect of endothelin-1 is partially blunted by endothelial ETB-receptor mediated NO production, in essential hypertensive patients this protective mechanism is lacking on account of impaired NO availability. This alteration in the NO pathway could be the main mechanism through which a dysfunctional endothelium could be a promoter of atherosclerosis and thrombosis and therefore lead to cardiovascular events in essential hypertensive patients.
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PMID:Endothelial dysfunction in hypertension. 1181 68

The relationship of two apolipoprotein (apo) E gene polymorphisms and coronary heart disease (CHD) was investigated in 118 Finnish families with premature CHD and in 110 healthy control subjects. Affected siblings and probands with premature CHD had higher frequencies of the T allele of the -219G/T promoter polymorphism and the epsilon 4 allele (genotypes epsilon 4/3 or epsilon 4/4) of the apo epsilon 2/epsilon 3/ epsilon 4 polymorphism than those of healthy control subjects. Additionally, when the two apo E gene polymorphisms were combined, affected siblings and probands had a higher frequency of the -219T allele and the epsilon 4 allele combinations than did healthy controls. The -219T and the epsilon 4 alleles both separately and together were associated with higher levels of 2-h glucose in an oral glucose tolerance test. These results indicate that the two polymorphisms of the apo E gene have similar effects on the risk of coronary atherosclerosis in families with premature CHD. This risk was not explained by the effect of apo E gene polymorphisms on cholesterol metabolism, but their effect on cardiovascular risk factor clustering with insulin resistance may be of importance. We conclude that in addition to the epsilon 4 allele, also the -219G/T promoter polymorphism of the apo E gene is associated with early onset CHD.
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PMID:Apolipoprotein E gene promoter (-219G/T) polymorphism is associated with premature coronary heart disease. 1186 16

The purpose of this study was to evaluate risk factors predicting restenosis and primary patency after percutaneous transluminal angioplasty. Follow-up data (including cardiovascular risk factor scores according to SCVIR criteria, preinterventional and postinterventional clinical data and patient history) of all patients who underwent successful percutaneous transluminal angioplasty for lower limb ischemia were analyzed retrospectively and patients, relatives, or referring physicians underwent a telephone interview. Patients with incomplete follow-up data were examined by means of a clinical examination, including Doppler measurements and treadmill test. Additionally all angiograms were evaluated to calculate lesion length, number of treated lesions, lesion type (SCVIR score), and runoff. The outcome was categorized into four groups: early recurrence (< 1 month, group I), mean recurrence (1-6 months, group II), late recurrence (>6 months, group III), and no recurrence (group IV). According to common concepts group I was defined as early (thrombotic) reocclusion, group II as clinically defined restenosis, and group III as progression of atherosclerosis. One hundred thirty-seven patients underwent percutaneous transluminal angioplasty of 148 extremities. The groups differ significantly only with respect to a higher diabetes score for group I in comparison to group IV (p=0.002, Kruskal-Wallis test), and a worse runoff of group I compared with group IV (p =0.008). There was a trend toward a higher diabetes score for group II in comparison to group IV (p = 0.014). There were no differences with regard to hyperlipemia, hypertension, and tobacco use between patient groups. Mean primary patency was 436 days. Predictors for lower patency rates were diabetes mellitus (p<0.001), runoff (p=0.005), and number of treated lesions (p=0.007) in a stepwise, multiple regression analysis. Patients with clinically defined restenosis showed no specific risk factor profile in this study. Predictors for lower primary patency were diabetes mellitus, number of treated lesions, and runoff.
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PMID:Cardiovascular risk factors do not predict clinically defined restenosis after percutaneous transluminal angioplasty for lower limb ischemia. 1186 5

A positive family history is a recognized cardiovascular risk factor, and genome-wide scans may reveal susceptibility loci for coronary artery disease. The acute coronary syndrome, consisting of myocardial infarction and unstable angina, is the most important manifestation of coronary disease and is characterized by atherosclerotic plaque disruption and coronary thrombosis. From approximately 6000 hospital admissions to cardiology units, we identified affected sibling pairs (n=61) who had documented acute coronary syndrome before the age of 70 years. A 10-cM resolution genetic map and MAPMAKER/SIBS were used for genome-wide linkage analysis. One locus on chromosome 2q36-q37.3 showed linkage with a lod score of 2.63 (P<0.0001). Separate multipoint fine-mapping of this locus with independent markers replicated the linkage results (lod 2.64). Two other regions on chromosomes 3q26-q27 and 20q11-q13 showed lod scores in excess of 1.5 (P<0.005). This genome scan in acute coronary syndrome suggests 1 locus that encompasses the gene encoding the insulin receptor substrate-1 gene. Two other potential loci were identified. These data imply that a limited number of potent susceptibility genes exist for the acute coronary syndrome. Such genes are likely to be relevant to the combined processes of atherosclerosis, plaque instability, and coronary thrombosis.
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PMID:Genome-wide linkage analysis of the acute coronary syndrome suggests a locus on chromosome 2. 1200 6

To be appropriately labelled as a 'risk factor' any putative risk factor should increase the prediction power of standard statistical models based on 'traditional' (Framingham) risk factors. In end-stage renal disease (ESRD), Framingham risk factors do not fully explain the cardiovascular burden of these patients. Inflammation, hyperhomocysteinemia and anemia contribute to the high cardiovascular risk of ESRD, but knowledge is still incomplete. We suspected that asymmetric dimethylarginine (ADMA) is an important cardiovascular risk factor in dialysis patients. This substance inhibits nitric oxide synthase thus triggering a series of pathophysiological events leading to atherosclerosis. To test this hypothesis, we studied the relationship between ADMA and intima media thickness (IMT) in the carotid artery. ADMA was found to be strongly and independently related to IMT. More importantly we found that patients with relatively higher plasma ADMA had shorter survival and a higher rate of incident cardiovascular complications in comparison to those with a relatively lower plasma concentration. These data represent a sound basis for intervention studies aimed at modifying the plasma ADMA concentration in ESRD patients.
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PMID:Endothelial damage, asymmetric dimethylarginine and cardiovascular risk in end-stage renal disease. 1220 95

Serum total sialic acid has recently been shown to be a cardiovascular risk factor. Increased levels of this substance are associated with higher cardiovascular mortality and with cerebrovascular disease. It has also been shown that serum concentrations of total and lipid-associated sialic acid are significantly increased in hypertriglyceridemia. On the other hand, several circulating lipoproteins have been suggested to be related to the severity of coronary atherosclerosis, but contradictory results have been reported in the possible relationship between the concentrations of sialic acid and the severity of coronary lesions in patients with coronary heart disease. The purpose of this study was to investigate the possible relationship between serum total sialic acid concentration, recently shown to be a cardiovascular risk factor, and serum lipid-bound sialic acid concentration and the severity of coronary lesions. The study comprised 90 subjects, divided into three subgroups according to angiography results: 30 patients with no vessel disease, 30 patients with single-vessel disease, and 30 patients with double/triple-vessel disease. Serum total sialic acid determination was carried out with the thiobarbituric acid method of Warren; lipid-associated sialic acid was assayed with the method of Katopodis. Mean serum total sialic acid levels in patients with single-vessel disease (P <.05) and patients with double/triple-vessel disease (P <.001) were found to be significantly increased compared with that in patients with no vessel disease, whereas mean serum lipid-bound sialic acid levels were found to be significantly different between patients with double- or triple-vessel disease and patients with no vessel disease (P <.001). We also noted a significant difference between the levels of serum total sialic acid (P <.001) and lipid-bound sialic acid (P <.001) in patients with single-vessel disease and patients with double/triple-vessel disease. We found a significant correlation only between serum lipid-bound sialic acid and coronary angiographic score in patients with double/triple-vessel disease (r = 0.425, P <.05). Although the concentration of serum total sialic acid is increased proportionally with the number of diseased coronary arteries, only the concentration of serum lipid-bound sialic acid is related to the severity of coronary atherosclerosis, especially in patients with double/triple-vessel disease.
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PMID:Association between serum total and lipid-bound sialic acid concentration and the severity of coronary atherosclerosis. 1222 67

Coronary heart disease is a leading cause of death in industrialized nations. Hyperlipidemia with elevated serum total cholesterol, LDL cholesterol, and triglycerides is a known major cardiovascular risk factor. HDL cholesterol is considered to be protective, so low HDL cholesterol is being recognized as an independent cardiovascular risk factor that contributes to the development of atherosclerosis and related adverse cardiovascular events. The recognition of insulin resistance and metabolic syndrome is a step further in understanding these risk factors. Attempts at reducing serum cholesterol with different strategies in the past have met with limited success until the development of statins. The advent of statins has revolutionized the management of hyperlipidemia. The post-statins era has seen major clinical trials demonstrating the benefit of cholesterol reduction in the setting of both primary and secondary prevention. In general, there appears to be a 25% to 40% relative risk reduction in major adverse cardiovascular events such as death, myocardial infarction, and stroke. The recent megatrials further suggest that aggressive management of cholesterol in patients with high cardiovascular risk may be beneficial. Though the concept of the-lower-the-better may be looming, the question of "How low is good enough?" remains controversial. The results of recent megatrials such as the Heart Protection Study go a step further than the NCEP guidelines and suggest that statin therapy may benefit patients at high risk of cardiovascular disease regardless of their baseline values. We summarize the results of the available large clinical trials in our understanding of the management of dyslipidemia in a setting of primary prevention.
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PMID:Management of dyslipidemia in the primary prevention of coronary heart disease. 1235 27

Women with polycystic ovary syndrome (PCOS) have a clustering of cardiovascular risk factors, such as obesity, lipid abnormalities, impaired glucose tolerance, insulin resistance, and hypertension. Exercise is reported to lower the incidence of cardiac events. The effect of exercise on plasma homocysteine concentrations, an independent cardiovascular risk factor, has not been previously reported in women with PCOS. We examined the effects of exercise on plasma total homocysteine concentrations in young overweight or obese PCOS women [age (mean +/- SD), 30.6 +/- 6.6 yr; body mass index, 35.49 +/- 7.57 kg/m(2)]. Twenty-one women consented to a 6-month exercise program; 12 women (exercisers) adhered to the program, whereas 9 (nonexercisers) did not. In both groups of women, the following parameters were recorded at baseline and 6 months: body mass index, waist-to-hip ratio, and aerobic capacity (maximal oxygen consumption); blood samples were taken after an overnight fast for plasma total homocysteine, insulin, and other biochemical parameters. A significant decrease in plasma total homocysteine concentrations (P < 0.001) and waist-to-hip ratio (P = 0.041) and a significant increase in maximal oxygen consumption (P = 0.019) were recorded at 6 months, compared with baseline in the exercise group. This decrease in homocysteine was not explained by changes in anthropometric or biochemical parameters. In contrast, no significant changes in any of the variables were observed in the nonexercise group. Our study has provided the first evidence that regular exercise significantly lowers plasma homocysteine in young overweight or obese women with PCOS, a group at increased risk of premature atherosclerosis. The precise mechanism by which exercise is associated with a reduction in homocysteine remains to be elucidated.
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PMID:Exercise decreases plasma total homocysteine in overweight young women with polycystic ovary syndrome. 1236 25

High-density lipoproteins (HDLs) are strongly related to risk of atherosclerotic cardiovascular disease. Low levels of HDL cholesterol are a major cardiovascular risk factor, and overexpression of the major HDL protein, apolipoprotein (apo) A-I, markedly inhibits progression and even induces regression of atherosclerosis in animal models. Clinical data regarding the effect of increasing HDL cholesterol on vascular events are limited. HDL remains an important potential target for therapeutic intervention. A variety of gene products are involved in the regulation of HDL metabolism. Yet, the mechanisms by which HDL inhibits atherosclerosis are not yet fully understood. There remains much to be learned about HDL metabolism and its relation to atherosclerosis and other cardiovascular risk factors.
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PMID:High-density lipoproteins and atherosclerosis. 1241 82


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