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)

Atherosclerotic changes have not been demonstrated directly in asymptomatic hyperglycaemic non-diabetic subjects, although high mortality due to coronary heart disease has been reported. We measured arterial wall thickness non-invasively, in order to directly demonstrate atherosclerosis of the carotid arteries of hyperglycaemic non-diabetic subjects and to evaluate its risk factors. The thicknesses of the intimal plus medial complex (IMT) of the carotid arteries of 112 asymptomatic hyperglycaemic non-diabetic subjects (aged 22-81, 95 males and 17 females) were compared with those of 55 healthy male subjects and 211 non-insulin-dependent NIDDM male diabetic patients. The subjects were subgrouped into impaired glucose-tolerant (IGT) subjects who had a 2-h glycaemic level of more than 7.8 mmol/l, and non-IGT subjects whose 2-h glycaemic levels were within 6.7-7.7 mmol/l. Non-IGT and IGT subjects showed significantly greater IMTs than age-matched healthy males and showed no significant differences compared to age-matched NIDDM patients. Multivariate analysis demonstrated that the risk factors for IMT of non-IGT and IGT subjects were age and systolic blood pressure. According to data on the accumulation of atherogenic risks (hypertension, dyslipidaemia, and smoking), IMT increased linearly in non-IGT and IGT subjects. However, non-IGT and IGT subjects without hyperlipidaemia, hypertension, or smoking risk still had significantly greater IMT than age-matched normal males (1.019 +/- 0.063 vs 0.770 +/- 0.111 mm, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Asymptomatic hyperglycaemia is associated with increased intimal plus medial thickness of the carotid artery. 748 42

We have evaluated quantitatively the thickness of intimal plus median wall of the carotid arteries (IMT) in subjects with mild hyperglycemia determined by the OGTT recommendation criteria of Japanese Diabetes Association, consisting of IGT and non IGT. IMTs of IGT and non IGT hyperglycemic subjects were significantly thicker than those of normal volunteers with any decade and were quite comparable with those of diabetics. Accumulation of risk factors of atherosclerosis linearly increased IMT in subjects with mild hyperglycemia. IMT of subjects with hyperglycemia and hyperin-sulinemia after OGTT was significantly higher than that with relatively hypoglycemia and hypoinsulinemia. IMT was inversely related with insulin resistance but not with endogenous insulin secretory ability. These data indicate that insulin resistance is one of major risk factor for advancing carotid arteriosclerosis in subjects with mild hyperglycemia.
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PMID:[Atherosclerosis in subjects with mild hyperglycemia]. 891 30

The characteristics of NIDDM seen in Japanese is coexistence of diminished insulin secretion and the impaired sensitivity to insulin in the target tissues. Thus, insulin resistance does not mean hyperinsulinemia. To investigate the organ-specific insulin action on glucose homeostasis, we developed an innovative non-invasive method, using an euglycemic hyperinsulinemic clamp combined with oral glucose load. With this procedure, we could reveal muscle glucose uptake and hepatic glucose uptake following oral glucose load, quantitatively, separately and simultaneously. The effect of strict glycemic control in non-obese NIDDM who were secondary failure to sulfonylurea with 3 times prandial regular insulin injections, on glucose disposals are investigated. Glucose disposal by peripheral tissues was not altered (clamped blood glucose and insulin concentration are, 90 mg/dl and 200 microU/ml, respectively). The ratio of splanchnic glucose disposal to the amount of ingested glucose, on the other hand, significantly increased to 33.1% from 14.5%. Therefore, short-term strict glycemic control appears to improve glucose handling by splanchnic tissues without affecting insulin sensitivity of peripheral tissues in NIDDM. This method would be feasible to investigate whether insulin resistance seen in hypertensive patients, is located only in peripheral tissues or is also in the liver. To find patients with asymptomatic atherosclerosis, we routinely apply a noninvasive maneuver using high resolution B-mode imaging of the carotid artery, to determine atherosclerosis quantitatively. Impaired glucose tolerance (IGT) male subjects showed significantly greater thickness of the intimal plus medial complex (IMT) than age-matched healthy males and showed no significant differences compared to age-matched NIDDM patients. Among IGT, those with exaggerated insulin secretion (average serum insulin concentration was 100 microU/ml at 1 and 2 h after), in other words, insulin resistant, showed thicker IMT. The characteristics of IGT groups with high insulin level were, BMI more than 25, diastolic blood pressure more than 83 mmHg, serum triglyceride more than 215 mg/dl. Thus, among mildly obese, mild hypertensive, mild glucose intolerant, slightly hypertriglyceridemic Japanese male subjects, there exist advanced atherosclerotic subjects.
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PMID:Insulin resistance seen in non-insulin dependent diabetes mellitus and hypertension. 924 Jul 67

To establish the prevalence of carotid atherosclerosis and its relation to aging in Japanese population, 270 participants in voluntary health screening at our hospital were studied with 7.5 MHz B-mode ultrasonography and accelerated plethysmography (APG), and their levels of serum lipids were measured. The subjects consisted of 84 people in the fifth decade of life, 89 in the sixth decade, 67 in the seventh decade, and 30 in the eighth decade. Carotid lesions were deemed to be present when occlusion, atheromatous plaque, or both were found. Atheromatous plaque was defined as a thickened intima-media complex of 2.1 mm or more. Plaques were divided into two types based on morphometric criteria, and into three types based on echogenic criteria. Thickness of the intimamedia complex (IMT) was measured at two randomly chosen points along the common carotid artery. APG was obtained by double-differentiation of finger-plethysmograph record, and the APG index was calculated as (-b+c+d)/a, where the letters are the distances from the baseline to the peaks of each wave (a, b, c, and d waves) on the APG waveform. Carotid lesions were seen in 5% of subjects in the fifth decade of life, 7% of subjects in the sixth decade, 24% of those in the seventh decade, and 27% of those in the eighth decade. All the lesions were plaques, and neither plaque type nor size differed between young-adult and elderly subjects. Multiple regression analysis revealed that the thickness of the intima-media complex correlated significantly with age, but not with carotid lesions, sex, body weight, serum lipid levels, hemoglobin A1 level, or uric acid level. The APG index also decreased significantly with age, but no correlation was seen with carotid lesions or with the thickness of the intima-media complex. These findings indicate that people aged 60 or over could be at risk for plaque formation in the carotid arteries and their carotid arteries should be examined carefully even in the absence of risk factors for vascular disease. These findings also suggest that both increased thickness of the intima-media complex and a low APG index arise via pathophysiologic mechanisms different from those that lead to atheromatous plaque.
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PMID:[Aging and ultrasonographic findings of carotid atherosclerosis]. 938 76

Vascular cell adhesion molecule-1 (VCAM-1) has been shown to be highly expressed in atherosclerotic lesions. Although the soluble form of VCAM-1 (sVCAM-1) is detected in human sera, the relation between the degree of atherosclerosis and serum sVCAM-1 level has not been defined. In the present study, sVCAM-1 concentrations were measured in sera from 101 Japanese NIDDM patients. The mean +/- SD serum sVCAM-1 concentration in 26 patients with symptomatic atherosclerotic vascular diseases (789 +/- 187 ng/ml) was higher than that in 75 patients without the disease (664 +/- 175 ng/ml). Among the 101 NIDDM patients, 56 had atherosclerotic change of the carotid arteries, based on the evaluation by high-resolution B-mode ultrasonography. Their sVCAM-1 level was 759 +/- 201 ng/ml, higher than that in 45 patients without any detectable atherosclerosis of the carotid arteries (619 +/- 130 ng/ml). In addition, there was a positive correlation between sVCAM-1 concentration and thickness of the intimal plus medial complex (IMT) of the carotid arteries in the NIDDM patients (r = 0.41, P < 0.0001). Multivariate regression analysis revealed significant predictors of mean IMT value to be sVCAM-1 concentration (F = 62.88, P = 0.0001) and age (F = 9.59, P = 0.0026). By contrast, sVCAM-1 concentration was not increased in nondiabetic patients with atherosclerotic change of the carotid arteries (668 +/- 191 ng/ml; n = 36) compared with those without the atherosclerotic change (632 +/- 177 ng/ml; n = 28), and there was no correlation between sVCAM-1 level and IMT of the carotid arteries in the nondiabetic subjects. These results indicate that circulating sVCAM-1 may be a marker of atherosclerotic lesions in NIDDM patients with symptomatic and asymptomatic atherosclerosis.
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PMID:Circulating vascular cell adhesion molecule-1 (VCAM-1) in atherosclerotic NIDDM patients. 1044 41

Studies have shown the presence of insulin resistance together with compensatory hyperinsulinemia in vasospastic angina as well as obstructive coronary artery disease. There is growing evidence that the development of coronary atherosclerosis may be closely related to systemic atherosclerosis as well as coronary spasm. However, no information is available about the possible relationship between insulin resistance and the existence of carotid atherosclerosis in vasospastic angina without segmental stenosis or luminal irregularities in coronary angiograms. To evaluate the independent effect of insulin resistance on carotid intima media thickening, we performed insulin sensitivity tests (steady-state plasma glucose method) on 40 patients with vasospastic angina and 24 control subjects with angiographically intact coronary arteries. Both oral glucose tolerance tests and lipid analyses were performed. Using B-mode ultrasonography, we assessed intima media thickness and plaque formation of common carotid arteries in these subjects. The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. The patients with vasospastic angina showed a significant increase in the average intima media thickness of the carotid wall and frequency of plaque formation, although they were comparable to the control subjects in risk factors other than insulin resistance. The intima media thickness was correlated with age (r = .62, P < .001), 2-hour insulin area (r = .45, P < .01), and steady-state plasma glucose level (r = .68, P < .0001) in patients with vasospastic angina. Similar correlations were observed in the control subjects. Multiple regression analyses of data indicated that 67% of the variation in the intima media thickness could be accounted for by age, steady-state plasma glucose level, and cigarette-years in vasospastic angina. In addition, differences in IMT were independently related to vasospastic angina. These results suggest that insulin resistance in association with compensatory hyperinsulinemia may be an important pathogenic factor for the development of coronary artery spasms and systemic early atherosclerosis.
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PMID:Insulin resistance as an independent risk factor for carotid artery wall intima media thickening in vasospastic angina. 940 26

The purpose of this study was to assess the effect of the main risk factors for cardiovascular disease on the process of subclinical atherosclerosis in originally borderline hypertensives. The relation of far wall common carotid artery intima-media thickness (IMT CCA) measured by B-mode ultrasound to smoking, body mass index (BMI), blood pressure, lipids, and angiotensin-converting enzyme (ACE) gene polymorphism was analyzed. In 48 subjects examined (mean age, 61.9 +/- 2.54 years), median IMT CCA was 0.708 mm. Statistically significant differences in BMI (26.5 vs. 29.2 kg/m2, p < 0.025) and HDL-cholesterol level (1.42 vs. 1.1 mmol/l, p < 0.025) between the first and third tertile of IMT CCA were found. No differences were observed between "controls" and "cases" in blood pressure, total cholesterol, and triacylglycerols. No significant differences in IMT CCA were found between smokers and nonsmokers and among different alleles of the ACE gene. These data reflect the importance of HDL-cholesterol and BMI on the process of atherosclerosis within an otherwise homogeneous group of patients.
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PMID:Intima-media thickness of carotid arteries in borderline hypertensives. 992 19

The primary objective of the present study was to investigate the cholesterol-lowering effect of fluvastatin on the incidence of cardiac events in hyperlipidaemic patients with symptomatic, clinically-diagnosed (exercise-ECG) coronary heart disease (CHD) during 1 year of treatment. Exercise tolerance, incidence of angina pectoris episodes, use of anti-anginal medication and intimal-medial-thickness (IMT subgroup) of the A. carotis were secondary endpoints. In the double-blind trial a total of 365 male and female patients with stable symptomatic CHD and a low-density lipoprotein cholesterol (LDL-C) above 160 mg/dl on a lipid-lowering diet were randomised to fluvastatin 40 mg (o.a.d. or b.i.d.) or placebo for 1 year. Fluvastatin lowered total cholesterol by 17% and LDL-C by 27%. There was a significantly lower incidence of cardiac events (cardiac death, nonfatal myocardial infarction, unstable angina pectoris) in the fluvastatin group (3 events) as compared to the placebo group (10 events) (P < 0.05). Exercise tolerance improved and the incidence of angina pectoris episodes decreased in both groups, but more pronounced on fluvastatin (n.s.). Exercise-ECG discontinuation due to angina pectoris and ST-segment depression decreased in the fluvastatin group by 55.6 and 70.9%, respectively, and in the placebo group by 39.6 and 46.5% (n.s.). At baseline, a subgroup of 76 patients showed a mean IMT value of 0.73 mm which remained uninfluenced in the fluvastatin and the placebo groups. Fluvastatin was safe and well tolerated. In conclusion, patients with symptomatic CHD get cardiovascular benefit from lipid-lowering therapy with fluvastatin even during the first year of treatment.
Atherosclerosis 1999 May
PMID:The effect of fluvastatin on cardiac events in patients with symptomatic coronary artery disease during one year of treatment. 1038 Dec 99

The aim of this study was to clarify whether insulin resistance contributes to atherosclerosis in patients with non-insulin-dependent diabetes mellitus (NIDDM). Fifty-three NIDDM patients (36 males and 17 females, 53+/-10 years old (mean+/-SD)) were studied. As an index of atherosclerosis, we measured the average thickness (IMT) as well as basal thickness excluding the maximum thickness and the height of the maximum thickness of the carotid artery wall. Euglycemic hyperinsulinemic glucose clamp was conducted for 90 min to evaluate average glucose infusion rate (GIR) as an index of insulin sensitivity in the peripheral tissues. For another 180 min after intake of oral glucose load with 0.3 g/kg, the euglycemic hyperinsulinemic clamp was continued to measure ratio of splanchnic glucose uptake (SGU) as an index of insulin sensitivity of the liver. The patients were separated into three activity groups according to the grade of their leisure-time physical activity. GIR (r = -0.32, p < 0.05) but not SGU (r=0.139) showed a significant inverse relationship with IMT. Multivariant regression analysis indicated that age and total cholesterol remain as independent risk factors for basal thickness and GIR as only independent risk factor for the height of the maximum thickness. Paralleling the degrees of habitual exercise (low, moderate, and high active group), GIR was higher (6.19+/-1.02, 6.38+/-1.38, 7.44+/-1.80, respectively) and IMT was lower (1.34+/-0.33 mm, 1.20+/-0.31 mm, and 1.12+/-0.29 mm, respectively) in male NIDDM as well as in female NIDDM. These data suggest that insulin resistance in the peripheral tissues but not the splanchnic tissues may independently contribute to carotid arterial wall thickness and especially to plaque lesion, and that habitual exercise might reduce insulin resistance leading to attenuation of atherosclerosis.
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PMID:Insulin resistance contributes to carotid arterial wall thickness in patients with non-insulin-dependent-diabetes mellitus. 1067 Jul 47

Oxidation of LDLs plays an important role in atherosclerosis, and immune response to oxidized LDL (oxLDL) may modulate atherogenesis. Although immunization with oxLDL is shown to suppress atherogenesis in animal models, the role of the immune response to oxLDL is not well established in humans. We investigated the relationship between the titer of anti-oxLDL antibody (oxLDL Ab) and arterial wall thickness in a healthy population with no clinical signs of atherosclerosis. Intima-media thickness of the carotid arteries (CA-IMT) was measured by high-resolution B-mode ultrasonography in 446 healthy subjects. The titer of IgG-class oxLDL Ab was measured by a solid-phase ELISA. In univariate analysis, CA-IMT correlated positively with age, systolic blood pressure, total cholesterol, triglyceride, LDL cholesterol, body mass index, and waist-to-hip ratio, whereas it correlated negatively with HDL cholesterol and oxLDL Ab titer. The inverse association between oxLDL Ab titer and CA-IMT remained significant in multiple regression analysis, which took other confounding variables into account. These results indicate an independent inverse relationship between oxLDL Ab titer and CA-IMT in healthy subjects, supporting the hypothesis that immune response to oxLDL may have a protective role at an early stage of human atherosclerosis.
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PMID:Antibodies against oxidized LDL and carotid artery intima-media thickness in a healthy population. 1071 94


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