The Experts below are selected from a list of 32598 Experts worldwide ranked by ideXlab platform
Eliseo Guallar - One of the best experts on this subject based on the ideXlab platform.
-
persistent nonalcoholic fatty liver disease increases risk for Carotid Atherosclerosis
2016Co-Authors: Dong Hyun Sinn, Soo Jin Cho, Donghyeong Seong, Danbee Kang, Hyunkyoung Kim, Seung Woon Paik, Eliseo GuallarAbstract:Background & Aims Nonalcoholic fatty liver disease (NAFLD) has been associated with subclinical Atherosclerosis in cross-sectional studies. We investigated the longitudinal association of NAFLD with the development of subclinical Carotid Atherosclerosis. Methods We performed a retrospective cohort study of 8020 adult men (average age, 49.2 y) without Carotid Atherosclerosis at baseline who underwent repeated health check-up examinations from January 1, 2005, through December 31, 2013. NAFLD status was diagnosed by ultrasonography and classified into 4 groups based on baseline and follow-up findings: none, developed, regressed, or persistent NAFLD. Subclinical Carotid Atherosclerosis was measured by ultrasound. Results The age-adjusted hazard ratio for subclinical Carotid Atherosclerosis development comparing participants with persistent NAFLD with those without NAFLD was 1.23 (95% confidence interval [CI], 1.13–1.35; P P = .014), but disappeared after adjustment for metabolic variables. The hazard ratio, comparing subjects with regression of NAFLD vs those with persistent NAFLD, was 0.82 (95% CI, 0.69–0.96; P = .013). The risk of subclinical Carotid Atherosclerosis development also was higher among participants with a high NAFLD fibrosis score, fibrosis-4 scores, or levels of γ-glutamyl transferase at baseline. Conclusions In a large cohort study, persistent NAFLD was associated with an increased risk of subclinical Carotid Atherosclerosis development. This association was explained by metabolic factors that could be potential mediators of the effect of NAFLD. Markers of liver fibrosis also were associated with subclinical Carotid Atherosclerosis development. Prospective studies are needed to determine whether treatment of NAFLD can reduce this risk.
Ward A Riley - One of the best experts on this subject based on the ideXlab platform.
-
effect of lovastatin on early Carotid Atherosclerosis and cardiovascular events asymptomatic Carotid artery progression study acaps research group
1994Co-Authors: Curt D Furberg, Donald B Hunninghake, Harold P Adams, William B Applegate, Robert P Byington, Mark A Espeland, T Hartwell, David Lefkowitz, J Probstfield, Ward A RileyAbstract:BACKGROUND HMG CoA reductase inhibitors (or statins), a new class of lipid-lowering compounds, have raised expectations for more widespread use than that of the older lipid-lowering drugs. Not only are they more effective in lowering LDL cholesterol, but they are better tolerated as well. No data exist concerning the effect of statins on early Carotid Atherosclerosis and clinical events in men and women who have moderately elevated LDL cholesterol levels but are free of symptomatic cardiovascular disease. METHODS AND RESULTS Lovastatin (20 to 40 mg/d) or its placebo was evaluated in a double-blind, randomized clinical trial with factorial design along with warfarin (1 mg/d) or its placebo. This report is limited to the lovastatin component of the trial. Daily aspirin (81 mg/d) was recommended for everyone. Enrollment included 919 asymptomatic men and women, 40 to 79 years old, with early Carotid Atherosclerosis as defined by B-mode ultrasonography and LDL cholesterol between the 60th and 90th percentiles. The 3-year change in mean maximum intimal-medial thickness (IMT) in 12 walls of the Carotid arteries was the primary outcome; change in single maximum IMT and incidence of major cardiovascular events were secondary outcomes. LDL cholesterol fell 28%, from 156.6 mg/dL at baseline to 113.1 mg/dL at 6 months (P < .0001), in the lovastatin groups and was largely unchanged in the lovastatin-placebo groups. Among participants not on warfarin, regression of the mean maximum IMT was seen after 12 months in the lovastatin group compared with the placebo group; the 3-year difference was statistically significant (P = .001). A larger favorable effect of lovastatin was observed for the change in single maximum IMT but was not statistically significant (P = .12). Five lovastatin-treated participants suffered major cardiovascular events--coronary heart disease mortality, nonfatal myocardial infarction, or stroke--versus 14 in the lovastatin-placebo groups (P = .04). One lovastatin-treated participant died, compared with eight on lovastatin-placebo (P = .02). CONCLUSIONS In men and women with moderately elevated LDL cholesterol, lovastatin reverses progression of IMT in the Carotid arteries and appears to reduce the risk of major cardiovascular events and mortality. Results from ongoing large-scale clinical trials may further establish the clinical benefit of statins.
-
effect of lovastatin on early Carotid Atherosclerosis and cardiovascular events asymptomatic Carotid artery progression study acaps research group
1994Co-Authors: Curt D Furberg, Donald B Hunninghake, Harold P Adams, William B Applegate, Robert P Byington, Mark A Espeland, T Hartwell, David Lefkowitz, J Probstfield, Ward A RileyAbstract:BACKGROUNDHMG CoA reductase inhibitors (or statins), a new class of lipid-lowering compounds, have raised expectations for more widespread use than that of the older lipid-lowering drugs. Not only are they more effective in lowering LDL cholesterol, but they are better tolerated as well. No data exist concerning the effect of statins on early Carotid Atherosclerosis and clinical events in men and women who have moderately elevated LDL cholesterol levels but are free of symptomatic cardiovascular disease.METHODS AND RESULTSLovastatin (20 to 40 mg/d) or its placebo was evaluated in a double-blind, randomized clinical trial with factorial design along with warfarin (1 mg/d) or its placebo. This report is limited to the lovastatin component of the trial. Daily aspirin (81 mg/d) was recommended for everyone. Enrollment included 919 asymptomatic men and women, 40 to 79 years old, with early Carotid Atherosclerosis as defined by B-mode ultrasonography and LDL cholesterol between the 60th and 90th percentiles. Th...
Jioh Mok - One of the best experts on this subject based on the ideXlab platform.
-
contribution of subcutaneous abdominal fat on ultrasonography to Carotid Atherosclerosis in patients with type 2 diabetes mellitus
2014Co-Authors: Chanhee Jung, Boyeon Kim, Kyujin Kim, Sanghee Jung, Chulhee Kim, Sungkoo Kang, Jioh MokAbstract:Background Whereas visceral abdominal adipose tissue (VAT) is associated with cardiometabolic risk, there is debate regarding the role of subcutaneous abdominal adipose tissue (SAT). The aim of this study was to investigate the relationships of subcutaneous and visceral abdominal fat with Carotid Atherosclerosis in patients with type 2 diabetes mellitus (T2DM).
-
contribution of subcutaneous abdominal fat on ultrasonography to Carotid Atherosclerosis in patients with type 2 diabetes mellitus
2014Co-Authors: Chanhee Jung, Boyeon Kim, Kyujin Kim, Sanghee Jung, Chulhee Kim, Sungkoo Kang, Jioh MokAbstract:Whereas visceral abdominal adipose tissue (VAT) is associated with cardiometabolic risk, there is debate regarding the role of subcutaneous abdominal adipose tissue (SAT). The aim of this study was to investigate the relationships of subcutaneous and visceral abdominal fat with Carotid Atherosclerosis in patients with type 2 diabetes mellitus (T2DM). A total of 234 patients (men 131, women 103, mean age: 53 years) with T2DM were enrolled. Carotid intima-media thickness (CIMT), abdominal subcutaneous fat thickness (SFT) and visceral fat thickness (VFT) were assessed by high-resolution B-mode ultrasonography (US). Compared to women, men had significantly higher VFT and lower SFT (p = 0.002, p = 0.04, respectively). In partial correlation coefficient analyses between CIMT and abdominal fat thickness after adjustment for body mass index (BMI), SFT showed a negative correlation with CIMT in men (r = -0.27, p = 0.03). VFT was not correlated with CIMT in either men or women. In women, SFT was not correlated with CIMT (r = -0.01, p = 0.93). VFT/SFT ratio was not correlated with CIMT in either men or women. In multivariate regression analyses adjusted for BMI and other CVD risk factors, SFT but not VFT was independently inversely associated with CIMT in men but not in women (p < 0.001). SFT assessed by US was inversely associated with Carotid Atherosclerosis in patients with T2DM, particularly men. Further research into the different roles of the two types of abdominal adipose tissue in both men and women is warranted.
-
association between cardiac autonomic neuropathy diabetic retinopathy and Carotid Atherosclerosis in patients with type 2 diabetes
2013Co-Authors: Chanhee Jung, Boyeon Kim, Kyujin Kim, Chulhee Kim, Sungkoo Kang, Aerin Baek, Jioh MokAbstract:Background: It is not clear whether microangiopathies are associated with subclinical Atherosclerosis in type 2 diabetes mellitus (T2DM). We investigated the relation of cardiac autonomic neuropathy (CAN) and other microangiopathies with Carotid Atherosclerosis in T2DM. Methods: A total of 131 patients with T2DM were stratified by mean Carotid intima-media thickness (CIMT) ≥ or <1.0 mm and the number of Carotid plaques. CAN was assessed by the five standard cardiovascular reflex tests according to the Ewing’s protocol. CAN was defined as the presence of at least two abnormal tests or an autonomic neuropathy points ≥2. Diabetic microangiopathies were assessed. Results: Patients with CAN comprised 77% of the group with mean CIMT ≥1.0 mm, while they were 29% of the group with CIMT <1.0 mm (P=0.016). Patients with diabetic retinopathy (DR) comprised 68% of the group with CIMT ≥1.0 mm, while they were 28% of the group without CIMT thickening (P=0.003). Patients with CAN comprised 51% of the group with ≥2 Carotid plaques, while they were 23% of the group with ≤1 Carotid plaque (P=0.014). In multivariable adjusted logistic regression analysis, the patients who presented with CAN showed an odds ratio [OR] of 8.6 (95% confidence interval [CI], 1.6 to 44.8) for CIMT thickening and an OR of 2.9 (95% CI, 1.1 to 7.5) for Carotid plaques. Furthermore, patients with DR were 3.8 times (95% CI, 1.4 to 10.2) more likely to have CIMT thickening. Conclusion: These results suggest that CAN is associated with Carotid Atherosclerosis, represented as CIMT and plaques, independent of the traditional cardiovascular risk factors in T2DM. CAN or DR may be a determinant of subclinical Atherosclerosis in T2DM.
Curt D Furberg - One of the best experts on this subject based on the ideXlab platform.
-
effect of lovastatin on early Carotid Atherosclerosis and cardiovascular events asymptomatic Carotid artery progression study acaps research group
1994Co-Authors: Curt D Furberg, Donald B Hunninghake, Harold P Adams, William B Applegate, Robert P Byington, Mark A Espeland, T Hartwell, David Lefkowitz, J Probstfield, Ward A RileyAbstract:BACKGROUND HMG CoA reductase inhibitors (or statins), a new class of lipid-lowering compounds, have raised expectations for more widespread use than that of the older lipid-lowering drugs. Not only are they more effective in lowering LDL cholesterol, but they are better tolerated as well. No data exist concerning the effect of statins on early Carotid Atherosclerosis and clinical events in men and women who have moderately elevated LDL cholesterol levels but are free of symptomatic cardiovascular disease. METHODS AND RESULTS Lovastatin (20 to 40 mg/d) or its placebo was evaluated in a double-blind, randomized clinical trial with factorial design along with warfarin (1 mg/d) or its placebo. This report is limited to the lovastatin component of the trial. Daily aspirin (81 mg/d) was recommended for everyone. Enrollment included 919 asymptomatic men and women, 40 to 79 years old, with early Carotid Atherosclerosis as defined by B-mode ultrasonography and LDL cholesterol between the 60th and 90th percentiles. The 3-year change in mean maximum intimal-medial thickness (IMT) in 12 walls of the Carotid arteries was the primary outcome; change in single maximum IMT and incidence of major cardiovascular events were secondary outcomes. LDL cholesterol fell 28%, from 156.6 mg/dL at baseline to 113.1 mg/dL at 6 months (P < .0001), in the lovastatin groups and was largely unchanged in the lovastatin-placebo groups. Among participants not on warfarin, regression of the mean maximum IMT was seen after 12 months in the lovastatin group compared with the placebo group; the 3-year difference was statistically significant (P = .001). A larger favorable effect of lovastatin was observed for the change in single maximum IMT but was not statistically significant (P = .12). Five lovastatin-treated participants suffered major cardiovascular events--coronary heart disease mortality, nonfatal myocardial infarction, or stroke--versus 14 in the lovastatin-placebo groups (P = .04). One lovastatin-treated participant died, compared with eight on lovastatin-placebo (P = .02). CONCLUSIONS In men and women with moderately elevated LDL cholesterol, lovastatin reverses progression of IMT in the Carotid arteries and appears to reduce the risk of major cardiovascular events and mortality. Results from ongoing large-scale clinical trials may further establish the clinical benefit of statins.
-
effect of lovastatin on early Carotid Atherosclerosis and cardiovascular events asymptomatic Carotid artery progression study acaps research group
1994Co-Authors: Curt D Furberg, Donald B Hunninghake, Harold P Adams, William B Applegate, Robert P Byington, Mark A Espeland, T Hartwell, David Lefkowitz, J Probstfield, Ward A RileyAbstract:BACKGROUNDHMG CoA reductase inhibitors (or statins), a new class of lipid-lowering compounds, have raised expectations for more widespread use than that of the older lipid-lowering drugs. Not only are they more effective in lowering LDL cholesterol, but they are better tolerated as well. No data exist concerning the effect of statins on early Carotid Atherosclerosis and clinical events in men and women who have moderately elevated LDL cholesterol levels but are free of symptomatic cardiovascular disease.METHODS AND RESULTSLovastatin (20 to 40 mg/d) or its placebo was evaluated in a double-blind, randomized clinical trial with factorial design along with warfarin (1 mg/d) or its placebo. This report is limited to the lovastatin component of the trial. Daily aspirin (81 mg/d) was recommended for everyone. Enrollment included 919 asymptomatic men and women, 40 to 79 years old, with early Carotid Atherosclerosis as defined by B-mode ultrasonography and LDL cholesterol between the 60th and 90th percentiles. Th...
Johann Willeit - One of the best experts on this subject based on the ideXlab platform.
-
Carotid Atherosclerosis and coronary heart disease in the metabolic syndrome prospective data from the bruneck study
2003Co-Authors: Enzo Bonora, Johann Willeit, Stefan Kiechl, Friedrich Oberhollenzer, Georg Egger, Riccardo C Bonadonna, Michele MuggeoAbstract:OBJECTIVE — The present study aimed at prospectively evaluating Carotid Atherosclerosis and coronary heart disease (CHD) in subjects with the metabolic syndrome. RESEARCH DESIGN AND METHODS — Within a prospective population-based survey examining 888 subjects aged 40–79 years, 303 subjects were identified as fulfilling World Health Organization (WHO) criteria and 158 as fulfilling the National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP)-III criteria for diagnosing the metabolic syndrome. The 5-year change in Carotid status, as assessed by echo-duplex scanning, and incident fatal and nonfatal CHD, as assessed by medical history and death certificates, were compared in subjects with the metabolic syndrome and in the rest of the sample (control subjects). RESULTS — Compared with the control subjects, subjects with the metabolic syndrome by WHO criteria had an increased 5-year incidence and progression of Carotid Atherosclerosis: 51 vs. 35% developed new plaques ( P = 0.021) and 34 vs. 19% developed Carotid stenosis >40% ( P = 0.002) after adjusting for several confounders. Subjects with the metabolic syndrome by these criteria also had an increased incidence of CHD during follow-up: 8 vs. 3% in control subjects ( P = 0.012). Similar results were found when the NCEP-ATPIII criteria were used. CONCLUSIONS — Subjects with the metabolic syndrome are at increased risk for both progressive Carotid Atherosclerosis and CHD.
-
chronic infections and the risk of Carotid Atherosclerosis prospective results from a large population study
2001Co-Authors: Stefan Kiechl, Friedrich Oberhollenzer, Enzo Bonora, Georg Egger, Michele Muggeo, Manuel Mayr, Christian J Wiedermann, Georg Wick, Werner Poewe, Johann WilleitAbstract:Background—Chronic infections have been implicated in the pathogenesis of Atherosclerosis, yet from an epidemiological perspective, this concept remains controversial. Methods and Results—The Bruneck Study is a prospective population-based survey on the pathogenesis of Atherosclerosis. In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in Carotid Atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of Atherosclerosis development in the Carotid arteries. The association was most pronounced in subjects free of Carotid Atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; P<0.0001) and applied to all types of chronic (bacterial) infections. It remained independently significant after adjustment for classic vascular risk attribu...
-
body iron stores and the risk of Carotid Atherosclerosis prospective results from the bruneck study
1997Co-Authors: Stefan Kiechl, Johann Willeit, Georg Egger, Werner Poewe, Friedrich OberhollenzerAbstract:Background Fe2+ released from tissue iron stores may accelerate lipid peroxidation by virtue of its pro-oxidant properties and thus promote early atherogenesis. Methods and Results The present prospective survey addresses the potential association between serum ferritin concentrations and the 5-year progression of Carotid Atherosclerosis as assessed by ultrasonographic follow-up evaluations. The study population comprises a random sample of 826 men and women 40 to 79 years old. Serum ferritin was one of the strongest risk predictors of overall progression of Atherosclerosis. The main part of this association appeared to act through modification of the atherogenic potential of LDL cholesterol (OR [95% CI] for a 1–SD unit increase in ferritin at LDL levels of 2.5, 3.6, and 4.9 mmol/L: 1.55 [1.30 to 1.85], 1.77 [1.40 to 2.24], and 2.05 [1.50 to 2.80]; P=.0012 for effect modification). Changes in iron stores during the follow-up period modified Atherosclerosis risk, in that a lowering was beneficial and furth...
-
increased concentrations of neopterin in Carotid Atherosclerosis
1994Co-Authors: Gunter Weiss, Johann Willeit, Stefan Kiechl, Dietmar Fuchs, Elmar Jarosch, Friedrich Oberhollenzer, Gilbert Reibnegger, Gernot P Tilz, Franz Gerstenbrand, Helmut WachterAbstract:Activation of T-cells and macrophages may play a role in the pathogenesis of Atherosclerosis. Therefore, serum concentrations of the immune activation markers neopterin and soluble interleukin-2 receptor were compared with routine laboratory parameters, candidate risk variables and degree of Carotid Atherosclerosis. Study subjects were 561 individuals (293 men and 268 women) aged between 50 and 79 years who were enrolled in a cross-sectional community based study (Ischemic Heart Disease and Stroke Prevention Study, Bruneck, Italy). Extent of Carotid Atherosclerosis was quantitated by an ultrasound B-mode procedure based scoring system. Detailed physical examination and quantification of laboratory and candidate risk variables were performed. By univariate as well as multivariate statistical analyses, serum concentrations of neopterin but not soluble interleukin-2 receptor were significantly higher in subjects with Carotid Atherosclerosis (men, 8.5 +/- 2.7 nmol/l neopterin; women, 9.6 +/- 3.3) than in those without (men, 6.7 +/- 2.3, P < 0.0001; women, 7.5 +/- 2.3, P < 0.0001). The data show that the macrophage-derived immune activation marker neopterin is closely correlated with the extent of Carotid Atherosclerosis. Chronic activation of immune cells, preferentially of macrophages, may play a key role in atherogenesis and/or progression of Atherosclerosis.