Search

Impact of Alcohol Intake on Measures of Lipid Metabolism Depends on Context Defined by Gender, Body Mass Index, Cigarette Smoking, and Apolipoprotein E Genotype
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 22, Issue 51 May 2002

Abstract Export Citations PDF/EPUB

Abstract
Hyperlipidemia, smoking, and obesity are well-known risk factors for cardiovascular disease. Conversely, moderate alcohol intake is associated with lower atherosclerosis risk. However, the influence of taking alcohol on the interrelationships of these factors in a particular context has not been thoroughly investigated. In this study, we asked whether the association between plasma measures of lipid metabolism and alcohol intake is dependent on context defined by gender, age, body mass index (BMI), smoking, and apolipoprotein E (APOE) genotype. Data were obtained in a sample of 869 women and 824 men who participated in the Quebec Heart Health Survey. There was no evidence that variation among APOE genotypes influenced the association between LDL cholesterol (LDL-C) or HDL cholesterol (HDL)-C and alcohol, after adjustment for age and BMI. Further, the positive (LDL-C and BMI) and the negative (HDL-C and BMI) associations that were observed in men and women with the ε3/2 and ε3/3 genotypes were not modified by alcohol intake. However, in women with the ε4/3 genotype only, we found a significant influence of an alcohol by BMI interaction on the prediction of total cholesterol, LDL-C, HDL-C, apoA-I, and apoB, and this interaction was influenced by the status of smoking. Whereas the influence of an alcohol by BMI interaction on total cholesterol and LDL-C was significant in smokers, its influence on HDL-C was significant only in non-smokers. This study emphasizes the context dependency of the influence of alcohol on lipid metabolism and demonstrates how biological, environmental, and genetic factors interact to determine cardiovascular disease risk.
Interrelationships Among Circulating Interleukin-6, C-Reactive Protein, and Traditional Cardiovascular Risk Factors in Women
- Edmund A. Bermudez,
- Nader Rifai,
- Julie Buring,
- JoAnn E. Manson and
- Paul M. Ridker
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 22, Issue 101 October 2002

Abstract Export Citations PDF/EPUB

Abstract
Objective— Interleukin-6 (IL-6) and C-reactive protein (CRP) are markers of systemic vascular inflammation that herald atherothrombosis and may have important interrelationships with traditional cardiovascular risk factors.Methods and Results— We conducted a cross-sectional analysis among 340 apparently healthy women enrolled in the Women’s Health Study. In unadjusted analyses, higher levels of IL-6 and CRP were seen with increasing body mass index (BMI), systolic and diastolic blood pressure, and smoking exposure. IL-6 levels were related to the frequency of alcohol intake (P=0.002) and showed an inverse relationship with exercise frequency and hormone replacement therapy (P<0.0001 for both). CRP levels increased with hormone replacement therapy (P=0.0002). Associations among IL-6, CRP, and lipid levels were minimal. Overall, mean levels of IL-6 and CRP increased with increasing numbers of clinical risk factors (P<0.0001). In multivariate analyses, independent relationships were seen between levels of IL-6 and age, BMI, smoking, systolic blood pressure, alcohol use, presence of diabetes, and frequency of exercise. CRP was associated with age, BMI, systolic blood pressure, high density lipoprotein, smoking, and hormone replacement therapy in adjusted analyses.Conclusions— Plasma levels of IL-6 and CRP are independently related to several clinical cardiovascular risk factors in women.
Heme Oxygenase-1 Gene Promoter Polymorphism Is Associated With Coronary Artery Disease in Japanese Patients With Coronary Risk Factors
- Hideaki Kaneda,
- Minoru Ohno,
- Junichi Taguchi,
- Masako Togo,
- Hideki Hashimoto,
- Ken Ogasawara,
- Tadanori Aizawa,
- Nobukazu Ishizaka and
- Ryozo Nagai
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 22, Issue 101 October 2002

Abstract Export Citations PDF/EPUB

Abstract
Objective— Heme oxygenase (HO) is important in the defense against oxidative stress and as a factor in an antiatherogenic mechanism. Compared with long (GT)_n repeats, short (GT)_n repeats in the human HO-1 gene promoter were shown to have higher transcriptional activity in response to oxidative stress. There is a strong link between oxidative stress and the pathogenesis of coronary artery disease (CAD).Methods and Results— We screened the allelic frequencies of (GT)_n repeats in the HO-1 gene promoter in 577 patients who underwent coronary angiography. Because the distribution of numbers of (GT)_n repeats was bimodal, we divided the alleles into 2 subclasses: class S included shorter (<27) repeats, and class L included longer (≥27) repeats. Multivariate logistic regression models including standard coronary risk factors revealed that the genotypes were significantly related to CAD status in hypercholesterolemic, diabetic patients or in smokers. In this study, the patients with shorter GT repeats were less likely to have CAD.Conclusions— Length polymorphism in the HO-1 gene promoter is related to CAD susceptibility in Japanese people who also have coronary risk factors such as hypercholesterolemia, diabetes, and smoking. HO-1 may play an antiatherogenic role in Japanese patients with these coronary risk factors.
Association of C-Reactive Protein With Carotid Atherosclerosis in Men and Women: The Framingham Heart Study
- Thomas J. Wang,
- Byung-Ho Nam,
- Peter W.F. Wilson,
- Philip A. Wolf,
- Daniel Levy,
- Joseph F. Polak,
- Ralph B. D’Agostino and
- Christopher J. O’Donnell
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 22, Issue 101 October 2002

Abstract Export Citations PDF/EPUB

Abstract
Objective— The objective of this study was to examine the relationship between C-reactive protein (CRP) and carotid atherosclerosis.Background— Levels of CRP, a nonspecific marker of inflammation, predict risk for cardiovascular events. However, the association between CRP and direct measures of atherosclerosis is not well established.Methods and Results— Subjects (n=3173, 52% women, mean age 55) in the offspring cohort of the Framingham Heart Study received a CRP measurement and then underwent carotid ultrasonography 4 years later. Carotid stenosis (≥25%) was present in 24% of men and 14% of women. Age-adjusted odds ratios for carotid stenosis were 1.62 (95%CI 1.12 to 2.36) for men and 3.90 (CI 2.44 to 6.44) for women in the fourth quartile of CRP compared with those in the lowest quartile. After further adjustment for traditional cardiovascular disease risk factors, the odds ratio remained significant for women (2.97, CI 1.72 to 5.25) but not for men. Similarly, after multivariable adjustment, women in the fourth CRP quartile had a higher mean internal carotid intima-media thickness than those in the lowest CRP quartile (P≤0.001). There was no association between common carotid intima-media thickness and CRP.Conclusions— There is a graded association between CRP and carotid atherosclerosis in women but not in men. The significance of this difference between sexes merits further investigation.
Smallest LDL Particles Are Most Strongly Related to Coronary Disease Progression in Men
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 21 February 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— LDLs include particle subclasses that have different mobilities on polyacrylamide gradient gels: LDL-I (27.2 to 28.5 nm), LDL-IIa (26.5 to 27.2 nm), LDL-IIb (25.6 to 26.5 nm), LDL-IIIa (24.7 to 25.6 nm), LDL-IIIb (24.2 to 24.7 nm), LDL-IVa (23.3 to 24.2 nm), and LDL-IVb (22.0 to 23.3 nm in diameter). We hypothesized that the association between smaller LDL particles and coronary artery disease (CAD) risk might involve specific LDL subclasses.Methods and Results— Average 4-year onstudy lipoprotein measurements were compared with annualized rates of stenosis change from baseline to 4 years in 117 men with CAD. The percentages of total LDL and HDL occurring within individual subclasses were measured by gradient gel electrophoresis. Annual rate of stenosis change was related concordantly to onstudy averages of total cholesterol (P=0.04), triglycerides (P=0.05), VLDL mass (P=0.03), total/HDL cholesterol ratio (P=0.04), LDL-IVb (P=0.01), and HDL_3a (P=0.02) and inversely to HDL₂-mass (P=0.02) and HDL_2b (P=0.03). The average annual rate in stenosis change was 6-fold more rapid in the fourth quartile of LDL-IVb (≥5.2%) than in the first quartile (<2.5%, P=0.03). Stepwise multiple regression analysis showed that LDL-IVb was the single best predictor of stenosis change.Conclusions— LDL-IVb was the single best lipoprotein predictor of increased stenosis, an unexpected result, given that LDL-IVb represents only a minor fraction of total LDL.
Hypercholesterolemia and Hypertension Have Synergistic Deleterious Effects on Coronary Endothelial Function
- Martin Rodriguez-Porcel,
- Lilach O. Lerman,
- Joerg Herrmann,
- Tatsuya Sawamura,
- Claudio Napoli and
- Amir Lerman
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 51 May 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— Coronary endothelial dysfunction is associated with an increase in cardiac events. Hypercholesterolemia (HC) and hypertension (HT) are both associated with endothelial dysfunction, and their coexistence is associated with an increased incidence of cardiac events in epidemiological studies. However, pathogenic mechanisms are poorly understood. Here we studied the effects of coexisting HC and HT on coronary endothelial function.Methods and Results— Four groups of pigs were studied after 12 weeks of a normal diet (n=9), a 2% HC diet (n=9), HT (achieved by unilateral renal artery stenosis, n=8), or HC+HT (n=6). Coronary endothelial function was tested, in epicardial arteries and arterioles, by using organ chamber techniques. Oxidative stress was measured in coronary artery tissue. Vasodilatory response to bradykinin and calcium ionophore was significantly impaired in animals with HC+HT compared with each risk factor alone (P<0.05 for both). In animals with coexistent HC and HT, the increase in oxidative stress was more pronounced compared with each risk factor alone (P<0.05). Furthermore, chronic antioxidant supplementation significantly improved coronary artery vasoreactivity.Conclusions— These results suggest that HC and HT have a synergistic deleterious effect on coronary endothelial function, associated with increased oxidative stress. This interaction may contribute to the increased incidence of coronary heart disease and cardiac events seen when HC and HT coexist.
Effects of Cyclooxygenases Inhibitors on Vasoactive Prostanoids and Thrombin Generation at the Site of Microvascular Injury in Healthy Men
- Ewa Tuleja,
- Filip Mejza,
- Adam Cmiel and
- Andrzej Szczeklik
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 61 June 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— Balance between vasoactive prostanoids that contribute to homeostasis of the circulatory system can be affected by cyclooxygenases inhibitors. Results of a recent large clinical trial show that myocardial infarction was more frequent among patients with rheumatoid arthritis treated with the selective cyclooxygenase-2 inhibitor rofecoxib compared with those treated with naproxen. Whether this difference was attributable to deleterious cardiovascular effects of rofecoxib or cardioprotective effects of naproxen has not been determined. We tested the hypothesis that naproxen, contrary to rofecoxib, exerts antithrombotic effects.Methods and Results— Forty-five healthy men were randomized to receive a 7-day treatment with rofecoxib (50 mg/d), naproxen (1000 mg/d), aspirin (75 mg/d), or diclofenac (150 mg/d). Formation of thromboxane, prostacyclin, and thrombin in the bleeding-time blood at the site of standardized microvascular injury was assessed before and after treatment. Naproxen, like aspirin, caused significant reduction of both thromboxane and prostacyclin, whereas diclofenac depressed prostacyclin synthesis but had no effect on tromboxane formation. Naproxen and aspirin significantly suppressed thrombin generation. Diclofenac showed a similar tendency, which did not reach statistical significance. Rofecoxib had no effect on any variables measured.Conclusions— In healthy men, naproxen exerts an antithrombotic effect at least as potent as aspirin, whereas rofecoxib does not affect hemostatic balance.
Regulation and Mechanisms of ATP-Binding Cassette Transporter A1-Mediated Cellular Cholesterol Efflux
- Nan Wang and
- Alan R. Tall
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 71 July 2003

Abstract Export Citations PDF/EPUB

Abstract
ATP-binding cassette transporter A1 (ABCA1) plays a major role in cholesterol homeostasis and HDL metabolism. ABCA1 mediates cellular cholesterol and phospholipid efflux to lipid-poor apolipoproteins, and upregulation of ABCA1 activity is antiatherogenic. ApoA-I, the major apolipoprotein component of HDL, promotes ABCA1-mediated cholesterol and phospholipid efflux, probably by directly binding to ABCA1. ABCA1 gene expression is markedly increased in cholesterol-loaded cells as a result of activation of LXR/RXR. ABCA1 protein turnover is rapid. ABCA1 contains a PEST—proline (P), glutamate (E), serine (S), and threonine (T)—sequence in the intracellular segment that mediates ABCA1 degradation by a thiol protease, calpain. ApoA-I and apoE stabilize ABCA1 in a novel mode of regulation by decreasing PEST sequence-mediated calpain proteolysis. ABCA1-mediated cholesterol and phospholipid efflux are distinctly regulated and affected by the activity of other gene products. Stearyol CoA desaturase decreases ABCA1-mediated cholesterol efflux but not phospholipid efflux, likely by decreasing the cholesterol pool available to ABCA1. This and other evidence suggest that ABCA1 promotes cholesterol and phospholipid efflux, probably by directly transporting both lipids as substrates.
Human CRP Gene Polymorphism Influences CRP Levels: Implications for the Prediction and Pathogenesis of Coronary Heart Disease
- D.J. Brull,
- Norma Serrano,
- F. Zito,
- Lisa Jones,
- H.E. Montgomery,
- A. Rumley,
- Pankaj Sharma,
- G.D.O. Lowe,
- M.J. World,
- S.E. Humphries and
- A.D. Hingorani
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 111 November 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— C-reactive protein (CRP) concentrations are predictive of cardiovascular disease, and levels are heritable, in part. We identified novel polymorphisms in the CRP gene and assessed their influence on CRP level.Methods and Results— CRP was measured in 250 male army recruits before and after strenuous exercise and perioperatively in 193 coronary artery bypass graft (CABG) patients. Two novel polymorphisms were identified in the CRP gene, −717G>A in the promoter and +1444C>T in the 3′UTR. Among army recruits, CRP was higher in +1444TT homozygotes than +1444 C-allele carriers at baseline (1.04±0.38 versus 0.55±0.06, P=0.014) and at all time points after exercise (2.35±0.68 versus 1.07±0.12, 2.11±0.53 versus 0.88±0.09, and 1.77±0.44 versus 0.71±0.09, P=0.034, P=0.007, and P=0.013, at 2, 48, and 96 hours after exercise, respectively). In the CABG patients, mean CRP (mg/L) rose from 1.97±0.36 at baseline to 167.2±5.0 72 hours postoperatively. Genotype did not influence CRP at baseline; however, peak post-CABG CRP levels were higher in +1444TT homozygotes compared with +1444C-allele carriers (198±17 versus 164±5, P=0.03).Conclusions— The CRP gene +1444C>T variant influences basal and stimulated CRP level. These findings have implications both for the prediction and pathogenesis of coronary heart disease.
C-Reactive Protein and Coronary Artery Calcification: The Study of Inherited Risk of Coronary Atherosclerosis (SIRCA)
- Muredach P. Reilly,
- Megan L. Wolfe,
- A. Russell Localio and
- Daniel J. Rader
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 101 October 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— Circulating levels of C-reactive protein (CRP) predict cardiovascular events. In contrast, an association between CRP and direct measures of atherosclerosis has not been established clearly. In the largest study to date, we examined the association of plasma CRP with coronary artery calcification (CAC) in 914 asymptomatic subjects in the Study of Inherited Risk of Coronary Atherosclerosis (SIRCA).Methods and Results— In age-adjusted, cross-sectional analysis, there was a weak association between plasma CRP levels and CAC in women (odds ratio [OR] for ordinal regression, 1.1 [1.04 to 1.17] per 1.0 mg/L increase in CRP; P=0.005) but not in men. The association between CRP and CAC in women remained significant after adjusting for traditional risk factors (OR, 1.08 [1.00 to 1.14]; P=0.048) but was lost after further adjustment for body mass index (BMI) (OR, 1.02 [0.94 to 1.08]; P=0.7).Conclusions— In SIRCA, CRP was not associated with CAC in men, and a weak association in women was lost after adjustment for BMI. The relation between CRP and clinical events might not be related to atherosclerotic burden. Measures of inflammation, such as CRP, and indices of atherosclerosis, such as CAC, are likely to provide distinct information regarding cardiovascular risk.
High Plasma Phospholipid Transfer Protein Levels as a Risk Factor for Coronary Artery Disease
- Axel Schlitt,
- Christoph Bickel,
- Prathima Thumma,
- Stefan Blankenberg,
- Hans J. Rupprecht,
- Juergen Meyer and
- Xian-Cheng Jiang
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 101 October 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— Plasma phospholipid transfer protein (PLTP) mediates both net transfer and exchange of phospholipids between different lipoproteins. Animal studies have shown that it is closely related to the development of atherosclerosis. PLTP-deficient mice have demonstrated increased antioxidation potential as well as a decrease in apolipoprotein B secretion and atherosclerotic lesions. In humans, high PLTP is associated with type II diabetes and obesity.Methods and Results— To assess the relationship between PLTP activity and coronary artery disease (CAD), a novel, high-throughput method to measure plasma PLTP activity was used, relating it to CAD in 1102 cases and 444 controls. This demonstrated that PLTP activity in patients with CAD was significantly higher than in controls (25.5 versus 22.4 pmol/μL per h; P<0.0001). Using multivariate logistic regression analysis, PLTP activity was found to have independent predictive value for CAD. Patients within the highest quintile of PLTP activity revealed a 1.9-fold increase in risk for CAD compared with patients within the lowest quintile.Conclusions— These findings indicate that PLTP activity is positively and independently related to CAD and suggest that (1) prospective studies to evaluate this relationship are warranted and (2) PLTP should be considered a therapeutic target.
Linkage and Association Between Distinct Variants of the APOA1/C3/A4/A5 Gene Cluster and Familial Combined Hyperlipidemia
- Sophie Eichenbaum-Voline,
- Michael Olivier,
- Emma L. Jones,
- Rossitza P. Naoumova,
- Bethan Jones,
- Brian Gau,
- Hetal N. Patel,
- Mary Seed,
- D. John Betteridge,
- David J. Galton,
- Edward M. Rubin,
- James Scott,
- Carol C. Shoulders and
- Len A. Pennacchio
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 11 January 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— Combined hyperlipidemia is a common disorder, characterized by a highly atherogenic lipoprotein profile and a substantially increased risk of coronary heart disease. The purpose of this study was to establish whether variations of apolipoprotein A5 (APOA5), a newly discovered gene of lipid metabolism located 30 kbp downstream of the APOA1/C3/A4 gene cluster, contributes to the transmission of familial combined hyperlipidemia (FCHL).Methods and Results— We performed linkage and association tests on 128 families. Two independent alleles, APOA5^c.56G and APOC3^c.386G, of the APOA1/C3/A4/A5 gene cluster were overtransmitted in FCHL (P=0.004 and 0.007, respectively). This was paired with reduced transmission of the common APOA1/C3/A4/A5 haplotype (frequency 0.4461) to affected subjects (P=0.012). The APOA5^c.56G genotype accounted for 7.3% to 13.8% of the variance in plasma triglyceride levels in probands (P<0.004). The APOC3^c.386G genotypes accounted for 4.4% to 5.1% of the variance in triglyceride levels in FCHL spouses (P<0.007), suggesting that this allele marks a FCHL quantitative trait as well as representing a susceptibility locus for the condition.Conclusions— A combined linkage and association analysis establishes that variation at the APOA1/C3/A4/A5 gene cluster contributes to FCHL transmission in a substantial proportion of northern European families.
Inflammation-Sensitive Plasma Proteins and Incidence of Myocardial Infarction in Men With Low Cardiovascular Risk
- Gunnar Engström,
- Lars Stavenow,
- Bo Hedblad,
- Peter Lind,
- Patrik Tydén,
- Lars Janzon and
- Folke Lindgärde
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 23, Issue 121 December 2003

Abstract Export Citations PDF/EPUB

Abstract
Objective— Myocardial infarction (MI) is sometimes experienced by individuals without any traditional risk factor. This prospective study explored whether incidence of MI in nonsmoking, nondiabetic men with normal blood pressure and serum lipids is related to inflammation-sensitive plasma proteins (ISPs).Methods and Results— Five ISPs (α1-antitrypsin, haptoglobin, ceruloplasmin, fibrinogen, orosomucoid) were analyzed in 6075 men, 47±3.6 years old. A low-risk group (no traditional risk factor, n=1108) and a high-risk group (≥2 major risk factors, n=1011) were defined. Incidence of MI (n=227) was monitored over 18.1±4.3 years of follow-up. In the low-risk group, the age-adjusted relative risks (RRs) were 1.00 (reference), 1.9 (95% CI, 0.8 to 4.2), 1.8 (95% CI, 0.6 to 5.4), and 2.9 (95% CI, 1.05 to 8.1), respectively, for men with 0, 1, 2 and ≥3 ISPs in the top quartile (trend: P=0.03). In this group, the increased risk was observed only after ≥10 years of follow-up. In the high-risk group, the age-adjusted RRs were 1.00, 1.4 (95% CI, 0.9 to 2.2), 1.9 (95% CI, 1.2 to 3.1), and 2.0 (95% CI, 1.3 to 3.1), respectively, for men with 0, 1, 2, and ≥3 ISPs in the top quartile (trend: P=0.0004).Conclusion— Incidence of MI in nonsmoking, nondiabetic men with normal blood pressure and lipids was related to ISPs. The causes for this relationship remain to be explored.
Site Specificity of Atherosclerosis: Site-Selective Responses to Atherosclerotic Modulators
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 11 January 2004

Abstract Export Citations PDF/EPUB

Abstract
Atherosclerosis is a complex disease process that affects very specific sites of the vasculature. It is recognized that hemodynamic forces are largely responsible for dictating which vascular sites are either susceptible or resistant to developing atherosclerosis. In addition, a number of systemic and local factors also modulate the pathogenesis of the disease. By studying the development of atherosclerosis in mice, investigators have gained insights into the molecular mechanisms of this disease, although studies have largely focused on a single vascular site. Here, we review those recent studies in which vascular site-specific effects on atherosclerosis were reported when more than 1 site was examined. We assess the hypothesis that regional differences in the hemodynamic profile prime the endothelial phenotype to respond distinctly to such systemic risk factors as hypercholesterolemia, genetics, immune status, gender, and oxidative stress. Because a given treatment may differentially affect the development of atherosclerotic lesions throughout the vasculature, the sites chosen for study are critically important. By accounting for the complex interplay of factors that may operate at these different sites, a more complete understanding of the overriding mechanisms that control the initiation and progression of the atherosclerotic lesion may be realized.
Weight Reduction With Very-Low-Caloric Diet and Endothelial Function in Overweight Adults: Role of Plasma Glucose
- Maria Raitakari,
- Thomas Ilvonen,
- Markku Ahotupa,
- Terho Lehtimäki,
- Aimo Harmoinen,
- Pauli Suominen,
- Juhani Elo,
- Jaakko Hartiala and
- Olli T. Raitakari
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 11 January 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— Obesity is associated with endothelial dysfunction that may contribute to the development of atherosclerosis. We studied whether weight reduction improves endothelial function in overweight individuals.Methods and Results— Flow-mediated endothelium-dependent vasodilation of the brachial artery was measured in 67 adults (age: 46±7 years, body mass index: 35.2±5.4 kg/m²) before and after a 6-week weight reduction program induced by very-low-calorie diet (daily energy: 580 kcal/2.3 MJ). Caloric restriction reduced body weight from 101±18 to 90±17 kg. Flow-mediated vasodilation increased from 5.5%±3.7 to 8.8%±3.7% (P<0.0001). Nitrate-mediated vasodilation was not significantly affected. The improvement in flow-mediated dilation was associated with the reduction in plasma glucose concentration (P=0.0003). This relationship was independent of changes in weight, serum lipids, oxidized LDL, C-reactive protein, adiponectin, blood pressure, and insulin.Conclusions— Weight reduction with very-low-calorie diet improves flow-mediated vasodilation in obese individuals. This improvement is related to the reduction in plasma glucose concentration. These observations suggest that changes in glucose metabolism may determine endothelial vasodilatory function in obesity.
Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women
- ,
- Lori Mosca,
- Lawrence J. Appel,
- Emelia J. Benjamin,
- Kathy Berra,
- Nisha Chandra-Strobos,
- Rosalind P. Fabunmi,
- Deborah Grady,
- Constance K. Haan,
- Sharonne N. Hayes,
- Debra R. Judelson,
- Nora L. Keenan,
- Patrick McBride,
- Suzanne Oparil,
- Pamela Ouyang,
- Mehmet C. Oz,
- Michael E. Mendelsohn,
- Richard C. Pasternak,
- Vivian W. Pinn,
- Rose Marie Robertson,
- Karin Schenck-Gustafsson,
- Cathy A. Sila,
- Sidney C. Smith,
- George Sopko,
- Anne L. Taylor,
- Brian W. Walsh,
- Nanette K. Wenger and
- Christine L. Williams
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 31 March 2004

Export Citations PDF/EPUB

Abstract
Regional Body Composition Changes Exhibit Opposing Effects on Coronary Heart Disease Risk Factors
- Tomohiro Okura,
- Yoshio Nakata,
- Keisuke Yamabuki and
- Kiyoji Tanaka
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 51 May 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— We investigated how regional body composition measured by dual-energy X-ray absorptiometry (DXA) is associated with risk factors for coronary heart disease (CHD) during weight reduction in obese women.Methods and Results— Data were gathered from 128 overweight and obese women, aged 34 to 66 years, during a 14-week intervention study with diet and exercise. Regional (arms, legs, and trunk) fat tissue (FT) and lean soft tissue (LST) were measured by DXA. The FT change in legs correlated negatively with changes in diastolic blood pressure, low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), and the number of CHD risk factors per subject (r=−0.17, P<0.05 to −0.26, P<0.01) in response to weight reduction, whereas truncal FT change had positive correlations with changes in triglycerides, LDL-C, FPG, and the number of CHD risk factors per subject (r=0.17, P<0.05 to 0.25, P<0.01). LST change in legs correlated negatively with changes in systolic blood pressure, FPG, and the number of risk factors (r=−0.20 to −0.21, P<0.05).Conclusions— Regional body composition information is important for evaluating improvement of CHD risk factors during weight-reduction treatment for obesity; differential FTs had opposing effects on CHD risk factors during weight reduction in obese women.
Large Artery Stiffness Is Not Related to Plasma Cholesterol in Older Subjects with Hypertension
- Anthony M. Dart,
- Christoph D. Gatzka,
- James D. Cameron,
- Bronwyn A. Kingwell,
- Yu-Lu Liang,
- Karen L. Berry,
- Christopher M. Reid and
- Garry L. Jennings
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 51 May 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— Previous studies have demonstrated a prognostic role of large artery stiffness in hypertensive subjects and increased stiffness in subjects with coronary artery disease. Although plasma cholesterol is an established risk factor for cardiovascular disease, its relationship with large artery properties in a hypertensive population is unclear.Methods and Results— Plasma cholesterol and large artery properties were measured at baseline in a subset of participants of a randomized controlled trial (ANBP2) evaluating hypertension treatment in older (65 to 84 years) subjects. Noninvasive measures of large artery behavior were central augmentation index (AI), systemic arterial compliance (SAC), and transverse expansion of the aortic arch (aortic distensibility). Arterial waveforms acceptable for analysis were obtained in ≈80% of cases yielding valid measurements of AI in 868, SAC in 846, and aortic distensibility in 680 subjects. Mean total and high-density lipoprotein (HDL) concentrations were 5.5±1.0 and 1.4±0.5 mmol L⁻¹. Total and HDL cholesterol and AI were greater in females than males, whereas SAC and aortic distensibility were greater in males. In multiple regression analyses there were no significant associations between stiffness parameters and total or HDL cholesterol. Significant independent associations in such analyses were found for mean arterial blood pressure, gender, age, height, and heart rate, in keeping with previous findings.Conclusions— In the largest cohort of elderly hypertensive subjects studied to date, plasma cholesterol per se was not associated with large artery stiffness. Such independence from cholesterol increases the potential for artery stiffness measurements to additionally contribute to cardiovascular risk assessment in this population.
Decreased Number and Impaired Angiogenic Function of Endothelial Progenitor Cells in Patients With Chronic Renal Failure
- Jin-Ho Choi,
- Koung Li Kim,
- Wooseong Huh,
- Beom Kim,
- Jonghoe Byun,
- Wonhee Suh,
- Jidong Sung,
- Eun-Seok Jeon,
- Ha-Young Oh and
- Duk-Kyung Kim
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 71 July 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— Increased risk of cardiovascular disease in patients with chronic renal failure (CRF) has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) may play key roles. We hypothesized that altered EPC biology may contribute to the pathophysiology of CRF.Methods and Results— EPCs were isolated from CRF patients on maintenance hemodialysis (n=44) and from a normal control group (n=30). CRF patients showed markedly decreased numbers of EPC (44.6%) and colonies (75.3%) when compared with the controls (P<0.001). These findings were corroborated by 30.5% decrease in EPC migratory function in response to vascular endothelial growth factor (VEGF) (P=0.040) and 48.8% decrease in EPC incorporation into human umbilical vein endothelial cells (HUVEC) (P<0.001). In addition, Framingham’s risk factor score of both CRF (r=−0.461, P=0.010) and normal group (r=−0.367, P=0.016) significantly correlated with the numbers of EPC. Indeed, the number of circulating EPC was significantly lower in CRF patients than in normal group under the same burden of risk factors (P<0.001). A significant correlation was also observed between dialysis dose (Kt/V) and EPC incorporation into HUVEC (r=0.427, P=0.004).Conclusions— EPC biology, which is critical for neovascularization and the maintenance of vascular function, is altered in CRF. Our data strongly suggest that dysfunction of circulating EPC has a role in the progression of cardiovascular disease in patients with CRF.Our study shows that EPC is numerically and functionally impaired in CRF. This may contribute to the accelerated atherosclerosis and impaired angiogenesis observed in patients with CRF. Altered biology of EPC may therefore account for the increased cardiovascular disease risk in CRF.
Can Exercise Training With Weight Loss Lower Serum C-Reactive Protein Levels?
- Koichi Okita,
- Hirotaka Nishijima,
- Takeshi Murakami,
- Tatsuya Nagai,
- Noriteru Morita,
- Kazuya Yonezawa,
- Kenji Iizuka,
- Hideaki Kawaguchi and
- Akira Kitabatake
Arteriosclerosis, Thrombosis, and Vascular Biology Volume 24, Issue 101 October 2004

Abstract Export Citations PDF/EPUB

Abstract
Objective— C-reactive protein (CRP), an obesity-related inflammatory marker, is a promising predictor for cardiovascular disease and may be a mediator for atherogenesis. It has been reported that diet-induced weight loss lowered CRP levels. However, the effect of exercise training, another therapy that can reduce weight, on CRP is still unclear. We examined effects of exercise training with weight loss on CRP levels and conventional cardiovascular risks.Methods and Results— A total of 227 apparently healthy women were recruited, and 199 subjects (average age 52 years) completed a 2-month weight reduction program consisting of supervised aerobic exercises. After the program, weight was reduced from 65.8 to 62.8 kg (P<0.0001), and all conventional variables were remarkably improved. Similarly, CRP levels were significantly decreased, from 0.63 (0.28 to 1.19) to 0.41 (0.18 to 0.80) mg/L (P<0.0001). However, in contrast to other variables, the changes in CRP levels were not proportionally associated with the extent of weight reduction. In the quartile analysis of % weight reduction, the largest weight reduction quartile did not show significant decreases in CRP levels, whereas moderate quartile showed remarkable CRP decreases.Conclusions— Exercise training with weight reduction disproportionately lowered CRP levels. Considering inflammatory status, there might be an optimal pace of exercise with weight loss.C-reactive protein (CRP) is a promising predictor for cardiovascular disease and may be a mediator for atherogenesis. Although it has been reported that diet-induced weight loss lowered CRP levels, the effect of exercise training on CRP is still unclear. We examined effects of exercise training with weight loss on CRP levels, finding that exercise training with weight reduction disproportionately lowered CRP levels. Considering inflammatory status, there might be an optimal pace of exercise with weight loss.

Search

Narrow Results

Applied FiltersReset all

Journal Title

Article Type

Subject

Date Range

Author

Export Citation

Advanced

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Export Citation