Showing papers by "Gerardo Heiss published in 1999"
TL;DR: Markers of inflammation are associated with the development of diabetes in middle-aged adults, and autoimmunity may partly explain these associations, which probably reflect the pathogenesis of type 2 diabetes.
1,021 citations
TL;DR: It is suggested that lower arterial elasticity is related to the development of hypertension, independent of established risk factors for hypertension and the level of baseline blood pressure.
Abstract: Decreased elasticity in large and medium-sized arteries has been postulated to be associated with cardiovascular diseases. We prospectively examined the relation between arterial elasticity and the development of hypertension over 6 years of follow-up in a cohort of 6992 normotensive men and women aged 45 to 64 years at baseline from the biracial, population-based Atherosclerosis Risk in Communities (ARIC) Study. Arterial elasticity was measured from high-resolution B-mode ultrasound examination of the left common carotid artery as adjusted arterial diameter change (in micrometers, simultaneously adjusted for diastolic blood pressure, pulse pressure, pulse pressure squared, diastolic arterial diameter, and height), Peterson's elastic modulus (in kilopascals), Young's elastic modulus (in kilopascals), and beta stiffness index. Incident hypertension (n=551) was defined as systolic blood pressure >/=160 mm Hg, diastolic blood pressure >/=95 mm Hg, or the use of antihypertensive medication at a follow-up examination conducted every 3 years. The age-, ethnicity-, center-, gender-, education-, smoking-, heart rate-, and obesity-adjusted means (SE) of baseline adjusted arterial diameter change, Peterson's elastic modulus, Young's elastic modulus, and beta stiffness index were 397 (5), 148 (2.0), 787 (12.7), and 11.43 (0.16), respectively, in persons who developed hypertension during follow-up, in contrast to 407 (1), 124 (0.6), 681 (3.7), and 10.34 (0.05), respectively, for persons who did not. The similarly adjusted cumulative incident rates of hypertension from the highest to the lowest quartiles of arterial elasticity were 6.7%, 8.0%, 7.3%, and 9.6%, respectively, when measured by adjusted arterial diameter change (P<0.01). One standard deviation decrease in arterial elasticity was associated with 15% greater risk of hypertension, independent of established risk factors for hypertension and the level of baseline blood pressure. These results suggest that lower arterial elasticity is related to the development of hypertension.
530 citations
TL;DR: Diabetes is a strong risk factor for ischemic stroke and aspects of insulin resistance, as reflected by elevated waist-to-hip ratios and elevated fasting insulin levels, may also contribute to a greater risk of isChemic stroke.
Abstract: OBJECTIVE: We tested the hypothesis that diabetes, body fat distribution, and (in nondiabetic subjects) fasting insulin levels are positively associated with ischemic stroke incidence in the general population. RESEARCH DESIGN AND METHODS: As part of the Atherosclerosis Risk in Communities (ARIC) Study, we measured diabetes by using fasting glucose criteria, waist and hip circumferences, and fasting insulin levels with a radioimmunoassay in > 12,000 adults aged 45-64 years who had no cardiovascular disease at baseline. We followed them for 6-8 years for ischemic stroke occurrence (n = 191). RESULTS: After adjustment for age, sex, race, ARIC community, smoking, and education level, the relative risk of ischemic stroke was 3.70 (95% CI 2.7-5.1) for diabetes, 1.74 (1.4-2.2) for a 0.11 increment of waist-to-hip ratio, and 1.19 (1.1-1.3) for a 50-pmol/l increment of fasting insulin among nondiabetic subjects. Ischemic stroke incidence was not statistically significantly associated with BMI (comparably adjusted relative risk = 1.15, 95% CI 0.97-1.36). With adjustment for other stroke risk factors (some of which may mediate the effects of diabetes, fat distribution, and hyperinsulinemia), the relative risks for diabetes, waist-to-hip ratio, and fasting insulin level were 2.22 (95% CI 1.5-3.2), 1.08 (0.8-1.4), and 1.14 (1.01-1.3), respectively. CONCLUSIONS: Diabetes is a strong risk factor for ischemic stroke. Aspects of insulin resistance, as reflected by elevated waist-to-hip ratios and elevated fasting insulin levels, may also contribute to a greater risk of ischemic stroke.
344 citations
TL;DR: Factor VIII and other hemostasis variables are associated with the development of diabetes in middle-aged adults and support a role for inflammation and, particularly in women, endothelial dysfunction in the pathogenesis of type 2 diabetes.
Abstract: OBJECTIVE: Our objective was to evaluate whether selected hemostasis variables, some of which may reflect inflammation or endothelial dysfunction, are independently associated with the development of diabetes. RESEARCH DESIGN AND METHODS: We studied a biethnic cohort of 12,330 men and women, 45-64 years of age, of the Atherosclerosis Risk in Communities Study. New cases of diabetes were diagnosed by a reported physician diagnosis, hypoglycemic medication use, or a casual or fasting serum glucose level of > or = 11.1 or > or = 7 mmol/l, respectively. RESULTS: Over an average follow-up of 7 years, 1,335 new cases of diabetes were detected. The odds ratios (4th versus 1st quartile) of developing diabetes, adjusted by logistic regression for age, sex, race, study center, family history of diabetes, fasting glucose, physical activity, and smoking, were 1.2 (95% CI 1.0-1.5) for fibrinogen and 1.4 (1.1-1.6) for factor VII. Associations for factor VIII, von Willebrand factor, and activated partial thromboplastin time were found to be 1.8 (1.3-2.3), 1.4 (1.1-1.8), and 0.63 (0.49-0.82), respectively, in women. Although further adjustment for BMI and waist-to-hip ratio diminished the relationships, a highly statistically significant association (P = 0.001) remained for factor VIII (1.6 [1.2-2.1]) in women. CONCLUSIONS: Factor VIII and other hemostasis variables are associated with the development of diabetes in middle-aged adults. These findings support a role for inflammation and, particularly in women, endothelial dysfunction in the pathogenesis of type 2 diabetes.
117 citations
TL;DR: Cardiovascular morbidity, sociodemographic factors, and cigarette smoking were associated with the magnitude and direction of the postural change in DeltaSBP.
Abstract: The epidemiology of a common measure of cardiovascular reactivity, the change in systolic blood pressure (DeltaSBP) from the supine to the standing position, is described in a cohort of 13 340 men and women aged 45 to 65 years enrolled in the Atherosclerosis Risk in Communities (ARIC) Study. The distribution of DeltaSBP was found to be symmetrical and unimodal, with a mean value near zero (-0.45 mm Hg). The range of DeltaSBP was from -63.2 to 54.3 mm Hg, and the standard deviation was 10.8. Stratification of DeltaSBP by race and gender shows a slight shift in distribution toward higher values for black men and women. DeltaSBP was categorized into deciles. Participants in the top 30% and bottom 30% of the distribution were compared with individuals in the middle 40% of the distribution, who had little or no change in SBP on standing. Participants in the bottom 30% (ie, SBP decreased on standing) were significantly older, had a greater prevalence of hypertension and peripheral vascular disease, had higher values of SBP, and had more cigarette-years of smoking. Among participants in the top 30% (ie, SBP increased on standing), a significantly larger proportion were black, mean seated SBP was higher, and the predicted risk of developing coronary heart disease after 8 years was greater. The response of SBP to change in posture showed considerable variability in a population sample of middle-aged adults. Cardiovascular morbidity, sociodemographic factors, and cigarette smoking were associated with the magnitude and direction of the postural change.
114 citations
TL;DR: The results suggest that the high triglyceride-low HDL cholesterol pattern is involved in the transition from atheroma to atherothrombosis, and that control of this pattern may be important in persons with detectable subclinical disease.
Abstract: Major risk factors for coronary heart disease are also associated with early carotid artery thickening, but no studies have yet examined patterns of risk factors to see whether they differ for the two outcomes. Assuming similar pathogenesis for both coronary and carotid atherosclerosis, one could interpret risk factor pattern differences as relating to differences in staging, i.e., early atheroma versus later stenotic or occlusive atherothrombosis. This study included 12,193 Atherosclerosis Risk in Communities Study participants aged 45-64 years who were free of clinical cardiovascular disease in 1987-1989, in whom 420 myocardial infarctions or coronary heart disease deaths occurred over the next 6 years. Plasma low density lipoprotein cholesterol, systolic blood pressure, and smoking were major risk factors for both outcomes. Compared with these factors, triglycerides and high density lipoprotein (HDL) cholesterol were associated only weakly with carotid atherosclerosis but were associated strongly with coronary heart disease incidence. No other risk factors, including those associated with diabetes mellitus, hemostasis, and inflammation, differed in their relative contribution to the two outcomes. These results suggest that the high triglyceride-low HDL cholesterol pattern is involved in the transition from atheroma to atherothrombosis, and that control of this pattern may be important in persons with detectable subclinical disease.
100 citations
TL;DR: The results from this population-based study suggest that lower pulmonary function is associated with subclinical cerebral abnormalities, and patterns of association were found among current smokers.
68 citations
TL;DR: The results are consistent with the concept of an aetiological heterogeneity for hypertension and may explain previously reported inconsistent findings on the association of insulin with incident hypertension.
Abstract: OBJECTIVE The prospective association of insulin and hypertension has been under debate in the context of the development of the insulin resistance or multiple metabolic syndrome. We examined the predictive associations of fasting serum insulin with incident hypertension occurring alone or as part of the multiple metabolic syndrome. DESIGN Analyses were restricted to 5221 middle-aged participants of the Atherosclerosis Risk in Communities Study cohort who were free of component disorders of the multiple metabolic syndrome (hypertension; diabetes; high triglycerides and/or low HDL cholesterol (dyslipidaemias)) at baseline. OUTCOME A total of 1018 individuals developed hypertension, 801 in the absence of components of the metabolic syndrome and 217 in combination with diabetes or dyslipidaemias, between 1987 and 1993. RESULTS Elevated fasting insulin (top quartile versus lowest quartile) was associated with overall incident hypertension in European Americans [hazard rate ratio (HRR) 2.0, 95% confidence interval (CI) 1.7-2.4] but the results were inconclusive in African Americans (HRR 1.3, 95% CI 0.9-1.8) after adjustment for age, gender and study centre. Among European Americans, body mass index and abdominal girth only partly explained the observed association. Elevated fasting insulin was more strongly predictive of hypertension occurring as a component of the multiple metabolic syndrome (HRR 2.4, 95% CI 1.5-3.9) than of hypertension occurring alone (HRR 1.3, 95% CI 1.0-1.7) adjusting statistically for age, gender, study centre, body mass index and abdominal girth. CONCLUSIONS The results are consistent with the concept of an aetiological heterogeneity for hypertension and may explain previously reported inconsistent findings on the association of insulin with incident hypertension.
57 citations
TL;DR: Data patterns suggest the absence of a race effect onMaximum inspiratory pressure (MIP), an indicator of inspiratory muscle strength, is reported on 13,005 African-American and white participants from the Atherosclerosis Risk in Communities Study.
Abstract: Maximum inspiratory pressure (MIP), an indicator of inspiratory muscle strength, is reported on 13,005 African-American and white participants from the Atherosclerosis Risk in Communities Study Sex-specific associations between MIP and age, anthropometric measures, physical activity, health status, smoking status, and education level are presented In this cohort of subjects 47 to 68 yr of age, MIP decreased 093 cm H2O (p
53 citations
TL;DR: The associations between carotid IMT and LDL cholesterol, HDL cholesterol, and other lipid measurements were significantly weaker in African Americans than whites, and analysis of many potential cofactors have not provided an explanation for the weaker association.
24 citations
TL;DR: Using parameters for major gene transmission estimated in the segregation analysis, LDL‐C showed no linkage to the LDL receptor gene (LDLR), nor to the apolipoprotein E gene (APOE), norto the cholesterol 7α‐hydroxylase gene (CYP7A1), indicating the major gene effect influencing mild elevation in LDL‐ C is not explained by any of these candidate loci.
Abstract: Studies of rare Mendelian disorders of low density lipoprotein cholesterol (LDL-C) metabolism have identified specific genetic mutations in the LDL receptor and apolipoprotein B. Although these rare mutations account for a small proportion of LDL-C variation, twin and adoption studies indicate that at least 50% of the overall LDL-C observed variation is genetically determined. In a heterogeneous sample of 3227 subjects from the NHLBI Family Heart Study collected from four US centres, we find evidence for a common major gene accounting for mild elevations (1.25 standard deviations) in LDL-C. The analysis favored a recessive model with a frequency of 0.52 for the gene influencing elevated LDL-C, phenotypic means of 113 mg/dl for the normal genotypes and 146 mg/dl for the abnormal genotype, and a significant polygenic heritability. This statistically-inferred major gene accounted for 24% of the variation in LDL-C, with polygenes accounting for another 28% of the variation. Using parameters for major gene transmission estimated in the segregation analysis, LDL-C showed no linkage to the LDL receptor gene ( LDLR ), nor to the apolipoprotein E gene ( APOE ), nor to the cholesterol 7α-hydroxylase gene ( CYP7A1 ), indicating the major gene effect influencing mild elevation in LDL-C is not explained by any of these candidate loci.