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Gerardo Heiss

Publications and source records attributed to Gerardo Heiss.

At least 37 records · Page 2Linked to original sources

Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.

CONTEXT: Observational studies and polyp recurrence trials are not conclusive regarding the effects of a low-fat dietary pattern on risk of colorectal cancer, necessitating a primary prevention trial. OBJECTIVE: To evaluate the effects of a low-fat eating pattern on risk of colorectal cancer in postmenopausal women. DESIGN, SETTING, AND PARTICIPANTS: The Women's Health Initiative Dietary Modification Trial, a randomized controlled trial conducted in 48,835 postmenopausal women aged 50 to 79 years recruited between 1993 and 1998 from 40 clinical centers throughout the United States. INTERVENTIONS: Participants were randomly assigned to the dietary modification intervention (n = 19,541; 40%) or the comparison group (n = 29,294; 60%). The intensive behavioral modification program aimed to motivate and support reductions in dietary fat, to increase consumption of vegetables and fruits, and to increase grain servings by using group sessions, self-monitoring techniques, and other tailored and targeted strategies. Women in the comparison group continued their usual eating pattern. MAIN OUTCOME MEASURE: Invasive colorectal cancer incidence. RESULTS: A total of 480 incident cases of invasive colorectal cancer occurred during a mean follow-up of 8.1 (SD, 1.7) years. Intervention group participants significantly reduced their percentage of energy from fat by 10.7% more than did the comparison group at 1 year, and this difference between groups was mostly maintained (8.1% at year 6). Statistically significant increases in vegetable, fruit, and grain servings were also made. Despite these dietary changes, there was no evidence that the intervention reduced the risk of invasive colorectal cancer during the follow-up period. There were 201 women with invasive colorectal cancer (0.13% per year) in the intervention group and 279 (0.12% per year) in the comparison group (hazard ratio, 1.08; 95% confidence interval, 0.90-1.29). Secondary analyses suggested potential interactions with baseline aspirin use and combined estrogen-progestin use status (P = .01 for each). Colorectal examination rates, although not protocol defined, were comparable between the intervention and comparison groups. Similar results were seen in analyses adjusting for adherence to the intervention. CONCLUSION: In this study, a low-fat dietary pattern intervention did not reduce the risk of colorectal cancer in postmenopausal women during 8.1 years of follow-up. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.

Adenoma↗

Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.

CONTEXT: Multiple epidemiologic studies and some trials have linked diet with cardiovascular disease (CVD) prevention, but long-term intervention data are needed. OBJECTIVE: To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk. DESIGN, SETTING, AND PARTICIPANTS: Randomized controlled trial of 48,835 postmenopausal women aged 50 to 79 years, of diverse backgrounds and ethnicities, who participated in the Women's Health Initiative Dietary Modification Trial. Women were randomly assigned to an intervention (19,541 [40%]) or comparison group (29,294 [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998 in 40 US clinical centers; mean follow-up in this analysis was 8.1 years. INTERVENTION: Intensive behavior modification in group and individual sessions designed to reduce total fat intake to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received diet-related education materials. MAIN OUTCOME MEASURES: Fatal and nonfatal coronary heart disease (CHD), fatal and nonfatal stroke, and CVD (composite of CHD and stroke). RESULTS: By year 6, mean fat intake decreased by 8.2% of energy intake in the intervention vs the comparison group, with small decreases in saturated (2.9%), monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d). Low-density lipoprotein cholesterol levels, diastolic blood pressure, and factor VIIc levels were significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%, respectively; levels of high-density lipoprotein cholesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention vs comparison groups. The numbers who developed CHD, stroke, and CVD (annualized incidence rates) were 1000 (0.63%), 434 (0.28%), and 1357 (0.86%) in the intervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. The diet had no significant effects on incidence of CHD (hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI, 0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05). Excluding participants with baseline CVD (3.4%), the HRs (95% CIs) for CHD and stroke were 0.94 (0.86-1.02) and 1.02 (0.90-1.17), respectively. Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits. CONCLUSIONS: Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.

Aged↗

Long-term adherence with cardiovascular drug regimens.

BACKGROUND: An increasing number of medications are prescribed for patients with coronary artery disease, but poor adherence may limit realization of their benefits. OBJECTIVE: To characterize adherence to evidence-based cardiovascular medications prescribed at hospital discharge at 1 year. METHODS: We studied 1326 patients with coronary artery disease undergoing cardiac catheterization between 1998 and 2001. We examined adherence to angiotensin-converting enzyme (ACE) inhibitors, aspirin, beta-blockers (BBs), and statins by comparing baseline prescription at hospital discharge to self-reported medical regimen at 12 months. Patients who reported use of each cardiac medication at 1 year were considered adherent. Clinical and demographic predictors of nonadherence are described. RESULTS: The population had a mean age of 65.7 +/- 10.5 years, and 36% were women. At discharge, aspirin was prescribed in 95%, BBs in 86%, ACE inhibitors in 65%, and statins in 55%. The proportion of patients who discontinued medications was lowest for aspirin (18%) and BBs (22%) and highest for ACE inhibitors/angiotensin receptor blockers (28%) and statins (28%). Only 54% were adherent to all of their initial medications. Patients who discontinued medications were more likely to be older, women, unmarried, and less educated. Multivariable predictors of better adherence were higher mental health, education level, marital status, and no antidepressant use. A higher number of prescribed medications were associated with lower adherence to the recommended regimen. Insurance coverage and physical function did not correlate with adherence. CONCLUSIONS: Patients frequently stop medications within 1 year of prescription. Adherence is influenced by marital status, mental health, education, and total number of medications prescribed. Physicians need to be aware of patient factors which influence adherence to facilitate higher use of evidence-based medications.

Adrenergic beta-Antagonists↗

Kidney function and anemia as risk factors for coronary heart disease and mortality: the Atherosclerosis Risk in Communities (ARIC) Study.

BACKGROUND: Kidney failure causes anemia and is associated with a very high risk of coronary heart disease (CHD). Mildly to moderately decreased kidney function is far more common and also is associated with an elevated prevalence of anemia and CHD risk. Recent data suggest an even higher risk of CHD when both conditions are present. METHODS: We investigated the association of kidney dysfunction and anemia with CHD events (fatal or nonfatal CHD or coronary revascularization procedures) and CHD and all-cause mortality over 12 years of follow-up in 14971 adults aged 45 to 64 years in the ARIC Study. Glomerular filtration rate (GFR) was estimated from calibrated serum creatinine using the MDRD Study equation (< 30 mL/min per 1.73 m2 excluded, n = 32). Anemia was defined as hemoglobin level < 13.5 g/dL in men (648/6746, 9.6%) and < 12 g/dL in women (1049/8225, 12.8%). RESULTS: The prevalence of anemia was progressively higher at lower estimated GFR < 75 mL/min per 1.73 m2 (both P < .001) for both men and women. A total of 1635 (10.9%) participants had a CHD event, 360 (2.4%) died of CHD, and 1722 (11.5%) died of any cause during follow-up. After adjustment for known risk factors, including diabetes, lipid levels, blood pressure, and use of antihypertensive medication, decreased kidney function was associated with a higher risk of recurrent CHD events and mortality from CHD and all causes. These associations were significantly stronger among participants with anemia. The adjusted relative hazards of all-cause mortality associated with moderately decreased versus normal kidney function (GFR 30-59 vs > or = 90 mL/min per 1.73 m2) were 1.7 (95% CI 1.3-2.2) in the absence of anemia and 3.5 (95% CI 2.4-5.1) in the presence of anemia (P interaction = .001). CONCLUSIONS: The combination of moderately decreased kidney function and anemia is associated with an increased risk of CHD events and mortality, emphasizing the need to identify individuals with these conditions and evaluate interventions to treat anemia and slow the progression of chronic kidney disease.

Anemia↗

NOS3 polymorphisms, cigarette smoking, and cardiovascular disease risk: the Atherosclerosis Risk in Communities study.

OBJECTIVE: Endothelial nitric oxide synthase (NOS3) activity and cigarette smoking significantly influence endothelial function. We sought to determine whether cigarette smoking modified the association between NOS3 polymorphisms and risk of coronary heart disease or stroke. METHODS: All 1085 incident coronary heart disease cases, all 300 incident ischemic stroke cases, and 1065 reference individuals from the Atherosclerosis Risk in Communities study were genotyped for the T-786C and E298D polymorphisms in NOS3. Using a case-cohort design, associations between genotype/haplotype and disease risk were evaluated by multivariable proportional hazards regression. Multiplicative scale interaction testing evaluated the influence of cigarette smoking history at baseline on these associations. RESULTS: In Caucasians, association between E298D genotype and risk of coronary heart disease was significantly modified by current smoking status (interaction P=0.013), with the highest risk observed in smokers carrying the variant D298 allele relative to nonsmokers carrying two E298 alleles (adjusted hazard rate ratio 2.07, 95% confidence interval 1.39-3.07). In African-Americans, association between T-786C genotype and risk of ischemic stroke was significantly modified by pack-year smoking history (interaction P=0.037), with the highest risk observed in >or=20 pack-year smokers carrying the variant C-786 allele relative to <20 pack-year smokers carrying two T-786 alleles (adjusted hazard rate ratio 4.03, 95% confidence interval 1.54-10.6). CONCLUSIONS: An interaction between the E298D and T-786C polymorphisms in NOS3, cigarette smoking, and risk of incident coronary heart disease and ischemic stroke events appears to exist, suggesting a potential complex interplay between genetic and environmental factors and cardiovascular disease risk.

Black or African American↗

GIS approaches for the estimation of residential-level ambient PM concentrations.

Spatial estimations are increasingly used to estimate geocoded ambient particulate matter (PM) concentrations in epidemiologic studies because measures of daily PM concentrations are unavailable in most U.S. locations. This study was conducted to a) assess the feasibility of large-scale kriging estimations of daily residential-level ambient PM concentrations, b) perform and compare cross-validations of different kriging models, c) contrast three popular kriging approaches, and d) calculate SE of the kriging estimations. We used PM data for PM with aerodynamic diameter </= 10 microm (PM10) and aerodynamic diameter </= 2.5 microm (PM2.5) from the U.S. Environmental Protection Agency for the year 2000. Kriging estimations were performed at 94,135 geocoded addresses of Women's Health Initiative study participants using the ArcView geographic information system. We developed a semiautomated program to enable large-scale daily kriging estimation and assessed validity of semivariogram models using prediction error (PE) , standardized prediction error (SPE) , root mean square standardized (RMSS) , and SE of the estimated PM. National- and regional-scale kriging performed satisfactorily, with the former slightly better. The average PE, SPE, and RMSS of daily PM10 semivariograms using regular ordinary kriging with a spherical model were 0.0629, -0.0011, and 1.255 microg/m3, respectively ; the average SE of the estimated residential-level PM10 was 27.36 microg/m3. The values for PM2.5 were 0.049, 0.0085, 1.389, and 4.13 microg/m3, respectively. Lognormal ordinary kriging yielded a smaller average SE and effectively eliminated out-of-range predicted values compared to regular ordinary kriging. Semiautomated daily kriging estimations and semivariogram cross-validations are feasible on a national scale. Lognormal ordinary kriging with a spherical model is valid for estimating daily ambient PM at geocoded residential addresses.

Air Movements↗

Socioeconomic disadvantage and periodontal disease: the Dental Atherosclerosis Risk in Communities study.

OBJECTIVES: We used data from the Dental Atherosclerosis Risk in Communities study to examine whether individual- and neighborhood-level socioeconomic characteristics were associated with periodontal disease. METHODS: We assessed severe periodontitis with a combination of clinical attachment loss and pocket depth measures. Marginal logistic regression modeling was used to estimate the association between individual and neighborhood socioeconomic indicators and prevalence of severe periodontitis before and after control for selected covariates. Residual intraneighborhood correlations in outcomes were taken into account in the analyses. RESULTS: Individual-level income and education were associated with severe periodontitis among Whites and African Americans, and these associations remained significant after adjustment for age, gender, recruitment center, and neighborhood socioeconomic score. Low-income Whites residing in disadvantaged neighborhoods had 1.8-fold (95% confidence interval=1.2, 2.7) higher odds of having severe periodontitis than high-income Whites residing in advantaged neighborhoods. CONCLUSIONS: Individual income and education were associated with severe periodontitis independently of neighborhood socioeconomic circumstances. Although the association between neighborhood socioeconomic status and severe periodontitis was not statistically significant, poverty and residence in a disadvantaged neighborhood were associated with higher odds of severe periodontitis among Whites.

Atherosclerosis↗

Haplotype association analysis of AGT variants with hypertension-related traits: the HyperGEN study.

OBJECTIVE: Function of the renin-angiotensin system is important to human hypertension, but its genetic etiology remains elusive. We set out to examine a hypothesis that multiple genetic variants in the system act together in blood pressure regulation, via intermediate phenotypes such as blood pressure reactivity. METHODS: A sample of 531 hypertensive cases and 417 controls was selected from the HyperGEN study. Hypertension-related traits including blood pressure responses to challenges to math test, handgrip and postural change (mathBP, gripBP, and postBP), and body mass index (BMI) were analyzed for association with 10 single nucleotide polymorphisms (SNPs) in the angiotensinogen (AGT) gene. Single-marker and haplotype analyses were performed to examine the effects of both individual and multiple variants. Multiple-trait profiling was used to assess interaction of latent intermediate factors with susceptible haplotypes. RESULTS: In Blacks, two SNPs in exon 5 and 3'UTR showed significant association with gripBP, and two promoter SNPs were strongly associated with postBP. In Whites, only borderline association was found for 2 promoter SNPs with mathBP. Haplotype analyses in Blacks confirmed association with gripBP, and detected significant association of a haplotype to BMI (p=0.029). With the interactions modeled, haplotype associations found in Blacks remain significant, while significant associations to BMI (p=0.009) and gripSBP emerged in Whites. CONCLUSION: Genetic variants in regulatory regions of AGT showed strong association with blood pressure reactivity. Interaction of promoter and genic SNPs in AGT revealed collective action of multiple variants on blood pressure reactivity and BMI both in Blacks and in Whites, possibly following different pathways.

Black or African American↗

Retinal microvascular abnormalities and MRI-defined subclinical cerebral infarction: the Atherosclerosis Risk in Communities Study.

BACKGROUND AND PURPOSE: Retinal microvascular abnormalities reflect cumulative small vessel damage from elevated blood pressure and may reflect subclinical cerebral microvascular changes. We examined their associations with MRI-defined cerebral infarcts. METHODS: Population-based, cross-sectional study of 1684 persons 55 to 74 years of age without a history of clinical stroke, sampled from 2 US southeastern communities. Retinal photographs were obtained and graded for presence of retinal microvascular abnormalities, including arteriovenous nicking, focal arteriolar narrowing, retinal hemorrhages, soft exudates and microaneurysms. Photographs were also digitized, and retinal vessel diameters were measured and summarized as the arteriole-to-venule ratio (AVR). Cerebral MRI scans were graded for presence of cerebral infarct, defined as a lesion > or =3 mm diameter in a vascular distribution with typical imaging characteristics. RESULTS: There were a total of 183 MRI cerebral infarcts. After adjustment for age, gender, race, 6-year mean arterial blood pressure, diabetes, and other stroke risk factors, cerebral infarcts were associated with retinal microvascular abnormalities, with odds ratios 1.90 (95% CI, 1.25 to 2.88) for arteriovenous nicking, 1.89 (95% CI, 1.22 to 2.92) for focal arteriolar narrowing, 2.95 (95% CI, 1.30 to 6.71) for blot hemorrhages, 2.08 (95% CI, 0.69, 6.31) for soft exudates, 3.17 (95% CI, 1.05 to 9.64) for microaneurysms, and 1.74 (95% CI, 0.95 to 3.21) for smallest compared with largest AVR. In stratified analyses, these associations were only present in persons with hypertension. CONCLUSIONS: Retinal microvascular abnormalities are associated with MRI-defined subclinical cerebral infarcts independent of stroke risk factors. These data suggest that retinal photography may be useful for studying subclinical cerebrovascular disease in population-based studies.

Aged↗

The soluble epoxide hydrolase gene harbors sequence variation associated with susceptibility to and protection from incident ischemic stroke.

Stroke is the leading cause of severe disability and the third leading cause of death, accounting for one of every 15 deaths in the USA. We investigated the association of polymorphisms in the soluble epoxide hydrolase gene (EPHX2) with incident ischemic stroke in African-Americans and Whites. Twelve single nucleotide polymorphisms (SNPs) spanning EPHX2 were genotyped in a case-cohort sample of 1336 participants from the Atherosclerosis Risk in Communities (ARIC) study. In each racial group, Cox proportional hazard models were constructed to assess the relationship between incident ischemic stroke and EPHX2 polymorphisms. A score test method was used to investigate the association of common haplotypes of the gene with risk of ischemic stroke. In African-Americans, two common EPHX2 haplotypes with significant and opposing relationships to ischemic stroke risk were identified. In Whites, two common haplotypes showed suggestive indication of an association with ischemic stroke risk but, as in African-Americans, these relationships were in opposite direction. These findings suggest that multiple variants exist within or near the EPHX2 gene, with greatly contrasting relationships to ischemic stroke incidence; some associated with a higher incidence and others with a lower incidence.

Black or African American↗

Periodontal disease and coronary heart disease: a reappraisal of the exposure.

BACKGROUND: Results from studies relating periodontal disease to cardiovascular disease have been mixed. Residual confounding by smoking and use of clinical measures of periodontal disease rather than measures of infection have been 2 major criticisms. The aims of this study were to investigate relationships between prevalent coronary heart disease (CHD) and 2 exposures, (1) clinical periodontal disease and (2) IgG antibodies to 17 oral organisms, and to evaluate the role of smoking in these relationships. METHODS AND RESULTS: Our study is based on a subset of participants in the Atherosclerosis Risk in Communities (ARIC) Study, who received a complete periodontal examination during visit 4 (1996-1998). The exposures were periodontal status and serum IgG antibody levels against 17 periodontal organisms, and the outcome was prevalent CHD at visit 4. Multivariable analyses indicate that periodontal status is not significantly associated with CHD in either ever smokers or never smokers. Similar analyses evaluating antibodies indicate that high antibodies (above the median) to Treponema denticola (odds ratio [OR]=1.7; 95% CI, 1.2 to 2.3), Prevotella intermedia (OR=1.5; 95% CI, 1.1 to 2.0), Capnocytophaga ochracea (OR=1.5; 95% CI, 1.1 to 2.1), and Veillonella parvula (OR=1.7; 95% CI, 1.2 to 2.3) are significantly associated with CHD among ever smokers, whereas Prevotella nigrescens (OR=1.7; 95% CI, 1.1 to 2.6), Actinobacillus actinomycetemcomitans (OR=1.7; 95% CI, 1.2 to 2.7), and Capnocytophaga ochracea (OR=2.0; 95% CI, 1.3 to 3.0) were associated with CHD among never smokers. CONCLUSIONS: Clinical signs of periodontal disease were not associated with CHD, whereas systemic antibody response was associated with CHD in ever smokers and never smokers. These findings indicate that the quality and quantity of the host response to oral bacteria may be an exposure more relevant to systemic atherothrombotic coronary events than clinical measures.

Antibodies, Bacterial↗

Impaired lung function and subclinical atherosclerosis. The ARIC Study.

An association between reduced pulmonary function and increased risk of atherosclerotic vascular events has been reported. The mechanisms underlying this association are unknown, but are unlikely to be entirely due to smoking given the presence of the association among non-smokers. Few studies have examined the cross-sectional association between subclinical atherosclerosis and pulmonary function. In 14,000 adults in the ARIC Study, we examined the cross-sectional relationship between lung function, measured by the forced expiratory volume at 1s (FEV(1)), and three markers of subclinical atherosclerosis: ankle-brachial index (ABI), carotid intimal-medial thickness (IMT), and presence of carotid plaques. Mean FEV(1) was computed by ABI category, IMT category, or plaque status, in the full cohort and after stratification by smoking status, adjusted for age, gender, race, study center, height, height-squared, smoking, and pack years. Decreased FEV(1) was associated with decreased ABI and increased IMT in the full cohort and in each smoking group. Further adjustment for CVD risk factors did not alter the ABI association, but attenuated the IMT association, eliminating it in never smokers. Plaque was not associated with FEV(1). These findings suggest a complex relationship between FEV(1) and atherosclerotic vascular disease that invites further study.

Arteriosclerosis↗

An evaluation of the metabolic syndrome in the HyperGEN study.

BACKGROUND: In 2001 the National Cholesterol Education Program (NCEP) provided a categorical definition for metabolic syndrome (c-MetS). We studied the extent to which two ethnic groups, Blacks and Whites were affected by c-MetS. The groups were members of the Hypertension Genetic Epidemiology Network (HyperGEN), a part of the Family Blood Pressure Program, supported by the NHLBI. Although the c-MetS definition is of special interest in particular to the clinicians, the quantitative latent traits of the metabolic syndrome (MetS) are also important in order to gain further understanding of its etiology. In this study, quantitative evaluation of the MetS latent traits (q-MetS) was based on the statistical multivariate method factor analysis (FA). RESULTS: The prevalence of the c-MetS was 34% in Blacks and 39% in Whites. c-MetS showed predominance of obesity, hypertension, and dyslipidemia. Three and four factor domains were identified through FA, classified as "Obesity," "Blood pressure," "Lipids," and "Central obesity." They explained approximately 60% of the variance in the 11 original variables. Two factors classified as "Obesity" and "Central Obesity" overlapped when FA was performed without rotation. All four factors in FA with Varimax rotation were consistent between Blacks and Whites, between genders and also after excluding type 2 diabetes (T2D) participants. Fasting insulin (INS) associated mainly with obesity and lipids factors. CONCLUSIONS: MetS in the HyperGEN study has a compound phenotype with separate domains for obesity, blood pressure, and lipids. Obesity and its relationship to lipids and insulin is clearly the dominant factor in MetS. Linkage analysis on factor scores for components of MetS, in familial studies such as HyperGEN, can assist in understanding the genetic pathways for MetS and their interactions with the environment, as a first step in identifying the underlying pathophysiological causes of this syndrome.

Journal Article↗

The association of spatial T wave axis deviation with incident coronary events. The ARIC cohort.

BACKGROUND: Although current evidence suggests that the spatial T wave axis captures important information about ventricular repolarization abnormalities, there are only a few and discordant epidemiologic studies addressing the ability of the spatial T wave axis to predict coronary heart disease (CHD) occurrence. METHODS: This prospective study analyzed data from 12,256 middle-aged African American and white men and women, from the Atherosclerosis Risk in Communities Study (ARIC). Following a standardized protocol, resting standard 12-lead, 10-second electrocardiograms were digitized and analyzed with the Marquette GE program. The median follow-up time was 12.1 years; incident coronary heart disease comprised fatal and non-fatal CHD events. RESULTS: The incidence rate of CHD was 4.26, 4.18, 4.28 and 5.62 per 1000 person-years respectively, across the spatial T wave axis quartiles. Among women for every 10 degrees increase in the spatial T wave axis deviation, there was an estimated increase in the risk of CHD of 1.16 (95% CI 1.04-1.28). After adjustment for age, height, weight, smoking, hypertension, diabetes, QRS axis and minor T wave abnormalities, this hazard rate ratio for women fell to 1.03 (0.92-1.14). The corresponding crude and adjusted hazard ratios for men were 1.05 (95% CI 0.96-1.15) and 0.95 (0.86-1.04) respectively. CONCLUSIONS: In conclusion, this prospective, population-based, bi-ethnic study of men and women free of coronary heart disease at baseline shows that spatial T wave axis deviation is not associated with incident coronary events during long-term follow up. It is doubtful that spatial T wave axis deviation would add benefit in the prediction of CHD events above and beyond the current traditional risk factors.

Black or African American↗

Lower extremity arterial disease assessed by ankle-brachial index in a middle-aged population of African Americans and whites: the Atherosclerosis Risk in Communities (ARIC) Study.

BACKGROUND: Lower extremity arterial disease (LEAD) is one of the most common manifestations of atherosclerosis. Its epidemiologic characteristics have not been well described, particularly in African Americans. Our purpose was to estimate the prevalence of LEAD and its associations with cardiovascular risk factors in a biracial population of men and women aged 45 to 64 years. METHODS: We examined 15,173 African-American and white men and women who participated in the baseline examination (1987-1989) of the Atherosclerosis Risk in Communities (ARIC) Study. LEAD was defined by a resting ankle-brachial index (ABI), the ratio of ankle systolic blood pressure to brachial systolic pressure, of < or = 0.90. Cross-sectional analyses were used to determine the association of LEAD with cardiovascular risk factors. RESULTS: The age-adjusted prevalence of ABI < or = 0.90 was 3.1% in African-American men, 4.4% in African-American women, 2.3% in white men, and 3.2% in white women. Cigarette smoking was the single most important risk factor for prevalent LEAD. The odds ratio estimate for LEAD in ever smokers versus never smokers was 6.6 (95% confidence interval [CI]=2.0-21.5) in African-American men, 2.3 (95% CI=1.5-3.5) in African-American women, 10.4 (95% CI=3.8-28.3) in white men, and 1.9 (95% CI=1.4-2.6) in white women, after adjustment for age, LDL cholesterol, hypertension, and diabetes. Prevalent LEAD was also associated with hypertension, diabetes, and higher concentrations of total cholesterol, triglycerides, LDL-cholesterol, and fibrinogen, and lower concentrations of HDL cholesterol, but the associations were not always significant across race/ethnic and gender groups. The associations of LEAD with plasma lipids were generally stronger in African Americans than whites. CONCLUSIONS: The prevalence of LEAD appears to be higher in African Americans than whites. Elevations in traditional cardiovascular risk factors are associated with a higher prevalence of LEAD across race/ethnic and gender groups.

Black or African American↗

Further evidence of a quantitative trait locus on chromosome 18 influencing postural change in systolic blood pressure: the Hypertension Genetic Epidemiology Network (HyperGEN) Study.

BACKGROUND: Postural change in systolic blood pressure (SBP) is prospectively associated with several disease outcomes including hypertension, stroke, and coronary heart disease. The objective of this study was to characterize further a possible quantitative trait locus on chromosome 18q21 influencing SBP response to a postural challenge. METHODS: A prior genome scan of postural SBP response in 636 subjects of white ethnicity from 285 hypertensive sibships in the Hypertension Genetic Epidemiology Network (HyperGEN) indicated suggestive evidence for linkage on chromosome 18q21. This study included a de novo set of 452 African American pedigrees from the HyperGEN study and an expanded set of 372 white pedigrees. Variance components linkage analysis of postural SBP change was conducted using microsatellite markers on chromosome 18, and association studies were performed with a common single nucleotide polymorphism (variant 13) in the gene encoding NEDD4L, a key regulator of fine sodium reabsorption in the distal nephron. RESULTS: Combined analysis of all white and African American pedigrees yielded a LOD score of 4.25 at 80 cM on chromosome 18q21, with at least nominal evidence of linkage at this position in both white (LOD: 3.43) and African American (LOD: 1.14) subjects. Postural SBP response was associated with variant 13 of the NEDD4L in a subset of white subjects taking medications effective in treating sodium volume-dependent hypertension (alpha1-blockers, calcium channel blockers, and/or diuretics). CONCLUSION: These data provide further evidence for a quantitative trait locus on chromosome 18q21 influencing postural change in SBP.

Adult↗

A summary of the effects of antihypertensive medications on measured blood pressure.

BACKGROUND: Epidemiologic analysis of family data on blood pressure (BP) is often compromised by the effects of antihypertensive medications. A review of numerous clinical trials that investigated the effects of BP-lowering medications is summarized here. METHODS: Published clinical trials, including 137 clinical trials with monodrug therapies and 28 clinical trials of combination drug therapies with a total of 11,739 participants, were reviewed from PubMed. Six major classes/groups of antihypertensive medications were categorized by ethnicity, including angiotensin-converting enzyme (ACE) inhibitors, alpha1-blockers, cardioselective beta-blockers (beta1-blockers), calcium channel blockers, thiazide and thiazide-like diuretics, and loop diuretics. RESULTS: Using sitting or supine BP, for ethnic groups combined, monodrug therapy with ACE inhibitors showed a weighted average effect of lowering the systolic and diastolic BP by 12.5/9.5 mm Hg; alpha1-blockers by 15.5/11.7 mm Hg; beta1-blockers by 14.8/12.2 mm Hg; calcium channel blockers by 15.3/10.5 mm Hg; thiazide diuretics by 15.3/9.8 mm Hg; and loop diuretics by 15.8/8.2 mm Hg. However, ACE inhibitors, alpha1-blockers, and beta1-blockers were less effective in African Americans than in non-African Americans, whereas calcium channel blockers, thiazide diuretics, and loop diuretics were more effective in African Americans than in non-African Americans. For two-drug combination therapy with ethnic groups combined, the BP-lowering effect of the second medication, when compared to its effect as monodrug therapy, was 84% and 65% for systolic and diastolic BP, respectively. CONCLUSIONS: The BP-lowering effects reported here may be used to impute the pretreatment BP levels, which can improve the information content and hence the power of epidemiologic analysis in studies where use of antihypertensive medications is a confounding factor in the BP measurements.

Adult↗

Associations between IgG antibody to oral organisms and carotid intima-medial thickness in community-dwelling adults.

AIMS: The aims of this study are to describe the relationships between IgG antibodies to 17 oral organisms and atherosclerosis as indexed by carotid intima-medial wall thickness (IMT) and to evaluate the role of smoking. METHODS AND RESULTS: Our study is based on a subset of participants in the Atherosclerosis Risk in Communities (ARIC) Study, who received a complete periodontal examination during visit 4 (1996-1998). The outcome was mean carotid IMT>/=1mm assessed by B-mode ultrasound. The exposures were serum IgG antibody levels against 17 periodontal organisms using a whole bacterial checkerboard immunoblotting technique. Evaluation of all 17 antibodies indicated that antibody to Campylobacter rectus resulted in the best-fitting model (OR=2.3, 95% CI=1.83-2.84) and individuals with both high C. rectus and Peptostreptococcus micros titers had almost twice the prevalence of IMT>/=1mm than those with only a high C. rectus antibody (8.3% versus 16.3%). Stratification by smoking indicated that all microbial models significant for smokers were also significant for never smokers except for Porphyromonas gingivalis (p=0.08). CONCLUSIONS: This is the first study to report a relationship between IgG antibody reactive to oral organisms and subclinical atherosclerosis with significant relationships evident in both ever and never smokers.

Antibodies, Anti-Idiotypic↗