Blood pressure and pulse responses to three stressors: associations with sociodemographic characteristics and cardiovascular risk factors.

Cardiovascular reactivity is hypothesized to increase the risk of hypertension and other CVD-related conditions. However, studies to date are inconclusive. We compared the association of blood pressure and pulse responses to three stressors (postural challenge, handgrip test, mental arithmetic) with sociodemographic characteristics and CVD risk factors. We included 782 participants from the Hypertension Genetic Epidemiology Study. Blood pressure and pulse responses to stressors were defined as the difference between post- and pre-stress measurements. Stepwise regression analyses examined change in SBP and pulse in response to stressors as a function of sociodemographic and CVD risk factors. Age, race, and gender were forced into models and other variables (education, BMI, waist circumference, resting SBP and DBP, cigarette smoking, LDL and HDL cholesterol, glucose, and antihypertensive medications (beta-blockers, calcium channel blockers, diuretics, ace inhibitors)) were retained if P<0.10. Age was a significant predictor of SBP response to all stressors. The SBP response to a change in posture was not related to other variables. The SBP response to mental arithmetic was significantly higher among men, those with larger waists, higher SBP, beta-blocker users, and lower among smokers. SBP response to the handgrip was significantly higher among those with higher SBP and beta-blocker users. Similarly, the association of the pulse response to the risk factors varied considerably across the stressors. Overall, the socio-demographic and CVD risk factors accounted for between 9 and 14% of the variance in the SBP response to the stressors and from between 4 and 12% of the variance in the pulse response to the three stressors. The associations between sociodemographic and CVD risk factors and the SBP and pulse response to stress were modest and inconsistent across stressors. The findings suggest that cardiovascular reactivity is a concept that needs to be defined in reference to specific stressors so that mechanisms leading to responses can be better understood.

Association between the blood pressure response to a change in posture and the 6-year incidence of hypertension: prospective findings from the ARIC study.

The association between the blood pressure response to a change from the supine to the standing position and the 6-year incidence of hypertension was studied in a bi-ethnic, middle-aged cohort of 6951 normotensive men and women free of coronary heart disease at baseline. Postural change in systolic blood pressure (SBP) was categorized into deciles, and the middle four deciles served as the referent (no change) group. In unadjusted analyses, the incidence of hypertension was higher among both those with SBP increases and decreases relative to those in the referent group. Associations were modestly attenuated after controlling for age, ethnicity, and gender and cardiovascular disease risk factors. However, after adjustment for baseline, seated SBP, a modest association with incident hypertension persisted only for SBP decreases. Orthostatic hypotension (upon standing) was associated with incident hypertension and isolated systolic hypertension and, unexpectedly, this increased risk was highest among those with the lowest levels of baseline, resting SBP.

Hypertensive retinopathy and incident coronary heart disease in high risk men.

BACKGROUND/AIM: Although routine ophthalmoscopy is recommended in the evaluation of people with hypertension, the prognostic significance of retinopathy is unknown. The purpose of this study is to determine if hypertensive retinopathy predicts coronary heart disease (CHD). METHODS: A prospective cohort study involving 560 hypertensive, hyperlipidaemic, middle aged men enrolled in the Lipid Research Clinic's Coronary Primary Prevention Trial. Signs of hypertensive retinopathy (generalised and focal arteriolar narrowing, arteriovenous nicking, widened arteriolar light reflex, retinal haemorrhage and exudates, microaneurysms, and disc swelling) were evaluated by direct funduscopy during a baseline examination by study physicians. Incident CHD events were ascertained from hospital records, necropsy reports, and death certificates, and reviewed by a masked panel of cardiologists. RESULTS: There were 51 definite CHD events (definite CHD deaths or myocardial infarctions) during a median follow up of 7.8 years. After adjusting for age, blood pressure, electrocardiographic manifestations of left ventricular hypertrophy, cholesterol levels and treatment, glucose and creatinine levels, and smoking status in proportional hazards analysis, the presence of hypertensive retinopathy predicted a doubling of the risk of definite CHD events (relative risk 2.1; 95% confidence interval (CI) 1.0 to 4.2 ). The presence of either generalised or focal arteriolar narrowing predicted almost a tripling of the risk (relative risk 2.9; 95% CI 1.3 to 6.2). Associations were similar for stage 1 hypertension (systolic and diastolic blood pressures of 140-159 and 90-99 mm Hg, respectively) and for other CHD end points. CONCLUSION: Hypertensive retinopathy predicts CHD in high risk men, independent of blood pressure and CHD risk factors. The data support the concept that retinal microvascular changes are markers of blood pressure damage and may be useful in risk stratification and in the tailoring of hypertension treatment decisions.

Associations between weight gain and incident hypertension in a bi-ethnic cohort: the Atherosclerosis Risk in Communities Study.

OBJECTIVE: To examine associations between weight gain and changes in blood pressure and the incidence of hypertension in four ethnicity-gender groups. DESIGN: Longitudinal closed cohort studied over an average of 6 y. SUBJECTS: Total of 9309 white and African-American men and women 45-64 y of age who participated in the Atherosclerosis Risk in Communities (ARIC) Study. METHODS: Weight and blood pressure were measured at baseline and after an average of 3 and 6 y of follow-up. Proportional hazard models with weight gain as a time-dependent variable were used to examine the association between weight gain and changes in blood pressure and hypertension. Multivariate models were used with baseline SBP, DBP, age, BMI, height, WHR, smoking, physical activity, education, caloric intake, fat intake and study center as covariates. RESULTS: Weight gain was associated with increases in SBP and DBP in all groups. Hazard ratios for hypertension associated with 1 kg annual weight gain were 1.36 (95% CI, 1.29, 1.45) in white women, 1.12 (95% CI, 1.03, 1.21) in African-American women, 1.35 (95% CI, 1.27, 1.43) in white men and 1.43 (95% CI, 1.27,1.61) in African-American men. CONCLUSION: Weight gain was associated with increased blood pressure and increased incidence of hypertension. The association was weaker among African-American women compared to other ethnicity-gender groups.

Sensitivity and specificity of anthropometrics for the prediction of diabetes in a biracial cohort.

OBJECTIVE: To evaluate the ability of body mass index, waist circumference, waist-to-hip ratio, and combinations of these variables to discriminate individuals who will develop diabetes in adulthood. RESEARCH METHODS AND PROCEDURES: Data were from 45- to 64-year-old men and women who were members of the Atherosclerosis Risk in Communities cohort. The analysis sample consisted of 12,814 African American and white participants who were free of diabetes at baseline. Body mass index, waist circumference, waist-to-hip ratio, and diabetes incidence (defined as one glucose measure > or =126 mg/dL after fasting for at least 8 hours, one nonfasting glucose measure > or =200 mg/dL, and self-report of diabetes or report of taking medication for diabetes). RESULTS: 1515 new cases of diabetes were identified over the 9-year follow-up. Areas under receiver operating characteristic curves ranged from 0.66 to 0.73 for single measures. The curves were smooth, with no indication of a threshold. Waist tended to have the highest receiver operating characteristic statistic in all groups, but differences were small. DISCUSSION: The three anthropometric indices tested were approximately equivalent in their ability to predict diabetes. Sensitivity and specificities differed among ethnic and gender groups.

Effects of an angry temperament on coronary heart disease risk : The Atherosclerosis Risk in Communities Study.

The objective of the study was to determine which component of an anger-prone personality more strongly predicts coronary heart disease (CHD) risk. Proneness to anger, as assessed by the Spielberger Trait Anger Scale, is composed of two distinct subcomponents-anger-temperament and anger-reaction. Participants were 12,990 middle-aged Black men and women and White men and women from the Atherosclerosis Risk in Communities Study who were followed for the occurrence of acute myocardial infarction (MI)/fatal CHD, silent MI, or cardiac revascularization procedures (average = 53 months; maximum = 72 months) through December 31, 1995. Among normotensive persons, a strong, angry temperament (tendency toward quick, minimally provoked, or unprovoked anger) was associated with combined CHD (acute MI/fatal CHD, silent MI, or cardiac revascularization procedures) (multivariate-adjusted hazard ratio = 2.10, 95% confidence interval: 1.34, 3.29) and with 'hard" events (acute MI/fatal CHD) (multivariate adjusted hazard ratio = 2.28, 95% confidence interval: 1.29, 4.02). CHD event-free survival among normotensives who had a strong, angry temperament was not significantly different from that of hypertensives at either level of anger. These data suggest that a strong, angry temperament rather than anger in reaction to criticism, frustration, or unfair treatment places normotensive, middle-aged persons at increased risk for cardiac events and may confer a CHD risk similar to that of hypertension.

Neighborhood of residence and incidence of coronary heart disease.

BACKGROUND: Where a person lives is not usually thought of as an independent predictor of his or her health, although physical and social features of places of residence may affect health and health-related behavior. METHODS: Using data from the Atherosclerosis Risk in Communities Study, we examined the relation between characteristics of neighborhoods and the incidence of coronary heart disease. Participants were 45 to 64 years of age at base line and were sampled from four study sites in the United States: Forsyth County, North Carolina; Jackson, Mississippi; the northwestern suburbs of Minneapolis; and Washington County, Maryland. As proxies for neighborhoods, we used block groups containing an average of 1000 people, as defined by the U.S. Census. We constructed a summary score for the socioeconomic environment of each neighborhood that included information about wealth and income, education, and occupation. RESULTS: During a median of 9.1 years of follow-up, 615 coronary events occurred in 13,009 participants. Residents of disadvantaged neighborhoods (those with lower summary scores) had a higher risk of disease than residents of advantaged neighborhoods, even after we controlled for personal income, education, and occupation. Hazard ratios for coronary events in the most disadvantaged group of neighborhoods as compared with the most advantaged group--adjusted for age, study site, and personal socioeconomic indicators--were 1.7 among whites (95 percent confidence interval, 1.3 to 2.3) and 1.4 among blacks (95 percent confidence interval, 0.9 to 2.0). Neighborhood and personal socioeconomic indicators contributed independently to the risk of disease. Hazard ratios for coronary heart disease among low-income persons living in the most disadvantaged neighborhoods, as compared with high-income persons in the most advantaged neighborhoods were 3.1 among whites (95 percent confidence interval, 2.1 to 4.8) and 2.5 among blacks (95 percent confidence interval, 1.4 to 4.5). These associations remained unchanged after adjustment for established risk factors for coronary heart disease. CONCLUSIONS: Even after controlling for personal income, education, and occupation, we found that living in a disadvantaged neighborhood is associated with an increased incidence of coronary heart disease.

Multi-country comparison of plasma lipid relationship to years of schooling in men and women.

BACKGROUND: The association between coronary heart disease (CHD) and social status has differed among societies in strength and direction. As years of schooling is a major determinant of socioeconomic status and dyslipidaemia a major CHD determinant, the purpose of this investigation is to estimate the association of years of schooling with plasma lipids and lipoproteins among samples from five countries representing different cultures, socio-political systems and stages of economic development. METHODS: Men and women from Chinese, Polish, Russian, Israeli and US samples were studied. Years of schooling were analysed both as a multi-category ordinal variable and divided into two strata: less than the equivalent of high school and greater than or equal to high school equivalence. Fasting plasma cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol and triglycerides were compared across years of schooling strata within each country. Lipid levels were computed unadjusted and then adjusted for age and lipid risk factor variables. RESULTS: Total cholesterol, LDL cholesterol, and triglycerides varied directly with years of schooling in Chinese, Polish and Russian men, and in contrast varied inversely with years of schooling among US white men. The HDL cholesterol varied inversely with years of schooling for Chinese, Polish, and Russian men, but varied directly with years of schooling among US white men. The lipid differences between men of high versus low years of schooling were not explained by age, body mass index, smoking, alcohol consumption or blood pressure medication use. Findings were less consistent for women and for Israelis and US blacks of both genders. CONCLUSIONS: Lipid and lipoprotein levels consistent with atherogenicity varied directly with years of schooling in Chinese, Polish, and Russian samples. Opposite trends were present in US whites. These findings are consistent with a hypothesized influence of social status on CHD risk differing among populations in relation to stages in societal economic development.

Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TEXCAPS): additional perspectives on tolerability of long-term treatment with lovastatin.

This study presents the long-term safety data from AFCAPS/TexCAPS, the first primary prevention trial to demonstrate that men and women with average levels of low-density lipoprotein cholesterol (LDL-C) and below average levels of high-density lipoprotein cholesterol (HDL-C) can significantly benefit from long-term treatment to lower LDL-C; lovastatin 20 to 40 mg/day reduced the risk of a first acute major coronary event (fatal or nonfatal myocardial infarction, unstable angina, or sudden death) by 37% (p = 0.00008). This double-blind randomized, placebo-controlled trial, in 6,605 generally healthy middle-aged and older men and women, had prespecified end point and cancer analyses. All analyses were intention-to-treat. Safety monitoring included history, physical examination, and laboratory studies (including hepatic transaminases and creatine phosphokinase [CPK]). All participants, even those who discontinued treatment, were contacted annually for vital status, cardiovascular events, and cancer history. After an average of 5.2 years of follow-up, there were 157 deaths (80 receiving lovastatin and 77 receiving placebo; relative risk [RR] 1.04; 95% confidence interval [CI] 0.76 to 1.42; p = 0.82); of which 115 were noncardiovascular (RR 1.21; CI 0.84 to 1.74; p = 0.31), and of these, 82 were due to cancer (RR 1.41; CI 0.91 to 2.19; p = 0.13). There were no significant differences between treatment groups in overall cancer rates, discontinuations for noncardiovascular adverse experiences, or clinically important elevations of hepatic transaminases or CPK. Among those who used cytochrome P450 isoform (CYP3A4) inhibitors, there were no treatment group differences in the frequency of clinically important muscle-related adverse events. Treatment with lovastatin 20 to 40 mg daily for primary prevention of coronary heart disease was well tolerated and reduced the risk of first acute coronary events without increasing the risk of either noncardiovascular mortality or cancer.

Interaction of the glutathione S-transferase genes and cigarette smoking on risk of lower extremity arterial disease: the Atherosclerosis Risk in Communities (ARIC) study.

Glutathione S-transferases M1 or T1 (GSTM1/GSTT1) affect the body's ability either to detoxify or to activate chemicals in cigarette smoke. Cigarette smoking increases the risk of lower extremity arterial disease (LEAD). We conducted a cross-sectional study to evaluate a hypothesized interaction of the genetic polymorphisms of GSTM1 and T1 with cigarette smoking in the risk of LEAD in the ARIC study. A stratified-random sample, including 212 LEAD cases (ankle-brachial index <0.9 in men or <0.85 in women) and 1277 non-cases, was selected from the ARIC cohort of 12041 middle-aged participants free of CHD, transient ischemic attack and stroke at baseline (1987-1989). Overall, the differences in the frequencies of GSTM1-0 and GSTT1-0 (the homozygous deletion genotype) were not statistically significant between cases and non-cases (44 vs. 41% and 28 vs. 18%). However, smoking was more prevalent among LEAD cases than non-cases. The results suggest that the non-deletion genotype GSTM1-1 interacts with smoking to increase the risk of LEAD, but this interaction was not statistically significant. The functional genotype GSTT1-1 was significantly associated with increased risk of LEAD given smoking after adjustment for other risk factors. In individuals with GSTT1-1, the odds ratios (ORs) (95% confidence intervals) of LEAD were 3.6 (1.4, 9.0) for current smoking and 5.0 (1.9, 13.0) for 20+ pack-years. However, in those with GSTT1-0, the ORs were 0.8 (0.2, 2.8) for current smoking and 0.6 (0.1, 2.1) for 20+ pack-years. The interaction was significant (P<0.05) on the additive scale for current smoking and on both the additive and multiplicative scales for 20+ pack-years. Among non-smokers, GSTT1-1 was not associated with LEAD. The results suggest that the GSTT1-1 polymorphism may be a susceptibility factor modifying the risk of LEAD associated with cigarette smoking.

Weight change among self-reported dieters and non-dieters in white and African American men and women.

Few studies have examined the association between dieting and weight change in general population and results have been inconsistent. To the best of our knowledge, no such study has been done in middle-aged African Americans. We examined 10,554 white and African American men and women who were participants in the Atherosclerosis Risk in Communities (ARIC) Study and attended examinations between 1986 and 1994. We found that the prevalence of dieting in white women, white men, African American women, and African American men was 6.5, 2.3, 3.5, and 0.9%, respectively. After controlling for the covariates, the difference in the mean annual weight gain between dieters and nondieters was 0.61, 0.46, and 0.59 kg/year among white women, white men, and African American women, respectively. In conclusion, in this cohort of white men and women and African American women aged 45-64 years, self-reported dieting was associated with a larger mean annual weight gain than non-dieting over a period of 6 years.

Association of educational achievement with pulsatile arterial diameter change of the common carotid artery: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1992.

Education is strongly inversely associated with common carotid artery intima-media thickness in the Atherosclerosis Risk in Communities (ARIC) Study. The authors extended the ARIC study of preclinical atherosclerosis by evaluating the cross-sectional association of education with common carotid artery elasticity. This study included 10,091 Black and White men and women aged 45-64 years who were free of clinical coronary heart disease and stroke/transient ischemic attack. Arterial elasticity was assessed by pulsatile arterial diameter change (PADC), derived from phase-locked echo-tracking. The smaller the PADC, the stiffer the artery. Education was categorized into grade school, high school without graduation, high school with graduation, vocational school, some college, and graduate/professional school. PADC was directly associated with educational attainment. The mean PADCs, adjusted for age, height, diastolic diameter, systolic blood pressure, pulse pressure (linear and squared), ethnicity, gender, and smoking status, in successively higher education strata were 402 (standard error (SE) 5), 403 (SE 4), 407 (SE 3), 413 (SE 4), 416 (SE 2), and 417 (SE 4) microm (p = 0.007). To the authors' knowledge, this is the first time such an association has been reported. If arterial dilation impairment precedes arterial wall thickening in the atherosclerotic process, as recent studies on endothelial dysfunction suggest, these results indicate that low socioeconomic status may be associated with early arterial pathophysiologic changes-an effect that appears to be mediated by established cardiovascular disease risk factors.

Orthostatic hypotension and the incidence of coronary heart disease: the Atherosclerosis Risk in Communities study.

We examined the association between orthostatic hypotension (OH) at baseline examination (1987-1989) and the incidence of coronary heart disease (CHD) over an average of 6 years, among 12,433 black and white middle-aged men and women participating in the Atherosclerosis Risk in Communities (ARIC) study. OH was defined as a SBP decrease > or = 20 mm Hg or a DBP decrease > or = 10 mm Hg after changing from supine to standing. CHD events included definite or probable myocardial infarctions (MI), silent MI, and fatal CHD. Five percent of participants had OH. Prevalence increased with advancing age and was more common among those with cardiovascular disease (CVD)-related comorbidities and risk factors. Those with OH had an increased risk of CHD (hazard ratio [HR] = 3.49, 95% confidence interval [CI] = 2.58, 4.73). This association was attenuated after controlling for age, ethnicity, gender, comorbid conditions, and CVD risk factors (HR = 1.85, 95% CI = 1.31, 2.63).

Anger proneness predicts coronary heart disease risk: prospective analysis from the atherosclerosis risk in communities (ARIC) study.

BACKGROUND: Increased research attention is being paid to the negative impact of anger on coronary heart disease (CHD). METHODS AND RESULTS: This study examined prospectively the association between trait anger and the risk of combined CHD (acute myocardial infarction [MI]/fatal CHD, silent MI, or cardiac revascularization procedures) and of "hard" events (acute MI/fatal CHD). Participants were 12 986 black and white men and women enrolled in the Atherosclerosis Risk In Communities study. In the entire cohort, individuals with high trait anger, compared with their low anger counterparts, were at increased risk of CHD in both event categories. The multivariate-adjusted hazard ratio (HR) (95% CI) was 1.54 (95% CI 1.10 to 2.16) for combined CHD and 1.75 (95% CI 1.17 to 2.64) for "hard" events. Heterogeneity of effect was observed by hypertensive status. Among normotensive individuals, the risk of combined CHD and of "hard" events increased monotonically with increasing levels of trait anger. The multivariate-adjusted HR of CHD for high versus low anger was 2.20 (95% CI 1.36 to 3.55) and for moderate versus low anger was 1.32 (95% CI 0.94 to 1.84). For "hard" events, the multivariate-adjusted HRs were 2.69 (95% CI 1.48 to 4.90) and 1.35 (95% CI 0.87 to 2.10), respectively. No statistically significant association between trait anger and incident CHD risk was observed among hypertensive individuals. CONCLUSIONS: Proneness to anger places normotensive middle-aged men and women at significant risk for CHD morbidity and death independent of the established biological risk factors.

Hypertension and arterial stiffness: the Atherosclerosis Risk in Communities Study. ARIC Investigators.

Our objective was to describe the relationship of arterial stiffness and hypertension in a large, population-based sample of men and women. Hypertension-related increases in arterial stiffness may reflect the distending pressure and/or structural alterations in the artery. Included were 10,712 participants, ages 45 to 64 years, of the Atherosclerosis Risk in Communities Study, free of prevalent cardiovascular disease. Hypertension was classified as systolic or diastolic blood pressure (BP) > or =140/90 mm Hg, respectively, or the current use of antihypertensive medications. Common carotid arterial diameter change was measured using B-mode ultrasound and an electronic device that utilized radio frequency signals to track the motion of the arterial walls. Using statistical models to control for diastolic BP and pulse pressure, arterial diameter change was calculated separately in normotensive/ nonmedicated and medicated hypertensives. Hypertension was associated with a smaller adjusted diameter change (ie, greater stiffness) in comparison to optimal blood pressure (BP < 120/80 mm Hg): normotensive/nonmedicated men, 0.33 versus 0.43 mm (P < 0.001); medicated men, 0.34 versus 0.42 mm (P < 0.001); normotensive/ nonmedicated women, 0.34 versus 0.40 mm (P < 0.001), and medicated women, 0.33 versus 0.40 mm (P < 0.001). The relationship between pulse pressure and diameter change (ie, the slope of pulse pressure and diameter change) did not differ between hypertensives and normotensives. These cross-sectional data suggest that hypertension is associated with carotid arterial stiffness; however, these differences in the calculated stiffness appear to be the effect of distending pressure rather than structural changes in the carotid artery.

Income inequality and all-cause mortality in the 100 counties of North Carolina.

BACKGROUND: This study evaluated the relationship between income inequality and all-cause mortality in the 100 counties of North Carolina. METHODS: Mortality data for 1985 to 1994 came from the National Center for Health Statistics and household income data from the 1990 Census. Associations between county-level income inequality and age-adjusted, all-cause mortality rates were evaluated in stratified and regression analyses. RESULTS: Stratified analyses suggest that all-cause mortality was directly related to income inequality in all 100 counties and in non-metropolitan statistical area (MSA) counties. This relationship was statistically significant, controlling for per capita income in regression analyses for all age groups except > or =65 years among all 100 counties and for all ages combined and for ages 35 to 64 among non-MSA counties. CONCLUSIONS: A relationship between income inequality and all-cause mortality previously identified nationally among states and MSAs was also found among all counties and non-MSA counties of North Carolina in 1985 to 1994.

Glutathione S-transferase genotype as a susceptibility factor in smoking-related coronary heart disease.

Cancer studies suggest that the null polymorphisms of glutathione S-transferase M1 or T1 (GSTM1/GSTT1) may affect the ability to detoxify or activate chemicals in cigarette smoke. The potential modification of the association between smoking and coronary heart disease (CHD) by GSTM1 and GSTT1 has not been studied in humans. A case-cohort study was conducted to test the hypotheses that specific genotypes of GSTM1 or GSTT1 affect susceptibility to smoking-related CHD. CHD cases (n=400) accrued during 1987-1993 and a cohort-representative sample (n=924) were selected from a biracial cohort of 15792 middle-aged men and women in four US communities. A significantly higher frequency of GSTM1-0 and a lower frequency of GSTT1-0 were found in whites (GSTM1-0=47.1%, GSTT1-0=16.4%) than in African-Americans (AAs) (GSTM1-0=17.5%, GSTT1-0=25.9%). A smoking-GSTM1-0 interaction for the risk of CHD was statistically significant on an additive scale, with ever-smokers with GSTM1-0 at a approximately 1.5-fold higher risk relative to ever-smokers with GSTM1-1 and a approximately 2-fold higher risk relative to never-smokers with GSTM1-0, after adjustment for other CHD risk factors. The interaction between having smoked >/=20 pack-years and GSTT1-1 was statistically significant on both multiplicative and additive scales. The risk of CHD given both GSTT1-1 and >/=20 pack-years of smoking was approximately three times greater than the risk given exposure to >/=20 pack-years of smoking alone, and approximately four times greater than the risk given exposure to GSTT1-1 alone. The modification of the smoking-CHD association by GSTM1 or GSTT1 suggests that chemicals in cigarette smoke that are substrates for glutathione S-transferases may be involved in the etiology of CHD.

Family risk score of coronary heart disease (CHD) as a predictor of CHD: the Atherosclerosis Risk in Communities (ARIC) study and the NHLBI family heart study.

Family history of coronary heart disease (CHD) has been found to be a risk factor for CHD in numerous studies. Few studies have addressed whether a quantitative measure of family history of CHD (family risk score, FRS) predicts CHD in African Americans. This study assessed the association between FRS and incident CHD of participants, and the variation of the association by gender and race. Participants in the study were a biracial population-based cohort with 3,958 African Americans and 10,580 Whites aged 45-64 years old in the ARIC baseline survey (1987-1989). They were randomly selected from four U. S. communities. During follow-up (1987-1993), 352 participants experienced the onset of CHD. Incidence density of CHD (per 1,000 person-years) was 7.8 and 3.6 among African-American men (AAM) and women (AAW), and 7.2 and 2.2 among White men (WM) and women (WW). The hazard rate ratio (HRR) of CHD associated with one standard deviation increase of FRS was 1.52 in AAW, 1.46 in AAM, 1.41 in WW, and 1.68 in WM. The HRRs decreased 4.6% in AAW, 1.4% in WW, 5.7% in AAM, and 3.0% in WM, but increased 2.1% in AAM after adjustment for selected covariates. FRS predicts incident CHD in African Americans and Whites, men and women. The relation of FRS to incident CHD can be only partially explained by the selected risk factors in the biological causal pathways: IMT, T-G, LDL, HDL, Lp(a), fibrinogen and hypertension. No significant difference by race has been found in this study.

Racial disparities in CHD mortality from 1968-1992 in the state economic areas surrounding the ARIC study communities. Atherosclerosis Risk in Communities.

PURPOSE: This study examined racial variations in CHD (coronary heart disease) mortality rates (1968-1992) of residents aged 35-84 in the state economic areas (SEAs) surrounding the ARIC (Atherosclerosis Risk in Communities) study. The quarter century of CHD mortality rates are discussed in relation to racial and gender differences in baseline risk factors measured in the ARIC cohort and to the incidence of hospitalized myocardial infarction and case fatality rates obtained from the community surveillance component of the ARIC study between 1987 and 1994, inclusive. METHODS: Five-year average annual, gender- and age-specific CHD mortality rates were compared across race groups, based on National Vital Statistics data for state economic areas. RESULTS: Five-year average annual CHD mortality declined 2.6% for white men and women and 1.6% and 2.2% for black men and women, respectively. The black-white mortality rate ratio increased over time for men and women. The black-white mortality age crossover (higher black than white mortality in young men, lower black than white mortality at older ages) had disappeared by the end of the observation. CHD mortality was markedly greater in black than white women at all ages and time periods. The black disadvantage in CHD mortality was increasingly greater in the ARIC SEAs than in the United States as a whole. CONCLUSIONS: Persistent and increasing racial disparities in CHD mortality occurred in the ARIC SEAs concurrently with racial differences in risk factors, the incidence of myocardial infarction, and case fatality rates.