Impact of Self-Preference Community Fitness Interventions in High-Risk African Americans.

African Americans have a high prevalence of obesity and physical inactivity, but few interventions have been successful in the long term. We describe a 1-year intervention program to increase physical activity and reduce cardiometabolic risk. Interventions incorporated the premise that self-selection into flexible venues and varying exercise modalities would result in improvement in fitness and risk factors. Results of this single-group pretest/posttest observational study show 1-year overall group reductions in body weight and body mass index and cardiometabolic factors including high-sensitivity C-reactive protein, and increases in dual-energy x-ray absorptiometry-derived absolute and percent lean mass and lean-fat ratio, and decreased fat mass.

Lean Mass and Fat Mass as Contributors to Physical Fitness in an Overweight and Obese African American Population.

OBJECTIVE: To determine the association of lean vs fat mass with fitness in healthy, overweight and obese African Americans from families with early-onset coronary disease. DESIGN: Cross-sectional study. SETTING: Baltimore, Maryland. PARTICIPANTS: 191 healthy, overweight, sedentary African Americans (69% women; aged 44.8 ± 11 years; body mass index 34 ± 5 kg/m2). MAIN OUTCOME MEASURES: Anthropometrics, smoking, blood pressure, lipids, c-reactive protein, and glucose were assessed with standard methods; body composition was determined by dual energy X-ray absorptiometry; cardiorespiratory fitness was expressed as VO(2peak) attained during a maximal treadmill test. RESULTS: In both men and women, greater lean mass was independently associated with higher VO(2peak) (P < .05) and explained > 21% of the variance in VO(2peak), adjusted for body mass index, fat mass, important covariables, and nonindependence of families. CONCLUSIONS: In this cross-sectional study, lean mass was the key determinant of cardiorespiratory fitness, independent of sex, age, and magnitude of obesity. These data provide a strong rationale for examining whether interventions that increase lean mass may also improve fitness, even among high-risk overweight and obese African Americans.

Extreme deep white matter hyperintensity volumes are associated with African American race.

BACKGROUND: African Americans (AAs) have a higher prevalence of extreme ischemic white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) than do European Americans (EAs) based on the Cardiovascular Health Study (CHS) score. Ischemic white matter disease, limited to the deep white matter, may be biologically distinct from disease in other regions and may reflect a previously observed trend toward an increased risk of subcortical lacunar infarcts in AAs. We hypothesized that extreme deep WMH volume (DWMV) or periventricular volume (PV) may also have a higher prevalence in AAs. Thus, we studied extreme CHS scores and extreme DWMV and PV in a healthy population enriched for cardiovascular disease risk factors. METHODS: We imaged the brains of 593 subjects who were first-degree relatives of probands with early onset coronary disease prior to 60 years of age. WMHs were manually delineated on 3-tesla cranial MRI by a trained radiology reader; the location and volume of lesions were characterized using automated software. DWMV and PV were measured directly with automated software, and the CHS score was determined by a neuroradiologist. Volumes were characterized as being in the upper 25% versus lower 75% of total lesion volume. Volumes in the upper versus the remaining quartiles were examined for AA versus EA race using multiple logistic regression (generalized estimating equations adjusted for family relatedness) and adjusted for major vascular disease risk factors including age ≥55 years versus <55, sex, current smoking, obesity, hypertension, diabetes and low-density lipoprotein >160 mg/dl. RESULTS: Participants were 58% women and 37% AAs, with a mean age of 51.5 ± 11.0 years (range, 29-74 years). AAs had significantly higher odds of having extreme DWMVs (odds ratio, OR, 1.8; 95% confidence interval, CI, 1.2-2.9; p = 0.0076) independently of age, sex, hypertension and all other risk factors. AAs also had significantly higher odds of having extreme CHS scores ≥3 (OR, 1.3; 95% CI, 1.1-3.6; p = 0.025). Extreme PV was not significantly associated with AA race (OR, 1.3; 95% CI, 0.81-2.1; p = 0.26). CONCLUSIONS: AAs from families with early-onset cardiovascular disease are more likely to have extreme DWMVs (a subclinical form of cerebrovascular disease) and an extreme CHS score, but not extreme PV, independently of age and other cardiovascular disease risk factors. These findings suggest that this AA population is at an increased risk for DWMV and may be at an increased risk for future subcortical stroke. Longitudinal studies are required to see if DWMV is predictive of symptomatic subcortical strokes in this population.

Heritability of platelet responsiveness to aspirin in activation pathways directly and indirectly related to cyclooxygenase-1.

BACKGROUND: The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness. METHODS AND RESULTS: We examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44+/-13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes (r2=0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not. CONCLUSIONS: Heritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA.

Platelet inhibition by aspirin 81 and 325 mg/day in men versus women without clinically apparent cardiovascular disease.

Compared with men, women have greater platelet aggregation before and after low-dose aspirin. It is not known whether high-dose aspirin therapy brings residual platelet aggregation in women closer to that in men. Our objective was to compare inhibition of platelet aggregation in women and men after low- and high-dose aspirin. We enrolled healthy subjects (n=106) in a trial of 14 days of aspirin 81 mg/day followed by 14 days of 325 mg/day. Platelet function was measured at baseline and after the 2 aspirin doses. Women had greater baseline platelet activation measurements. After the 2 aspirin doses, men and women had near complete suppression of platelet aggregation to arachidonic acid in whole blood and in platelet-rich plasma (PRP), the direct cyclo-oxygenase-1 pathway affected by aspirin. For indirect pathways, women had significantly greater residual platelet activation to collagen and adenosine diphosphate (ADP) in whole blood after the 2 aspirin doses and in response to collagen and ADP in PRP after aspirin 325 mg/day only. After aspirin 325 mg/day, women continued to have greater residual platelet aggregation compared with men after aspirin 81 mg/day in response to collagen (p=0.016 in whole blood, p=0.037 in PRP), ADP (p<0.001 in whole blood, p=0.012 in PRP), and epinephrine (p=0.03 in PRP). Excretion of urinary thromboxane metabolite (urinary 11-dehydrothromboxane B2) decreased after aspirin to a similar extent in men and women. In conclusion, women continue to have greater residual platelet activity after high-dose aspirin compared with men treated with a lower dose of aspirin.

Sustainability of a multiple risk factor intervention on cardiovascular disease in high-risk African American families.

OBJECTIVES: To determine the long-term effect of a community-based risk reduction intervention at five years after completion of a one-year randomized clinical trial and to determine the sustainability of the beneficial effects seen one year after the intervention. METHODS: 30- to 59- year-old African American siblings of probands with premature coronary heart disease (CHD) were randomized for care of multiple CHD risk factors to either one year of community-based care (CBC) provided by a nurse practitioner/community health worker team or enhanced usual care (EUC). At five years, 307 (84.6%) of the siblings returned for reevaluation. MAIN OUTCOME MEASURES: Changes in and achievement of goal levels of low-density lipoprotein cholesterol (LDL-C), systolic and diastolic blood pressure (SBP and DBP, respectively), and smoking cessation at five years. RESULTS: No significant differences were seen between groups in mean LDL-C, SBP, and DBP or in the overall percentages achieving goal LDL-C, blood pressure, or smoking status. Changes after completion of the intervention suggest that the CBC group lost the beneficial effects for mean LDL-C and for percentage at goal LDL-C, while the EUC group continued to improve. CBC was associated with greater sustainability and less refractoriness of one-year results for LDL-C and blood pressure goals. CONCLUSIONS: Although no group differences were found in mean risk factor levels at five years, data indicate that CBC is both feasible and associated with earlier sustainability of positive risk factor changes compared with EUC.

Incidence of coronary artery disease in siblings of patients with premature coronary artery disease: 10 years of follow-up.

Although family history of premature coronary artery disease (CAD) confers increased risk of CAD, the magnitude of this increase beyond that expected from the risk factors incorporated in the Framingham Risk Equation (FRE) remains unknown. We prospectively determined the accuracy of the FRE 10-year incident CAD events prediction in initially healthy siblings of patients with documented premature CAD. We recruited 784 siblings (30 to 59 years) of 449 patients hospitalized with CAD <60 years of age (1983 to 1995). We compared the estimated 10-year incidence of total CAD events by the gender-specific FREs at baseline, to the observed incidence at 10 years of follow-up. In men, the 10-year actual CAD event rate was 20%, only half of which was predicted by the FRE (12% vs 20%, p <0.001). In women, the observed CAD event rate was 7.1% (p <0.001 vs men), modestly but not significantly greater than the 6.3% predicted by the FRE (p = 0.34). Thus, there was a significant 66.6% excess risk in men, and a nonsignificant 12.7% excess risk in women beyond the risk predicted by the FRE for total CAD events. The FRE and its known classic risk factor profile failed to accurately predict total incident 10-year CAD events in individuals with a sibling history of premature CAD, most particularly in men. In conclusion, in families with a history of premature CAD, the excess risk observed cannot be attributed to traditional risk factors, suggesting a major role for as yet undetermined genetic and other susceptibility factors.

Casual chocolate consumption and inhibition of platelet function.

Observational studies have associated reduced cardiovascular mortality with chocolate consumption. Feeding studies of high-dose, flavanol-rich chocolate show antiplatelet effects, but the effect of casual chocolate consumption on platelet function is unknown. Healthy adults (N=1535) were proscribed from consuming foods affecting platelet function, including chocolate, for 48 hours and completed a 24-hour dietary recall before ex vivo platelet testing with the Platelet Function Analyzer (PFA)-100 (Dade Behring, Inc, Deerfield, IL) test and in vivo testing with urinary 11-dehydro thromboxane B2 (Tx-M) measurements. Some participants (n=141) reported ignoring the prohibition of consuming chocolate before platelet testing. Despite having similar baseline characteristics, chocolate consumers had longer PFA closure times (130 vs 123 seconds, P=.005) and decreased Tx-M levels (175 vs 290 ng/mol creatinine, P=.03). Chocolate remained a significant independent predictor of both ex vivo and in vivo platelet function testing after adjusting for confounders. The authors concluded that even consuming modest amounts of commercial chocolate has important antiplatelet effects.

Interaction of body mass index and framingham risk score in predicting incident coronary disease in families.

BACKGROUND: Siblings of individuals with premature coronary heart disease (CHD) have a marked excess risk of CHD risk factors and premature CHD. The impact of body mass index (BMI) on incident CHD in these families and the extent to which it may be mediated by associated risk factors are unknown. The aim of this study was to examine the effect of high BMI on incident CHD in white and black families with premature CHD and to estimate the heritability of BMI. METHODS AND RESULTS: Risk factors, BMI, and Framingham Risk Score (FRS) were assessed at baseline and incident CHD was determined prospectively in 827 apparently healthy siblings of probands with premature CHD aged <60 years. During a mean follow-up of 8.7 years, 13.3% of siblings had incident CHD events. Event rates were higher in obese and overweight siblings than in those with normal weight (15.3% and 16.0% versus 8.1%, respectively; P=0.01). Multivariable Cox proportional hazards analyses demonstrated the independent prognostic value of BMI when added to FRS (P=0.02). A marked interaction between obesity (BMI > or =30 kg/m2) and high FRS (>20%) was seen for incident CHD (P for interaction=0.008), with an adjusted hazard ratio compared with low-FRS/normal-weight siblings of 14.63 (95% CI, 6.40 to 33.44; P<0.0001). BMI heritability (h2) was moderate for whites and low for blacks (52% and 29%, respectively). CONCLUSIONS: High BMI contributed independently and significantly to incident CHD, beginning in the overweight range, and was most notable for obese siblings with a high-risk FRS.

Impact of a community-based multiple risk factor intervention on cardiovascular risk in black families with a history of premature coronary disease.

BACKGROUND: Black subjects with a family history of premature coronary heart disease (CHD) have a marked excess risk, yet barriers prevent effective risk reduction. We tested a community-based multiple risk factor intervention (community-based care [CBC]) and compared it with "enhanced" primary care (EPC) to reduce CHD risk in high-risk black families. METHODS AND RESULTS: Black 30- to 59-year-old siblings of a proband with CHD aged <60 years were randomized for care of BP > or =140/90 mm Hg, LDL cholesterol > or =3.37 mmol/L, or current smoking to EPC (n=168) or CBC (n=196) and monitored for 1 year. EPC and CBC were designed to eliminate barriers to care. The CBC group received care by a nurse practitioner and a community health worker in a community setting. The CBC group was 2 times more likely to achieve goal levels of LDL cholesterol and blood pressure compared with the EPC group (95% CI, 1.11 to 4.20 and 1.39 to 3.88, respectively) with adjustment for baseline levels of age, sex, education, and baseline use of medications. The CBC group demonstrated a significant reduction in global CHD risk, whereas no reduction was seen in the EPC group (P<0.0001). CONCLUSIONS: Eliminating known barriers may not be sufficient to reduce CHD risk in primary care settings. An alternative community care model that addresses barriers may be a more effective way to ameliorate CHD risk in high-risk black families.

Relation between atherosclerosis risk factors and aspirin resistance in a primary prevention population.

Resistance to inhibition of platelet function by aspirin may contribute to future myocardial infarction and stroke. Adverse cardiovascular outcomes have been associated with aspirin resistance on several different platelet function assays, including the level of urinary 11-dehydro thromboxane B2 (Tx-M), platelet aggregation to arachidonic acid and adenosine diphosphate, and closure time on the platelet function analyzer-100. We examined the concordance of these aspirin-resistance assays and their relation to cardiovascular risk factors in a primary prevention population. Asymptomatic patients (n = 1,311) at increased risk for coronary heart disease were evaluated before and after 2 weeks of aspirin (81 mg/day). Aspirin resistance was defined according to published criteria for these 3 assays of platelet function. Subjects were characterized for the presence of atherosclerosis risk factors. Agreement among the 3 assays was poor. Only 5 patients met aggregation criteria for aspirin resistance. Attenuated suppression of urinary Tx-M by aspirin was associated with a greater atherosclerotic risk profile and Framingham risk score in multivariable regression analysis. Aspirin resistance by platelet function analyzer-100 was associated only with increased von Willebrand factor levels and not with atherosclerotic risk profile. In conclusion, in a primary prevention population, different published criteria for aspirin resistance classify distinct groups of patients as aspirin resistant with very little overlap. Higher Tx-M, which reflects decreased suppression of thromboxane production in vivo, is the only criterion associated with atherosclerosis risk factors, suggesting that this measurement may represent the most relevant approach for identifying asymptomatic subjects whose aspirin treatment will "fail."

Comparison of coronary calcium and stress myocardial perfusion imaging in apparently healthy siblings of individuals with premature coronary artery disease.

Detection of subclinical coronary atherosclerosis is possible using exercise myocardial perfusion imaging for inducible ischemia or multidetector computed tomography for coronary artery calcium (CAC), which is used to detect subclinical coronary atherosclerosis. The extent to which these screening tests converge in an asymptomatic population that is at increased risk for coronary artery disease remains unknown. We compared the concordance of findings in 260 asymptomatic middle-age siblings of hospitalized index patients <60 years of age with documented coronary artery disease. All subjects underwent maximal exercise testing with postexercise and delayed attenuation-corrected thallium single-photon emission computed tomography and multidetector computed tomography for CAC. An abnormal exercise single-photon emission computed tomographic (SPECT) result occurred in >50% of subjects with a CAC score >100, but also in 12% with no CAC, 9% with CAC scores of 1 to 10, and 20% with CAC scores of 11 to 100. In subjects with an abnormal exercise SPECT result, 59% had CAC scores < or =100. Overall, there was only a modest agreement between an abnormal exercise SPECT result and high CAC scores. In conclusion, although moderate or severe CAC is often associated with inducible ischemia, the absence of CAC or the presence of only mild CAC by no means precludes inducible myocardial ischemia. These screening tests may reflect different aspects or stages of coronary disease in an asymptomatic middle-age population.

Glucose levels in the normal range predict incident diabetes in families with premature coronary heart disease.

PURPOSE: Little is known about excess risk of incident diabetes conferred by fasting plasma glucose (FPG) within the normal range (<5.6 mmol/l) for high risk families. METHODS: Healthy 30-59 year old non-diabetic siblings (N = 542) of index cases with documented premature coronary disease were followed prospectively for type 2 diabetes. RESULTS: During 8.7+/-3 years of follow-up, incident diabetes was identified in 7.8%. Rates were incremental with baseline non-diabetes FPG thresholds of 5.0, 5.6, 6.1, and 6.7 mmol/l (p for trend < 0.0001). FPG was the strongest predictor of incident diabetes even across levels within the normal range. The multivariable adjusted relative risk was 14.9 (95% CI = 3.4-65.2) at FPG thresholds > or =5.0 mmol/l versus FPG <5.0 mmol/l. The maximal diagnostic efficiency for FPG was 5.50 mmol/l; with sensitivity and specificity 0.782. All FPG thresholds in the normal range between 5.0 and 5.6 mmol/l showed efficiency levels >0.74. The overall area under the ROC curve predicting incident diabetes for normal and prediabetes ranges of FPG was 0.867. CONCLUSION: Higher FPG levels within the designated "normal" range in high risk families are a potent independent risk factor for type 2 diabetes and may serve as a sentinel to trigger primary preventive interventions.

Sex differences in platelet reactivity and response to low-dose aspirin therapy.

CONTEXT: Recent randomized trials suggest that women may not accrue the same cardioprotective benefits as men do from low-dose aspirin therapy used in primary prevention. Failure of aspirin to suppress platelet aggregation in women is one hypothesized mechanism. OBJECTIVE: To examine differential platelet reactivity to low-dose aspirin therapy by sex. DESIGN, SETTING, AND PARTICIPANTS: A clinical trial of aspirin at 81 mg/d for 14 days was conducted in 571 men and 711 women. Baseline and post-aspirin therapy measures included platelet aggregation to arachidonic acid, adenosine diphosphate, epinephrine, and platelet function analyzer closure time. MAIN OUTCOME MEASURE: Sex differences in cyclooxygenase 1 (COX-1) direct and indirect platelet activation pathways before and after administration of aspirin. RESULTS: In 10 of the 12 platelet agonist exposures, women's platelets were significantly more reactive at baseline. However, after aspirin therapy, the percent aggregation to arachidonic acid (the direct COX-1 pathway) decreased more in women than in men (P<.001) and demonstrated near total suppression of residual platelet reactivity in both men and women. In COX-1 indirect pathways, women experienced the same or more platelet inhibition than men in 8 of the 9 assays yet retained modestly greater platelet reactivity after aspirin therapy. In multivariable analysis, female sex significantly predicted aggregation to 2 muM and 10 muM of adenosine diphosphate (P = .02 and <.001, respectively) and collagen at 5 mug/mL (P<.001) independent of risk factors, age, race, menopausal status, and hormone therapy. CONCLUSIONS: Women experienced the same or greater decreases in platelet reactivity after aspirin therapy, retaining modestly more platelet reactivity compared with men. However, most women achieved total suppression of aggregation in the direct COX-1 pathway, the putative mechanism for aspirin's cardioprotection.

Detecting occult coronary disease in a high-risk asymptomatic population.

BACKGROUND: Exercise stress testing alone or with perfusion imaging is the standard screening method to determine the presence of obstructive coronary artery disease (CAD) in people with chest pain. In asymptomatic individuals with a family history of premature CAD, it is unclear whether abnormalities on these functional exercise tests represent significant coronary disease. METHODS AND RESULTS: An abnormal exercise test, thallium scan, or both occurred in 153 (21%) of 734 asymptomatic siblings of persons with documented CAD, of whom 105 underwent coronary angiography with quantitative analysis of stenosis severity. Overall, 95% had coronary atherosclerosis, but only 39% had 1 or more stenoses with >or=50% narrowing. Of 30 siblings in whom the exercise test and perfusion scan were both abnormal, 70% had >or=50% stenoses. The mean stenosis in arteries that fed perfusion defects was only 43+/-31%, and 68% of such stenoses were <50%. However, in 71% of all defects, the location matched arteries with the most severe stenoses. CONCLUSIONS: In asymptomatic persons with a family history of CAD, abnormal exercise scintigraphy identifies predominantly mild coronary atherosclerosis. Perfusion defects may be caused by coronary vasomotor dysfunction in addition to atherosclerotic plaque.

Women with a low Framingham risk score and a family history of premature coronary heart disease have a high prevalence of subclinical coronary atherosclerosis.

BACKGROUND: The Framingham risk estimation (FRE) serves as the basis for identifying which asymptomatic adults should be treated with aspirin and lipid-lowering therapy in primary prevention. However, the FRE generally yields low estimates of 10-year "hard" coronary heart disease (CHD) event risk with few women (< 70 years) qualifying for preventive pharmacologic therapy despite relatively high lifetime risk. We postulated that traditional risk factor assessment might fail to identify a sizeable portion of women with a sibling history for premature CHD as having advanced subclinical atherosclerosis. METHODS: We studied 102 asymptomatic women (mean age 51 +/- 7 years) who were the sisters of a proband hospitalized with documented premature CHD. Participants underwent risk factor assessment and multidetector computed tomography for coronary artery calcium (CAC) scoring. Based on FRE prediction of 10-year risk for hard CHD events, participants were classified as low risk (< 10%) (n = 100), intermediate risk (10%-20%) (n = 2), or high risk (> 20%) (n = 0). Significant subclinical atherosclerosis was defined as age-sex adjusted > 75th percentile CAC scores. RESULTS: Ninety-eight percent were at low risk (mean FRE of only 2% +/- 2%). However, 40% had detectable CAC, 12% had CAC > 100, and 6% had CAC > or = 400. Based on CAC score percentiles, 32% had significant subclinical atherosclerosis and 17% ranked above the 90th percentile. CONCLUSION: Among women classified as low risk by FRE, a third had significant subclinical atherosclerosis. Sisters of probands with premature CHD appear to be a high-risk group and may warrant noninvasive screening for subclinical atherosclerosis to appropriately target individuals for more aggressive primary prevention therapy than what is currently recommended.

Predictors of low-density lipoprotein particle size in a high-risk African-American population.

A predominance of small, dense, low-density lipoprotein particles (pattern B) has been associated with increased cardiovascular risk independent of absolute cholesterol levels in primarily white populations. Because of the putative association of pattern B with increased risk, some investigators have proposed that routine measurement of low-density lipoprotein particle size may be beneficial for cardiovascular risk assessment. Because no studies have specifically examined this possibility in African-Americans, it remains unclear whether measurement of low-density lipoprotein particle size adds information beyond that of traditional lipid risk factors. We compared standard lipid profile measurements with extended measurements concurrently in an apparently healthy, high-risk population of African-American siblings of patients who had premature cardiovascular disease. We determined the extent to which patients who had pattern B would be identifiable from the usual lipid profile. A high triglyceride level alone was a strong independent correlate of pattern B. In subjects whose triglyceride level was >/=150 mg/dl, 67% had pattern B, whereas only 17% of subjects whose triglyceride level was <150 mg/dl had pattern B. The area under the receiver-operating characteristic curve was 0.77. Our data suggest that the standard lipid profile, primarily fasting triglyceride measurement, appears to be a useful surrogate for direct measurement of particle size in a high-risk African-American population.

Age differences in periventricular and deep white matter lesions.

Deep white matter hyperintensity (DWMH) and periventricular (PV) white matter lesion volumes are associated with age and subsequent stroke. We studied age differences in these volumes accounting for collinearity and risk factors. Subjects were 563 healthy family members of early-onset coronary artery disease patients. Using 3T magnetic resonance imaging, lesions were classified as DWMH or PV. Age association with lesion classification was analyzed using random effects Tobit regression, adjusting for intracranial volume (ICV) and risk factors. Subjects were 60% women, 36% African-American, mean age 51 ± 11 years. In multivariable analysis adjusted for PV and ICV, DWMH was associated with age (p < 0.001) and female sex (p = 0.003). PV, adjusted for DWMH and ICV, was age associated (p < 0.001). For each age decade, DWMH showed 0.07 log units/decade greater volume (95% CI = 0.04-0.11); PV was 0.18 log units/decade greater (95% CI = 0.14-0.23); slope differences (p < 0.001). In people with a family history of coronary artery disease, PV and DWMH are independently and differentially associated with age controlling for traditional risk factors.

Sociodemographic, behavioral, and psychological correlates of current overweight and obesity in older, urban african american women.

To better understand obesity and overweight among urban African American women, the authors examined sociodemographic, behavioral, and psychological factors within body mass index (BMI) categories. A total of 496 women were recruited for cardiovascular risk factor screening from 20 urban African American churches. Study participants had a mean age of 52.8 years, 13.5 years of education, and an average BMI of 32 kg/m2. Bivariate analyses showed increased overall energy intake and decreased physical performance on a walk test, and general well-being declined as the BMI class increased; obese women had the lowest physical performance and well-being levels and the highest energy intake levels. There was no difference by BMI category, however, in social variables such as educational attainment, employment, marital status, or household income. This study suggests that although women with increasing BMI have some physical and well-being concerns, the major social variables are not differentially distributed by BMI in this sample of women.