Neli Stoyanova

Racial differences in arterial stiffness and microcirculatory function between Black and White Americans.

Background Compared with whites, black Americans suffer from a disproportionate burden of cardiovascular disease (CVD). We hypothesized that racial differences in the prevalence of CVD could be attributed, in part, to impaired vascular function in blacks after adjustment for differences in risk factor burden. Methods and Results We assessed vascular function in 385 black and 470 white subjects (mean age, 48±11 years; 45% male). Using digital pulse amplitude tonometry (EndoPAT) we estimated the reactive hyperemia index (RHI), a measure of microvascular endothelial function, and peripheral augmentation index (PAT‐AIx). Central augmentation index (C‐AIx) and pulse‐wave velocity (PWV) were measured as indices of wave reflections and arterial stiffness, respectively, using applanation tonometry (Sphygmocor). Compared with whites, blacks had lower RHI (2.1±0.6 versus 2.3±0.6, P<0.001), greater arterial wave reflections assessed as both PAT‐AIx (20.4±21.5 versus 17.0±22.4, P=0.01) and CAIx (20.8±12.3 versus 17.5±13.3, P=0.001), and greater arterial stiffness, measured as PWV (7.4±1.6 versus 7.1±1.6 m/s, P=0.001). After adjustment for traditional CVD risk factors, black race remained a significant predictor of lower RHI and higher PAT‐AIx and CAIx (all P<0.001) in all subjects and of higher PWV in men (P=0.01). Furthermore, these associations persisted in a subgroup analysis of “healthy” individuals free of CVD risk factors. Conclusion Black race is associated with impaired microvascular vasodilatory function, and greater large arterial wave reflections and stiffness. Because impairment in these vascular indices may be associated with worse long‐term outcomes, they may represent underlying mechanisms for the increased CVD risk in blacks.

Association between Depression and Inflammation - Differences by Race and Sex: The META-Health Study

Objective: To test whether the association between depression and inflammation differs by race and sex. Depressive symptoms have been associated with higher levels of C-reactive protein (CRP). However, few studies have examined this association in samples including a significant number of African Americans, or examined whether the association differs by race and sex. Methods: Depressive symptoms and CRP were assessed in 512 African American and white participants, age 30 to 65 years, as part of the community-based Morehouse and Emory Team up to Eliminate Health Disparities (META-Health) Study. Depression was determined by responses to the Beck Depression Inventory II (BDI-II). Multivariable linear regression models were used to adjust for demographic and metabolic risk factors. Results: African American men had higher total BDI-II scores than white men (p =.03), whereas there was no difference in women. There was a significant race-sex-depression interaction in predicting CRP levels (p =.02). White women with mild to severe depressive symptoms had higher levels of CRP compared with those with minimal to no depressive symptoms (p <.05). There were no differences in levels of CRP by severity of depressive symptoms in white men or African Americans of either sex. Higher BDI-II scores were related to higher CRP levels in white women after adjusting for age and level of education (&bgr; = 0.227, p =.006). However, the association was eliminated after further adjustment for metabolic risk factors (&bgr; = 0.077, p =.35). Conclusions: Although depressive symptoms are associated with inflammation, the association varies by race and sex.CVD = cardiovascular disease; BDI-II = Beck Depression Inventory II; CRP = C-reactive protein; BMI = body mass index; HDL-C = high-density lipoprotein cholesterol

The Association between Depression and Leptin is Mediated by Adiposity

Objective Animal models suggest that impaired leptin production, or leptin resistance despite increased leptin levels, may contribute to depression. The link between leptin and depression could be mediated by obesity, which is more common in depression and increases leptin production. Methods We administered the Beck Depression Inventory–II (BDI-II) to 537 participants (mean [standard deviation (SD)] age = 51 [9] years; female, 61%) enrolled in the Morehouse and Emory Team up to Eliminate Health Disparities (META-Health) study. Leptin levels were examined as continuous log-transformed values. Results Participants with moderate to severe depression had higher levels of leptin (median [interquartile range] 37.7 [17.6–64.9] ng/mL) than those with mild depression (22.9 [7.0–57.9] ng/mL) or minimal to no depression (19.8 ng/mL [7.8–39.1], p = .003). Participants with moderate to severe depression had higher body mass index (BMI) than those with mild or minimal depression (mean [SD] = 33 [8] versus 31 [9] versus 29 [7] kg/m2, p = .001). After multivariate adjustment for age, sex, race, smoking status, hypertension, diabetes, blood pressure, lipids, and C-reactive protein, the BDI-II score remained a significant predictor of leptin levels (&bgr; = 0.093, p = .01). Further adjustment for BMI eliminated the association between the BDI-II score and leptin (&bgr; = 0.03, p = .3). Adjusting for waist circumference in place of BMI revealed similar findings. Conclusions The association between depression and leptin seems to be mediated by increased adiposity in depressed individuals. Abbreviations BDI-II = Beck Depression Inventory–II BMI = body mass index HDL-C = high-density lipoprotein cholesterol

Differences in Systemic Oxidative Stress Based on Race and the Metabolic Syndrome: The Morehouse and Emory Team up to Eliminate Health Disparities (META-Health) Study

BACKGROUND Classification schema such as metabolic syndrome may underestimate cardiovascular disease (CVD) risk in African Americans, despite a higher burden of CVD in African Americans. Oxidative stress results from an imbalance of prooxidants and antioxidants and leads to endothelial dysfunction that promotes vascular inflammation and atherosclerosis. Aminothiol markers of oxidative stress are associated with CVD risk factors and metabolic syndrome; however, little is known about racial differences in levels of oxidative stress. We sought to investigate whether oxidative stress would be higher in African Americans compared to whites independently of traditional risk factor burden. METHODS We assessed oxidative stress in a biracial, community-based cohort. In 620 subjects (59% female, 52% African American) in the Morehouse and Emory Team up to Eliminate Health Disparities (META-Health) study, we measured plasma levels of glutathione, an intracellular antioxidant, and its redox potential as a ratio of reduced and oxidized glutathione (E(h) glutathione). RESULTS African Americans had lower glutathione levels (P<0.001) compared to whites. There was a trend toward more oxidized E(h) glutathione (P = 0.07) in African Americans; however, this did not reach statistical significance. After adjustment for demographics and CVD risk factors, African-American race remained a significant correlate of lower glutathione levels (P<0.001) and a more oxidized E(h) glutathione (P = 0.04). After further adjustment for high-sensitivity C-reactive protein (hsCRP), glutathione remained significantly lower in African Americans (P = 0.001). African Americans with or without metabolic syndrome had lower glutathione levels compared to whites with or without metabolic syndrome, respectively (both P ≤ 0.001), and African Americans without metabolic syndrome had a more oxidized E(h) glutathione compared to whites without metabolic syndrome (P = 0.003). CONCLUSIONS African Americans have higher levels of oxidative stress than whites, even after adjustment for differences in CVD risk factors and inflammation. Racial differences in oxidative stress may play a key role in understanding observed racial disparities in CVD.

Association between vitamin D and adiponectin and its relationship with body mass index: the META-Health Study

Background: Low vitamin D and adiponectin levels are both associated with obesity and cardiovascular disease. Previous studies have indicated that vitamin D levels are directly associated with adiponectin, and that this association varies across body mass index (BMI) categories; stronger with increasing BMI. Few studies examined this association in African-Americans (AA), known to have lower levels of vitamin D and adiponectin, and in whites. Methods: We assessed whether serum vitamin D is associated with serum adiponectin in a biracial population-based sample. Cross-sectional analyses were performed on 426 non-diabetic participants (218 whites and 208 AA) from the META-Health Study, a random sample from the metro Atlanta. Age-adjusted correlations and multivariable linear regression were used for analyses. We investigated the effect modification of the BMI categories of lean, overweight, and obese as defined by standard cut-points (25 and 30 kg/m2). Results: The mean (SD) age of our study sample was 50.5 (9) years. The mean (SD) levels of vitamin D were 27.4 (9.8) ng/mL in white women, 25.5 (9.3) ng/mL in white men, 16.9 (7.3) ng/mL in AA women, and 18.8 (7.3) ng/mL in AA men. The mean (SD) levels of adiponectin were 17.0 (17.1) μg/mL in white women, 9.9 (11.3) μg/mL in white men, 6.6 (4.8) μg/mL in AA women, and 9.4 (11.6) μg/mL in AA men. Among lean white women (n = 63), there was a significant direct association between vitamin D and adiponectin (β = 0.02, p = 0.04) after adjustment for age, systolic blood pressure, HDL-cholesterol, triglycerides, income, and season of blood drawing. On the contrary, in lean AA women (n = 23), there was a significant inverse association (β = −0.06, p = 0.01). Conclusion: The association of vitamin D and adiponectin is dependent on race, gender, and BMI category. Among lean white women, there was a significant direct association, whereas in lean AA women the association was inverse. No association was present among obese individuals.