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Increased height is a known independent risk factor for atrial fibrillation (AF). However, whether genetic determinants of height influence risk is uncertain. In this candidate gene study, we examined the association of 209 height-associated single-nucleotide polymorphisms (SNPs) with incident AF in 3,309 persons of European descent from the Cardiovascular Health Study, a prospective cohort study of older adults (aged ≥65 years) enrolled in 1989–1990. After a median follow-up period of 13.2 years, 879 participants developed incident AF. The height-associated SNPs together explained approximately 10% of the variation in height (P = 6.0 × 10−8). Using an unweighted genetic height score, we found a nonsignificant association with risk of AF (per allele, hazard ratio = 1.01, 95% confidence interval: 1.00, 1.02; P = 0.06). In weighted analyses, we found that genetically predicted height was strongly associated with AF risk (per 10 cm, hazard ratio = 1.30, 95% confidence interval: 1.03, 1.64; P = 0.03). Importantly, for all models, the inclusion of actual height completely attenuated the genetic height effect. Finally, we identified 1 nonsynonymous SNP (rs1046934) that was independently associated with AF and may warrant future study. In conclusion, we found that genetic determinants of height appear to increase the risk of AF, primarily via height itself. This approach of examining SNPs associated with an intermediate phenotype should be considered as a method for identifying novel genetic targets. [ABSTRACT FROM PUBLISHER]

Abstract: Objectives: HIV disease is associated with increased arterial stiffness, which may be related to inflammation provoked by HIV-related immune perturbation. We assessed the association of T cell markers of immune activation and immunosenescence with carotid artery stiffness among HIV-infected women. Methods: Among 114 HIV-infected and 43 HIV-uninfected women, we measured CD4+ and CD8+ T cell populations expressing activation (CD38+HLA-DR+) and senescence (CD28-CD57+) markers. We then related these measures of immune status with parameters of carotid artery stiffness, including decreased distensibility, and increased Young''s elastic modulus, as assessed by B-mode ultrasound. Results: HIV infection was associated with increased CD4+ T cell activation, CD8+ T cell activation and CD8+ T cell senescence. Among HIV-infected women, adjusted for age, HIV medications, and vascular risk factors, higher CD4+CD38+HLA-DR+ T cell frequency was associated with decreased carotid artery distensibility (β =−2.00, 95% confidence interval [CI]=−3.86, −0.14, P =0.04) and increased Young''s modulus (β =1.00, 95% CI=0.03, 1.97, P =0.04). These associations were affected little by further adjustment for CD4+ T cell count and viral load. Among HIV-infected women, higher frequencies of immunosenescent T cells, including CD4+CD28-CD57+ and CD8+CD28-CD57+ T cells, were also associated with decreased arterial distensibility. Among HIV-uninfected women, frequencies of activated or senescent T cells were not significantly associated with measures of carotid stiffness. Discussion: T cell activation and senescence are associated with arterial stiffness, suggesting that pro-inflammatory populations of T cells may produce functional or structural vascular changes in HIV-infected women. [Copyright &y& Elsevier]

The Hispanic/Latino population experiences socioeconomic adversities across the lifespan and is at greater risk of cognitive impairment, yet little is known about the role of life-course socioeconomic position (SEP) in cognitive function in this population. Using baseline data (2008–2011) from adults (aged 45–74 years) of the Hispanic Community Health Study/Study of Latinos, we assessed the association between childhood SEP and socioeconomic mobility with cognitive function, and whether this association was mediated by midlife SEP. Childhood SEP was assessed using parental education. An index combining participants' education and household income represented midlife SEP. Socioeconomic mobility was categorized as stable low, downward or upward mobility, and stable high-SEP. Cognitive function measures were modeled using survey linear regression with inverse-probability weighting, accounting for covariates. We used mediation analysis to estimate the indirect effect of childhood SEP on cognition through midlife SEP. High childhood SEP was associated with global cognition in adulthood (coefficient for parental education beyond high school vs. less than high school = 0.26, 95% confidence interval: 0.15, 0.37). This association was partially mediated through midlife SEP (indirect effect coefficient = 0.16, 95% confidence interval: 0.15, 0.18). Low SEP through the life course was associated with the lowest cognitive function. This study provides evidence that life-course SEP influences cognitive performance in adulthood. [ABSTRACT FROM AUTHOR]

Background Human immunodeficiency virus (HIV) may affect the risk of death due to cardiovascular disease (CVD) differently in men versus women. Methods We examined CVD mortality rates between 2007 and 2017 among all New York City residents living with HIV and aged 13+ by sex, using data from city HIV surveillance and vital statistics and the National Death Index. Residents without HIV were enumerated using modified US intercensal estimates. We determined associations of HIV status with CVD mortality by sex and neighborhood poverty, defined as the percent of residents living below the federal poverty level, after accounting for age, race/ethnicity, and year. Results There were 3234 CVD deaths reported among 147 915 New Yorkers living with HIV, with the proportion of deaths due to CVD increasing from 11% in 2007 to 22% in 2017. The age-standardized CVD mortality rate was 2.7/1000 person-years among both men and women with HIV. The relative rate of CVD mortality associated with HIV status was significantly higher among women (adjusted rate ratio [aRR] 1.7, 95% confidence interval [CI] 1.6–1.8) than men (aRR 1.2, 95% CI 1.1–1.3) overall, and within strata defined by neighborhood poverty. Sex differences in CVD mortality rates were the greatest when comparing individuals living with HIV and having detectable HIV RNA and CD4+ T-cell counts <500 cells/uL with individuals living without HIV. Conclusions Among people with HIV, 1 in 5 deaths is now associated with CVD. HIV providers should recognize the CVD risk among women with HIV, and reinforce preventive measures (eg, smoking cessation, blood pressure control, lipid management) and viremic control among people living with HIV regardless of neighborhood poverty to reduce CVD mortality. Human immunodeficiency virus (HIV) increases cardiovascular disease mortality risks to a greater degree among women than men, even after accounting for neighborhood poverty. HIV providers should emphasize cardiovascular disease prevention (eg, smoking cessation, hypertension control, lipid management) and viremic control. [ABSTRACT FROM AUTHOR]

Background Estrogen-based hormone therapy (HT) may have beneficial cardiovascular effects when initiated in early menopause. This has not been examined in women with human immunodeficiency virus (HIV), who have heightened immune activation and cardiovascular risks. Methods Among 609 postmenopausal women (1234 person-visits) in the Women's Interagency HIV Study, we examined the relationship of ever HT use (oral, patch, or vaginal) with subclinical atherosclerosis: carotid artery intima-media thickness (CIMT), distensibility, and plaque assessed via repeated B-mode ultrasound imaging (2004–2013). We also examined associations of HT with cross-sectional biomarkers of immune activation and D-dimer. Statistical models were adjusted for sociodemographic, behavioral, and cardiometabolic factors. Results Women (mean age, 51 years; 80% HIV positive) who ever used HT at baseline were older, and more likely to be non-Hispanic White and report higher income, than never-users. Women who ever used HT had 43% lower prevalence of plaque (prevalence ratio, 0.57 [95% confidence interval {CI},.40–.80]; P <.01), 2.51 µm less progression of CIMT per year (95% CI, –4.60, to –.41; P =.02), and marginally lower incidence of plaque over approximately 7 years (risk ratio, 0.38 [95% CI,.14–1.03; P =.06), compared with never-users, adjusting for covariates; ever HT use was not associated with distensibility. These findings were similar for women with and without HIV. Ever HT use was associated with lower serum D-dimer, but not with biomarkers of immune activation after covariate adjustment. Conclusions HT may confer a subclinical cardiovascular benefit in women with HIV. These results begin to fill a knowledge gap in menopausal care for women with HIV, in whom uptake of HT is very low. [ABSTRACT FROM AUTHOR]

Background People with human immunodeficiency virus (HIV) have been reported to have increased risk of clinical and subclinical cardiovascular disease. Existing studies have focused on men and often have been uncontrolled or lacked adequate HIV-negative comparators. Methods We performed echocardiography in the Women's Interagency HIV Study to investigate associations of HIV and HIV-specific factors with cardiac phenotypes, including left ventricular systolic dysfunction (LVSD), isolated LV diastolic dysfunction (LVDD), left atrial enlargement (LAE), LV hypertrophy (LVH), and increased tricuspid regurgitation velocity (TRV). Results Of 1654 participants (age 51 ± 9 years), 70% had HIV. Sixty-three (5.4%) women with HIV (WWH) had LVSD; 71 (6.5%) had isolated LVDD. Compared with women without HIV (WWOH), WWH had a near-significantly increased risk of LVSD (adjusted relative risk = 1.69; 95% confidence interval = 1.00 to 2.86; P =.051). No significant association was noted for HIV seropositivity with other phenotypes, but there was a risk gradient for decreasing CD4+ count among WWH that approached or reached significance for isolated LVDD, LAE, and LVH. WWH with CD4+ count <200 cells/mm3 had significantly higher prevalence of LAE, LVH, and high TRV than WWOH. There were no consistent associations for viral suppression or antiretroviral drug exposure. Conclusions This study suggests that WWH have a higher risk of LVSD compared with sociodemographically similar WWOH, but their risk for isolated LVDD, LAE, LVH, and high TRV is increased only with reduced CD4+ count. Although these findings warrant replication, they support the importance of cardiovascular risk-factor and HIV-disease control for heart disease prevention in this population. [ABSTRACT FROM AUTHOR]

Objectives How insulin-like growth factor-1 (IGF-1) is related to OA is not well understood. We determined relationships between IGF-1 and hospital-diagnosed hand, hip and knee OA in UK Biobank, using Mendelian randomization (MR) to determine causality. Methods Serum IGF-1 was assessed by chemiluminescent immunoassay. OA was determined using Hospital Episode Statistics. One-sample MR (1SMR) was performed using two-stage least-squares regression, with an unweighted IGF-1 genetic risk score as an instrument. Multivariable MR included BMI as an additional exposure (instrumented by BMI genetic risk score). MR analyses were adjusted for sex, genotyping chip and principal components. We then performed two-sample MR (2SMR) using summary statistics from Cohorts for Heart and Aging Research in Genetic Epidemiology (CHARGE) (IGF-1, N  = 30 884) and the recent genome-wide association study meta-analysis (N  = 455 221) of UK Biobank and Arthritis Research UK OA Genetics (arcOGEN). Results A total of 332 092 adults in UK Biobank had complete data. Their mean (s. d.) age was 56.5 (8.0) years and 54% were female. IGF-1 was observationally related to a reduced odds of hand OA [odds ratio per doubling = 0.87 (95% CI 0.82, 0.93)], and an increased odds of hip OA [1.04 (1.01, 1.07)], but was unrelated to knee OA [0.99 (0.96, 1.01)]. Using 1SMR, we found strong evidence for an increased risk of hip [odds ratio per s. d. increase = 1.57 (1.21, 2.01)] and knee [1.30 (1.07, 1.58)] OA with increasing IGF-1 concentration. By contrast, we found no evidence for a causal effect of IGF-1 concentration on hand OA [0.98 (0.57, 1.70)]. Results were consistent when estimated using 2SMR and in multivariable MR analyses accounting for BMI. Conclusion We have found evidence that increased serum IGF-1 is causally related to higher risk of hip and knee OA. [ABSTRACT FROM AUTHOR]

Background: The relationship between alcohol consumption and atherosclerosis has not been sufficiently examined among people living with HIV (PLWH). Methods: We analyzed data from PLWH in the Women's Interagency HIV Study (WIHS; n = 1,164) and the Multicenter AIDS Cohort Study (MACS; n = 387) with no history of cardiovascular disease (CVD). Repeated measures of intima‐media thickness of the right common carotid artery (CCA‐IMT) were assessed using B‐mode ultrasound from 2004 to 2013. Current alcohol consumption was collected at time of CCA‐IMT measurement and was categorized according to gender‐specific weekly limits. Group‐based trajectory models categorized participants into past 10‐year consumption patterns (1994 to 2004). Multivariate generalized estimating equations were conducted to assess the association of past and current alcohol use patterns on change in CCA‐IMT by cohort, controlling for age, race, cigarette and illicit drug use, probable depression, HIV RNA viral load, antiretroviral therapy exposure, and hepatitis C coinfection. Results: Among the WIHS, past heavy alcohol consumption was associated with increased CCA‐IMT level over time (β = 8.08, CI 0.35, 15.8, p = 0.04), compared to abstinence. Among the MACS, compared to abstinence, all past consumption patterns were associated with increased CCA‐IMT over time (past low: β = 15.3, 95% CI 6.46, 24.2, p < 0.001; past moderate: β = 14.3, CI 1.36, 27.2, p = 0.03; past heavy: β = 21.8, CI 4.63, 38.9, p = 0.01). Current heavy consumption was associated with decreased CCA‐IMT among the WIHS (β = −11.4, 95% CI −20.2, −2.63, p = 0.01) and MACS (β = −15.4, 95% CI −30.7, −0.13, p = 0.04). No statistically significant time by consumption pattern effects were found. Conclusions: In both cohorts, 10‐year heavy consumption was associated with statistically significant increases in carotid artery thickness, compared to abstinence. Long‐term patterns of drinking at any level above abstinence were particularly significant for increases in IMT among men, with heavy consumption presenting with the greatest increase. Our results suggest a potentially different window of risk among past and current heavy drinkers. Further studies are needed to determine whether alcohol consumption level is associated with intermediate measures of atherosclerosis. Alcohol screening and interventions to reduce heavy consumption may benefit PLWH who are at risk of CVD. The relationship between alcohol consumption and atherosclerosis has not been sufficiently examined among people living with HIV (PLWH). We analyzed data from PLWH with no history of cardiovascular disease (CVD) using repeated measures of intima‐media thickness and alcohol consumption. Our results suggest a potentially different window of risk among past and current heavy drinkers. Alcohol screening and interventions to reduce heavy consumption may benefit PLWH who are at risk for CVD. [ABSTRACT FROM AUTHOR]

Abstract: Aim: We investigated the cross‐sectional association between diet quality and severe periodontitis in a sample of diverse Hispanics from the Hispanic Community Health Study/Study of Latinos. Materials and methods: A total of 13,920 Hispanic/Latinos aged 18–74 years of different heritages underwent a full‐mouth oral examination and completed two 24‐hr dietary recalls during 2008–2011. Severe periodontitis was defined as having ≥30% tooth sites with clinical attachment loss ≥5 mm. Diet quality was assessed using the Alternative Healthy Eating Index (AHEI‐2010). We evaluated the association of diet quality with severe periodontitis adjusting for age, sex, nativity status, income, education, last dental visit, current insurance, cigarette smoking, diabetes, and energy intake. Results: Relative to those at the lowest quartile of diet quality, individuals at the highest quartile had significantly lower odds of severe periodontitis (adjusted OR = 0.57, 95% CI: 0.39–0.82), with evidence of a dose–response relationship across AHEI quartiles. Among AHEI‐2010 components, higher consumption of whole grains and fruits, and lower consumption of red/processed meats were associated with lower odds of severe periodontitis. Conclusion: Better‐quality diet was associated with lower prevalence of severe periodontitis although the causal pathways need to be clarified in future work. [ABSTRACT FROM AUTHOR]

Reports on the associations between multiple clinical and behavioral health indicators and major health outcomes among older adults are scarce. We prospectively examined concordance with guidelines from the American Cancer Society and American Heart Association for disease prevention in relation to cancer, cardiovascular disease (CVD), and mortality among Cardiovascular Health Study enrollees aged 65-98 years who, at baseline assessment in 1989-1996 (n = 3,491), were free of CVD and cancer. Total and cause-specific mortality, as well as incidence of cancer and CVD, were lower with higher guideline concordance. Independent of body mass index, blood pressure, total cholesterol, and fasting plasma glucose, better health behaviors (diet, physical activity, and alcohol consumption) were associated with lower mortality (2-sided P < 0.0001). Among individuals with ideal levels for 3-4 of these 4 cardiometabolic biomarkers, those with poor concordance with health behavior recommendations had higher mortality compared with those who had the highest concordance with these behavioral recommendations (adjusted mortality hazard ratio = 1.82,95% confidence interval: 1.25,2.67). Older adults who are concordant with recommendations for cancer and CVD prevention have reduced rates of chronic disease and mortality. Interventions to achieve and maintain healthy lifestyle behaviors may offer benefits both in the presence and absence of adverse traditional clinical risk factors. [ABSTRACT FROM AUTHOR]

Objectives To ascertain whether older adults with extensive disease but relative vigor (adapters) shorten the period at the end of life in which they live with morbidity (compress morbidity). Design Prospective, community-based cohort study in four U.S. cities. Setting Cardiovascular Health Study. Participants Individuals aged 65 and older. Measurements Participants were categorized into three groups according to extent of disease (assessed noninvasively), vigor, and frailty (expected agers (n = 3,528, extent of disease similar to vigor and frailty-reference group), adapters (n = 882, higher disease but vigorous), and prematurely frail (n = 855, lower disease but frail)) and compared according to years of able life ( YAL), years of self-reported healthy life ( YHL), and mortality using multivariable regression and survival analysis. Results After adjustment, adapters had 0.97 (95% confidence interval ( CI) = 0.60-1.33) more YAL and 0.54 (95% CI = 0.19-0.90) more YHL than expected agers, and those who were prematurely frail had −0.99 (95% CI = −1.36 to −0.62) fewer YAL and −0.53 (95% CI = −0.89 to −0.17) fewer YHL than expected agers. Adapters had 0.9 more and prematurely frail had 1.5 fewer years of total life than expected agers ( P < .001). Adapters spent 55% of their remaining life able and healthy, those who were prematurely frail spent 37%, and of expected agers spent 47% ( P < .001). Conclusion Despite similar levels of disease burden, older adults who were more vigorous appeared to compress morbidity and live longer. Older adults with higher frailty lengthened morbidity and had greater mortality. Adaptive factors may compress morbidity and decrease mortality. [ABSTRACT FROM AUTHOR]

The study examined the association of childhood and current economic hardship with anthropometric indices in Hispanic/Latino adults, using data from the HCHS/SOL Socio-cultural ancillary study (N = 5,084), a community-based study of Hispanic/Latinos living in four urban areas (Bronx, NY, Chicago, IL, Miami, FL, and San Diego, CA). Childhood economic hardship was defined as having experienced a period of time when one’s family had trouble paying for basic needs (e.g., food, housing), and when this economic hardship occurred: between 0–12, 13–18 years old, or throughout both of those times. Current economic hardship was defined as experiencing trouble paying for basic needs during the past 12 months. Anthropometry included height, body mass index (BMI), waist circumference (WC), and percentage body fat (%BF). Complex survey linear regression models were used to test the associations of childhood economic hardship with adult anthropometric indices, adjusting for potential confounders (e.g., age, sex, Hispanic background). Childhood economic hardship varied by Hispanic background, place of birth, and adult socio-economic status. Childhood economic hardship during both periods, childhood and adolescence, was associated with shorter height. Childhood economic hardship was associated with greater adiposity among US born individuals only. Current economic hardship was significantly associated with all three measures of adiposity (BMI, WC, %BF). These findings suggest that previous periods of childhood economic hardship appear to influence adult height more than adiposity, whereas current economic hardship may be a better determinant of adult adiposity in Hispanics. [ABSTRACT FROM AUTHOR]

Objectives. We assessed risk of cigarette smoking initiation among Hispanics/ Latinos during adolescence by migration status and gender. Methods. The Hispanic Community Health Study/Study of Latinos (HCHS/ SOL) surveyed persons aged 18 to 74 years in 2008 to 2011. Our cohort analysis (n = 2801 US-born, 13 200 n on-US-born) reconstructed participants' adolescence from 10 to 18 years of age. We assessed the association between migration status and length o f US residence and risk of cigarette smoking initiation during adolescence, along with effects o f gender and Hispanic/Latino background. Results. Among individuals who migrated by 18 years of age, median age and year of arrival were 13 years and 1980, respectively. Among women, but not men, risk o f smoking initiation during adolescence was higher among the US-born (hazard ratio [HR] = 2.10; 95% confidence interval [Cl] = 1.73, 2.57; P<.001), and those who had resided in the United States for 2 or more years (HR = 1.47; 95% Cl = 1.11, 1.96; P= .01) than among persons who lived outside the United States. Conclusions. Research examining why some adolescents begin smoking after moving to the United States could inform targeted interventions. [ABSTRACT FROM AUTHOR]