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Individuals with prediabetes and diabetes are at increased risk of atherosclerotic cardiovascular disease (ASCVD) and heart failure (HF). Whether ASCVD or HF is more likely to occur first in these populations within different race-sex groups is unknown.Determine the competing risk for the first cardiovascular event by subtype in Black and White men and women with prediabetes and diabetes.Individual-level data from adults without ASCVD or HF were pooled from 6 population-based cohorts. We estimated the competing cumulative incidences of ASCVD, HF, and non-cardiovascular death as the first event in middle-aged (40-59 years) and older (60-79 years) adults, stratified by race and sex, with normal fasting plasma glucose (FPG100 mg/dL), prediabetes (FPG 100-125 mg/dL) and diabetes (FPG ≥126 mg/dL or on antihyperglycemic agents) at baseline. Within each race-sex group, we estimated risk (aHR) of ASCVD, HF, and non-cardiovascular death in adults with prediabetes and diabetes relative to adults with normoglycemia after adjusting for cardiovascular risk factors.In 40,117 participants with 638,910 person-years of follow-up, 5,781 cases of incident ASCVD and 3,179 cases of incident HF occurred. In middle-aged adults with diabetes, competing cumulative incidence of ASCVD as first event was higher than HF in White men (35.4% vs. 11.6%), Black men (31.6% vs. 15.1%), and White women (24.3% vs 17.2%), but not in Black women (26.4% vs 28.4%). Within each group, aHR of ASCVD and HF was significantly higher in adults with diabetes compared with adults with normal FPG. Findings were largely similar in middle-aged adults with prediabetes and older adults with prediabetes or diabetes.Black women with diabetes are more likely to develop HF as their first CVD event, while individuals with diabetes from other race-sex groups are more likely to present first with ASCVD. These results can inform tailoring primary prevention therapies for either HF- or ASCVD-specific pathways based on individual-level risk.

Background: Social and psychosocial factors are associated with cardiovascular health (CVH) and may underlie race/ethnic differences in CVH. Quantifying the contribution of individual-level social and psychosocial factors to racial and ethnic differences in CVH may guide strategies to reduce disparities. Methods: In the MESA and MASALA cohorts, Kitagawa-Blinder-Oaxaca decomposition quantified the contributions of social and psychosocial factors to differences in mean CVH score (range 0-14, with 14 indicating optimal CVH) in Black, Chinese, Hispanic, or South Asian compared with White participants. Results: Among 7,978 adults (mean age 61 [SE 10] years, 52% female), there were 1,892 Black (mean CVH score 7.96), 804 Chinese (CVH 9.69), 1,496 Hispanic (CVH 8.00), 1,164 South Asian (CVH 9.16), and 2,622 White (CVH 8.91) participants. The factors that statistically contributed the most to explained differences in mean CVH score were income for Black participants (if mean income in Black participants were equivalent to White participants, Black participants’ mean CVH score would be 0.14 points higher, p Conclusions: In this multiethnic US cohort, social and psychosocial factors statistically explained racial and ethnic differences in CVH. Socioeconomic and immigration-related factors contributed the largest magnitude to CVH differences between race and ethnic groups.

Introduction: Over 50% of US adults older than 75 live free of atherosclerotic cardiovascular disease (ASCVD) and diabetes (DM), yet data on incident statin use among this population are lacking. Our objective was to assess statin initiation by age among the Women’s Health Initiative cohort free of ASCVD and DM at baseline (1993). Hypothesis: Statin initiation is higher at older ages and differs by race/ethnicity. Methods: Exclusions were statin use at baseline, known ASCVD, DM, and no follow-up after baseline. Self-reported medication use was assessed in 1996 and 2008. Specific statin and dose prescribed at the time of initiation were identified using National Drug Codes and determined statin intensity, defined by the ACC/AHA guidelines. We estimated the adjusted association between age group ( Results: Over 12 years of follow-up, 27% of 99,631 women free of ASCVD and DM at baseline initiated a statin; initiation was lower with older age (Table). This association remained after adjustment for ASCVD risk factors and did not differ by race/ethnicity (p for interaction >0.5). Moderate intensity dose was most common at statin initiation overall, and moderate and high intensity dose were both lower with older age. Conclusion: Of women free of ASCVD and DM, women older than 75 were least likely to start a statin and most likely to start low intensity statin therapy at initiation than younger women. We identified a potential clinical gap for investigation: whether lower overall use of statins and lower intensity statin therapy among older women are associated with preventable ASCVD.

Objectives: To assess whether T2D subgroups are associated with MCI/dementia, and whether the Action for Health in Diabetes (Look AHEAD) intensive lifestyle intervention (ILI) differs in prevention of MCI/dementia by T2D subgroup. Methods: Included 3760 participants (73% of original cohort after death and attrition) with T2D and overweight/obesity randomized to years of ILI or diabetes support and education. We characterized T2D subgroups at randomization using k-means clustering methods and data on age of T2D diagnosis, BMI, waist circumference, and HbA1c. We estimated marginal probabilities for prevalent MCI/dementia 10-13 years post-randomization by T2D subgroup with adjustment for cohort attrition and covariates (Table) and assessed for differential effects of ILI on MCI/dementia by T2D subgroup. Results: T2D subgroups were characterized by (1) older and (2) younger age at T2D onset, (3) high HbA1c, and (4) severe obesity (Table) . Prevalence of MCI/dementia was 8.4% and differed by T2D subgroup. After adjustment, rate of MCI/dementia was highest for the severe obesity and lowest for the younger onset subgroups. There were no differences in MCI/dementia rates between intervention arms for any T2D subgroup (interaction p-value=0.84) . Conclusions: T2D subgroups differ in rate of MCI/dementia, with the highest rate for a subgroup of participants with severe obesity. Lifestyle intervention did not modify rate of MCI/dementia in any T2D subgroup. Disclosure M.Bancks: None. J.Lovato: None. A.Balasubramanyam: None. M.Coday: None. K.C.Johnson: None. M.Munshi: Consultant; Sanofi. C.J.Rebello: None. L.E.Wagenknecht: None. M.Espeland: None.

Background: Higher visit-to-visit variability in fasting glucose (GV) and HbA1c (A1cV), indicating worse glycemic control, is associated with incident dementia in adults with type 2 diabetes (T2D). Few studies have investigated the relationship of GV and A1cV with cognitive decline in the general population. Hypothesis: Higher visit-to-visit GV and A1cV are associated with decline in global cognitive performance. Methods: Fasting glucose (FG) was measured in MESA participants at Exam 1 (2000-02) and each of 5 follow-up exams, and HbA1c was measured at Exam 2 (2002-04), Exam 5 (2010-12), and Exam 6 (2016-18). Global cognitive performance was assessed by the Cognitive Abilities Screening Instrument (CASI; scored 0-100) at Exam 5 and re-administered to a subset at Exam 6. We calculated GV and A1cV as the SD (SD GV ; SD A1c ), coefficient of variation (CV GV ; CV A1c ), and average real variability (ARV GV ; ARV A1c ), and defined global cognitive decline as a ≥1 race/ethnicity-specific SD decrease in CASI score from Exam 5 to Exam 6 (-5.9 to -8.2 points across 4 races/ethnicities). We report the CASI point-change and relative odds of decline (OR) from Exam 5 to Exam 6 (95% CI) associated with continuous log 2 -normalized and highest quartile (Q4 vs. quartiles 1-3 for potential floor effects) of GV and A1cV from inverse probability of censor-weighted linear and logistic regression adjusted for Exam 5 CASI score, age, sex, race/ethnicity, education, vascular risk factors, and APOE ε4 status. Results: A total of 1834 Exam 6 participants (aged 73±8 years; 47% men; 43% White; 7% with T2D at Exam 1; 13% with incident T2D over follow-up) had ≥3 FG measurements and repeat CASI data. The overall 6-year mean (SD) change in CASI was +0.1 (6.6) points. Q4 of SD GV , CV GV , and ARV GV was associated with 0.8 (0.1, 1.5), 0.9 (0.2, 1.6), and 0.7 (0.03, 1.4) point decreases in CASI, respectively, and Q4 of CV GV was associated with higher odds of global cognitive decline (OR = 1.5 [1.1, 2.1]); continuous GV indices were not associated with CASI change. Associations with SD GV and CV GV were driven by participants with incident T2D (interaction P A1c was associated with a 0.5 (0.1, 0.9) point decrease in CASI. However, in participants with incident T2D, 2-fold increments in SD A1c , CV A1c , and ARV A1c were associated with 1.3 (0.2, 2.4), 1.4 (0.2, 2.6), and 1.8 (0.6, 3.0) point decreases in CASI, respectively, and a 2-fold increment in ARV A1c was associated with greater odds of decline (OR = 2.1 [1.1, 3.8]) (interaction P all Conclusions: Poor glycemic control over 14-16 years is associated with modest cognitive decline over the subsequent 6-8 years, particularly among adults at high risk for T2D during mid- to late-life.

Introduction: Body mass index (BMI) does not capture tissue composition and thus is unable to assess the contribution of each tissue type to cardiometabolic health. This limitation of BMI may explain the paradoxical association of BMI-weight status with mortality for those with type 2 diabetes (T2D), and merits investigation of individual tissues. We assessed the relationship between body composition and incident T2D and assessed for differences by BMI-weight status. We hypothesized that greater lean mass (LM) would be associated with lower risk for T2D for all BMI groups. Methods: Black and White participants from CARDIA without T2D in 2005-06 (baseline) were included in this longitudinal analysis ( N =2,473). LM and fat mass (FM) were assessed via dual-energy X-ray absorptiometry. Incident T2D was defined using American Diabetes Association cut points for fasting and post-load glucose, glycated hemoglobin, and diabetes medication use. We used Cox proportional hazards regression to estimate hazard ratios (HR) for incident T2D over 10 years according to 1-standard deviation (SD) increment in LM (1 SD=1g) and assessed for potential effect measure modification (EMM) of this association by weight status. We assessed a secondary exposure, LM:FM ratio, in relation to incident T2D. Results: Mean baseline age was 45.2±3.6 years (57% White and 57% female). The cumulative incidence of T2D was 7.2% (178 events, total person years=21,421.7). Before and after adjustment, neither LM nor LM:FM were significantly associated with T2D (Table), and we did not observe evidence for EMM by weight status for any association. Conclusions: LM in middle adulthood does not appear to be associated with T2D risk. Whether incorporation of data for other tissue depots is informative to T2D risk merits evaluation.

Introduction: Black adults experience higher rates of cardiovascular disease (CVD) compared with White adults, particularly across young adulthood. To identify intervention targets to reduce disparities, we quantified the contribution of individual- and neighborhood-level determinants across young adulthood to Black-White differences in incidence of premature CVD. Methods: In Black and White adults (baseline age 18-30 years) in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, the associations of clinical, lifestyle, psychosocial, socioeconomic, and neighborhood determinants with racial disparities in incident CVD were evaluated with sex-stratified Cox proportional hazards models adjusted for time-updated risk factors. Percent reduction in the ß estimate (log-hazard ratio [HR]) for race quantified the contribution of each risk factor group, individually and combined, to incident CVD racial disparities. Results: In 1707 Black and 2001 White young adults followed for median 33.9 (IQR 33.7-34.0) years, Black adults had higher risk of incident CVD than White adults (Figure). The fully adjusted model yielded significant attenuation of the disparity: HR 1.22 (0.68-2.21) for Black vs. White women, HR 1.42 (0.91-2.23) for Black vs. White men. In women, clinical risk factors were associated with the largest percent reduction in the ß estimate (83%) for race. In men, socioeconomic, lifestyle and clinical risk factors were each associated with significant percent reductions in ß estimates (45%, 37%, and 28%, respectively). Conclusions: In CARDIA, risk for premature CVD was no longer significantly higher in Black vs. White adults after adjustment for upstream determinants across multiple domains. The largest contribution to racial disparities was from clinical factors in women and socioeconomic factors in men. These findings may inform earlier-life interventions to reduce disparities in premature CVD.

OBJECTIVE Patients with type 2 diabetes are encouraged to lose weight, but excessive weight loss in older adults may be a marker of poor health and subsequent mortality. We examined weight change during the postintervention period of Look AHEAD, a randomized trial comparing intensive lifestyle intervention (ILI) with diabetes support and education (DSE) (control) in overweight/obese individuals with type 2 diabetes and sought to identify predictors of excessive postintervention weight loss and its association with mortality. RESEARCH DESIGN AND METHODS These secondary analyses compared postintervention weight change (year 8 to final visit; median 16 years) in ILI and DSE in 3,999 Look AHEAD participants. Using empirically derived trajectory categories, we compared four subgroups: weight gainers (n = 307), weight stable (n = 1,561), steady losers (n = 1,731), and steep losers (n = 380), on postintervention mortality, demographic variables, and health status at randomization and year 8. RESULTS Postintervention weight change averaged −3.7 ± 9.5%, with greater weight loss in the DSE than the ILI group. The steep weight loss trajectory subgroup lost on average 17.7 ± 6.6%; 30% of steep losers died during postintervention follow-up versus 10–18% in other trajectories (P < 0001). The following variables distinguished steep losers from weight stable: baseline, older, longer diabetes duration, higher BMI, and greater multimorbidity; intervention, randomization to control group and less weight loss in years 1–8; and year 8, higher prevalence of frailty, multimorbidity, and depressive symptoms and lower use of weight control strategies. CONCLUSIONS Steep weight loss postintervention was associated with increased risk of mortality. Older individuals with longer duration of diabetes and multimorbidity should be monitored for excessive unintentional weight loss.