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Purpose: Cardiovascular disease is a major contributor to morbidity and mortality, and prevention relies on accurate identification of those at risk. Studies of the association between quality of life (QOL) and mortality and vascular events incompletely accounted for depression, cognitive status, social support, and functional status, all of which have an impact on vascular outcomes. We hypothesized that baseline QOL is independently associated with long-term mortality in a large, multi-ethnic urban cohort.Methods: In the prospective, population-based Northern Manhattan Study, Spitzer QOL index (SQI, range 0-10, with ten signifying the highest QOL) was assessed at baseline. Participants were followed over a median 11 years for stroke, myocardial infarction (MI), and vascular and non-vascular death. Multivariable Cox proportional hazards regression estimated hazard ratio and 95% confidence interval (HR, 95% CI) for each outcome, with SQI as the main predictor, dichotomized at 10, adjusting for baseline demographics, vascular risk factors, history of cancer, social support, cognitive status, depression, and functional status.Results: Among 3298 participants, mean age was 69.7 + 10.3 years; 1795 (54.5%) had SQI of 10. In fully adjusted models, SQI of 10 (compared to SQI <10) was associated with reduced risk of all-cause mortality (HR 0.80, 95% CI 0.72-0.90), vascular death (0.81, 0.69-0.97), non-vascular death (0.78, 0.67-0.91), and stroke or MI or death (0.82, 0.74-0.91). In fully adjusted competing risk models, there was no association with stroke (0.93, 0.74-1.17), MI (0.98, 0.75-1.28), and stroke or MI (1.03, 0.86-1.24). Results were consistent when SQI was analyzed continuously.Conclusion: In this large population-based cohort, highest QOL was inversely associated with long-term mortality, vascular and non-vascular, independently of baseline primary vascular risk factors, social support, cognition, depression, and functional status. QOL was not associated with non-fatal vascular events. [ABSTRACT FROM AUTHOR]

We hypothesized that tumor necrosis factor receptor 1 (TNFR1) levels are associated with long-term trajectories of functional status independently of vascular risk factors and the occurrence of stroke and myocardial infarction (MI) during follow-up. In the Northern Manhattan Study, stroke-free persons aged ≥40 years in northern Manhattan (New York, New York) had annual assessments with the Barthel index (BI) for a median of 13 years (1993-2015). Assessment of baseline demographic factors, risk factors, and laboratory studies included measurement of TNFR1 (n = 1,863). Generalized estimating equations models were used to estimate standardized associations between TNFR1 and 1) baseline functional status and 2) change in function over time, adjusting for demographic factors, vascular risk factors, social variables, cognition, and depression, as well as stroke and MI occurrence during follow-up. The mean age of participants was 70 (standard deviation (SD), 10) years; 66% were women, and 55% were Hispanic. The mean TNFR1 level was 2.57 mg/L. TNFR1 was associated with baseline BI (-0.93 BI points per SD increment in TNFR1; 95% confidence interval: -1.59, -0.26) and change over time (-0.36 BI points per year per SD increment in TNFR1; 95% confidence interval: -0.69, -0.03). In this large population-based study, higher TNFR1 levels were associated with greater baseline disability and disability over time, even with adjustment for baseline covariates and stroke and MI occurrence during follow-up. [ABSTRACT FROM AUTHOR]

Background: Previous studies of exercise have focused on measuring physical activity in totality using summary statistics such as metabolic equivalent score for total intensity or total energy count.Objective: We aimed to examine the multidimensionality of leisure-time physical activity (LTPA) and to identify the specific LTPA components that were associated with cardiovascular mortality in the elderly.Design and Participants: The Northern Manhattan Study (NOMAS) is a multiethnic prospective cohort of elderly stroke-free individuals consisting of a total of 3298 participants recruited between 1993 and 2001, with a median follow-up of 17 years.Main Measures: Physical activity questionnaire data were available in 3293 NOMAS participants, who were categorized into subgroups with similar exercise patterns by model-based cluster analysis. Three subgroup-defining LTPA features were identified and were considered as primary exposures in Cox proportional hazard models: frequency of activity, number of activity types (variety), and energy-to-duration ratio (EDR). We considered cardiovascular mortality and non-cardiovascular mortality as outcomes in Cox cause-specific proportional hazard models, and all-cause mortality as outcome in Cox models.Key Results: A high activity frequency was associated with reduced cardiovascular mortality (hazard ratio, HR = 0.93, P = 0.03), but demonstrated no effect on non-cardiovascular death. A high EDR was associated with increased risk of cardiovascular death (HR = 1.30, P = 0.01). A high number of activity types was beneficial in reducing all-cause mortality (HR = 0.87, P = 0.01).Conclusions: Exercise frequency was protective against cardiovascular mortality, and a high variety of activity was protective against all-cause mortality. The performance of frequent and varied non-intense exercise in an elderly population such as ours is achievable and can reduce the risk of death. [ABSTRACT FROM AUTHOR]

Background: high-sensitivity C-reactive protein (CRP) has been associated with cardiovascular events and mortality, but the association of CRP with functional status is not well defined. We hypothesised that serum levels of high-sensitivity CRP are associated with long-term trajectories of functional status independently of vascular risk factors and stroke and myocar-dial infarction (MI) occurring during follow-up. Design: prospective, population-based. Setting: northern Manhattan Study. Participants: stroke-free participants aged ≥40 years. Measurements: annual assessments of disability with the Barthel index (BI) for a median of 13 years. BI was analysed as a continuous variable (range 0-100). Baseline demographics, risk factors and laboratory studies were collected, including CRP (n = 2,240). Separate generalised estimating equation models estimated standardised associations between CRP and (i) baseline functional status and (ii) change in function over time, adjusting for demographics, vascular risk factors, social variables, cognition, and depression measured at baseline, and stroke and MI occurring during follow-up. Results: mean age was 69 (SD 10) years, 36% were male, 55% Hispanic, 75% hypertensive and 21% diabetic; 337 MIs and 369 first strokes occurred during follow-up. Mean CRP level was 5.24 mg/l (SD 8.86). logCRP was associated with baseline BI (-0.34 BI points per unit logCRP, 95% confidence interval -0.62, -0.06) but not with change over time. Conclusions: in this large population-based study, higher serum CRP levels were associated with higher baseline disability, even when adjusting for baseline covariates and stroke and MI occurring during follow-up. Systemic inflammation may contribute to disability independently of clinical vascular events. [ABSTRACT FROM AUTHOR]

Purpose: To identify risk factors (RF) for diabetes within a multiethnic cohort and to examine whether race-ethnicity modified their effects.Methods: Participants in the Northern Manhattan Study without diabetes at baseline were studied from 1993 to 2014 (n=2430). Weibull regression models with interval censoring data were fit to calculate hazard ratios and 95% confidence intervals for incident diabetes. We tested for interactions between RF and race-ethnicity.Results: During a mean follow-up period of 11years, there were 449 diagnoses of diabetes. Being non-Hispanic black (HR 1.69 95% CI 1.11-2.59) or Hispanic (HR 2.25 95% CI 1.48-3.40) versus non-Hispanic white, and body mass index (BMI; HR 1.34 per SD 95% CI 1.21-1.49) were associated with greater risk of diabetes; high-density lipoprotein cholesterol (HR 0.75 95% CI 0.66-0.86) was protective. There were interactions by race-ethnicity. In stratified models, the effects of BMI, current smoking, and C-reactive protein (CRP) on risk of diabetes differed by race-ethnicity (p for interaction <0.05). The effects were greater among non-Hispanic whites than non-Hispanic blacks and Hispanics.Conclusions: Although Hispanics and non-Hispanic blacks had a greater risk of diabetes than whites, there were variations by race-ethnicity in the association of BMI, smoking, and CRP with risk of diabetes. Unique approaches should be considered to reduce diabetes as traditional RF may not be as influential in minority populations. [ABSTRACT FROM AUTHOR]