BACKGROUND: We wished to determine if a marker of endothelial dysfunction/activation soluble vascular cell adhesion molecule (s-VCAM)-was related to functional status and mortality in community-dwelling older adults independent of the known effects of markers of inflammation and coagulation. METHODS: Data came from the third and fourth in-person waves of the Duke Established Populations for Epidemiologic Studies of the Elderly. Participants (aged ≥ 71 years) had participated in a blood draw (N = 1,551) from which concentrations of s-VCAM, interleukin-6, and D-dimer were determined. Information was gathered in-person on demographics, health behaviors, chronic health conditions, and functional status (Katz, Rosow-Breslau, Nagi). Death was determined through the National Death Index. Multivariable regression analysis was used to examine the adjusted association of s-VCAM with functional status; Cox proportional hazards models ascertained hazard of mortality. RESULTS: Controlled analyses indicated that cross-sectionally, but not longitudinally (4 years later), greater s-VCAM concentrations were associated with poorer function as measured by the Katz and Rosow-Breslau scales (p < .05 for both), independent of interleukin-6 and D-dimer. In controlled analyses, s-VCAM (p = .002), D-dimer (p = .008), and interleukin-6 (p = .01) were independently related to 4-year mortality; 1 SD increase in log concentration conferred 1.2-, 1.1-, and 1.2-fold increases in mortality, respectively. The greatest hazard of mortality was observed within the first year after measurement. s-VCAM concentrations were not predictive of 15-year mortality. CONCLUSIONS: Independent of inflammation and coagulation markers, endothelial dysfunction serves as a marker of, and potentially contributes causally to, poor function and death in community-dwelling older adults.
BACKGROUND: We wished to determine if a marker of endothelial dysfunction/activation soluble vascular cell adhesion molecule (s-VCAM)-was related to functional status and mortality in community-dwelling older adults independent of the known effects of markers of inflammation and coagulation. METHODS: Data came from the third and fourth in-person waves of the Duke Established Populations for Epidemiologic Studies of the Elderly. Participants (aged ≥ 71 years) had participated in a blood draw (N = 1,551) from which concentrations of s-VCAM, interleukin-6, and D-dimer were determined. Information was gathered in-person on demographics, health behaviors, chronic health conditions, and functional status (Katz, Rosow-Breslau, Nagi). Death was determined through the National Death Index. Multivariable regression analysis was used to examine the adjusted association of s-VCAM with functional status; Cox proportional hazards models ascertained hazard of mortality. RESULTS: Controlled analyses indicated that cross-sectionally, but not longitudinally (4 years later), greater s-VCAM concentrations were associated with poorer function as measured by the Katz and Rosow-Breslau scales (p < .05 for both), independent of interleukin-6 and D-dimer. In controlled analyses, s-VCAM (p = .002), D-dimer (p = .008), and interleukin-6 (p = .01) were independently related to 4-year mortality; 1 SD increase in log concentration conferred 1.2-, 1.1-, and 1.2-fold increases in mortality, respectively. The greatest hazard of mortality was observed within the first year after measurement. s-VCAM concentrations were not predictive of 15-year mortality. CONCLUSIONS: Independent of inflammation and coagulation markers, endothelial dysfunction serves as a marker of, and potentially contributes causally to, poor function and death in community-dwelling older adults.
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