Stamatelopoulos, Kimon and Sibbing, Dirk and Rallidis, Loukianos S and Georgiopoulos, Georgios and Stakos, Dimitrios and Braun, Siegmund and Gatsiou, Aikaterini and Sopova, Kateryna and Kotakos, Christos and Varounis, Christos and Tellis, Constantinos C and Kastritis, Efstathios and Alevizaki, Maria and Tselepis, Alexandros D and Alexopoulos, Panagiotis and Laske, Christoph and Keller, Till and Kastrati, Adnan and Dimmeler, Stefanie and Zeiher, Andreas M and Stellos, Konstantinos (2015) Amyloid-beta (1-40) and the risk of death from cardiovascular causes in patients with coronary heart disease. Journal of the American College of Cardiology, 65 (9). pp. 904-916. ISSN 1558-3597
Full text not available from this repository.Abstract
BACKGROUND: The amyloid beta peptide is the major protein constituent of neuritic plaques in Alzheimer disease and appears to play a central role in vascular inflammation pathophysiology. OBJECTIVES: This study sought to determine the clinical value of amyloid-beta 1-40 (Abeta40) measurement in predicting cardiovascular (CV) mortality in patients with coronary heart disease (CHD) and arterial stiffness progression in young healthy subjects. METHODS: Abeta40 was retrospectively measured in blood samples collected from 3 independent prospective cohorts and 2 case-control cohorts (total N = 1,464). Major adverse cardiac events (MACE) were assessed in the 2 prospective cohorts (n = 877) followed for a median of 4.4 years. To look at effects on subclinical disease, arterial stiffness was evaluated at baseline and after 5-year follow-up (n = 107) in young healthy subjects. The primary endpoint was the predictive value of Abeta40 for CV mortality and outcomes in patients with CHD. RESULTS: In Cox proportional hazards models adjusted for age, sex, estimated glomerular filtration rate, left ventricular ejection fraction, high-sensitivity C-reactive protein, and high-sensitivity troponin T, Abeta40 independently predicted CV death and MACE in patients with CHD (p < 0.05 for all). After multivariate adjustment, Abeta40 levels conferred a substantial enhancement of net reclassification index and integrated discrimination improvement of individuals at risk in the total combined CHD cohort over the best predictive model. Further cohort-based analysis revealed that Abeta40 levels were significantly and independently associated with arterial stiffness progression, incident subclinical atherosclerosis, and incident CHD. CONCLUSIONS: Measuring blood levels of Abeta40 identified patients at high risk for CV death.