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Revista Española de Cardiología (English Edition) Revista Española de Cardiología (English Edition)

Bloodstream Amyloid-beta (1-40) Peptide, Cognition, and Outcomes in Heart Failure

Antoni Bayes-Genis a,b,c,, Jaume Barallat d, Marta de Antonio a,b, Mar Domingo a,c, Elisabet Zamora a,c, Joan Vila e,f, Isaac Subirana e,f, Paloma Gastelurrutia a,c, M. Cruz Pastor b, James L. Januzzi g, Josep Lupón a,b,c

a Unidad de Insuficiencia Cardiaca, Servicio de Cardiología, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain
b Departamento de Medicina, Universidad Autónoma de Medicina, Barcelona, Spain
c CIBERCV (CB16/11/00403), Instituto de Salud Carlos III, Madrid, Spain
d Servicio de Bioquímica, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, Spain
e CIBER de Epidemiología y Salud Pública, Barcelona, Spain
f Grupo de estudio en Genética y Epidemiología Cardiovascular, Grupo de estudio REGICOR, IMIM (Instituto de Investigación Médica del Hospital del Mar), Barcelona, Spain
g Cardiology Division, Massachusetts General Hospital, Harvard Clinical Research Institute, Boston, Massachusetts, United States

Refers to

Circulating Amyloid-Beta (1-40) Predicts Clinical Outcomes in Patients With Heart Failure
Kimon Stamatelopoulos, Konstantinos Stellos
Rev Esp Cardiol. 2017;70:905-6
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Amyloid-beta. Heart failure. Cognition. Prognosis. Biomarkers.


Introduction and objectives

In the brain, amyloid-beta generation participates in the pathophysiology of cognitive disorders; in the bloodstream, the role of amyloid-beta is uncertain but may be linked to sterile inflammation and senescence. We explored the relationship between blood levels of amyloid-beta 1-40 peptide (Aβ40), cognition, and mortality (all-cause, cardiovascular, and heart failure [HF]-related) in ambulatory patients with HF.


Bloodstream Aβ40 was measured in 939 consecutive patients with HF. Cognition was evaluated with the Pfeiffer questionnaire (adjusted for educational level) at baseline and during follow-up. Multivariate Cox regression analyses and measurements of performance (discrimination, calibration, and reclassification) were used, with competing risk for specific causes of death.


Over 5.1 ± 2.9 years, 471 patients died (all-cause): 250 from cardiovascular causes and 131 HF-related. The median Aβ40 concentration was 519.1 pg/mL [Q1-Q3: 361.8-749.9 pg/mL]. The Aβ40 concentration correlated with age, body mass index, renal dysfunction, and New York Heart Association functional class (all P < .001). There were no differences in Aβ40 in patients with and without cognitive impairment at baseline (P = .97) or during follow-up (P = .20). In multivariable analysis, including relevant clinical predictors and N-terminal pro-B-type natriuretic peptide, Aβ40 remained significantly associated with all-cause death (HR, 1.22; 95%CI, 1.10-1.35; P < .001) and cardiovascular death (HR, 1.18; 95%CI, 1.03-1.36; P = .02), but not with HF-related death (HR, 1.13; 95%CI, 0.93-1.37; P = .22). Circulating Aβ40 improved calibration and patient reclassification.


Blood levels of Aβ40 are not associated with cognitive decline in HF. Circulating Aβ40 was predictive of mortality and may indicate systemic aging.


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1885-5857/© 2017 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved