Amiloide beta (1-40) en sangre, cognición y pronóstico en insuficiencia cardiaca / Bloodstream amyloid-beta (1-40) peptide, cognition, and outcomes in heart failure

Introducción y objetivos: A nivel cerebral, el amiloide-beta participa en la fisiopatología de trastornos cognitivos; en la circulación, el papel del amiloide-beta es incierto pero podría estar relacionado con procesos de inflamación estéril y senescencia. Se ha analizado la relación entre concentraciones circulantes de amiloide-beta 1-40 (Aβ40), cognición y mortalidad (global, cardiovascular y por insuficiencia cardiaca [IC]) en pacientes ambulatorios con IC. Métodos: El Aβ40 circulante se midió en 939 pacientes consecutivos con IC. El estado cognitivo se evaluó con el cuestionario de Pfeiffer (ajustado al nivel educacional) en condiciones basales y durante el seguimiento. Se utilizaron análisis de regresión múltiple de Cox y medidas de función (discriminación, calibración y reclasificación), ajustando por riesgos competitivos para causas de muerte específicas. Resultados: Durante 5.1 ± 2.9 años, 471 pacientes murieron: 250 de causa cardiovascular y 131 por IC. La mediana de Aβ40 circulante fue de 519,1 pg/ml [Q1-Q3: 361,8-749,9 pg/ml]. La concentración de Aβ40 correlacionó con la edad, índice de masa corporal, insuficiencia renal y clase funcional de la New York Heart Association (todas p < 0,001). No hubo diferencias en Aβ40 en pacientes con y sin trastorno cognitivo a nivel basal (p = 0,97) o durante el seguimiento (p = 0,20). En el análisis multivariado, que incluye predictores clínicos relevantes y la fracción aminoterminal del propéptido natriurético cerebral, Aβ40 permaneció asociado a mortalidad global (HR = 1,22; IC95%, 1,10-1,35; p < 0,001) y cardiovascular (HR = 1,18; IC95%, 1,03-1,36; p = 0,02), pero no con mortalidad por IC (HR = 1,13; IC95%, 0,93-1,37; p = 0,22). El Aβ40 circulante mejoró la calibración y reclasificación de los pacientes. Conclusiones: Las concentraciones circulantes de Aβ40 no se asocian a trastorno cognitivo en la IC. Aβ40 fue predictor de mortalidad y podría indicar envejecimiento sistémico (AU)

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. Methods: 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. Results: 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. Conclusions: Blood levels of Aβ40 are not associated with cognitive decline in HF. Circulating Aβ40 was predictive of mortality and may indicate systemic aging (AU)

The Dynamics of Cardiovascular Biomarkers in non-Elite Marathon Runners.

The number of recreational/non-elite athletes participating in marathons is increasing, but data regarding impact of endurance exercise on cardiovascular health are conflicting. This study evaluated 79 recreational athletes of the 2016 Barcelona Marathon (72% men; mean age 39 ± 6 years; 71% ≥35 years). Blood samples were collected at baseline (24-48 h before the race), immediately after the race (1-2 h after the race), and 48-h post-race. Amino-terminal pro-B type natriuretic peptide (NT-proBNP, a marker of myocardial strain), ST2 (a marker of extracellular matrix remodeling and fibrosis, inflammation, and myocardial strain), and high-sensitivity troponin T (hs-TnT, a marker of myocyte stress/injury) were assayed. The median (interquartile range, IQR) years of training was 7 (5-11) years and median (IQR) weekly training hours was 6 (5-8) h/week, respectively. The median (IQR) race time (h:min:s) was 3:32:44 (3:18:50-3:51:46). Echocardiographic indices were within normal ranges. Immediately after the race, blood concentration of the three cardiac biomarkers increased significantly, with 1.3-, 1.6-, and 16-fold increases in NT-proBNP, ST2, and hs-TnT, respectively. We found an inverse relationship between weekly training hours and increased ST2 (p = 0.007), and a direct relationship between race time and increased hs-TnT (p < 0.001) and ST2 (p = 0.05). Our findings indicate that preparation for and participation in marathon running may affect multiple pathways affecting the cardiovascular system. More data and long-term follow-up studies in non-elite and elite athletes are needed.

[Updating of relative data on tocopherols in clinical biochemistry]. / Actualisation des données relatives aux tocophérols en biochimie clinique.

The working group on lipophilic vitamins of the FSBC has reviewed current knowledge in the field of tocopherols and tried to summarize the most important and recent aspects that may be useful to clinical practitioners. The molecular structure of tocopherols and tocotrienols, their biogenesis, their analysis in foods, their metabolism in humans, their measurement in biological fluids, and the organism's needs and dietary requirements are reviewed. Their main functions as antioxidants and free radical scavengers are described at the molecular, ultra-structural, cellular and organ levels. The interest of these vitamins in three pathologies in which oxidative-stress has been implicated (atherosclerosis, cancer, kidney failure) is discussed.