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1.
Chest ; 156(3): 544-552, 2019 09.
Artículo en Inglés | MEDLINE | ID: mdl-30825445

RESUMEN

BACKGROUND: Short sleep may be a risk factor for atrial fibrillation. However, previous investigations have been limited by lack of objective sleep measurement and small sample size. We sought to determine the association between objectively measured sleep duration and atrial fibrillation. METHODS: All 31,079 adult patients undergoing diagnostic polysomnography from 1999 to 2015 at multiple sites within a large hospital network were identified from electronic medical records. Prevalent atrial fibrillation was identified by continuous ECG during polysomnography. Incident atrial fibrillation was identified by diagnostic codes and 12-lead ECGs. Logistic regression and Cox proportional hazards modeling were used to examine the association of sleep duration and atrial fibrillation prevalence and incidence, respectively, adjusting for age, sex, BMI, hypertension, coronary artery disease, cerebrovascular disease, peripheral vascular disease, heart failure, and sleep apnea severity. RESULTS: We identified 404 cases of prevalent atrial fibrillation among 30,061 individuals (mean age ± SD, 51.0 ± 14.5 years; 51.6% women) undergoing polysomnography. After adjustment, each 1-h reduction in sleep duration was associated with a 1.17-fold (95% CI, 1.11-1.30) increased risk of prevalent atrial fibrillation. Among 27,589 patients without atrial fibrillation at baseline, we identified 1,820 cases of incident atrial fibrillation over 4.6 years median follow-up. After adjustment, each 1-h reduction in sleep duration was associated with a 1.09-fold (95% CI, 1.05-1.13) increased risk for incident atrial fibrillation. CONCLUSIONS: Short sleep duration is independently associated with prevalent and incident atrial fibrillation. Further research is needed to determine whether interventions to extend sleep can lower atrial fibrillation risk.


Asunto(s)
Fibrilación Atrial/epidemiología , Síndromes de la Apnea del Sueño/complicaciones , Adulto , Anciano , Fibrilación Atrial/diagnóstico , Estudios Transversales , Femenino , Humanos , Incidencia , Modelos Logísticos , Estudios Longitudinales , Masculino , Persona de Mediana Edad , Polisomnografía , Prevalencia , Factores de Riesgo , Síndromes de la Apnea del Sueño/diagnóstico
2.
J Clin Lipidol ; 11(2): 328-337, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28502488

RESUMEN

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that exhibits proinflammatory properties and has been associated with subclinical cardiovascular disease. OBJECTIVE: The relationship between Lp-PLA2 and subclinical CVD remains unclear. The goal of this systematic review was to clarify this relationship. METHODS: An extensive literature search of the MEDLINE database using Ovid and PubMed was performed. From an initial search of 444 articles, 13 met the inclusion and exclusion criteria and were included in the review. RESULTS: Of the 13 studies included in the review, 6 examined the relationship between Lp-PLA2 and coronary artery calcification, of which 3 showed a significant correlation. Two studies examined the relationship between Lp-PLA2 and endothelial dysfunction, and 1 reported a significant relationship. Five studies investigated the association of Lp-PLA2 with carotid intima-media thickness (CIMT), and 3 reported a significant relationship. CONCLUSIONS: This review shows a variable association between Lp-PLA2 and subclinical disease. This finding has broad implications for the future of public health and clinical practice. Future research is needed to clarify what role Lp-PLA2 has in guiding treatment and if it is involved in plaque instability, which would make it a useful tool for risk prognostication.


Asunto(s)
1-Alquil-2-acetilglicerofosfocolina Esterasa/metabolismo , Enfermedades Cardiovasculares/metabolismo , Biomarcadores/metabolismo , Calcio/metabolismo , Enfermedades Cardiovasculares/diagnóstico por imagen , Enfermedades Cardiovasculares/enzimología , Enfermedades Cardiovasculares/patología , Grosor Intima-Media Carotídeo , Células Endoteliales/patología , Humanos
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