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1.
Article de Anglais | WPRIM | ID: wpr-152281

RÉSUMÉ

BACKGROUND/AIMS: Poor sleep quality (SQ) is associated with increased cardiovascular mortality and morbidity. Additionally, asymmetric dimethylarginine (ADMA) is an independent predictor of cardiovascular mortality and morbidity. However, no sufficient data regarding the relationship between ADMA levels and SQ have been reported. The goal of the current study was to evaluate the association between SQ and ADMA levels in normotensive patients with type 2 diabetes mellitus. METHODS: The study participants consisted of 78 normotensive type 2 diabetics. The SQ of all participants was assessed using the Pittsburgh Sleep Quality Index (PSQI). Patients with a global PSQI score > 5 were defined as "poor sleepers." Factors associated with poor SQ were analyzed using a multiple regression model. Serum ADMA levels were measured using high performance liquid chromatography. RESULTS: The median ADMA levels of the poor sleepers were increased compared with patients defined as good sleepers (5.5 [4.2 to 6.6] vs. 4.4 [2.9 to 5.4], p < 0.01, respectively). However, the L-arginine/ADMA ratio was decreased in poor sleepers (p < 0.01). Global PSQI scores were positively correlated with ADMA levels (p < 0.01) and negatively correlated with the L-arginine/ADMA ratio (p = 0.02). ADMA levels were correlated with sleep latency (p < 0.01) and sleep efficiency (p = 0.01). Logistic regression analysis showed that ADMA levels (odds ratio [OR], 1.68; 95% confidence interval [CI], 1.16 to 2.44; p = 0.01) and body mass index (OR, 1.15; 95% CI, 1.01 to 1.31; p = 0.04) were associated with poor SQ independently of glomerular filtration rate, sex, age, duration of diabetes, hemoglobin A1c, total cholesterol, and systolic blood pressure. CONCLUSIONS: Self-reported SQ was independently associated with ADMA levels in normotensive patients with diabetes mellitus.


Sujet(s)
Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Arginine/analogues et dérivés , Marqueurs biologiques/sang , Maladies cardiovasculaires/sang , Loi du khi-deux , Chromatographie en phase liquide à haute performance , Études transversales , Diabète de type 2/sang , Modèles logistiques , Odds ratio , Facteurs de risque , Sommeil , Troubles de la veille et du sommeil/sang , Enquêtes et questionnaires
2.
Medical Principles and Practice. 2011; 20 (5): 464-469
de Anglais | IMEMR | ID: emr-136703

RÉSUMÉ

In this study, our aim was to evaluate the effect of a higher dose of atorvastatin on the recurrence rate of atrial fibrillation [AF] after electrical cardioversion [EC] in addition to antiarrhythmic therapy. 48 patients with persistent AF were included in this study. The patients were randomized to an atorvastatin 40-mg treatment group and a control group. Atorvastatin was started 3 weeks before EC and was continued for 2 months after EC. EC was performed using biphasic shocks after 3 weeks of treatment with the orally administered anticoagulant warfarin. Lipid and inflammatory parameters [high-sensitivity C-reactive protein, white blood cell count and fibrinogen level] were evaluated at the baseline and before EC. The endpoint of this study was electrocardiographically confirmed recurrence of AF of>10 min. There were no significant differences in baseline characteristics and lipid and inflammatory marker levels between the treatment and control groups. Total cholesterol and low-density lipoprotein levels were significantly decreased in patients taking atorvastatin for 2 months compared with baseline values [174 +/- 31 vs. 129 +/- 25 mg/dl, p=0.001, and 112 +/- 23 vs. 62 +/- 20 mg/dl, p=0.001, respectively], while no significant change occurred in control patients [168 +/- 26 vs. 182 +/- 29 mg/dl, p=0.07, and 99 +/- 18 vs. 108 +/- 26 mg/dl, p=0.1, respectively]. At the end of the 2-month follow-up period, 9 patients [20.5%] experienced AF recurrence, and there was no significant difference in AF recurrence rate between the treatment and control groups [26 vs. 13%; p=0.2]. Atorvastatin therapy prior to EC does not prevent the recurrence of arrhythmia in patients with persistent AF who are receiving antiarrhythmic therapy

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