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Central sleep apnoea and inflammation are independently associated with arrhythmia in patients with heart failure
Author(s) -
Sano Kan,
Watanabe Eiichi,
Hayano Junichiro,
Mieno Yuuki,
Sobue Yoshihiro,
Yamamoto Mayumi,
Ichikawa Tomohide,
Sakakibara Hiroki,
Imaizumi Kazuyoshi,
Ozaki Yukio
Publication year - 2013
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hft066
Subject(s) - medicine , atrial fibrillation , heart failure , hazard ratio , cardiology , odds ratio , confidence interval , premature atrial contraction , ventricular tachycardia
Aims We examined whether the severity of central sleep apnoea (CSA) and the level of C‐reactive protein are associated with the prevalence and complexity of arrhythmias, and whether these factors contribute to increased risk of nocturnal sudden death. Methods and results We prospectively examined 178 patients (age 70 ± 1 years) who were admitted to our hospital due to worsening heart failure. We recorded a simultaneous overnight cardiorespiratory polygraph and Holter ECG. Obstructive sleep apnoea was excluded and patients were dichotomized based on the median value of the central apnoea index (CAI) of 7.5/h. The prevalence and complexity of arrhythmias were compared between daytime (06:00 h to 15:00 h) and night‐time (21:00 h to 06:00 h). A multivariate logistic regression analysis revealed that the CAI was associated with prevalence of atrial fibrillation (AF) [odds ratio 1.03, 95% confidence interval (CI) 1.02–2.51)] and sinus pause during the night‐time period (1.12, 95% CI 1.08–1.35). The CAI and C‐reactive protein were independently associated with non‐sustained ventricular tachycardia during both daytime (1.22, 95% CI 1.00–6.92; and 5.82, 2.58–56.1, respectively) and night‐time periods (3.57, 95% CI 1.06–13.1; and 10.7, 3.30–44.4, respectively). During a mean follow‐up period of 22 months, 30 (17%) patients had cardiovascular deaths and the CSA was an independent predictor (hazard ratio 1.29, 95% CI 1.16–2.32); only 5 (2.8%) of them died due to ventricular tachyarrhythmia, occurring during wakefulness. Conclusions We demonstrated that the severity of CSA and C‐reactive protein levels are independently associated with the prevalence and complexity of arrhythmias. CSA was associated with increased mortality risk, but it was not related directly to nocturnal death due to ventricular tachyarrhythmia.