QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension

Dursunoğlu, Dursun; Dursunoğlu, Neşe; Evrengül, Harun; Özkurt, Sibel; Kılıç, Mustafa; Fişekçi, Fatma Evyapan; Kuru, Ömür; Delen, O

doi:10.1183/09031936.05.00067104

Cited by 37 publications

(24 citation statements)

References 38 publications

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“…7 In contrast to the present investigation, they showed that corrected QTd is increased in patients with severe OSA. The high value of AHI (42.4 ± 17.6/ h) can be the reason for the difference between the 2 studies (we assessed only 25.83 ± 18.5/ h AHI).…”

Section: Discussioncontrasting

confidence: 53%

The Effect of Sleep Apnea on QT Interval, QT Dispersion, and Arrhythmias

Barta

Szabó

Kun

et al. 2010

Clinical Cardiology

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Background: QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. Hypothesis: The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. Methods: A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. Results: Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 ± 34.6 ms, daytime QT interval: 381.6 ± 33.8 ms, 24-hour QT interval: 394.7 ± 31.1 ms). However, during the nighttime QT interval (422.8 ± 14.9 ms), QTd (31.2 ± 11.0 ms) and QT dispersion (30.5 ± 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 ± 14.2 ms, QTd: 28.8 ± 9.4 ms, QTcd: 30.5 ± 9.43 ms) and daytime levels (QTc interval: 423.9 ± 14.3 ms, QTd: 27.3 ± 10.7 ms, QTcd: 29.9 ± 11.1 ms). None of the patients had ventricular arrhythmias. Conclusions: QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period.

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Section: Discussioncontrasting

confidence: 53%

The Effect of Sleep Apnea on QT Interval, QT Dispersion, and Arrhythmias

Barta

Szabó

Kun

et al. 2010

Clinical Cardiology

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“…It has also been implicated as an independent risk factor for cardiovascular diseases such as myocardial infarction, hypertension, heart failure, arrhythmias, and stroke [6][7][8][9][10][11]. We showed that, especially in females with metabolic syndrome risk, evaluation of metabolic syndrome criteria may play an important role in predicting OSA severity with high sensitivity (86.6%) and high negative predictivity (85.7%) [12].…”

Section: Introductionmentioning

confidence: 74%

Is the clinical presentation different between men and women admitting to the sleep laboratory?

2009

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“…61 The QT interval dispersion, (difference between the longest and shortest QT intervals) a marker of vulnerability to ventricular arrhythmias and risk for sudden cardiac death, 62 is increased in OSA patients. 63 During sleep apneic episodes, cardiac arrhythmias are fairly common but in most cases benign, especially if the cardiac substrate is normal. Bradycardia prevalence and severity appears to correlate with worsening OSA severity.…”

Section: Sleep Apnea and Arrhythmiasmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

Patel¹,

Rosen²

2007

Clinical Pulmonary Medicine

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Obstructive sleep apnea (OSA), a widely prevalent disease, is the most frequent form of sleep-disordered breathing encountered by adults of all age groups and is associated with serious medical, public health, and economic sequelae. During the last 2 decades, the cardiovascular consequences associated with OSA continue to unfold. These include hypertension, coronary artery disease, congestive heart failure, arrhythmia, stroke, insulin resistance/diabetes, and pulmonary hypertension. The association with systemic hypertension is most compelling and believed to be causal. Increasing evidence accrues for the remaining cardiovascular spectrum. Myocardial infarction, stroke, arrhythmia, and death appear to be more common or premature in those afflicted with OSA than the general population. Although the mechanisms underpinning the relationships with cardiovascular disease are not fully elucidated, investigators propose that the consequences of chronic, intermittent hypoxemia, and repetitive apnea include fluctuations in sympathetic drive, endothelial dysfunction, and inflammatory mediators. A large proportion of patients remain undiagnosed and untreated despite an increasing understanding of the deleterious health and economic effects of OSA.T he advancement in our understanding of cardiovascular pathophysiology has led to the recognition of the importance of sleep-disordered breathing (SDB) and its role in cardiovascular disease. Positive cardiovascular outcomes have been reported anecdotally by treating sleep apnea with tracheostomies. 1,2 Since then, the field of sleep and cardiovascular medicine has exploded with a multitude of experimental, cross-sectional, case-controlled, randomized, and longitudinal studies to address a range of associations between the 2 disease entities. The main areas of interest have focused on SDB's link with several cardiovascular disorders including hypertension, coronary artery disease (CAD), and congestive heart failure (CHF), as well as potential mechanisms of association such as endothelial dysfunction, inflammation, and hypercoagulability.A number of factors have hampered the establishment of associations and causality in the field of SDB and cardiovascular disease. First, the definition of SDB, especially hypopneas, has not been standardized. In addition, the cut-off point for a given number of apnea events to define a sleep disorder is inconsistent. Further complication is anticipated with increasing demand for evaluation and the resultant expansion in use of home-based diagnostic techniques. Cardiovascular disease and SDB populations share many common attributes such as body mass index (BMI), age, and sex that can confound interpretations and results. Moreover, sleep apnea, in and of itself, is a disorder that is plagued by under diagnosis and lack of an aggressive approach to treatment. 3 Nonetheless, the relationship between SDB and cardiovascular disease is clinically relevant since patients with SDB have a 13.4% increased risk for developing a cardiovascular event over a peri...

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QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension

Cited by 37 publications

References 38 publications

The Effect of Sleep Apnea on QT Interval, QT Dispersion, and Arrhythmias

The Effect of Sleep Apnea on QT Interval, QT Dispersion, and Arrhythmias

Is the clinical presentation different between men and women admitting to the sleep laboratory?

Sleep Apnea and Cardiovascular Disease

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