The effects of continuous positive airway pressure therapy withdrawal on cardiac repolarization: data from a randomized controlled trial

Rossi, Valentina A.; Stoewhas, Anne-Christin; Camen, Giovanni; Steffel, Jan; Bloch, Konrad E.; Stradling, John; Kohler, Malcolm

doi:10.1093/eurheartj/ehs073

Cited by 63 publications

(42 citation statements)

References 45 publications

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“…The increase in the length of these intervals was positively correlated with the change in the severity of OSA, suggesting that the risk for malignant dysrhythmias increases with the severity of OSA. In addition, there was a correlation between the change in the QTc and change in the urinary noradrenaline levels, suggesting that increased sympathetic nervous system activity may be one of the underlying mechanisms between OSA and the increased dispersion of cardiac repolarisation [89]. According to PANIKKATH et al [83] an uncorrected TpTe interval .100 ms, and a QTc interval .430 ms in the resting ECG, are associated with an increased risk of SCD.…”

Section: Interventional Studiesmentioning

confidence: 99%

“…In a randomised-controlled trial, analysis of QTc and TpTec (TpTe corrected for heart rate) intervals from a 12-lead ECG found that CPAP withdrawal for 2 weeks was associated with both prolongation, and an increase in dispersion, of repolarisation, providing a possible mechanistic link between OSA, cardiac arrhythmias and SCD [89]. The increase in the length of these intervals was positively correlated with the change in the severity of OSA, suggesting that the risk for malignant dysrhythmias increases with the severity of OSA.…”

Section: Interventional Studiesmentioning

confidence: 99%

“…According to PANIKKATH et al [83] an uncorrected TpTe interval .100 ms, and a QTc interval .430 ms in the resting ECG, are associated with an increased risk of SCD. Using these thresholds in the latter randomised controlled trial, more than 50% of patients with OSA were found to be at increased risk for SCD after 2 weeks of CPAP therapy withdrawal [89].…”

Section: Interventional Studiesmentioning

confidence: 99%

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Effects of obstructive sleep apnoea on heart rhythm

2012

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Symptomatic obstructive sleep apnoea (OSA) has been proven to be a risk factor for hypertension and vascular dysfunction, and has been proposed to be causally related with cardiac arrhythmias and sudden cardiac death.Searches of bibliographical databases revealed that several mechanisms seem to underpin the association between OSA and cardiac arrhythmias: intermittent hypoxia associated with autonomic nervous system activation and increased oxidative stress, which may lead to cardiac cellular damage and alteration in myocardial excitability; recurrent arousals, resulting in sympathetic activation and coronary vasoconstriction; and increased negative intrathoracic pressure which may mechanically stretch the myocardial walls and, thus, promote acute changes in myocardial excitability as well as structural remodelling of the myocardium.Findings from cross-sectional studies suggest a high prevalence of cardiac arrhythmias in patients with OSA and a high prevalence of OSA in those with cardiac arrhythmias. Preliminary evidence from uncontrolled interventional studies suggests that treatment of OSA may prevent cardiac arrhythmias.In conclusion, there is preliminary evidence that OSA is associated with the development of cardiac arrhythmias. Data from randomised controlled studies are needed to definitively clarify the role of OSA in arrhythmogenesis.

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Section: Interventional Studiesmentioning

confidence: 99%

Section: Interventional Studiesmentioning

confidence: 99%

Section: Interventional Studiesmentioning

confidence: 99%

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Effects of obstructive sleep apnoea on heart rhythm

2012

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“…ECG was recorded with a 12-lead ECG (AT 104 PC, Schiller-Reomed AG, Switzerland) set at 25-mm/s paper speed and 10-mm/mV amplitude. Measurements of the ECG intervals were performed twice with dedicated ECG analysis software (DatInf® Measure 2.1d, DatInf GmbH, Tübingen, Germany) by two investigators who were blinded to the patient's data as previously described [23]. The mean of the ECG interval measurements by the two investigators was calculated and used for statistical analysis.…”

Section: Methodsmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease and Cardiac Repolarization: Data from a Randomized Controlled Trial

2016

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Background: Altered cardiac repolarization is a risk factor for sudden cardiac death and seems to be increased in chronic obstructive pulmonary disease (COPD) patients. Objective: Lung volume reduction surgery (LVRS) has been shown to improve breathing mechanics and lung function in patients with severe COPD and emphysema and possibly also improve altered cardiac repolarization. Methods: Thirty patients scheduled for LVRS were randomized to LVRS or to the control group. We investigated the treatment effect 3 months after LVRS on measures of cardiac repolarization and dispersion of repolarization (QTc interval, QT dispersion) derived from electrocardiography. Univariable and multivariable analyses were used to identify possible confounders influencing the treatment effect. Results: LVRSwas associated with an improvement in lung function (mean ± SD residual volume/total lung capacity of -9 ± 11% and forced expiratory volume in 1 s of +30 ± 29%). LVRS did not significantly reduce QTc (median -5.3 ms, 95% confidence interval, CI -15.5 to 3.7, p = 0.214) and QT dispersion (median -3.0 ms, 95% CI -13.0 to 7.0, p = 0.536) compared to the control group. No significant association between change in QTc and change in QT dispersion, respectively, and change in possible confounders was found. Conclusion: LVRS seems to have no effect on cardiac repolarization in patients with COPD. Thus, lung hyperinflation seems not to be a causal mechanism for altered cardiac repolarization in COPD patients.

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“…An analysis of the dynamics of the QT interval before and after the treatment of OSA by continuous positive airway pressure (CPAP) is given in a study by Rossi et al [28]. This study characterized the trend towards a significant QT interval elongation among patients who discontinued therapy.…”

Section: Electrical Myocardial Instabilitymentioning

confidence: 99%

Clues to the Pathophysiology of Sudden Cardiac Death in Obstructive Sleep Apnea

Grishina¹,

Перетолчина²,

Solenskaia³

et al. 2018

Cardiology

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Background: Risk assessment of sudden cardiac death (SCD) is multifactorial and complex, especially among individuals without established cardiovascular disease. There are insufficiently investigated conditions that can affect arrhythmogenesis. One such condition is obstructive sleep apnea (OSA) syndrome, which is not on the list of risk factors of the Russian National Society of Arrhythmology. Objective: The aim of this review article is to discuss clues to the pathophysiology of SCD in OSA subjects. Methods: We searched the literature for data reporting the impact of apnea on arrhythmogenesis. The preferred languages were English and Russian. The most important clinical reports, as well as biochemistry and pathophysiology guides, were selected for inclusion in the review. Results: It was clearly observed in the searched literature that OSA is the crucial aspect of arrhythmogenesis. Among the clues are intermittent nocturnal hypoxia, reactive oxygen species, cardiomyocyte metabolism disturbances, myocardial electric heterogeneity, and intrathoracic pressure changes. Conclusion: This review emphasizes the importance of the inclusion of OSA in the list of risk factors of the Russian National Society of Arrhythmology.

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The effects of continuous positive airway pressure therapy withdrawal on cardiac repolarization: data from a randomized controlled trial

Abstract: Continuous positive airway pressure withdrawal is associated with the prolongation of the QT(c) and TpTe(c) intervals and TpTe/QT ratio, which may provide a possible mechanistic link between OSA, cardiac dysrhythmias, and thus sudden cardiac death.

Cited by 63 publications

References 45 publications

Effects of obstructive sleep apnoea on heart rhythm

Effects of obstructive sleep apnoea on heart rhythm

Chronic Obstructive Pulmonary Disease and Cardiac Repolarization: Data from a Randomized Controlled Trial

Clues to the Pathophysiology of Sudden Cardiac Death in Obstructive Sleep Apnea

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