Sleep apnoea therapy reverses atrial remodelling in AF

CPAP therapy has been shown to reverse atrial remodelling in the first study to evaluate the impact of obstructive sleep apnoea treatment (OSA) on the hearts of patients with atrial fibrillation.

The Australian randomised Sleep Apnoea and Atrial Fibrillation: The Effect of Treatment of Sleep Apnoea on Atrial Fibrillation Burden (SLEEP-AF) study, published in JACC Clinical Electrophysiology, found mechanistic evidence of improved atrial function among OSA patients who used CPAP therapy for six months.

These included faster conduction velocity, significantly higher atrial voltage and lower proportion of complex points compared to the non-treatment group.

Lead author Dr Chrishan Nalliah of the Department of Cardiology, Royal Melbourne Hospital, said the study provided RCT evidence of an improvement in atrial remodelling with OSA treatment.

“There was a modest but significant change in electrophysiologic parameters with CPAP therapy that implies an anti-arrhythmic benefit for putting patients on that therapy that may reduce the atrial fibrillation burden or recurrence rate,” he told the limbic.

“It’s a nice piece of mechanistic data that prompts further clinical evaluation to determine whether or not this translates to a clinical benefit.”

The study was based on the hypothesis that OSA is a major ‘upstream’ risk factor for AF, with epidemiologic studies showing that OSA is independently associated with incidence, prevalence, and severity of the condition. Several observational studies have shown that OSA management is associated with improved rates of freedom from arrhythmia, and conversely that untreated OSA negates the efficacy of AF rhythm control strategies.

However, until now there have been no randomised trials evaluating the impact of OSA management on the atrial substrate.

Dr Nalliah’s study recruited 24 patients from two major hospitals in Melbourne who were being managed for atrial fibrillation and moderate to severe OSA. All underwent atrial mapping of the right atrium at the start of the trial, and again at six months.

Twelve were assigned to the CPAP group, of whom 10 were deemed to have good compliance to the therapy. In the usual care group, none used CPAP. At six months atrial mapping revealed improvements in conduction and voltage in the CPAP group that were not found in the control group.

These included conduction velocity increase in the CPAP group from 0.67m/s to 0.86m/s, compared to 0.68m/s to 0.69 in the control; bipolar voltage of 2.17mV to 2.30mV, compared to 2.16mV to 1.96mV; and reduced complex points 9.17% to 8.87%, compared to 7.49% to 11.93%.

It found the differences were due to improvements in the CPAP group, progression in the non-CPAP group, or a combination of both.

“The present study shows that CPAP therapy has potent mechanistic impacts that are observable even in a relatively small group. Larger randomised trials are required to determine their clinical relevance,” the paper’s authors said.

If replicated, the findings suggested that OSA may be considered along with alcohol, smoking and obesity, as a potentially modifiable risk factor for AF management, the authors concluded.

However, Dr Nalliah also drew attention to the study’s limitations, noting the small size from a single centre, and the high motivation of the CPAP group as evidenced by their strong adherence to the treatment. Further studies were required to determine clinical impacts, he said.

“Whether the treatment of a single risk factor, sleep apnoea, is able to drive a clinically meaningful results, need to be the subject of a robust, randomised trial. That is something that we are looking into,” he told the limbic.

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