Please login or register to print this page.

Clinical Articles, Lead Article

Novel device for central sleep apnoea in heart failure

A novel device (remede®, Respicardia, Inc.) implanted under the skin like a pacemaker successfully treats central sleep apnoea (CSA) in heart failure patients, according to research presented recently at the Heart Failure Congress 2014, in Athens, Greece.

The system uses unilateral transvenous phrenic nerve stimulation to prevent CSA before it occurs. The pulse generator is implanted under the skin, just below the collar bone, and a wire is threaded into one of the veins near the phrenic nerve.

The pilot study was a prospective, multicentre trial in 46 patients with moderate to severe CSA who were implanted with the system. The primary endpoint was a reduction in apnoea hypopnea index (AHI) at three months compared to baseline with six and 12 month data also collected.

The one year results show that implantation led to substantial benefits in sleep parameters including a reduction in AHI, a reduction in the time spent with low blood oxygen levels overnight, and improvements in sleep efficiency and REM sleep.

The system also improved important cardiac endpoints such as heart rate variability. Patients were less fatigued and their quality of life improved, according to the Minnesota Living with Heart Failure Quality of Life questionnaire.

slpThe results were revealed for the first time by lead author Professor William T Abraham (Ohio State University, USA). He said that the system “is the first fully implantable device to treat central sleep apnoea in heart failure patients”.

He added: “Patients using the device tell us they haven’t slept so well in years. They have more energy and can do their normal daily activities without falling asleep. They also don’t have to fight with a mask.”

“The device stimulates the diaphragm via the phrenic nerve, causing the diaphragm to contract. It regularises the patient’s breathing pattern throughout the night, rather than waiting until the patient stops breathing to react,” Professor Abraham added.

He concluded: “The major problem with mask based therapies such as continuous positive airway pressure (CPAP) is patient acceptance and compliance. Up to 50% of patients can’t or won’t wear a mask so their sleep apnoea is untreated or inadequately treated.”

The pivotal trial for USA regulatory approval is ongoing and is set to enroll around 150 patients in the US and Europe. Results are expected by the end of 2015.

Sleep apnoea affects heart rate regulation

Sufferers of obstructive sleep apnoea (OSA) have diminished activity among neurons responsible for keeping heart rate low, according to a study published recently in the Journal of Physiology.1

In OSA, neurons in the brainstem that control heart rate experience a blunting of their activity. The reduction of neuronal activity likely contributes to the increased heart rate, blood pressure and risk of adverse cardiovascular events that occur in patients with OSA.

The authors explored these mechanisms in rats, by mimicking OSA for four weeks and studying the changes in blood pressure, heart rate, and synaptic activity in parasympathetic neurons that control heart rate.

Dr David Mendelowitz, who led the study at the George Washington University USA, says: “Lack of sleep leaves the mind and body tired, leading to poor mental and physical performance, and if untreated OSA increases a person’s risk of developing hypertension and irregular heartbeats. Therefore it is very important that we have discovered some of the underlying mechanisms that could injure the heart and other cardiovascular tissues.”

“Our study shows that progression of blunted cardiovascular reflexes is accompanied, and likely maintained by, inhibition of neurons in the brainstem that protect the heart and normally maintain a low resting heart rate. This study would predict that patients who have OSA, and also take sleep medicines, might be at heightened risk for an exaggerated reduction of essential neuronal activity that protects the heart,” Dr Mendelowitz added.

Future work will need to build from this foundation and focus on finding targets to restore the usual cardio-protective function of these neurons to help reduce the risk of arrhythmias, elevated heart rate, and blood pressure that occur with this disease, the authors conclude.

References

1. Dyavanapalli J, Jameson H, Dergacheva O, Jain V, Alhusayyen M, Mendelowitz D. Chronic intermittent hypoxia‐hypercapnia blunts heart rate responses and alters neurotransmission to cardiac vagal neurons. J Physiol 2014. http://dx.doi.org/10.1113/jphysiol.2014.273482

Published on: May 28, 2014

Members Area

Log in or Register now.

 For healthcare professionals only
Angina book sky

SEARCH THE SITE

RSS FEED

Subscribe to our RSS feed
home

GET EXCLUSIVE UPDATES

Sign up for our regular email newsletters & be the first to know about fresh articles and site updates.

RECENT COMMENTS

    None Found

ENDORSED BY

  • ArrhythmiaAlliance
  • Stars
  • Anticoagulation Europe
  • Atrial Fibrillation Association
 

You are not logged in

You need to be a member to print this page.
Sign up for free membership, or log in.

You are not logged in

You need to be a member to download PDF's.
Sign up for free membership, or log in.