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Case Study

Use of Closed Loop Stimulation for Rate-Responsive Pacing in an AAI Pacemaker

December 2020

There is limited information and data on the use of Closed Loop Stimulation (CLS, BIOTRONIK) in myocardial regions not at the right ventricular (RV) apex. In fact, we found only 1 case study using CLS derived from the atrium.1 Thus, we looked at evaluating its use in a patient with a AAI pacemaker (Entovis SR-T, BIOTRONIK) due to limited response from her traditional accelerometer. 

Case Presentation

The patient is an 89-year-old female with a past medical history of hypertension and dyslipidemia. She had a single-lead atrial pacemaker implanted in 2011 for sick sinus syndrome (her underlying rhythm is sinus bradycardia <30 bpm), with symptoms of lethargy. A year and a half ago, she began reporting dyspnea on exertion and occasional dizzy spells. With a poor heart rate spread observed on the pacemaker histograms and previous optimization attempted of the accelerometer settings, it was decided, with agreement of the patient and her daughter, to try CLS with the stipulation that she would return for reprogramming if there were any issues.

 Rate response using an accelerometer is derived from movement of the generator in the anterior-posterior axis, and is more sensitive to motion, providing a more proportional and quicker response. However, it is not based on any physiological changes and can be inaccurate in its regulation of the heart rate. Many sensors are now adaptive and incorporate auto-calibration to optimize response to each individual patient, and have been found to be superior to previous manually calibrated sensors. However, accelerometers have limitations in their ability to match varying activities to an appropriate chronotropic response (eg, ascending vs descending stairs).2 Some research suggests there is little benefit of one sensor over another, and that the use of blended sensors has not only little benefit over single sensors,3 but is also potentially detrimental.4

CLS has a demonstrated physiological response to not only exertion, but also emotional or mental stress5,6 as well as orthostatic hypotension and vasovagal syncope.7-10 CLS measures multiple unipolar impedances to assess changes in myocardial contractility from intrathoracic impedance changes. Variations in the autonomic nervous system can be sensed by the device and preempt changes in heart rate and blood pressure that may cause presyncope or syncope. This response can also be used to adapt the heart rate in a more physiological manner in patients with chronotropic incompetence.11

The sensor histogram refers to the accelerometer’s measurements, and therefore, can be used as a comparison to the CLS response over the same period of time. We can see a much more varied heart rate spread with CLS (Figures 1-4). Accelerometer trends show ~70% of heart rates at base rate, whereas with CLS, heart rates are predominantly 70-120 bpm with ~40% of heart rates at base rate. 

According to the pacemaker clinic report from a check 6 months later, the patient reported “feeling great with exertion” and a “big improvement with current programming.” The patient also had no further syncopal or presyncopal episodes since reprogramming.

Discussion

The use of CLS for vasovagal syncope patients is well documented,7-10 but does not come without issues when programmed on for atypical use.The histogram reports it as ventricular due to a programming change to CLS, as the only available programming option in a single-chamber pacemaker is VVI-CLS. This is where potential issues may arise, as CLS is designed to derive its data from the RV apex. However, theoretically, if a baseline response curve is taken from the atrium, the reduced contractility should have little effect on the CLS response. Further research has shown a similarly good response with CLS in atypical lead positions such as on the epicardium, the His bundle, or the high RV septum.1,12-15

However, patients may find the CLS response too aggressive with data suggesting the potential for inappropriate increases in heart rate, which may cause patients to become symptomatic.16 Another drawback of CLS is that it is not available during mode switching. It has also been suggested that if the device has failed to mode switch, CLS could result in inappropriate maximum sensor pacing,17 which is thought to be due to the reduced contractility and filling seen as a result of atrial fibrillation (AF), triggering the CLS response. However, CLS can replace normal chronotropy lost by medications and slowed conduction, which can be seen with AF treatment. This also potentially reduces AF burden by detecting precursors to AF and pacing the heart faster in an attempt to prevent its onset.18-20

CLS could also prove to be beneficial for cardiac resynchronization therapy (CRT) patients, who are often limited by chronotropic incompetence, meaning that CLS could relieve some of the symptoms associated with heart failure.21 When combined with intrathoracic impedance monitoring, it can indicate fluid overload and other heart failure diagnostics provided by the device. 

The patient did not experience these issues as she had an AAI device, and had seen improvements with her symptoms and her heart variability. But as there is limited data on the effects of using CLS in the atrium, we will need to continue to monitor the patient’s progress and the pacemaker’s function with CLS.

Conclusion

CLS for rate-responsive pacing in patients with AAI programming, or an AAI pacemaker, may be a viable option and results appear comparable to pacing from the apex. Further data is required to confirm these early findings, but it may prove challenging to gain suitable numbers due to AAI devices falling out of favor in recent years. However, as more data is published on other novel sites, such as in conjunction with His bundle pacing, knowledge of how CLS works and its additional uses will be developed. The ultimate aim of rate response is to improve patient symptoms, and CLS could be another tool to utilize to help increase quality of life in patients. 

Acknowledgements: With thanks to Graham Orsbourn (Cardiac Physiologist at Auckland Hospital) for his support with this case.

Disclosures: The author has no conflicts of interest to report regarding the content herein.

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