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EP-4566656-B1 - SYSTEMS FOR MANAGING ATRIAL-VENTRICULAR DELAY

EP4566656B1EP 4566656 B1EP4566656 B1EP 4566656B1EP-4566656-B1

Inventors

  • MANGUAL-SOTO, Jan O
  • Simonetti, Angelo

Dates

Publication Date
20260513
Application Date
20241204

Claims (15)

  1. An implantable medical device (IMD) (210) for managing therapy comprising: a connector coupleable to a lead (220, 224) with an electrode (222, 232); a memory (294) configured to store program instructions; and one or more processors (260) configured to execute the program instructions to: determine a sensed right atrium (RAs) event or a paced right atrial (RAp) event (RAs,p event) (412); determine a sensed right ventricle (RVs) event (414) by detecting a cardiac activity (CA) signal (402) reaches a threshold amplitude (410) and determine a maximum amplitude (420) in a determined period of time (418) after the CA signal (402) reaches the threshold amplitude (410); determine an RAs,p-RVs interval (404) between the RAs,p event (412) and RVs event (414); calculate an atrioventricular delay (AV) delay based on the RAs,p-RVs interval (404); and manage therapy, provided by the IMD (210), based on the AV delay that is calculated.
  2. The IMD of claim 1, wherein the one or more processors (260) are configured to manage the therapy by controlling the electrode (222, 232) to deliver left bundle branch area pacing therapy based on the AV delay.
  3. The IMD of claim 1 or 2, wherein the IMD (210) is a dual chamber implantable pulse generator (IPG).
  4. The IMD of any one of claims 1 to 3, wherein the one or more processors (260) are configured to calculate the AV delay by subtracting a determined percentage of the RAs,p-RVs interval (404) from the RAs,p-RVs interval (404).
  5. The IMD of any one of claims 1 to 4, wherein the CA signal (402) is an intrinsic CA signal (402).
  6. The IMD of any one of claims 1 to 5, wherein the one or more processors (260) are further configured to: after calculating the AV delay, set the AV delay as an initial AV delay; and utilize the initial AV delay to manage the therapy for a determined number of CA signals.
  7. The IMD of claim 6, wherein the one or more processors (260) are further configured to: count a number of the CA signals after a first CA signal; compare a number of counted CA signals to the determined number of CA signals; repeat determination of the RAs,p event (412), determination of the RVs event (414), determination of the RAs,p-RVs interval (404) and calculation of the AV delay after the number of counted CA signals matches the determined number of CA signals, to calculate an updated AV delay; and manage the therapy provided by the IMD (210), based on the updated AV delay.
  8. The IMD of claim 7, wherein the one or more processors (260) are further configured to reset a count of the number of counted CA signals in response to calculating the updated AV delay.
  9. The IMD of any one of claims 1 to 7, wherein the one or more processors (260) are further configured to: after calculating the AV delay, determine a second RAs,p-RVs interval based on a second CA signal, compare the second RAs,p-RVs interval to the AV delay; and responsive to the second RAs,p-RVs interval being less than the AV delay, calculate an updated AV delay based on the second RAs,p-RVs interval.
  10. The IMD of claim 9, wherein the one or more processors (260) are further configured to: count a number of CA signals obtained after a first CA signal, compare a counted number of CA signals to a determined number of CA signals; and reset the counted number of the CA signals in response to calculating the updated AV delay.
  11. The IMD of claim 9 or 10, wherein the one or more processors (260) are further configured to manage the therapy, provided by the IMD (210), based on the updated AV delay, wherein the one or more processors (260) are configured to manage the therapy by controlling the electrode (222, 224) to deliver left bundle branch area pacing therapy based on the updated AV delay.
  12. The IMD of any one of claims 1 to 11, further comprising a sensing circuitry (230) configured to be coupled to the electrode (222, 232) to detect the CA signal (402).
  13. The IMD of any one of claims 1 to 12, further comprising a pulse generator (270) controlled by the one or more processors (260) to deliver pacing stimulation pulses via the electrode (222, 232).
  14. The IMD of claim 13, wherein the one or more processors (260) are further configured to control the pulse generator (270) to deliver a pacing stimulation pulse via the electrode (222, 232) at the expiry of the AV delay.
  15. The IMD of any one of claims 1 to 14, wherein the one or more processors (260) are configured to determine the RVs event (414) as the maximum amplitude (420) in the CA signal (402) in the determined period of time (418) after the CA signal (402) reaches the threshold amplitude (410).

Description

TECHNICAL FIELD This disclosure relates generally to implantable cardiac stimulating devices. BACKGROUND In a normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse, or excitation pulse, arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (AV) node and a ventricular conduction system, causing a depolarization and ventricular chamber contractions. The ventricular conduction system includes the bundle of HIS (also referred to as the HIS bundle), the left and right bundle branches, and the Purkinje fibers. The depolarization of the interventricular septum and ventricles is generally referred to as a QRS complex. The QRS complex is observed and measured through the use of electrocardiogram (ECG) machines and similar equipment for measuring electrical activity of the heart. Disruption of this natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators. The implantable cardiac stimulation devices deliver rhythmic electrical pulses or other anti-arrhythmia therapies to the heart at a desired energy and rate via electrodes implanted in contact with the heart tissue. To the extent the electrical pulses are sufficient to induce depolarization of the associated heart tissue, the heart tissue is said to be captured. The minimum electrical pulse resulting in capture is generally referred to as the capture threshold. In the majority of individuals, the most effective heartbeat is triggered by the patient's own natural pacing physiology. Implantable cardiac stimulation devices are intended as a back-up when the natural pacing functionality of the patient's heart fails or acts inefficiently (such as in cases of sinus arrest and symptomatic bradycardia, respectively) or when the heart's conduction system fails or acts inefficiently. In a large number of heart failure (HF) patients, natural conduction through the AV node and the HIS bundle are intact and disruption of ventricular rhythm is the result of conduction disorders residing in the left and/or right bundle branches. Dilation of the heart due to congestive heart failure (CHF) has been associated with delayed conduction through the ventricles. This delayed conduction leads to reduced hemodynamic efficiency of the failing heart because of the resulting poor synchronization of the heart chambers. Direct stimulation of the HIS bundle has been found to provide hemodynamic improvement for various patients including those suffering from dilated cardiomyopathy but having normal ventricular activation. However, a significant learning curve remains in connection with the implant procedure and in some instances involves a higher rate of lead placement adjustment. HIS bundle pacing (HBP) is also associated with higher capture thresholds and lower ventricular sensing amplitudes as compared to other pacing modes, which can be challenging for device functionality and battery longevity. Further, HBP may exhibit lower success in patients with His-Purkinje conduction disease when the conduction block is more distal in the conduction system. Transvenous left bundle branch (LBB) pacing has been proposed where the lead is implanted from the right ventricle and screwed deep into the septum to deliver pacing stimuli at the LBB. The LBB area pacing technique has been shown to be associated with an easier implant procedure, lower capture thresholds, and higher ventricular sensing amplitudes compared to HBP. LBB area pacing has been proposed to be used in parallel or in lieu of HBP to increase overall success of physiological pacing. In addition, the narrowing of QRS duration (QRSd) has been proven to predict long-term mortality reduction in patients utilizing LBB pacing. A dynamic atrioventricular delay (AVD) optimization algorithm based on the promoting of biventricular fusion pacing has been proven to narrow QRSd over biventricular pacing with fixed AVD. In HF patients treated with LBB area pacing, QRSd narrowing may be a predictor of patient outcome and a target. As a result, a need exists for systems and methods that utilize a dynamic algorithm for AVD optimization that narrows QRSd in patients treated with LBB area pacing. US9220905 discloses an implantable medical device for managing therapy. SUMMARY The present invention is defined in the independent claim. Further embodiments are defined in dependent claims. In accordance with embodiments herein, an implantable medical device (IMD) for managing therapy is provided that comprises a connector