Atrial pacing and sensing in cardiac resynchronization therapy

Details Atrial pacing and sensing in cardiac resynchronization therapy Atrial pacing and sensing in cardiac resynchronization therapy

2001-09-13

2004-03-02

Layno, Carl (Department: 3762)

Surgery: light, thermal, and electrical application

Light, thermal, and electrical application

Electrical therapeutic systems

C607S017000

Reexamination Certificate

active

06701186

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates to cardiac resynchronization therapy in heart failure patients. More specifically, the present invention relates to using both atrial pacing and atrial sensing when applying cardiac resynchronization therapy.
BACKGROUND OF THE INVENTION
Cardiac resynchronization therapy (CRT) is a well-known method of treating heart failure patients. Oftentimes, a heart failure patient will experience a conduction disorder in a chamber of the heart caused by damage to the high-speed conduction fiber network, such as the Purkinje Fibers or Bachmann's Bundle, that is responsible for providing an electrical signal to excite a chamber, causing contraction. One form of CRT involves the use of a pacing device to provide the otherwise-faulty electrical stimulation of the chamber(s) to counteract the effects of the damaged conduction fibers. When the high-speed conduction fibers are damaged, electrical signals traveling through the heart no longer travel quickly through the high-speed fibers. The electrical signals travel much slower, because they are forced to propagate sequentially through muscle conduction, rather than high-speed fiber conduction. This results in an attenuation of the signal propagation speed and the delivery of the depolarization signal to the chamber is delayed.
This attenuation of the signal propagation speed to and through the chamber may cause the chamber to contract asynchronously relative to other chambers, or may cause one part of the chamber (e.g., the septum between the ventricles) to contract first and begin to relax before another part (e.g., the freewall of the left ventricle) contracts. This asynchronous operation can have deleterious hemodynamic effects.
CRT generally improves the pumping efficiency of the heart by providing an electrical stimulation to a later-contracting chamber, or to a later-contracting chamber portion (e.g., the left ventricle freewall) contemporaneously with the natural contraction of the earlier contracting portion, such as the septum. Because adjacent chambers and/or both walls of a ventricle contract at approximately the same time with CRT, the pumping efficiency of the heart may be significantly improved. To provide such electrical stimulation, an electrode connected to a CRT pacing device must be positioned near the delayed chamber or chamber region (e.g., the left ventricle freewall). For example, the delayed region of the left ventricle freewall may be stimulated via a branch of the coronary sinus vein that extends over the portions of the left ventricle, and a delayed region of the left atrium may be stimulated via Bachmann's bundle, the coronary sinus vein passing beneath the left atrium, or the Triangle of Koch.
When applying CRT to synchronize ventricle contraction that is otherwise asynchronous due to a bundle branch block, such as a left bundle branch block (LBBB) of the left ventricle delaying freewall contraction, the stimulation is provided synchronously with the natural conduction of the septum between the right and left ventricles. For many patients, there is no block of Bachmann's bundle between the right and left atria so no stimulation is necessary at the left atrium when the heart is beating at the natural pulse rate created by depolarization at the sino-atrial node. The right and left atria have sufficient conduction paths to the sino-atrial node and contract before the ventricles contract.
Some of these patients requiring ventricular resynchronization may also require a pacing stimulation to improve the pulse rate of the heart, such as for the bradycardia condition. Some patients requiring ventricular resynchronization may also require a rate responsive pacing device to dynamically advance the pulse rate for particular physical states of their body (e.g., during exercise) when their pulse rate does not adequately advance naturally. When controlling the pulse rate, such as for the bradycardia patient and/or for a patient requiring a rate responsive pacing device, the pulse rate is advanced through a stimulation applied by the device to the right atrium. This stimulation causes a cardiac cycle to occur sooner relative to a previous cycle than would happen naturally. These patients requiring ventricular resynchronization therapy and pulse rate control may not have an interatrial block, so that during cardiac cycles when the pulse rate is not being controlled, the conduction between the atria occurs quickly. In this case, the left atrium contracts sufficiently early so that ventricular contraction does not conflict with atrial contraction.
However, application of this stimulation by the lead also used for atrial sensing in the right atrium creates an interatrial block in most patients because the conduction from the right atrium to the left atrium will occur through muscle conduction rather than through high-speed fiber conduction. Therefore, the left atrium will contract after a delay relative to the initial stimulation. If the conduction from the right atrium proceeds quickly through the atrio-ventricular node to the septum between the ventricles, then the freewall must also be quickly paced for bundle block patients in order to maintain synchronization between the ventricular walls. However, the ventricular contraction may occur before the left atrium has completed its contraction.
Once the ventricles begin to contract, the mitral valve will be forced into a closed position. If the left atrium is contracting as the mitral valve closes in response to left ventricle contraction, then the left atrium will no longer be able to expel blood into the left ventricle and will instead pump blood back into the lungs. This condition leads to additional health problems for the patient.
If the lead used for sensing and pacing is placed in proximity to the left atrium to reduce the stimulation delay of the left atrium, then the sensing of the natural conduction will be delayed during cardiac cycles when the natural pulse rate is otherwise sufficient. This delay in sensing the natural depolarization at the left atrium location will delay the stimulation being provided to the ventricle's freewall for the bundle block patient. Ventricular contraction will remain asynchronous, and the heart's pumping efficiency will remain unimproved.
Therefore, there is a need for a cardiac resynchronization method and device that can stimulate one or more ventricular walls to synchronize ventricular contractions without creating mitral valve closure during left atrium contraction, either when allowing a natural pulse rate or when controlling the pulse rate.
SUMMARY OF THE INVENTION
Embodiments of the present invention improve cardiac resynchronization therapy by sensing a natural depolarization at the right atrium when allowing a natural pulse rate and by pacing the left atrium when controlling the pulse rate. These embodiments detect a depolarization at the sino-atrial node or other right atrium location for purposes of timing a ventricular stimulation when allowing the natural pulse rate and provide a pacing signal at the coronary sinus adjacent the left atrium or other left atrium location and a subsequent ventricular stimulation when controlling the pulse rate.
The present invention may be viewed as a method for providing resynchronization therapy to a heart. The method involves detecting whether to allow the heart to proceed at a natural pulse rate. The method also involves sensing a natural depolarization event with a first electrode in a right atrium, not stimulating a left atrium, and subsequently stimulating one or more ventricular walls with at least a second electrode during a cardiac cycle when allowing the heart to proceed at the natural pulse rate. The method additionally involves stimulating a left atrium with a third electrode and subsequently stimulating one or more ventricular walls with at least the second electrode during a cardiac cycle when not allowing the heart to proceed at the natural pulse rate.
The present invention may also be viewed as a device for

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