Linear stimulation of the heart for improved hemodynamic...

Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems

Reexamination Certificate

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Reexamination Certificate

active

06829506

ABSTRACT:

TECHNICAL FIELD
This invention relates to cardiac rhythm management devices for the heart. In addition, the invention relates to linear stimulation of the heart in order to provide improved hemodynamic benefits.
BACKGROUND
A normal human heart
100
, as illustrated in
FIG. 1
, includes a right atrium
106
, a left atrium
110
, a right ventricle
131
, and a left ventricle
132
. The ventricles
131
,
132
further comprise a right ventricular free wall
133
, a left ventricular free wall
134
, and an interventricular septum
135
dividing the ventricles. The electrical propagation system of the heart includes a sinoatrial (SA) node
120
, an atrioventricular (AV) node
122
, a bundle of His
124
dividing into a right branch of bundle of His
126
and left branch
128
, and a plurality of Purkinje fibers
112
dispersed throughout ventricular myocardium
136
.
During normal contraction, the SA node
120
initiates the excitation of the heart
100
, sending an electrical cardiac pulse through the atria and ventricles. Once initiated by the SA node
120
, the cardiac pulse is transmitted through right and left atria
106
,
110
, causing the atria to contract and pump blood from the atria to the ventricles. The cardiac pulse is then further transmitted through the AV node
122
to ventricles
131
,
132
. Transmission in the ventricles
131
,
132
is accomplished using a conduction system including the bundle of His
124
, which divides into the right branch
126
and left branch
128
, and finally the Purkinje fibers positioned throughout the ventricular myocardium
136
. The transmitted cardiac pulse causes the ventricles to contract, pushing the blood from the ventricles out into the pulmonary and systemic circulatory systems.
In patients with certain heart abnormalities, such as, for example, congestive heart failure and left bundle branch block, the electrical conduction patterns of the left ventricle
132
can be altered or impaired. These abnormalities can in turn cause the interventricular septum
135
to contract before the left ventricular free wall
134
, creating asynchronous left ventricular contraction and causing impaired hemodynamic function.
Recently, it has been demonstrated that through the use of atrial synchronous ventricular pacing, the left ventricular contractions in patients with the heart abnormalities described above can be resynchronized. Resynchronization differs from typical pacing performed by devices such as a pacemaker in that the goal of resynchronization is not to alter the rate at which the heart is contracting, but instead to alter the manner in which the contraction occurs. Resynchronization is a process that can involve the application of an electrical stimulus to the left ventricle or both the left and right ventricles after pacing has been detected in the atria. This electrical stimulus forces the septum
135
and free wall
134
to contract at approximately the same time, thereby resynchronizing left ventricular contraction. This resynchronization provides both acute and chronic hemodynamic benefits.
At present, resynchronization has been implemented by resynchronizing the left ventricle or both ventricles using a single point source for each ventricle. An example of a prior art cardiac rhythm management (CRM) device using a single point source is shown in FIG.
2
. The left ventricle
132
illustrated in
FIG. 2
includes the interventricular septum
135
and interventricular free wall
134
with free wall points
236
,
237
noted. The resynchronization system
200
includes CRM device
201
, lead
203
, and single point source
205
. The single point source
205
is typically coupled via the lead
203
to the CRM device
201
, with the CRM device
201
providing the electrical stimulus for resynchronization. Single point source
205
is constructed with a small surface area such that single point source
205
contacts only a small region of the surface of the left ventricular free wall
134
where point source
205
is located, such as at free wall point
237
.
Electrical propagation using a single point source differs from that of the propagation of a cardiac pulse during normal sinus rhythm. In normal sinus rhythm, the bundle of His
124
and Purkinje fibers
112
enhance conduction so that the entire ventricle is activated almost instantaneously, thereby causing the left ventricular contraction time to be very short in duration. In contrast, using a single point source, such as
205
as shown in
FIG. 2
, electrical propagation from the site at which the single point source contacts the surface of the left ventricle
132
at free wall point
237
to the rest of the ventricular muscle, such as free wall point
236
, is much slower, prolonging the left ventricular contraction time. This prolongation of contraction time compared to normal contraction makes the ventricle less efficient.
A further limitation of resynchronization through use of a single point source is the inability to adequately alleviate local wall stress. Local wall stress is a phenomenon that occurs when the interventricular septum
135
contracts before the ventricular free wall
134
, forcing the blood contained within ventricle
132
that is displaced by the septum
135
to push against and distend free wall
134
. A reduction in local wall stress has been shown through use of a single point source
205
, as shown in FIG.
2
. However, this reduction in local wall stress is limited to the area immediately adjacent to free wall point
237
, and other remote areas of the ventricular free wall, such as free wall region
236
, may still exhibit local wall stress.
Therefore, although some advantage may be gained through use of a single point source to assist in resynchronization of the left ventricular free wall and interventricular septum contractions, use of a single point source may still result in a hemodynamically suboptimal situation.
SUMMARY
Generally, the present invention relates to cardiac rhythm management devices for the heart. In addition, the invention relates to linear stimulation of the heart in order to provide improved hemodynamic benefits. In one aspect of the disclosure, a method of resynchronization of a heart may comprise the steps of coupling a linear source to a cardiac rhythm management device via a lead, coupling the linear source to a surface of the heart; and resynchronizing a contraction of the heart through linear excitation of the surface by the linear source.
In another aspect, the disclosure provides another method of resynchronization of a heart comprising the steps of coupling a first linear source to a left ventricular free wall nearer an apex of the heart and sending a first electrical stimulus to the first linear source.
In still yet another aspect, the disclosure provides an apparatus to resynchronize a heart by using atrial synchronous ventricular pacing comprising a cardiac rhythm management device, linear source coupled to a portion of a ventricular myocardium surface of the heart, and a lead coupled at a first lead end to the cardiac rhythm management device and at a second lead end to the linear source.
In still yet another aspect, the disclosure further provides an apparatus to resynchronize a heart comprising first means for providing an electrical stimulus to stimulate the heart, second means for exciting a linear region of a surface of the left ventricle, and means for electrically coupling the first means to the second means.
In still yet another aspect, the disclosure provides an apparatus to resynchronize contraction of a left ventricular free wall of a heart using atrial synchronous ventricular pacing, the apparatus comprising a cardiac rhythm management device for creating an electrical stimulus, a lead coupled to the cardiac rhythm management device at a first lead end, and a linear source coupled to the lead at a second lead end. Further in this aspect, the linear source may comprise a contact surface coupled to the left ventricular free wall at a free wall region, wherein the contact surface spans in a linear dire

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