Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
2000-12-21
2002-11-19
Layno, Carl (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C607S004000, C607S122000
Reexamination Certificate
active
06484057
ABSTRACT:
FIELD OF THE INVENTION
The present invention is related to methods and apparatus for treating arrhythmias such as atrial and/or ventricular fibrillation in subjects.
BACKGROUND OF THE INVENTION
The heart is a muscular organ which is covered by a fibrous sac known as the pericardium. The space between the pericardium and the muscular organ is called the pericardial space. The walls of the heart are substantially formed from muscle (the myocardium) which differs from either skeletal or smooth muscle. The heart comprises atria and ventricles, each of which is composed of layers of myocardium which are formed to encase the blood-filled chambers. In operation, when the walls of a chamber contract, they come together similar to a squeezing fist. This contraction of the cardiac muscle is triggered by depolarization of the muscle membrane. To operate properly, the muscle contractions should be coordinated.
If the muscle contractions are not coordinated within the ventricles, blood may be sloshed back and forth within the ventricular cavities instead of being ejected into the aorta and pulmonary arteries. Thus, the complex muscle masses forming the ventricular pumps should contract substantially simultaneously for efficient pumping.
The heart is able to achieve this coordination because of (a) the tight junctions formed between adjacent cardiac fibers (the fibers are joined end to end at structures known as intercalated disks, which provide the points or junctions) which allow action potentials to be transmitted from one cardiac cell to another; and (b) the specialized muscle fibers in certain areas of the heart which provide the conducting system for proper excitation of the heart. The specialized fibers are in contact with fibers of the cardiac muscles to form gap junctions, which permit passage of action potentials from one cell to another. The specialized conduction system is configured, in normal operation, to provide a rapid and coordinated spread of excitation.
Cardiac muscle cells are autorhythmic, i.e., capable of spontaneous, rhythmical self-excitation. The sinoatrial (SA) node is the normal pacemaker for the entire heart or smooth muscle, and it is from this region that the excitation wave starts; it then moves or propagates through the remainder of the myocardium in a synchronized manner. The SA node region of the heart contains a small mass of specialized myocardial cells in the right atrial wall near the entrance of the superior vena cava which have a fast inherent rhythm, which allows the SA node to be the normal pacemaker. In unusual circumstances, other regions of the heart can become more excitable and provide a faster spontaneous rhythm. In this situation, this other region can become the pacemaker and the rhythm for the entire heart.
In normal operation, the cells of the SA node make contact with the surrounding atrial myocardium fibers. Thus, from the SA node, a wave of excitation spreads throughout the right atrium along the atrial myocardial cells via the gap junctions. In addition, the specialized conducting system directs the impulse from the SA node directly to the left atrium, to simultaneously contract both atria.
The excitation wave then is distributed to the ventricles by way of a second small mass of specialized cells located at the base of the right atrium near the wall between the ventricles (the atrioventricular (AV) node). The AV node is configured to delay the propagation of action potentials (the wavefront) by about 0.1 second, to allow the atria to contract and empty the blood into the ventricle before ventricular contraction. The wavefront is then quickly dispersed along the specialized conducting fibers (down the interventricular septum) and then through unspecialized (typical) myocardial fibers in the remaining myocardium.
The pumping of blood includes alternate periods of contraction and relaxation. The cardiac muscle has a relatively long refractory period (on the order of about 250 ms). This refractory period is a time during which the membrane is insensitive to stimulus (either totally unable to propagate an excitation wave or only able to do so upon exposure to an increased level of stimulation).
During ventricullar fibrillation (VF) a number of independent activation wavefronts propagate simultaneously through the mycodardium. It has been suggested that as soon as the myocardium becomes excitable, it is excited by a wandering wavefront. See Lammers et al.,
The use of fibrillation cycle length to determine spatial dispersion in eletrophysiologic properties used to characterize the underlying mechanism of fibrillation
, 2 N. Trends Arrhythmia, pp. 109-112 (1986); Opthof, et al.,
Dispersion of refracteries in canine ventricular myocardium: Effects of sympathetic stimulation
, 68 Circ. Res., pp. 1204-1215 (1991). This proposition would indicate that there is no excitable gap between activations and would preclude the possibility of capturing fibrillation with exogenously generated electrical stimuli. However, pacing stimuli have been shown to be able to capture the myocardium during fibrillation. For example, Allesie et al and Kirchhof et al. report successful pacing of the canine left atrium during atrial fibrillation; and Daoud et al. and Capucci et al. report successful pacing of the human right atrium during atrial fibrillation. Others report pacing of right ventricular free wall during VF, although capture of the fibrillating myocardium was only successful in about 36% of the episodes. See KenKnight et al.,
Regional capture of fibrillating ventricular myocardium: Evidence of an excitable gap
, 77 Circ. Res. 849-855 (1995). In addition, in the past, the amount of myocardium captured by pacing via a single electrode has been relatively modest.
SUMMARY OF THE INVENTION
The present invention provides improved methods and devices for pacing the heart by increasing the number of pacing sites. Certain embodiments of the pacing systems of the present invention include a plurality of discrete electrodes, a single elongated electrode, or one or more line electrodes, arranged to direct at least one pacing train to multiple sites within a selected localized region or regions of the myocardium during a treatment window such as during an episodic onset of an arrhythmia or during a fibrillating event (whether in the atria, the ventricles, or both). In certain embodiments, the present invention can provide a plurality of pacing trains which transmit stimulation pulses to multiple proximately located sites in the myocardium at the time of the onset of a sensed or detected arrhythmia or fibrillation event. In certain embodiments, the timing and/or strength of the pacing trains and the position of the electrodes which transmit the stimuli may improve the likelihood that the arrhythmia will be halted and/or that fibrillating myocardium will be captured.
The pacing train stimuli can be configured with sufficient strength to control the excitation of the heart in the region undergoing stimulation. In certain embodiments, the pacing trains are sequentially delivered and each has an increased electrical strength (increased current) which is well above the lowest electrical stimulation needed to excite the myocardium in the region of interest during diastole of paced or sinus rhythm. In some embodiments, a diastolic pacing threshold (DPT) can be predetermined in situ (DPT is the lowest strength which is able activate the tissue during diastole of paced or sinus rhythm) and for pacing, a 5×-10×DPT stimulation strength can be employed.
Certain embodiments of the present invention are configured, by electrode placement and/or the selection of pacing signals, so that at least a 30-40 mm
2
region proximate the stimulus per pacing cycle may be captured, and typically the captured area is between 40 mm
2
-200 mm
2
and higher (such as about 500 mm
2
, or even up to about the area of substantially the entire myocardium).
One aspect of the invention is a method of pacing to treat arrhythmia in a patient, comprising the steps of: (a) positioning at least o
Ideker Raymond E.
Newton Jonathan C.
Layno Carl
Myers Bigel Sibley & Sajovec P.A.
UAB Research Foundation
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