Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
1999-06-17
2001-09-18
Schaetzle, Kennedy (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C607S099000, C607S113000, C607S122000, C607S148000
Reexamination Certificate
active
06292695
ABSTRACT:
BACKGROUND OF THE INVENTION
The field of the invention is the control of tachycardia, including fibrillation, and arrhythmias, particularly the control of atrial fibrillation and ventricular tachycardia.
Tachycardia is the rapid beating of the heart, caused by abnormalities in any part of the heart, for example the atria, Purkinje system, or ventricles. Often, the extremely rapid beating of the heart is uncoordinated, and leads to fibrillation or flutter. These conditions occur after myocardial infarctions, for example, or in various pathological conditions, such as a dilated heart, blockage of the Purkinje system, or following chemical therapies (e.g., epinephrine) or repetitive stimulation. Atrial flutter often becomes atrial fibrillation within a few days or weeks, and leads to a complete failure of the atria to pump blood.
Atrial fibrillation is the most frequent tachycardia in patients. It most frequently occurs in patients over the age of 60 years, and affects over 8% of patients with cardiovascular disease and people older than 80 years (
1
,
2
). Chronic atrial fibrillation doubles mortality (
3
), mostly due to an increased risk of stroke as well as other cardiovascular complications. Among other risk factors, congestive heart disease imposes the highest risk for developing atrial fibrillation (4.5-5.9 fold) (
4
). Therefore, restoration of normal sinus rhythm by pharmacological or electrical cardioversion is attempted in many patients with atrial fibrillation. Unfortunately, atrial fibrillation recurrence rates one year after successful cardioversion are high (75% without antiarrhythmic drug prophylaxis and 50% with aggressive antiarrhythmic medication; (
5
)). Moreover, the likelihood of cardioversion success is low in patients with chronic atrial fibrillation lasting longer than 2 years or who have enlarged atria (
6
). In many of these patients, therapy is directed toward ventricular rate control during atrial fibrillation in order to stabilize cardiac function. However, in patients with concomitant heart failure, drugs that slow the ventricular rate during atrial fibrillation may further depress ventricular contractility and cause arterial hypotension or be of limited use due to side effects.
Like atrial fibrillation, ventricular tachycardia can lead to fibrillation, which leads to failure of the ventricles to pump blood. Unlike atrial fibrillation, ventricular fibrillation cannot be compensated for by the rest of the heart and rapidly leads to sudden death if not reversed. Ventricular fibrillation is a common cause of death in patients (
7
). For example, patients who survive myocardial infarction often remain at risk for reentrant ventricular tachycardia. The sympathetic and parasympathetic nerves (autonomic innervation) of the heart influence susceptibility to spontaneous arrhythmias. Sympathetic stimulation can increase the risk of fatal arrhythmias during ischemic events and parasympathetic stimulation can decrease the risk (
8
). Current efforts to control this excess sympathetic tone include administration of &bgr;-adrenergic blocking drugs and surgical sympathectomy (
9
). Problems with these methods include contraindications for drug therapy in patients who are sensitive to the negative inotropic effects of &bgr;-adrenergic blockade and the inherent risks of thoracic surgery, which in this case also include pulmonary complications, injury to the brachial plexus, and upper extremity paresthesias.
Another common measure used to control atrial or ventricular tachycardia is ablation or modification of the His bundle or atrioventricular node and ablation of atrial or ventricular foci. Such ablation may abolish a tachycardia or slow the ventricular response during atrial fibrillation by blocking impulse conduction across the atrioventricular node. Ablation can be performed by introduction of a catheter into the heart through the venous system and subsequent ablation of the tissue.
In 1973, Lazzara and Scherlag reported that electrical stimulation of parasympathetic cardiac nerves at the junction of the right atrium and the inferior vena cava close to the coronary sinus ostium selectively prolonged atrio-ventricular (AV) conduction time (
10
). Chen et al. showed control of ventricular rate during atrial fibrillation by short bursts of stimulation to parasympathetic nerves in the fat pads to the AV node, but this method can lead to unwanted stimulation of myocardial muscle, and stimulation times are necessarily very brief because the electrode cannot be stably maintained in the appropriate location. Most recently, Reek et al. (
12
) reported that stimulation of the parasympathetic nerve fibers in the RPA with a conventional electrode catheter decreased the sinus rate in sheep. In addition, electrical stimulation of parasympathetic nerves either during coronary artery bypass grafting operation (CABG) (
13
) or after CABG operation (
14
) have demonstrated that parasympathetic fibers innervating the sinus and atrioventricular node can also be stimulated in humans. The stimulation electrodes, however, were only temporarily fixed at the outer surface of the heart or superior vena cava. Chiou et al. demonstrated that extracardiac electrical stimulation of parasympathetic fibers in fat pad between the superior vena cava, the aorta, and adjacent to the right pulmonary artery, diminished AV nodal conduction during sinus rhythm (
15
). These results required a thoracotomy. Most recently, Thompson and coworker reported that endovascular electrical stimulation of parasympathetic fibers in the superior vena cava with a conventional electrode catheter slows the sinus rate (
16
).
SUMMARY OF THE INVENTION
The present invention provides a method and system for controlling the heart rate of a patient and is particularly useful in controlling cardiac fibrillation and tachycardia. The method involves the intravascular stimulation and/or ablation of cardiac parasympathetic and sympathetic nerves sufficient to regulate or slow the heart rate or prevent the occurrence of these arrhythmias.
The method comprises providing an electrophysiology catheter comprising at least one electrode and preferably an electrode array, e.g., in an expandable electrode basket, at its distal end. The catheter is inserted into a blood vessel and directed to a location wherein the electrode through which a stimulus is delivered is adjacent to one or more predetermined cardiac parasympathetic or sympathetic nerves. A selected stimulus preferably a pulsed electrical signal, is then delivered through the electrode(s) to slow or regulate the beating rate of the heart. The stimulus is maintained for an extended period to provide a physician sufficient time to administer a drug, operate or take other appropriate measures to attempt to permanently or at least more permanently establish normal heart rhythm or slow the heart rate. Such a period may require several hours.
The selected stimulus is preferably below the threshold needed to depolarize the cardiac muscle or it is applied sufficiently far from the cardiac muscle so that depolarization does not occur. Alternatively, a stronger stimulus intensity may be used if it is timed to occur during the myocardial refractory period. The refractory period can be induced at regular intervals by pacing the contraction of the myocardium with electrical pulses applied from the same or a different electrode as is used to apply the nerve stimulation.
A preferred stimulus for stimulating a predetermined parasympathetic nerve is a pulsed electrical signal having a frequency of from about 1 to about 200 Hz, preferably about 20-30 Hz, having an intensity or strength of from about 1 to about 200 volts as measured at the electrode tissue interface, preferably from about 8 to about 15 volts. The duration of each stimulating pulse is from about 1 microsecond to about 10 milliseconds, preferably from about 50 &mgr;sec (0.05 ms) to about 600 Asec (0.6 ms), most preferably from about 50 &mgr;sec to about 100 &mgr;sec.
It is understood that the frequency, intensity and duration of t
Schauerte Patrick
Scherlag Benjamin J.
Scherlag Michael
Webster, Jr. Wilton W.
Christie Parker & Hale LLP
Schaetzle Kennedy
LandOfFree
Method and apparatus for transvascular treatment of... does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Method and apparatus for transvascular treatment of..., we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method and apparatus for transvascular treatment of... will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-2445827