Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
2001-02-28
2003-05-13
Bockelman, Mark (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C607S099000, C607S122000, C607S113000, C607S148000
Reexamination Certificate
active
06564096
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to an improved method and system for treating and controlling tachycardia and arrhythmias, and more particularly treating and controlling atrial fibrillation and ventricular tachycardia.
BACKGROUND OF THE INVENTION
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 or blockage of the Purkinje system. The conditions can also occur 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. Chronic atrial fibrillation doubles mortality, mostly due to an increased risk of stroke as well as other cardiovascular complications. Congestive heart disease imposes the highest risk for developing atrial fibrillation. 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). Moreover, the likelihood of cardioversion success is low in patients with chronic atrial fibrillation lasting longer than 2 years or in patients who have enlarged atria. 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. 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. Current efforts to control this excess sympathetic tone include administration of &bgr;-adrenergic blocking drugs and surgical sympathectomy. 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. (Lazzara R, Scherlag B J, Robinson M J et al. Selective in situ parasympathetic control of the canine sinuatrial and atrioventricular node. Circ Res 1973; 32:393-401.) 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. (Chen S A, Chiang C E, Tai C T et al. Intracardiac stimulation of human parasympathetic nerve fibers induces negative dromotropic effects: implication with the lesions of radio frequency catheter ablation. Cardiovasc. Electrophysiol. 1998;9: 245-252.) However, 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. More recently, Reek et al. reported that stimulation of the parasympathetic nerve fibers in the RPA with a conventional electrode catheter decreased the sinus rate in sheep. (Reek S, Geller J C, Hartung W M, Auricchio A. Einfluss transvenöser elektrischer Stimulation in der rechten Pulmonalarterie auf Sinusknotenläre und ventrikuläre Refraktärzeiten. Z Kardiologie 1999;88, Suppl. 1:10.) In addition, electrical stimulation of parasympathetic nerves either during or after coronary artery bypass grafting operation have demonstrated that parasympathetic fibers innervating the sinus and atrioventricular node can also be stimulated in humans. (Murphy D A, Johnstone D E, Armour J A. Preliminary observations on the effects of stimulation of cardiac nerves in man. Can J Physiol. Pharmacol. 1985;63:649-655; Quan K J, Mackall J A, Biblo L A, Van Hare G F, Carlson M d. Endocardial parasympathic stimulation slows the ventricular rate during atrial fibrillation in humans. PACE 1996;19:647 (abstract).) 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. (Chiou C W, Eble J N, Zipes D P. Efferent vagal innervation of the canine atria and sinus and atrioventricular nodes. Circulation 1997;95:2573-2584.) These results required a thoracotomy. Additionally, 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. (Thompson G W, Levett J M, Miller S M et al. Bradycardia induced by intravascular versus direct stimulation of the vagus nerve. Ann Thorac Surg 1998;65(3):637-42.)
Copending application Ser. No. 09/334,822, entitled Method and Apparatus for Transvascular Treatment of Tachycardia and Fibrillation, discloses the use of a catheter having an expandable basket-shaped electrode array for delivering a stimulus adjacent to one or more predetermined cardiac parasympathetic nerves to slow or regulate the beating rate of the heart. The basket-shaped electrode array provides excellent stability during stimulation.
SUMMARY OF THE INVENTION
The present invention is directed to an improved 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. In connection with the method and system, an improved catheter is provided having a generally circular electrode array that is generally transverse to the axis of the catheter. This improved design is smaller and less cumbersome than the basket-shaped electrode array, described above, and reduces the risk of clott
Bockelman Mark
Christie Parker & Hale LLP
Yu Jeanne
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