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C600S375000, C607S120000, C607S121000, C607S122000, C607S127000, C607S128000, C607S126000, C604S021000

Reissue Patent

active

RE037463

ABSTRACT:

BACKGROUND—FIELD OF INVENTION
This invention relates to the field of endocardial mapping, and more particularly to the new field of devices for non-destructive elimination of arrhythmogenic sites and inappropriate conduction pathways, catheter methods for implantation of such devices and the use of such devices as substrates for local controlled drug release therapy.
BACKGROUND—PRIOR ART
Cardiac arrhythmias are abnormal rhythmic contractions of the myocardial muscle, often introduced by electrical or irregularities in the heart tissue. A region of the heart that results in an arrhythmia is here defined as an arrhythmogenic site in that it introduces the arrhythmia. If a number of regions acting in unison introduce an arrhythmia, they are each considered arrhythmogenic sites. Types of arrhythmogenic sites include, but are not limited to: accessory atrioventricular pathways, ectopic foci, and reentrant circuits.
The anatomical causes of heart arrhythmias are numerous and not entirely understood. Disease and damage to the myocardium from a variety of causes introduce variations in parameters such as conduction and excitability of cells. In turn, such physiological disturbances introduce more complicated spatial and temporal disruption of the electrical synchronization of the heart cells necessary for proper heart function.
Arrhythmias are often classified by where they occur in the heart. Supraventricular arrhythmias occur above the ventricles especially in the atrium or atrio ventricular node. Ventricular arrhythmias occur in the ventricles.
Two of the more common mechanisms of supraventricular arrhythmia generation are accessory pathways and atrioventricular node reentry. Accessory pathways are anomalous bands of conducting tissue that form a connection to the normal atrioventricular conducting system. Typically, in healthy individuals, anatomical regions known as the AV node, His bundle, and bundle branches arc the only conduit for the transmission of signals between the atria and the ventricles. Inappropriate accessory pathways are often characterized by rapid conduction and can conduct from atrium to ventricles as well as from ventricle to atrium. These inappropriate conduction pathways result in premature stimuli to some region of the heart by bypassing the normal conduction pathways. Atrio Ventricular reentry tachycardia (AVNRT) has been described as consisting of 2 functionally distinct conduction pathways and has been observed during electrophysiology studies. The two functionally distinct pathways are a fast pathway in which there is rapid signal conduction and a long refractory period, and the second consists of a slow pathway with slow conduction and a short refractory period. In normal or sinus rhythm, the signal is transmitted from the atria to the ventricles via the fast pathway. AVNRT is initiated by atrial premature depolarization where the signal is blocked at the fast pathway because it is still in its longer refractory period. However, the slow conduction pathway has a short refractory period, and is capable of conducting the signal. This can set up a circuit stimulating the fast pathway from the ventricle side, and a reentry circuit within the atrioventricular node is set up. Ten percent of AVNRT cases are believed to be due to a reversal of this situation in which the signal is carried antegrade over the fast pathway and retrograde over the slow pathway. [Ganz, L., Friedman, P.: Supraventricular Tachycardia, New England Journal of Medicine, V. 332, No. 3, pp 162-173, Jan. 19, 1995.]
In general, reentry shall be referred to here as a mechanism whereby the signal propagating through the heart is conducted through a circuit such that it returns to the original site causing premature depolarization of the cardiac cells. Such premature depolarization of surrounding heart cells on a small scale is often sufficient to completely disrupt the action of the heart overall. Reentry can be initiated by fast pathways or by slow pathways caused by a variety of cardiac diseases and is believed to be the cause of many arrhythmias. Reentry can also happen in any region of the heart.
For example, in a myocardial infarction, or heart attack, cells die due to lack of nutrients because the blood vessel that provides the nutrients is obstructed. As the site of infarction heals, the dead myocardium is replaced by fibrous tissue and the residual viable myocardial cells become embedded in scar leading to non-uniform activation and slow conduction. These abnormalities provide a substrate for reentry which may initiate a ventricular arrhythmia. [Hsia, H. H. et. al., “Work-Up and Management of Patients with Sustained and Non sustained Monomorphic Ventricular Tachycardias”, Cardiology Clinics, Vol. 11, No. 1, pp 21-37, February, 1993].
A schematic of one such reentry circuit is shown in FIG.
1
. Because the surviving tissue
32
in the center of the necrotic tissue
30
a
and
30
b
has higher resistance to the incoming electrical signal
34
, the signal
36
travels around the necrotic region
30
b
, and excites the embedded surviving tissue
32
on the far side of the necrotic region. The excitation of surviving tissue
30
often results in stimulation of cells that have already fired when reentry of the signal
38
occurs. In turn, surrounding cells
28
are then affected.
Arrhythmias can result from the propagation of an impulse around a large necrotic scar in what can be called a macro reentrant circuit. In this type of circuit, the impulse propagates as a broad wave front around the obstacle. If the obstacle is sufficiently large, there is no need for a well defined area of slow conduction. Arrhythmias can also be due to a reentrant circuit where the impulse propagates around a fixed obstacle in which a well defined area of myocardium is a necessary path in the circuit. Other mechanisms are also possible. [Brugada, Josep, et. al., “The Complexity of Mechanisms in Ventricular Tachycardia”, Pace, March, Part 11, pp 680-686, 1993]. A simple schematic of a reentry circuit introduced by a fixed obstacle is shown in FIG.
2
. Here the necrotic tissue or region of slow conduction
30
results in a reentry signal
38
which disrupts the function of the surrounding myocardial cells
28
.
Necrotic regions that act as arrhythmogenic sites may depend upon other arrhythmogenic sites to introduce an arrhythmia, just as the presence of other arrhythmogenic sites may complicate an arrhythmia. In
FIG. 3
, a figure of eight functional circuit is shown. This circuit consists of two reentrant regions
38
a
and
38
b
that are essentially coupled. Here, a slightly more complicated reentrant circuit is shown to be introduced by two separate regions of dead tissue
30
c
and
30
d
. Although they act together, each of these regions is an arrhythmogenic site.
Surgical techniques exist to treat arrhythmias, and the selection of the most appropriate technique often depends upon the type of arrhythmia that is believed to be present. Most of these involve destroying the electrical action of the tissue to block one or more inappropriate conduction pathways. Interruption of a presumed reentrant circuit or complete isolation of the problem region have been attempted by a variety of techniques.
A surgical technique, called the Maze procedure, has been used for treating Supra Ventricular Tachycardias. In the Maze procedure, a number of incisions are made in an attempt to terminate inappropriate accessory pathways. [Furguson, T. Bruce; The Future of Arrhythmia Surgery, J. Cardiovascular E.P., Vol. 5, pp 621-634, July 1994.] This technique is hazardous for the patient in that it requires open heart surgery. The procedure is complex in that it required a number of precisely located delicately introduced incisions in the heart wall. The procedure is innovative in that it may result in a cure, but it is expensive and risky for the patient due to its complexity.
A new series of procedures and techniques for interrupting a current pathway in the heart or isolating tissue exist.

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