Prosthesis (i.e. – artificial body members) – parts thereof – or ai – Arterial prosthesis – Drug delivery
Reexamination Certificate
2000-10-13
2004-04-06
Isabella, David J. (Department: 3738)
Prosthesis (i.e., artificial body members), parts thereof, or ai
Arterial prosthesis
Drug delivery
C623S001440, C623S001460, C623S001150, C427S002250
Reexamination Certificate
active
06716242
ABSTRACT:
FIELD OF THE INVENTIONS
The inventions described below relate to the field of implantable medical devices. Specifically the invention relates to endoluminally placed prosthesis known as stents. More specifically, the invention relates to the placement of stents in the pulmonary veins which have advantages for the treatment of atrial fibrillation.
BACKGROUND OF THE INVENTIONS
Atrial fibrillation (AF) is a form of heart disease that afflicts millions of people. It is a condition in which the normal contraction of the heart is interrupted, primarily by abnormal and uncontrolled action of the atria of the heart. The heart has four chambers: the right atrium, right ventricle, the left ventricle, and the left atrium. The right atrium pumps de-oxygenated blood from the vena cava to the right ventricle, which pumps the blood to the lungs, necessary for return flow of de-oxygenated blood from the body. The right atrium contracts to squeeze blood into the right ventricle, and expands to suck blood from the vena cava. The left atrium pumps oxygenated blood from the pulmonary veins (returning from the lungs), necessary for flow of oxygenated blood from the lungs. The left atrium contracts to squeeze blood into the left ventricle, which then pumps the blood into the aorta and thence to the entire body, and expands to suck blood from the pulmonary veins. The contractions of the atria normally occur in a controlled sequence with the contractions of the other chambers of the heart. When the left atrium or the right atrium fails to contract, contracts out of sequence, or contracts ineffectively, blood flow within the heart is disrupted. The disruption of the normal rhythm of contraction is referred to as an arrhythmia. The arrhythmia, known as atrial fibrillation, can cause weakness of the heart due to reduced ventricular filling and reduced cardiac output, stroke due to clot formation in a poorly contracting atria, which may lead to brain damage and death, and even life threatening ventricular arrhythmias.
There is a broad spectrum of situations which fall under the broad heading of AF. For example, in older patients where there is substantial heterogeneity in the conduction within the atrial tissue, the patient is said to have the tissue substrate for AF such that any trigger will result in maintaining AF. In younger patients, the tissue may have more homogeneous conduction and be less likely to have sustained AF. In the younger patient it may be the often reoccurrence of a premature depolarizing tissue which acts as a trigger that causes the clinical manifestation of problematic episodes of AF. Clearly, there is a continuous spectrum of degrees of triggered AF and conduction heterogeneity which acts as a substrate for this arrhythmia, and it is appropriate that a number of medical therapies are being developed to treat this disease.
Atrial fibrillation may be treated with an atrial defibrillator. Atrial defibrillators are typically implantable electrical therapy devices which deliver defibrillating energy to the atrium to terminate arrhythmias. They sense the electrical activity of the atrium and deliver an electrical shock to the atrium when the electrical activity indicates that the atrium is in fibrillation. Electrical defibrillation has two major problems: the therapy causes substantial pain, and has the potential to initiate a life threatening ventricular arrhythmias. The pain associated with the electrical shock is severe and unacceptable for many patients. Unlike electrical ventricular defibrillators, where the patient loses consciousness prior to receiving therapy, the patient who suffers an atrial arrhythmia is conscious and alert when the device delivers electrical therapy.
The potential for inappropriate induction of ventricular fibrillation by the shock intended to defibrillate the atrium exists. The induction of ventricular fibrillation has great potential to result in death in just a few minutes if no intervening therapy is provided. Even with careful algorithms to deliver shocks to the periods in the ventricular contraction cycle when the heart is not susceptible to shock induced ventricular fibrillation, the risk of setting off a ventricular fibrillation remains substantial.
Doctors have treated atrial fibrillation with drugs injected intravenously or administered orally. Recent literature describes the potential for the delivery of drugs to the heart on demand to terminate arrhythmias. The concept has been suggested for use in the atrium to treat atrial fibrillation. Arzbaecher, Pharmacologic Atrial Defibrillator and Method, U.S. Pat. No. 5,527,344 (Jun. 18, 1996) describes a pharmacological atrial defibrillator and method for automatically delivering a defibrillating drug into the bloodstream of a patient upon detection of atrial arrhythmias in order to terminate the atrial arrhythmias. Arzbaecher teaches that unspecified defibrillating drugs should be injected into the bloodstream with a large initial dose followed by delivery of a continuous smaller dose (this is the “two-compartment pharmacokinetic model” discussed in the Arzbaecher patent). By delivering agents to a blood vessel and maintaining a therapeutic level of drugs in the blood stream, Arzbaecher requires systemic effects to be achieved in order to terminate atrial arrhythmias. In other words, if drugs injected according to Arzbaecher are to have any effective concentrations within the heart, then a large amount must be injected in the blood stream to ensure that an adequate dose is delivered to the affected area of the heart. While the drugs are in the blood stream, they are available throughout the body to cause side effects on all other organs.
There are several disadvantages to the transient introduction of systemic drug levels by an implantable device. Systemic effects resulting from such delivery may result in detrimental effects to ventricular cardiac conduction. These detrimental effects could be life threatening, and several studies suggest that use of these drugs actually leads to higher mortality. The large amount of drugs required for systemic delivery of therapeutic doses demands a larger, less comfortable device than smaller dosages would allow. The large quantity of drug in the implantable reservoir of such a system is potentially more dangerous if it develops a leak or is ruptured. Such a large single dosage requires a reservoir that requires frequent follow-ups for refilling post therapy by a clinician. Lastly, the large quantity of drugs required to obtain therapeutic levels in the entire body may cost substantially more than that required to treat a specific site within the heart.
Atrial fibrillation can be treated by atrial ablation. There are two general approaches for providing ablative therapy to the heart for the treatment of atrial fibrillation. These shall be called the long linear ablative lesion approach and the focal ablation approach.
In the long linear lesion approach, the heart tissue is killed along a linear pathway. The cardiac electrophysiologist does this to segment the heart into regions which are too small to sustain atrial fibrillation. Such an approach is very similar to performing the Maze procedure using radiofrequency, microwave, and ultrasound ablative energy sources on the end of catheters. In the Maze procedure, a number of incisions are made with a scalpel in an attempt to terminate inappropriate accessory pathways.
In the focal ablation approach, the heart tissue is killed at a single site. The cardiac electrophysiologist attempts to ablate the region of the heart that prematurely depolarizes, and which has been described as acting as a trigger for the initiation of atrial fibrillation. Recently, work in ablating regions at the junction of the pulmonary veins and the left atrium has been performed. Such ablations remove the possibility of triggers for AF initiating within the pulmonary veins, or at the region near the junction of the veins with the left atrial tissue. Such ablations may also remove disturbances introduced into the conduction pathway by the hetero
Chattopadhyay Urmi
Isabella David J.
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