Abstract:
A method is described for increasing the likelihood of the occurrence of an arrhythmia in a heart, particularly a ventricular arrhythmia of the type leading to Sudden Cardiac Death. The method includes the steps of creating an atrioventricular block in the heart of an animal test subject, inducing a myocardial infarction in the heart of the test subject, and then stimulating myocardial hyperinnervation the test subject. In a specific example described herein, the atrioventricular block is created by ablating the atrioventricular node of the heart using an ablation catheter. The myocardial infarction is induced by ligating the left anterior descending portion of the coronary artery. Myocardial hyperinnervation is stimulated by application of Nerve Growth Factor or other neurotrophic vectors to the left stellate ganglion. The test subject is an adult canine. By creating an atrioventricular block and a myocardial infarction within the heart of an adult canine test subject, then stimulating nerve growth within the left stellate ganglion of the subject using Nerve Growth Factor, it has been found that there is a significant increase in the likelihood of Sudden Cardiac Death arising from ventricular arrhythmias. It is believed that the Sudden Cardiac Death of the test subject arises in a manner very similar to circumstances wherein Sudden Cardiac Death occurs in human patients subject to a previous myocardial infarction, thus, an animal model system for artificially inducing a heart arrhythmia is also disclosed. Thus, the method and animal model system facilitate the collection of data pertinent to conditions within the heart arising prior to Sudden Cardiac Death and for developing and testing therapies intended to prevent Sudden Cardiac Death.
Abstract:
A system and method for predicting the defibrillation threshold energy of a defibrillation lead arrangement by determining the upper limit of vulnerability of the heart by shocking the heart at varying times during the T-wave at decreasing test shock energy levels until fibrillation is induced in the heart. The lowest energy level which fails to induce fibrillation is determined to be the upper limit of vulnerability and the defibrillation threshold is predicted to be an energy level incrementally higher in the range of about 5 Joules.
Abstract:
A method has been developed that detects cardiac arrhythmia from intrinsic cardiac nerve signals obtained from a heart in a patient. The method includes sampling intrinsic cardiac nerve activity at a high sample rate, filtering the sampled signal with a high pass filter, comparing the filtered signal to a predetermined threshold, and initiating a therapeutic action in response to the filtered signal exceeding the predetermined threshold. The intrinsic cardiac nerve activity may be received through an electrode implanted on the heart or from an electrode inserted into the venous structure of the heart.
Abstract:
An electrode for monitoring nerve activity has been developed. The electrode includes an array of electrically conductive projections extending from a surface of an electrical contact that enable the electrical contact to be connected directly to the nerve.
Abstract:
An XSLT method is used in a multi-thread environment. In the XSLT method, an XML file is analyzed in view of XSLT templates. Relationships between the transforming processes of the XSLT templates and the tree nodes of the XML file are built. Time for the execution of the transforming process of each of the XSLT templates and the number of a related one of the tree nodes are calculated. Threads are scheduled for the transforming processes of the XSLT templates. The transforming processes of the XSLT templates are executed.
Abstract:
Methods and systems are provided for determining an increased likelihood of the occurrence of a cardiac arrhythmia, myocardial ischemia, congestive heart failure and other diseased conditions of the heart associated with elevated sympathetic neural discharges in a patient. The methods and systems comprise monitoring the sympathetic neural discharges of a patient from the stellate ganglia, the thoracic ganglia, or both, and detecting increases in the sympathetic neural discharges. The methods and systems may further comprise delivering therapy to the patient in response to a detected increase in the sympathetic neural discharge, such as delivering one or more pharmacological agents; stimulating myocardial hyperinnervation in the sinus node and right ventricle of the heart of the patient; and applying cardiac pacing, cardioversion or defibrillation shocks. Pharmacologic agents which may be used in connection with the delivery of include those which are known to exert anti-arrhythmic effect and anti-convulsant agents, such as phenytoin, carbamazepine, valproate, and phenobarbitone. Other pharmacologic agents may be used to treat impending myocardial ischemia and other diseased conditions of the heart associated with elevated sympathetic neural discharges.
Abstract:
A system and method for monitoring nerve activity in a subject. The system includes a plurality of electrodes placed in proximity to skin of the subject, an amplifier electrically connected to the electrodes and configured to generate a plurality of amplified signals corresponding to electrical signals received from the subject through the electrodes, and a signal processor. The signal processor applies a high-pass filter to the amplified signals to generate filtered signals from the amplified signals, identifies autonomic nerve activity in the plurality of filtered signals; and generates an output signal corresponding to the filtered signals. The high-pass filter attenuates a plurality of the amplified signals having frequencies that correspond to heart muscle activity during a heartbeat.
Abstract:
A method of manufacturing a resistive memory device is provided. A bottom electrode and a cup-shaped electrode connected to the bottom electrode are formed in an insulating layer. A cover layer extends along a first direction is formed and covers a first area surrounded by the cup-shaped electrode and exposes a second area and a third area surrounded by the cup-shaped electrode. A sacrificial layer is formed above the insulating layer. A stacked layer extends along a second direction and covers the second area surrounded by the cup-shaped electrode and a portion of the corresponding cover layer is formed. A conductive spacer material layer is formed on the stacked layer and the sacrificial layer. By using the sacrificial layer as an etch stop layer, the conductive spacer material layer is etched to form a conductive spacer at the sidewall of the stacked layer.
Abstract:
Methods and kits are provided for determining an increased likelihood of the occurrence of a cardiac arrhythmia, myocardial ischemia, congestive heart failure and other diseased conditions of the heart. The methods and kits comprise measuring serum NGF levels in a subject and detecting increases in NGF levels over baseline. The methods may further comprise initiating preventive therapy in response to a detected increase in serum NGF levels.
Abstract:
A method is described for increasing the likelihood of the occurrence of an arrhythmia in a heart, particularly a ventricular arrhythmia of the type leading to Sudden Cardiac Death. The method includes the steps of creating an atrioventricular block in the heart of an animal test subject, inducing a myocardial infarction in the heart of the test subject, and then stimulating myocardial hyperinnervation the test subject. In a specific example described herein, the atrioventricular block is created by ablating the atrioventricular node of the heart using an ablation catheter. The myocardial infarction is induced by ligating the left anterior descending portion of the coronary artery. Myocardial hyperinnervation is stimulated by application of Nerve Growth Factor or other neurotrophic vectors to the left stellate ganglion. The test subject is an adult canine. By creating an atrioventricular block and a myocardial infarction within the heart of an adult canine test subject, then stimulating nerve growth within the left stellate ganglion of the subject using Nerve Growth Factor, it has been found that there is a significant increase in the likelihood of Sudden Cardiac Death arising from ventricular arrythmias. It is believed that the Sudden Cardiac Death of the test subject arises in a manner very similar to circumstances wherein Sudden Cardiac Death occurs in human patients subject to a previous myocardial infarction, thus, an animal model system for artificially inducing a heart arrhythmia is disclosed. Thus, the method and animal model system facilitate the collection of data pertinent to conditions within the heart arising prior to Sudden Cardiac Death and for developing and testing therapies intended to prevent Sudden Cardiac Death.