HK1088570A - Breaking reentry circuits by cooling cardiac tissue - Google Patents

Description

Interrupting reentry circuits by cooling cardiac tissue

Technical Field

The present invention relates generally to systems and methods for stimulating myocardial tissue. In particular, embodiments of the present invention provide a system and method for treating cardiac tissue by cooling the cardiac tissue to inhibit the conduction of specific electrical signals in the cardiac tissue and reduce the duration of tachycardia and increase the effectiveness of pacing and defibrillation stimulation.

Background

The role of the cardiovascular system is crucial for survival. Through blood circulation, human tissues receive necessary nutrients and oxygen and discharge waste. Without blood circulation, the cells begin to undergo irreversible changes and lead to death. The muscle contraction of the heart is the driving force behind the blood circulation.

Each heart contraction, or heartbeat, is triggered by an electrical impulse. These electrical impulses originate from the sinoatrial node (the heart's natural pacemaker), which is located at the top of the right superior chamber of the heart or the right atrium. From there, the electrical impulses pass through the superior chamber (atrium) and Atrioventricular (AV) node of the heart, passing through the "bundle branch" to the inferior chamber of the ventricle. In this way, electrical impulses are transmitted from the sinoatrial node to the ventricles, triggering and modulating the heartbeat.

An arrhythmia is an abnormality of the heartbeat caused by any change, deviation or malfunction of the heart conduction system that conducts normal electrical impulses to the heart. In general, each heart contraction, or heartbeat, is triggered by an electrical impulse. These electrical impulses originate from the sinoatrial node (the heart's natural pacemaker), which is located at the top of the right superior chamber of the heart or the right atrium. From there, the electrical impulses pass through the superior chamber (atrium) and Atrioventricular (AV) node of the heart, passing through the "bundle branch" to the inferior chamber of the ventricle. In this way, electrical impulses are transmitted from the sinoatrial node to the ventricles, triggering and modulating the heartbeat.

Arrhythmias occur when the electrical "circulation" of the heart does not operate optimally. Arrhythmias result in abnormally fast (tachycardia) or abnormally slow (bradycardia) heartbeats. The cause of the arrhythmia may involve a previous heart condition (e.g., damage due to a previous heart attack) or other factors (e.g., medication, stress, insufficient sleep). In most cases, missed beats are of no medical significance. The most severe arrhythmias, however, result in almost 500,000 deaths per year in the united states, as counted by the american heart society. Sudden heart disease ("cardiac arrest") accounts for almost half of the deaths due to heart disease and is the first cause of death in the united states, as determined by the statistics of north american pacing and electrophysiology societies.

Almost all clinically important tachyarrhythmias are due to the fact that the conduction pulse does not disappear but continues to propagate and re-excite the heart tissue (called "reentry activation"). Such tachyarrhythmias include sinus node reentry activation, atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular node reentry tachycardia, atrioventricular reentry activation (wolpa-white syndrome or occult extra-ventricular junction), ventricular tachycardia, and branchlet reentry tachycardia.

For reentry activation to occur, a matrix must be present in the cardiac tissue to support reentry activation ("reentry circuits"). The action wavefront must be able to circulate along the central region of the block and encounter a unidirectional block, thus forcing it to travel in one direction along the central block. (if the action wavefront were allowed to travel in both directions along the retardation region, the action wavefront would collide and fade away.) important is the speed of travel of the cyclic wavefront. If the conduction velocity is too fast, the cyclic wavefront will reach the point of origin before the tissue has substantially repolarized and become excited again. Thus, at least one region of slow conduction is part of the reentry circuit for virtually all clinical reentry laws. Eliminating the slow conduction component of the reentrant circuit disrupts the circuit.

Atrial Fibrillation (AF) is the most common type of the same arrhythmia, with 200 million episodes per year in the united states alone. Both atrial fibrillation and atrial flutter increase the risk of stroke. According to the statistics of the American Heart Association, they result in over 54,000 deaths annually in the United states. The increased risk of atrial fibrillation is significantly associated with age. As a result, almost 70% of patients with atrial fibrillation are between 65 and 85 years of age. Atrial fibrillation is a rapid, abnormal heart rhythm (arrhythmia) caused by the absence of electrical signals from the upper chambers of the heart (the atria). The electrical signal emanating from the sinoatrial node should normally be a fixed rhythm: about 60 to 100 times per minute. The heart undergoes atrial fibrillation appearing as two heart rates: one room rate and one heart rate. With atrial fibrillation, the atrial rate is 300-. This heart rate is a result of the atrioventricular node blocking most of the atrial impulses and allowing only a small fraction of them to appear in the ventricles.

Certain arrhythmias are associated with specific electrical problems within the heart. Atrioventricular nodal reentry tachycardia is caused by external conduction pathways within the atrioventricular node. This allows the heart to electrically activate to a "short circuit" or circulate in the sinoatrial region.

Atrioventricular nodal reentry tachycardia is caused by external conduction pathways that allow electrical activity of the heart to simultaneously reach the "short circuit" and the bypassed atrioventricular node. In this mode, the outer "loop" directly connects the atrium and ventricle. In more cases, this path can only conduct "backwards": from the ventricles to the atria. This is called the "insidious additional pathway" because it cannot be diagnosed from a conventional Electrocardiogram (EKG). These arrhythmias are medically treatable, but may also be treated by catheter ablation. Rarely, the external pathway is conducted in the forward direction (from the atrium to the ventricle) and is embodied on the EKG. One such condition is called Wolff-Paris-Huai syndrome (WPW). WPW syndrome is caused by a particularly rapid heart rate and is potentially lethal. Typical WPW syndrome usually requires catheter ablation therapy.

A very different (and life threatening) situation is ventricular fibrillation. Ventricular fibrillation includes fibrillation of the ventricles rather than the atria. Unlike atrial fibrillation, it is life-threatening because the result is 350 beats per minute or more. The heart does not persist for several minutes at this rhythm without treatment (e.g., with a defibrillator).

In some cases, the arrhythmia may be transient. For example, a patient may experience a period of stress, illness, or drug (legitimate or otherwise) response. In other cases, more invasive treatments are helpful. For a slow heart movement (bradycardia), the most common treatment is an electrical (artificial) pacemaker. The instrument, implanted subcutaneously and permanently into the heart, emits electrical impulses when a slow or irregular heart rate is detected. For abnormally fast heart rates, Implantable Cardioverter Defibrillators (ICDs) may be implanted. An ICD monitor may correct abnormally fast heartbeats, if desired. These devices are life-saving for patients with ventricular fibrillation or ventricular arrhythmias. Another approach is electrophysiological studies with catheter ablation. The method is to introduce a catheter from a leg and/or neck vessel into the heart and very carefully destroy (ablate) the arrhythmogenic cardiac abnormality with radiofrequency energy.

In the myocardium, muscle fibers are connected internally to a bundle branch network that is distributed in all directions of the heart. When any part of the network is stimulated, the depolarization wave propagates to all of its parts and the entire structure contracts as a whole. Before a muscle fiber is stimulated to contract, its membrane must be polarized. The muscle fiber is usually in a polarized state until it is stimulated by changes in the surrounding environment. The membrane may be stimulated electrically, chemically, mechanically or by temperature changes. The minimum stimulus required to cause a contraction is called the stimulation threshold. The maximum stimulation amplitude that can be controlled without causing contraction is the maximum subthreshold amplitude.

Throughout most of the heart are the massive and string-like structures of specialized myocardial tissue. This tissue comprises the cardiac conduction system and is responsible for initiating and propagating depolarization waves throughout the myocardium. Any interruption or block in the conduction of heart pulses can cause arrhythmias or significant changes in the heart rate or rhythm of the heart.

Biphasic (cathodic or anodic) currents are used to stimulate the myocardium. However, until work such as in us patents 5,871,506 and 6,141,586 was achieved, the anodic current was considered clinically useless. The cathodic current comprises an electrical pulse of negative polarity. This type of current depolarizes the cell membrane by discharge of the membrane capacitance, directly lowering the membrane potential to a threshold level. Cathodic current, by directly lowering the potential of the resting membrane to a threshold, is less than half to one third the threshold current than anodic current during the subsequent diastole. Currently, substantially all artificial pacing uses negative stimulation pulses, although the use of anodal pulses has been experimentally demonstrated.

A typical implantable cardioverter/defibrillator (ICD) emits an initial anti-shock within 10 to 20 seconds of the onset of arrhythmia, thereby saving a myriad of lives. The improved apparatus has anti-tachycardia pacing capabilities added to the cardioversion/defibrillation function. These ICDs can have different initial responses to one or more tachycardias, as well as a program sequence for a particular arrhythmia.

The output energy level is typically set by the physician according to a threshold experienced by the patient. The threshold represents a minimum pacing energy that reliably stimulates the patient's heart. However, due to trauma associated with stimulation, scar tissue can develop at the interface between the implanted pacemaker lead and the myocardium. This scar tissue increases the threshold experienced by the patient. To ensure reliable cardiac endurance, the output energy level is typically set at a minimum of twice the initial measured endurance threshold. The disadvantage of this method is that higher stimulation levels cause more trauma to the myocardial tissue than lower stimulation levels, thereby promoting scar tissue formation and increasing the tolerance threshold. Higher stimulation levels also shorten the useful life of the battery. This is undesirable because a shorter battery life requires more frequent surgical implantation of a new battery.

Another disadvantage is the potential discomfort to the patient associated with higher stimulation levels. This is because higher stimulation levels can stimulate the diaphragm or diaphragm plexus or cause twitching of the intercostal muscles. Finally, higher stimulation was less effective due to overall blockage.

The result of improvements to pacing technology is improved conduction of electrical impulses associated with the effective heart rate of patients with arrhythmias that are unable to respond to normal pacing. For example, us patent 6,343,232B1, filed by Morton m.mower m.d., entitled "increasing muscle contraction with biphasic stimulation". The invention describes increasing electrical conduction and contraction by biphasic pacing comprising an original anodic pulse followed by a cathodic pulse. This technique increases the conduction velocity of almost over 100% of the effective heartbeat over conventional pacing stimulators. However, this technique does not allow all patients with cardiac conduction disorders to recover sinus rhythm.

It would be truly useful to provide an alternative method of stimulating the myocardium and inhibiting the conduction of certain spurious electrical pulses in the heart, as an alternative or enhancement to conventional pacing and drug therapy, and/or to use this alternative in conjunction with conventional pacing and safe drug therapy, to provide another approach to overcoming the heart conduction problem.

Disclosure of Invention

Embodiments of the present invention include designing implantable cardiac treatment/stimulation devices for suppressing certain pseudo-electrical impulses, preferably without pacing. The technique applied in the implant device comprises a cooling element for cooling the heart tissue. Alternatively, the cooling treatment may be used in conjunction with biphasic stimulation of the heart tissue.

It is therefore an object of the present invention to inhibit the conduction of certain spurious electrical impulses caused by reentry circuits in cardiac tissue.

It is a further object of the present invention to inhibit the conduction of certain spurious electrical impulses in the heart caused by reentry circuits by cooling the heart tissue.

It is a further object of the present invention to selectively apply a cooling temperature to a region of cardiac tissue to inhibit the conduction of certain spurious electrical pulses in the cardiac tissue caused by reentry circuits.

It is another object of the invention to apply cooling over a larger area of cardiac tissue to inhibit the conduction of certain spurious electrical impulses in the cardiac tissue caused by reentry circuits.

It is yet another object of the present invention to affect the reentry circuit in a more effective manner than conventional cardiac pacing.

It is yet another object of the present invention to suppress certain spurious electrical pulses in a larger region of the heart, not just a smaller area of the pacing site.

It is a further object of the present invention to provide an implantable stimulation device for automatically cooling cardiac tissue affected by a reentry circuit.

It is yet another object of the present invention to provide a mobile device that can perform cooling of cardiac tissue in an operating room or trauma room.

It is yet another object of the present invention to provide an implant device that can combine cooling of cardiac tissue with stimulation of the cardiac tissue using conventional pacing.

It is yet another object of the present invention to provide an implant device that combines cooling of cardiac tissue with stimulation of the cardiac tissue using biphasic stimulation.

It is a further object of the present invention to provide an implantable cardiac stimulation device that senses the onset of fibrillation or other bradycardia arrhythmia and that can selectively apply cooling of cardiac tissue, pacing of cardiac tissue, defibrillation of cardiac tissue, or a combination thereof as a therapeutic modality.

In one object of the invention, both cooling and biphasic electrical stimulation are administered to the myocardium. The anodic component of biphasic electrical stimulation increases the contractile force of the heart, which is achieved by hyperpolarizing the tissue prior to activation, resulting in faster pulse conduction, more intracellular calcium release, and resulting in superior cardiac contraction. The cathodal stimulation component eliminates the disadvantages of anodal stimulation alone, with the result that cardiac stimulation requires a lower voltage level than anodal stimulation alone. Thereby extending the life of the pacemaker battery and reducing tissue damage.

In a second object of the invention, cooling is applied to the heart tissue while controlling the biphasic electrical stimulation to the heart's blood pool, i.e. the blood entering and surrounding the heart. This allows cardiac stimulation to be directly connected to the cardiac tissue without the need for pacing electrical leads, thereby reducing damage to the tissue. The stimulation threshold for a pool-controlled biphasic stimulation may be as wide as the range of standard stimulation directly to the myocardium. The use of biphasic electrical stimulation to the blood pool of the heart can enhance cardiac contraction without contraction of skeletal muscles, destruction of cardiac muscles or adverse effects on the blood pool.

Yet another embodiment of the present invention includes an implant device for the automated treatment of frequent recurrent atrial fibrillation or chronic atrial fibrillation. This embodiment includes a sensing system that monitors various parameters, such as the atrial PDF (probability density function) parameters that sense atrial fibrillation. By detecting the PDF of the atria, a detector for atrial fibrillation not previously considered may be provided. Upon sensing the atrial PDF and detecting the occurrence of atrial fibrillation, the implant device of the present invention begins cooling the heart tissue of the atrium. Cooling is applied across a wide area by a contact device to cover a wide area of cardiac tissue. The applied cooling temperature cools the cardiac tissue by contacting the device to the cardiac tissue, and thus inhibits the conduction of spurious signals through the tissue. This reduced temperature affects the foldback circuit in an efficient manner. Since this interference acts on large areas of tissue rather than small pacing sites, the suppression of glitches may act on a larger area than pacing sites of conventional pacing.

When the sensor detects a need for cooling application, cooling is applied to the heart tissue for a brief period of time that is programmable and adjustable. The amount of cooling applied and the overall temperature of the heart are monitored by the thermostat function of the device. Cooling may be achieved by a mechanical hydraulic system pumping cooling fluid into a sac at the atrial surface.

The heart rate is monitored and, if initially failed, the application of cooling temperature is repeated a number of times.

In the event that the present embodiment fails to lower the temperature of the cardiac tissue alone, alternative embodiments include both a cooling element in the form of a contact device and a more conventional cardiac stimulation element that applies an electrical pulse to the cardiac tissue in the form of a negative phase, an anodic pulse followed by a negative polarity pulse, or other stimulation methods known in the art.

This combination of cardiac tissue cooling combined with cardiac stimulation is also another embodiment of the invention. A processor in the implanted device detects the onset of fibrillation and first applies a cooling temperature to the heart tissue. If there is no effect on the reentry circuit of the heart, a combination of cooling and electrical stimulation and/or electrical stimulation alone may be applied. If this combined approach does not work on the reentry circuit, a more traditional pacing approach alone is used. Thus, the application of the detected and cooled temperature electrical stimulus, or a combination thereof, is provided by circuitry in the implanted device.

The above embodiments are applied without anesthesia and are potentially more effective than conventional cardioversion.

A further embodiment of the invention connects the implant device to a communication terminal, preferably wireless, so that a suitable caretaker can take care of the heart abnormality. The signal may be received by a physician for indicating the condition. The physician may remotely select control of the stimulation strategy of the implant device of the present invention.

Another embodiment of the invention relates to altering the conductivity of the heart by cooling the temperature and application of other forms of pacing (e.g., heart rate control, and defibrillation). Pacing includes, but is not limited to, bipolar, biphasic, unipolar, monophasic, overdrive, atrioventricular, and continuous pacing.

Embodiments of the invention provide methods of inhibiting spurious electrical impulse conduction in cardiac tissue, comprising: establishing a temperature that helps to inhibit conduction of electrical impulses to a target area of the heart; the temperature is lowered and maintained at an established temperature for the target area.

Another embodiment of the invention provides a method of inhibiting spurious electrical impulse conduction in cardiac tissue. The method comprises the following steps: detecting an onset of an arrhythmia, detecting a temperature of heart tissue at the onset of the arrhythmia, and lowering a current temperature of the heart tissue.

Another embodiment of the invention provides a method of inhibiting spurious electrical impulse conduction in cardiac tissue. A heat exchange operator is located at each of one or more target areas of the heart. In one embodiment of the invention, the heat exchange operator is a Peltier cooler. In another embodiment of the invention, the heat exchange manipulator is a heat sink, which is thermally coupled to the peltier cooler. A symptom associated with the arrhythmia is detected, and in response to the detection of the arrhythmia, heat is selectively removed from a target region of the heart associated with the arrhythmia by absorbing the heat into a heat-exchange operator located at the target region.

In another embodiment of the present invention, a method of suppressing arrhythmia in a patient is provided. A thermal exchange manipulator is implanted at each location in one or more target areas of the heart. Operating at least one thermal exchange operator to cool at least one target region of the heart to inhibit cardiac arrhythmia.

In another embodiment of the present invention, a method of inhibiting spurious electrical impulse conduction in cardiac tissue is provided. Detecting an episode of arrhythmia and evaluating the detected arrhythmia. The temperature of the heart tissue at the onset of the arrhythmia is also detected. One or more therapeutic measures are selected from applying a temperature reduction to the cardiac tissue and applying a pacing pulse to the cardiac tissue based on the detected arrhythmia and an estimate of the current temperature of the cardiac tissue. Applying the selected treatment.

In another embodiment the invention includes an apparatus for inhibiting false impulse conduction in cardiac tissue. The sensing element detects an episode of arrhythmia; the cooling element applies a cooling stimulus to the cardiac tissue in response to the sensing element. In another embodiment of the invention, a device is provided or spurious electrical impulse conduction in cardiac tissue is inhibited. The sensor detects a symptom associated with the arrhythmia. A heat exchange operator is located at each of one or more target areas of the heart. In another embodiment of the invention, the heat exchange operator is a peltier cooler. In another embodiment of the invention, the heat exchange operator is a heat sink that is thermally coupled to a peltier cooler implanted in the torso of the patient. The thermal exchange operators at each of the one or more target areas of the heart are adapted to respond to the sensors for dissipating heat from the target area for which the thermal exchange operator is responsible.

In another embodiment of the present invention, an apparatus for suppressing arrhythmia in a patient is provided. A thermal exchange manipulator is implanted at each location in one or more target areas of the patient's heart. In response to detection of an arrhythmia, a heat-exchanging operator at each location in one or more target regions of the heart is adapted to remove heat from the target region for which the heat-exchanging operator is responsible, whereby each location in the one or more target regions is cooled and the arrhythmia is suppressed.

Drawings

Fig. 1 illustrates a method of preventing spurious electrical impulse conduction in cardiac tissue, in accordance with an embodiment of the present invention.

Fig. 2 illustrates a method for suppressing spurious electrical impulse conduction in cardiac tissue by applying a temperature reduction to the cardiac tissue, in accordance with an embodiment of the present invention.

Fig. 3 illustrates a method for suppressing spurious electrical pulse conduction in cardiac tissue by applying a temperature decrease and at least one pacing pulse to the cardiac tissue, in accordance with an embodiment of the present invention.

Fig. 4 illustrates a method of suppressing arrhythmia by selectively applying a temperature reduction to a target region of the heart and a pacing pulse to cardiac tissue, in accordance with an embodiment of the present invention.

Fig. 5 illustrates an apparatus for inhibiting conduction of electrical impulses in cardiac tissue by applying a temperature reduction to a target region of the heart, in accordance with an embodiment of the present invention.

Detailed Description

One embodiment of the present invention includes an implantable cardiac treatment/stimulation device for inhibiting the conduction of spurious electrical signals in cardiac tissue without pacing. Techniques applied to implantable devices include cooling elements for cooling cardiac tissue. Alternatively, one or two cooling embodiments are provided in combination with single-cathode or two-phase stimulation of cardiac tissue.

One embodiment of the present invention provides a method of inhibiting the conduction of spurious electrical signal pulses in cardiac tissue. The method includes determining a temperature of conduction for inhibition of conduction of electrical impulses to a target region of a heart; and applying a temperature reduction to the target area to maintain the determined temperature. The temperature of the target area is detected. The application of the temperature reduction is stopped if the target zone has reached a determined temperature. If the target area does not reach the determined temperature, the application of the temperature reduction to the target area continues.

The temperature reduction of the heart tissue may be obtained by different means, including, by way of non-limiting example: applying a cooling fluid to the heart tissue, electrically cooling the heart tissue, and mechanically cooling the heart tissue.

Another embodiment of the present invention provides a method of inhibiting the conduction of spurious electrical impulses in cardiac tissue. The method includes detecting an onset of arrhythmia, determining a temperature of heart tissue at the onset of the arrhythmia, and applying a temperature reduction to the heart tissue. In another method, the function of cardiac tissue is detected. If the heart tissue returns to sinus rhythm, the application of the temperature decrease is stopped. If the heart tissue does not return to sinus rhythm, the temperature reduction applied to the heart tissue continues.

The temperature reduction of the heart tissue may be obtained by different means, including, by way of non-limiting example: applying a cooling fluid to the heart tissue, electrically cooling the heart tissue, mechanically cooling the heart tissue, and cooling the heart tissue by an endothermic chemical reaction. Examples of cooling devices suitable for implementing the invention are: evaporative coolers, radiant coolers, chillers, thermal holdover devices (e.g., thermal storage units, with or without phase change phenomena), and gas expansion coolers. Cooling may be achieved by heat exchange structures or by direct contact.

In another embodiment of the invention, detecting the onset of the arrhythmia includes detecting a symptom indicative of the arrhythmia. Detecting different symptoms indicative of cardiac arrhythmia, including by way of non-limiting example: electrical changes within the heart, and changes in cardiac function during measurement.

In another embodiment of the present invention, the method for inhibiting the conduction of spurious electrical pulses in cardiac tissue further comprises applying pacing pulses to the cardiac tissue. Pacing may be achieved by one or more electrodes that contact cardiac tissue, or electrodes placed within the blood pool of one or more heart chambers. In either method, pacing pulses are applied to one or more electrodes. The pacing pulse may be a cathodic electrical waveform or a biphasic electrical waveform comprising cathodic and anodic components.

Another embodiment of the present invention provides a method for inhibiting the conduction of spurious electrical impulses in cardiac tissue. One or more regions of the heart affected by one or more reentry circuits are targeted. In one embodiment of the invention, each of the one or more target regions is selected from one of a right anterior-lateral (lateral) atrial surface, a left anterior-lateral atrial surface, a right posterior-lateral atrial surface, and a left posterior-lateral atrial surface. A thermal exchange operator is located in each of one or more target areas of the heart. In one embodiment of the invention, the heat exchange operator is a peltier cooler. The peltier cooler may be electrically connected to a power source implanted in the patient's torso. In another embodiment of the invention, the heat exchange operator is a heat sink thermally coupled to a peltier cooler implanted in the torso of the patient. Alternatively, the heat sink is a thermocouple employing mechanical contact or a heat transfer liquid.

A symptom associated with the arrhythmia is detected, and in response to the detection of the symptom, heat is selectively transferred from a target region of the heart associated with the arrhythmia by a heat exchange operator that absorbs the heat into the target region.

Symptoms can be detected in the heart. The hot-swap operator is activated in response to detection of an arrhythmia. Different symptoms may be detected, including by way of non-limiting example: electrical changes within the heart and changes in the heart function in the measurement.

Another method includes detecting a function of the heart and ceasing heat removal from the at least one target area when a symptom associated with the arrhythmia is not detected.

In another embodiment of the present invention, the method for inhibiting the conduction of a spurious electrical pulse in cardiac tissue further comprises applying a pacing pulse to the cardiac tissue. Pacing may be achieved by one or more electrodes that contact cardiac tissue, or electrodes placed within the blood pool of one or more heart chambers. In either method, pacing pulses are applied to one or more electrodes. The pacing pulse may be a cathodic electrical waveform or a biphasic electrical waveform comprising cathodic and anodic components.

In another embodiment of the present invention, a method for inhibiting the conduction of a spurious electrical pulse in cardiac tissue includes applying a pacing pulse to the cardiac tissue. Pacing may be achieved by one or more electrodes that contact cardiac tissue, or electrodes placed within the blood pool of one or more heart chambers. In either method, pacing pulses are applied to one or more electrodes. The pacing pulse may be a cathodic electrical waveform or a biphasic electrical waveform comprising cathodic and anodic components.

In another exemplary embodiment of the present invention, a method of suppressing an arrhythmia in a patient is provided. The thermal exchange manipulator is implanted in each of one or more target areas of a heart of a patient. The at least one thermal exchange operator is used to cool at least one target area of the heart, thereby suppressing arrhythmia. In one embodiment of the invention, the heat exchange manipulator is a peltier cooler implanted in one or more target zones, each of the target zones being selected from one of a right anterior-lateral atrial surface, a left anterior-lateral atrial surface, a right posterior-lateral atrial surface, and a left posterior-lateral atrial surface. The peltier cooler may be electrically connected to a power source implanted in the patient's torso. In another embodiment of the invention, the thermal conversion manipulator is a heat sink implanted in one or more target areas, each of the target areas selected from one of a right anterior-lateral atrial surface, a left anterior-lateral atrial surface, a right posterior-lateral atrial surface, and a left posterior-lateral atrial surface, the heat sink thermally coupled to a peltier cooler implanted in the patient's torso. Alternatively, the heat sink is a thermocouple employing mechanical contact or a heat transfer liquid.

Another method of suppressing arrhythmia in a patient includes implanting at least one sensing-contact (sensing-contact) in the patient's heart for sensing a condition, and connecting the sensing-contact (sensing-contact) to a power source that provides power for operation of a thermal-exchange operator when the condition is sensed. Different symptoms may be detected, including by way of non-limiting example: electrical changes within the heart, and changes in cardiac function during measurement.

In another embodiment of the present invention, a method of suppressing arrhythmia in a patient further comprises applying pacing pulses to cardiac tissue. Pacing may be achieved by one or more electrodes that contact cardiac tissue, or electrodes placed within the blood pool of one or more heart chambers. In either method, pacing pulses are applied to one or more electrodes. The pacing pulse may be a cathodic electrical waveform or a biphasic electrical waveform comprising cathodic and anodic components.

In yet another embodiment of the present invention, a method of inhibiting the conduction of spurious electrical impulses in cardiac tissue is provided. Detecting an onset of an arrhythmia and evaluating the detected arrhythmia. The temperature of the heart tissue at the onset of the arrhythmia is also determined. Based on the evaluation of the detected arrhythmia and the temperature of the cardiac tissue, one or more therapeutic measures are selected from applying a temperature reduction to the cardiac tissue and applying a pacing pulse to the cardiac tissue. The selected treatment is applied. Alternatively, cardiac tissue function is detected and the application of therapeutic measures is stopped if the heart returns to sinus rhythm. Similarly, if the heart tissue does not return to sinus rhythm, the application of therapeutic measures continues.

In other embodiments of the present invention, an apparatus for inhibiting the conduction of spurious electrical pulses in cardiac tissue is provided. The apparatus includes a detection device for detecting an onset of arrhythmia and a cooling device responsive to the detection device to apply a cooling stimulus to the cardiac tissue. The apparatus further includes logic for detecting when a sinus rhythm in the heart tissue is reestablished and discontinuing the cooling stimulus when the sinus rhythm is reestablished. Additional devices are provided for continuing the cooling stimulation when the sinus rhythm is not reestablished.

The cooling device includes non-limiting examples: an apparatus for applying a cooling liquid to cardiac tissue, an electrical cooling device, and a mechanical cooling device. In addition, the detection device may be adapted to detect symptoms associated with the arrhythmia. By way of non-limiting example, the condition may be an electrical change in the heart, and a measure of cardiac function.

Another device of the present invention further includes a cardiac stimulation generator and one or more electrodes in contact with the cardiac tissue. The electrodes are connected to a cardiac stimulation generator adapted to apply pacing pulses of a cathodal electrical waveform or biphasic waveform to cardiac tissue. In an alternative embodiment of the invention, the electrodes are in contact with the heart blood pool. Alternatively, the cardiac stimulus generator is responsive to the detection device.

Another apparatus of the invention for inhibiting the conduction of spurious electrical pulses in cardiac tissue includes a sensor that detects a symptom associated with an arrhythmia. By way of non-limiting example, the condition may be an electrical change in the heart, a measure of cardiac function, and a change indicative of an arrhythmia. A thermal exchange operator is located in each of one or more target areas of the heart. In one embodiment of the invention, the heat exchange operator is a peltier cooler. The peltier cooler may be electrically connected to a power source implanted in the patient's torso. In another embodiment of the invention, the thermal conversion operator is a heat sink thermally coupled to a peltier cooler implanted in the torso of the patient. Alternatively, the heat sink is a thermocouple employing mechanical contact or a heat transfer liquid.

A thermal exchange operator located at each of the one or more target zones is adapted to remove heat from the target zone for which the thermal exchange operator is responsible in response to the sensor. The sensor is placed above the heat exchange operator.

An apparatus further includes a logic device to detect when a sinus rhythm is reestablished in the heart tissue and to suspend the cooling stimulus when the sinus rhythm is reestablished. Additional devices are provided for continuing the cooling stimulation when the sinus rhythm is not reestablished.

In another embodiment of the invention, the device further comprises a power source adapted to power the sensor and activate the heat exchange operator upon detection of the symptom. Alternatively, the power source stores sufficient energy to suppress the patient's arrhythmia for an extended period of time. In addition, the power supply automatically ceases to provide power to the heat exchange operator when one or more target zones have sufficiently cooled. In one embodiment of the invention, one or more target zones are sufficiently cooled when a symptomatic decay (decay) is detected by the sensing contact. Alternatively, one or more target zones are sufficiently cooled when each target zone reaches a predetermined temperature as measured by a thermocouple. In another alternative embodiment, one or more target areas are sufficiently cooled when the one or more target areas are cooled for a set period of time.

In one embodiment of the invention, each of the one or more target regions is selected from one of a right anterior-lateral atrial surface, a left anterior-lateral atrial surface, a right posterior-lateral atrial surface, and a left posterior-lateral atrial surface.

In another embodiment of the invention, the device further comprises a cardiac stimulation generator and one or more electrodes in contact with the cardiac tissue. The electrodes are connected to a cardiac stimulation generator adapted to apply pacing pulses of a cathodal electrical waveform or biphasic waveform to cardiac tissue. In an alternative embodiment of the invention, the electrodes are in contact with the heart blood pool. Alternatively, the cardiac stimulus generator is responsive to the detection device.

Another device of the invention is for suppressing arrhythmia in a patient. The device includes a sensor that detects a symptom associated with the arrhythmia. By way of non-limiting example, the condition may be an electrical change in the heart, a measure of cardiac function, and a change indicative of an arrhythmia. A thermal exchange operator is located at each of one or more target areas of the heart, and in response to detection of the arrhythmia, the thermal exchange operator located at each of the one or more target areas is adapted to transfer heat away from the target area for which the thermal exchange operator is responsible. As a result, each of the one or more target zones is partially cooled to suppress the arrhythmia.

In one embodiment of the invention, the thermal conversion operator is a peltier cooler. The peltier cooler may be electrically connected to a power source implanted in the patient's torso. The power source is adapted to provide power to the sensor and activate the heat-exchange operator upon detection of the symptom. In another embodiment of the invention, the heat exchange operator is a heat sink thermally coupled to a peltier cooler implanted in the torso of the patient. Alternatively, the heat sink is a thermocouple employing mechanical contact or a heat transfer liquid.

In another embodiment of the present invention, each of the one or more target regions is selected from one of a right anterior-lateral atrial surface, a left anterior-lateral atrial surface, a right posterior-lateral atrial surface, and a left posterior-lateral atrial surface.

In another embodiment of the invention, the device further comprises a power source adapted to power the sensor and activate the heat-exchange operator upon detection of the symptom.

In another embodiment of the invention, the device further comprises a cardiac stimulation generator and one or more electrodes in contact with the cardiac tissue. The electrodes are connected to a cardiac stimulation generator adapted to apply pacing pulses of a cathodal electrical waveform or biphasic waveform to cardiac tissue. In an alternative embodiment of the invention, the electrodes are in contact with the heart blood pool. Alternatively, the cardiac stimulus generator is responsive to the detection device.

Fig. 1 illustrates a method of preventing spurious electrical impulse conduction in cardiac tissue, in accordance with an embodiment of the present invention. Referring to fig. 1, a temperature 100 that helps to inhibit conduction of electrical impulses is determined for a target area of the heart. A temperature reduction is applied to the target area to maintain the determined temperature 110. The temperature of the target area is sensed 115 and a determination is made as to whether the target area has reached a determined temperature 120. If the target zone has reached the determined temperature, the application of the temperature decrease is stopped 125. If the target area has not reached the determined temperature, the temperature reduction applied to the target area continues 130. Although fig. 1 illustrates a single target area, the invention is not so limited. One or more target zones are the same and associated with the determined temperature 120 without departing from the scope of the present invention.

The temperature reduction of the heart tissue may be obtained by different means, including, by way of non-limiting example: applying a cooling fluid to the heart tissue, electrically cooling the heart tissue, and mechanically cooling the heart tissue.

Fig. 2 illustrates a method of inhibiting spurious electrical impulse conduction in cardiac tissue by applying a temperature reduction to the cardiac tissue, in accordance with an embodiment of the present invention. Referring to fig. 2, an episode of arrhythmia 200 and a temperature reduction applied to cardiac tissue 210 are detected. Detecting the function of the heart tissue 215 and determining whether the heart tissue has returned to sinus rhythm 220. If the heart tissue returns to sinus rhythm, the temperature decrease applied to the heart tissue ceases 225. If the heart tissue has not returned to sinus rhythm, the temperature decrease applied to the heart tissue continues 230.

Fig. 3 illustrates a method of suppressing spurious electrical pulse conduction in cardiac tissue by applying a decrease in temperature and at least one pacing pulse to the cardiac tissue, in accordance with an embodiment of the present invention. Referring to fig. 3, an episode of arrhythmia 300 is detected. At least one pacing pulse and temperature reduction is applied to cardiac tissue 310. Detecting the heart tissue 315 and determining whether the heart tissue has returned to sinus rhythm 320. If the heart tissue returns to sinus rhythm, the application of the at least one pacing pulse and the temperature decrease to the heart tissue is stopped 325. If the heart tissue has not returned to sinus rhythm, the at least one pacing pulse and the temperature decrease applied to the heart tissue continues 330. As described above, the pacing pulse may be cathodic or biphasic and may be applied to the cardiac tissue by contacting the electrodes with the blood pool of the heart or contacting the cardiac tissue.

Fig. 4 illustrates a method of suppressing arrhythmia by selectively applying a temperature reduction to a target region of the heart and pacing pulses to cardiac tissue in accordance with embodiments of the present invention. Referring to fig. 4, an episode of arrhythmia 400 is detected. The arrhythmia is evaluated and the temperature of the heart tissue is determined 405. Based on the evaluation of the detected arrhythmia and the temperature of the cardiac tissue, one or more therapeutic measures 410 are selected from applying a temperature reduction to the cardiac tissue and applying a pacing pulse to the cardiac tissue. The selected treatment is applied to cardiac tissue 415. The selective application of cardiac cooling and pacing pulses is determined by logic circuitry incorporated in a computer processor. In one embodiment of the invention, the processor is located in the device that provides the pacing pulses. Alternatively, the processor is located in the device that provides the cooling function. In another embodiment of the invention, the processor is a stand-alone device. Detecting the function of the heart tissue 420 and determining whether the heart tissue has returned to a sinus rhythm 425. If the heart tissue returns to sinus rhythm, application of the selected treatment is stopped 430. If the heart tissue has not returned to sinus rhythm, application of the selected treatment continues 435. In an alternative embodiment, the temperature and arrhythmia of the heart tissue are re-evaluated and one or more of the therapeutic measures are re-selected.

As described above, the pacing pulse may be cathodic or biphasic and may be applied to the cardiac tissue by contacting the electrodes with the blood pool of the heart or contacting the cardiac tissue.

Fig. 5 illustrates an apparatus for inhibiting conduction of electrical impulses in cardiac tissue by applying a temperature decrease to a target region of the heart, in accordance with embodiments of the present invention. Referring to fig. 5, a heart detection device 510 and a heart cooling device 515 are applied to a heart 505 of a patient 500. In one embodiment of the invention. The cardiac detection device 510 detects the onset of an arrhythmia. In response to the heart detecting means 510, the heart is cooled by heart cooling means 515. Logic 520 detects when the sinus rhythm is reestablished in the heart tissue. If the sinus rhythm is reestablished in the heart tissue, the logic 520 suspends the cooling activation of the cooling device 515. If the sinus rhythm is not reestablished in the heart tissue, the logic 520 continues the cooling activation of the cooling device 515.

In one embodiment of the present invention, cardiac cooling device 515 comprises a Peltier cooler. Such heat exchange operators pass electric current through the junctions between dissimilar metals. Atoms of different metals have different energy levels, resulting in a step difference between the energy levels at each metal junction. When a current passes through the metal, metal electrons having a low energy level flow to the metal having a higher energy level through the first order difference. In order to pass this step and continue the circuit, the electrons must absorb thermal energy, resulting in cooling of the metal at the first connection. At the opposite junction, the electrons migrate from a high level to a low level, releasing energy resulting in an increase in temperature at the junction.

As will be appreciated by those skilled in the art, other cooling devices may be used to accomplish this function of the invention without departing from the scope of the invention. By way of non-limiting illustration, the heart cooling device 515 may be another device or system that absorbs heat from a particular region and effects heat transfer by convection or conduction through a liquid. Alternatively, cooling may be achieved by a mechanical hydraulic system that pumps coolant into a sac on the atrial surface. The application of the amount of cooling and the overall temperature of the heart can be monitored by the "thermostat" function of the device.

In another embodiment of the invention, the heart cooling device further comprises a heat sink thermally coupled to the heat exchanging manipulator, such as a peltier cooler. The hot swap operator is electrically connected to a power source that provides an electrical current that flows through the hot swap operator to affect heat transfer. The power supply operates effectively by turning off the power to the hot swap operator when heat transfer is not required. When heat transfer is desired, the power supply can be activated to provide a direct current to the heat-exchange operator, which in turn initiates heat transfer from the target area through a cold connection in thermal contact with the heat-exchange operator.

In another embodiment of the invention, the thermal exchange operator is responsive to a cardiac detection device 510 that detects symptoms of cardiac arrhythmia. The symptom detected by the cardiac detection device may be an electrical or physiological measurement indicative of an arrhythmia.

In yet another embodiment of the present invention, the logic 520 determines when the heart is sufficiently cooled. The time required to sufficiently cool the heart may be programmed into logic 520 or calculated by logic 520 based on information obtained from heart detection device 510.

Referring again to fig. 5, in another embodiment of the present invention, cardiac stimulation generator 530 applies pacing pulses to the cardiac tissue via electrodes 525. Although fig. 5 shows a single electrode, the present invention is not limited thereto. As will be appreciated by those skilled in the art, multiple electrodes may also be used without departing from the scope of the invention. Additionally, the electrodes 525 may be placed in contact with cardiac tissue or within the blood pool of the heart. The cardiac stimulus generator 530 is responsive to the cardiac sensing device 510. The pacing pulses generated by cardiac stimulation generator 530 may be a cathodic electrical waveform or a biphasic electrical waveform including a cathodic and an anodic component.

Although embodiments of the present invention are directed to cooling cardiac tissue to inhibit the conduction of spurious electrical impulses, the present invention is not so limited. The influence of spurious signals on other parts of the human body (e.g. brain, skeletal muscles, pain receptors) can be suppressed by cooling. It will be apparent to those skilled in the art that embodiments of the present invention may be used to suppress spurious signals in other parts of the human body without departing from the invention

The scope of the invention.

Systems and methods for inhibiting the conduction of spurious electrical impulses within cardiac tissue have been described. It will be understood by those skilled in the art to which the invention pertains that other specific forms of the invention may be practiced without departing from the scope of the invention disclosed, the examples and embodiments of which are intended to be non-limiting examples. Those skilled in the art to which the invention relates will appreciate that other embodiments are possible which employ the concepts described herein.

Claims (46)

1. A device for inhibiting spurious electrical impulse conduction in cardiac tissue, comprising:

a sensor to detect a symptom associated with the arrhythmia; and

a thermal exchange manipulator located at each of one or more target areas of the heart;

wherein the thermal exchange operator is adapted to respond to the sensor at each of the one or more target zones for transferring heat away from the target zone for which the thermal exchange operator is responsible.

2. The apparatus of claim 1, further comprising:

logic to detect when a sinus rhythm is reestablished in the heart tissue; and

means to suspend the cooling stimulus when the sinus rhythm has been reestablished.

3. The apparatus of claim 2, wherein the logic element further comprises logic to continue to apply the cooling stimulus when the heart tissue does not restore sinus rhythm.

4. The apparatus of claim 1, wherein the symptom is an electrical change in the heart.

5. The apparatus of claim 1, wherein the symptom is a change in cardiac function in the measurement.

6. The apparatus of claim 1, wherein the symptom is a change indicative of an arrhythmia.

7. The apparatus of claim 1, wherein the sensor is located on the heat exchange operator.

8. The device of claim 1, wherein the device further comprises a power source, wherein the power source is adapted to power the sensor and activate the heat-exchange operator upon detection of the symptom.

9. The apparatus of claim 8, wherein the power source stores sufficient energy to suppress the patient's arrhythmia for an extended period of time.

10. The apparatus of claim 8, wherein the power supply automatically ceases to provide power to the thermal exchange operator after the one or more target zones have cooled sufficiently.

11. The apparatus of claim 10, wherein the one or more target areas are sufficiently cooled when the symptoms are reduced, the reduction being detected by the sensor.

12. The apparatus of claim 10, wherein the one or more target zones are sufficiently cooled when each of the one or more target zones reaches a predetermined temperature.

13. The apparatus of claim 12, wherein the temperature of the target zone is measured with a thermocouple.

14. The apparatus of claim 10, wherein the one or more target areas are sufficiently cooled when the one or more target areas are cooled for a set time.

15. The apparatus of claim 1, wherein the heat exchange operator is a peltier cooler.

16. The apparatus of claim 15, wherein the peltier cooler is electrically connected to a power source implanted in the patient's torso.

17. The apparatus of claim 1, wherein the heat exchange operator comprises a heat sink thermally coupled to a peltier cooler mounted within a housing implanted in the torso of the patient.

18. The apparatus of claim 17, wherein the heat sink is coupled to the peltier cooler by mechanical contact.

19. The apparatus of claim 17, wherein the heat sink is coupled to the peltier cooler by a thermally conductive liquid.

20. The apparatus of claim 17, wherein the peltier cooler is electrically connected to a power source located within the housing.

21. The device of claim 1, wherein each of the one or more target regions is selected from one of a right anterior atrial surface, a left anterior atrial surface, a right posterior atrial surface, and a left posterior atrial surface.

22. The apparatus of claim 1, further comprising:

a cardiac stimulus generator;

one or more electrodes in contact with cardiac tissue, wherein the electrodes are connected to the cardiac stimulation generator; and

wherein the cardiac stimulation generator is adapted to apply pacing pulses to cardiac tissue.

23. The apparatus of claim 22, wherein the cardiac stimulus generator is responsive to a sensing element.

24. The device of claim 23, wherein the pacing pulse is a cathodic electrical waveform.

25. The apparatus of claim 23, wherein the pacing pulse is a biphasic electrical waveform.

26. The apparatus of claim 1, further comprising:

a cardiac stimulus generator;

one or more electrodes in contact with a cardiac blood pool, wherein the electrodes are connected to the cardiac stimulation generator; and

wherein the cardiac stimulation generator is adapted to apply pacing pulses to a cardiac blood pool.

27. The device of claim 26, wherein the pacing pulse is a cathodic electrical waveform.

28. The apparatus of claim 27, wherein the pacing pulse is a biphasic electrical waveform.

29. An apparatus for suppressing arrhythmia in a patient, comprising:

a sensor to detect a symptom associated with the arrhythmia; and

a thermal exchange manipulator located at each of one or more target areas of the heart;

wherein, in response to detection of an arrhythmia, the thermal exchange operator at each location in the one or more target regions of the heart is adapted to remove heat from the target region for which the thermal exchange operator is responsible, whereby each location in the one or more target regions is cooled and the arrhythmia is suppressed.

30. The apparatus of claim 29, wherein the heat exchange operator is a peltier cooler.

31. The apparatus of claim 30, wherein the peltier cooler is electrically connected to a power source implanted in the patient's torso, and wherein the power source is adapted to power the sensor and activate the heat exchange operator upon detection of the symptom.

32. The apparatus of claim 29, further wherein the heat exchange operator comprises a heat sink thermally coupled to a peltier cooler mounted within a housing implanted in the torso of the patient.

33. The apparatus of claim 32, wherein the peltier cooler is electrically connected to a power source located within the housing.

34. The apparatus of claim 32, wherein the heat sink is coupled to the peltier cooler by mechanical contact.

35. The apparatus of claim 32, wherein the heat sink is coupled to the peltier cooler by a thermally conductive liquid.

36. The apparatus of claim 29, wherein the one or more target regions are each selected from one of a right anterior atrial surface, a left anterior atrial surface, a right posterior atrial surface, and a left posterior atrial surface.

37. The apparatus of claim 29, wherein the symptom is an electrical change in the heart.

38. The apparatus of claim 29, wherein the symptom is a change in cardiac function in the measurement.

39. The apparatus of claim 29, wherein the symptom is an alteration indicative of an arrhythmia.

40. The apparatus of claim 29, further comprising:

a cardiac stimulus generator;

one or more electrodes in contact with cardiac tissue, wherein the electrodes are connected to the cardiac stimulation generator; and

wherein the cardiac stimulation generator is adapted to apply pacing pulses to cardiac tissue.

41. The apparatus of claim 40, wherein the cardiac stimulus generator is responsive to the sensor.

42. The device of claim 41, wherein the pacing pulse is a cathodic electrical waveform.

43. The apparatus of claim 41, wherein the pacing pulse is a biphasic electrical waveform.

44. The apparatus of claim 29, further comprising:

a cardiac stimulus generator;

one or more electrodes in contact with a cardiac blood pool, wherein the electrodes are connected to the cardiac stimulation generator; and

wherein the cardiac stimulation generator is adapted to apply pacing pulses to a cardiac blood pool.

45. The device of claim 44, wherein the pacing pulse is a cathodic electrical waveform.

46. The apparatus of claim 45, wherein the pacing pulse is a biphasic electrical waveform.