KR20070062455A - A system and method for managing detrimental cardiac remodeling - Google Patents

Abstract

A system and method for managing and inhibiting cardiac remodeling in MI patients. Bi-ventricular stimulation is constantly provided with and without sensing to encourage normal pumping of the heart on a consistent basis. Pulses are administered using an anodal pulse followed by a cathodal pulse to stimulate cardiac muscle contraction. Stem cells are administered to MI areas to encourage regeneration of cardiac tissue in the damaged area. Stimulation may be provide to both healthy and compromised cardiac tissue.

Description

A SYSTEM AND METHOD FOR MANAGING DETRIMENTAL CARDIAC REMODELING

This application claims priority by 35 U.S.C. # 119 (e), based on provisional application No. 60 / 575,121, filed May 28, 2004.

Provisional Application No. 60 / 575,121 is incorporated by reference in its entirety for all purposes of the present application.

This application is a CIP application of US Application No. 10 / 053,750, filed Jan. 21, 2002, and is still pending.

Again, the latter is a continuation of US application Ser. No. 09 / 60,947, filed Oct. 18, 2000, and now US Pat. No. 6,341,235.

This is again a CIP application of 09 / 008,636 filed January 16, 1998, which is registered in US Patent 6 / 136,019.

This is again a CIP application of 08 / 699,552 filed on August 19, 1996 and registered in US Pat. No. 5,871,506.

Patent applications 10 / 053,750, 09 / 690,947, 09 / 008,636, 08 / 699,552 are incorporated by reference in their entirety for all purposes of the present application.

The present application relates generally to cardiac treatment, and more particularly to preventing and managing structural changes in the harmful heart following myocardial infarction.

Changes in the structure of the heart are organic changes in the heart that cause heart disease such as heart failure and heart attack.

Structural changes in the heart are characterized by enlargement of the heart and thinning of the heart wall.

For example, after a heart attack, normal heart muscle responds normally to excited pulses, but tissues damaged by a heart attack do not respond to excited pulses or respond more slowly than normal rates.

However, healthy tissue that tries to maintain its normal function provides greater stimulation to damaged and weakened tissues, causing them to stretch.

This elasticity increases the blood flow of the heart and in the short term increases the blood production in the heart through the so-called Frank-Sterling mechanism.

Thus, the more the heart muscle stretches like a rubber band, the more vital the heart becomes.

However, if the heart muscle is excessively stretched or repeatedly stretched over a long period of time, the heart gradually loses its vitality, slack and relaxes (a form of structural change).

The structural change proceeds in stages.

Following a heart attack, or as a result of heart disease, the heart becomes rounded and widened.

Cells in the heart muscle die and the heart pumps weaker. If a structural change is underway, the main atrium of the discharge, the left ventricle, expands and changes its shape.

The heart also undergoes changes at the cellular level. The heart is divided into right and left, and the right heart, which consists of the right atrium and the right ventricle, collects deoxygenated blood and discharges it into the lungs so that it can be combined with oxygen. Discharge.

Oxygen deprived blood from the body enters the right atrium through the vena cava.

The right atrium contracts and discharges blood to the right ventricle through the three thousand plates.

The right ventricle contracts and discharges blood through the pulmonary artery into the pulmonary artery connected to the lungs.

Blood is oxidized in the lungs and then returned to the heart through the pulmonary veins.

The pulmonary vein leads to the left atrium, which contracts and pushes oxidized blood into the left ventricle.

The left ventricle contracts and pushes blood through the aortic valve into the aorta, which is connected to the body's presence or absence.

The coronary artery extending from the aorta supplies blood to the heart.

The heart's unique pacemaker is located in the atrium and is responsible for causing the heartbeat.

The heartbeat begins with atrial tissue activation of the cardiac pacemaker region (ie SA node).

When atrial tissue is activated, excitability spreads to cells throughout the atrium.

The only link in the excitatory tissue that connects the atria and the ventricles is the AV node located at the boundary between the atria and the ventricles.

Propagation occurs at a slower rate, but at the end of the ventricles there is a bundle of tubules (i.e. electrical conduction passages located in the ventricular septum) and a bundle of branch lines at a relatively high rate of 1 to 2 m / s. Carries the state of excitement to various places.

Slow conduction at the AV junction results in a delay of about 0.1 seconds of atrial ventricular excitation.

This parallax facilitates terminal filling of the ventricles from contraction of the atria prior to ventricular contraction.

After the delay of the atrioventricular node, the tube is split into two left and right branch lines that run along each side of the septum.

The bundles are divided into Purkinjo fibers and branch inwardly to the ventricular wall.

This allows the conduction of the excitation pulse to proceed at a relatively faster rate than conducting through the atrium (AV) in the ventricular conduction system.

Symptoms of heart failure are a common form of various forms of heart disease.

Heart failure is thought to be a condition in which abnormal cardiac function causes blood to be discharged at a rate well suited to the needs of the metabolic tissue of the heart or to produce blood at abnormally high pressures.

In general, elevated pressure results in enlargement of the left ventricle.

The etiology leading to this paralysis form (dysplasia) is patient specific cardiomyopathy, including viral cardiomyopathy and ischemic cardiomyopathy.

Heart failure is a chronic disease that affects more than 5 million Americans and is the number one reason why older people are hospitalized.

Contrary to nomenclature, heart failure is not a heart attack, nor does the heartbeat stop suddenly.

Heart failure is the failure of the heart to release enough blood to meet the body's needs.

Heart failure often occurs when the heart is damaged or weakened due to a heart attack or other cause.

If heart failure persists, patients may have difficulty breathing, weak limbs, or severe fatigue.

Delayed response to the excited pulse diaphragm causes non-simultaneous contractions and thus deflects the pattern of ventricular contractions.

This causes the heart to beat inefficiently.

When the heart is working properly, the lower two chambers (ventricle) simultaneously drain blood, and the upper two chambers (atrium) simultaneously drain blood.

However, up to 40% of patients with heart failure have difficulty in shocking the ventricles (ie blockage of the coronary branch: bundle branch blocks or conduction delays in the ventricles).

As a result, the left and right ventricles act at different times.

If this happens, the wall of the left ventricle (eg the room responsible for blood draining throughout the body) does not contract at the same time and reduces cardiac efficiency as pumping.

The heart usually responds by pulsing or expanding quickly.

As a result, it causes a vicious cycle that causes further dilation, narrowing of blood vessels in the body, high salinity, or worsening of heart failure.

This delay in conduction does not respond to antiarrhythmic drugs or other drugs.

Heart failure patients are candidates for heart rate control.

Two ventricular heart rate control devices are implantable heart rate control devices designed to treat heart failure.

The two ventricular pacemakers send electrical signals to the left and right ventricles simultaneously, helping the lower ventricles to work simultaneously.

By stimulating the two ventricles (2 ventricular pacing), the pacemaker causes the walls of the left and right ventricles to drain blood together again.

In this way, the heart makes blood discharge more effective at the same time without fatigue of the heart muscle.

This is why two ventricular pacing is also referred to as cardiac resynchronization therapy (CRT).

For patients suffering from heart failure, the heart can be restructured.

Restructuring for heart failure may be characterized by left ventricular dilatation of the heart.

In addition, the left ventricular wall becomes thinner.

Increased use of oxygen, increased backflow of monk plates, and reduced emissions occur at this time.

Restructuring has a "domino effect" that counteracts continued damage to heart tissue and the development of more severe heart disease.

The 2 ventricular heart rate control device of the present invention can reverse the process.

Because of this effect, it is called "opposite structural change".

A typical 2-ventricular pacemaker uses a 2.5 volt bipolar pulse in the atrium and a 5 volt bipolar pulse in the ventricles.

heart attack

Heart attack is an event that results in permanent heart damage or functional disruption (death).

It is also known as myocardial infarction because part of the heart muscle (myocardium) is completely inactive (infarct).

Heart attack occurs when one of the coronary arteries is severely or wholly blocked by a thrombus.

The heart muscle begins to die when it does not receive the necessary blood filled with oxygen.

The severity of a heart attack depends on how much the heart muscle is damaged or dead during the heart attack.

Heart attacks are most common in chronic heart disease (eg, coronary artery disease), but the triggers for heart failure are often blood clots that block blood flow through the coronary arteries.

If the arterial vessels are already narrowed by atherosclerotic plaques (a disease called atherosclerosis), the blood clots are large enough to completely or severely block blood flow.

Patients may experience an example, such as myocardial ischemia in which the heart does not receive enough oxygen-filled blood.

Even asymptomatic ischemia, which does not show any signs, often involves angina (in the form of chest discomfort, pressure, pain).

Severe or prolonged cardiac ischemia leads to a heart attack.

Depending on the severity of the seizure and subsequent wounds, a heart attack results in the following symptoms:

＊ Heart failure. Chronic situation where at least one heart chamber fails to drain blood to meet the needs of the body.

＊ Electrical instability of the heart. Causes of potentially dangerous abnormal heart rhythm (arrhythmia).

＊ Cardiac arrest. Cardiac arrest, sudden cardiac death if no action is taken immediately.

＊ cardiac shock. Injured myocardium is impaired normally and enters a shock state, often fatal.

* Dead.

After a heart attack, whether the heart muscle continues to function depends on how much the heart muscle is damaged or how much cardiac death occurs before the patient receives medical treatment.

The location of harm in the heart muscle is also important.

Because different coronary arteries supply different parts of the heart, and the depth of injury depends on the degree of blockage and the amount of part of the heart muscle that depends on the blocked artery. As previously described, tissues damaged by a heart attack do not respond or respond slower than normal to excitable pulses.

Healthy tissues work normally, but as a result, the stimulation increases in these marginal marginal tissues, causing the tissue to stretch.

When treating a heart attack, it is desirable to minimize the sustainability of harmful structural alterations.

So this should reduce the contractile force of healthy heart tissue, increase the contractile force of peripheral marginal cardiac tissue, or combine the two therapies.

Heart disease and arrhythmia

Diseases affecting the AV junctions interfere with normal AV conduction.

This is explained by the different degrees of blocking (blocking).

The first level of blockage is that the conduction is simply slow, and the second level of blockage is intermittent pulsation, but the third level of blockage shows no signs of the ventricles.

This last situation is represented by complete seam blockage.

In this case, the ventricles are completely isolated from the atria.

The heart rate of the atria is still determined at the AV node, while the ventricle is determined by ventricular locations outside the ventricular place.

Because under normal (standard) conditions, the ventricles are operated by the atria and the potential ventricular pacemakers have slow beats.

As a result, there is a low rate of ventricular rhythm in complete atrial blockage (blockage).

This situation does not require medical treatment, but if the heart rate is low heart rate with a condition known as Stokes-Adams Syndrome, the situation is life-threatening. Will be.

In the case of complete heart blockage and Stokes-Adams syndrome, the prognosis is that 50% die within one year.

In this case, subcutaneous injection of the pacemaker is essential.

In another situation, also known as The Sick Sinus Syndrome, an artificial pacemaker is also a treatment option.

In this situation, the atrial rhythm becomes abnormally low, resulting in bradycardia.

As such, even if the AV junction is normal, the ventricles show very low beats.

Acute myocardial infarction is prone to many arrhythmia symptoms.

The tachyarrhythmias of the supra ventricular, including sinus tachycardia, atrial fibrillation, and atrial flutter, are relatively large but usually life-threatening. Not enough to threaten.

Ventricular arrhythmias are quite common. Premature Ventricular Beats occur in over 90% of patients, Ventricular Tachycardias occur in over 40% of patients, and Ventricular Fibrillation occurs in over 5% of patients.

Ventricular fibrillation occurs most commonly in the first 24 to 48 hours after myocardial infarction and is life-threatening.

Non-persistent ventricular tachycardias have prognostic significance in the late infarction period, but it is uncertain whether treatment will change the prognosis.

In the case of abnormal conduction and bradyarrhythmias, the frequent occurrence of acute myocardial infarction also requires pulsed therapy depending on the condition.

Temporary beats are generally used first.

If symptoms persist, a permanent pacemaker is needed.

Heart rate control devices are artificial devices that help the heart beat electrically to help the heart drain blood more efficiently.

Implantable electrical designs have been developed to treat both bradycardia, an abnormally slow heart rate, and tachycardia, an excessively fast heart rate.

The heart pacemaker's job is to maintain a safe heartbeat by guiding the pumping of the room properly in response to an electrical pulse that replaces the heart's normal pulse.

Designed to fulfill this role of life extension, the device is powered by silver-sized power (including batteries), control circuits that connect to the power source of the atrium, and wires or "wires" that connect power and heart chambers. Consists of.

The lead is usually located in contact with the right atrium or the right ventricle, or both of the atrium.

The lead allows the heart pacemaker to detect and stimulate in different combinations depending on where the beat is needed.

Without symptoms of arrhythmia, anti-arrhythmic pacing is not commonly used to treat myocardial infarction patients.

Whether myocardial infarction leads to heart failure depends largely on how the remaining normal muscles move.

Ventricular hypertrophy processes (structural changes) are usually manifested as abnormal damage to the myocardium or chronic overload.

Even a normal heart, if exposed to prolonged overload, for example in the athlete's heart, undergoes a process of adaptation to some ventricular and muscle hypertrophy.

As such, the heart fully compensates for the increased heart burden.

However, myocardial damage or chronic overload may not be fully compensated and the heart may continue to enlarge.

The major problem of the enlarged left ventricle is that there is a significant increase in wall tension and stress during cardiac dilatation and cardiac contraction.

In a normal heart, adaptation to muscle and ventricular hypertrophy maintains a constant wall tension for cardiac contraction.

However, in heart failure, continued dilation is greater than hypertrophy, which in turn increases the demands on the heart wall for cardiac contractility.

This means more damage to the muscles and more damage to the heart muscle cells.

Increased Wall Stress is also the same as fullness of the cardiac dilator.

In addition, the lack of cardiac output increases the filling pressure of the ventricles according to some physiological mechanisms.

Furthermore, in the cardiac dilator, the diameter increases and the pressure increases beyond normal, and the level of the wall stress is high.

Increased wall stress in the diastolic phase is considered to be a major contributor to the continued enlargement of the heart chamber.

Inadequate blood discharge to the atrial system of the heart is called "forward failure", and to cause high pressure in the veins of the system leading to the lungs and digestion is called "backward failure".

Posterior decline is a natural consequence of anterior decline because it prevents blood from the lungs and veins from draining.

Anterior decline is caused by poor ventricular function and reduced contractility or increased postload (i.e., forces that impede blood drainage),

For example, there are some causes of hypertension or pathological disorders of the heart valves.

One physiological compensatory mechanism that increases the heart's blood output is due to posterior gas decline, which increases the filling pressure of the ventricles of the diastolic heart and thereby causes full load (ie, by the enlarged volume of the ventricles at the end of the dilator). Increase the ventricles).

An increase in full load increases the amount of heart rate during cardiac contractors, a phenomenon known as the Frank-Sterling principle.

As such, heart failure may be at least partially compensated for by this mechanism, but at the cost of redness of the lung or body tissue.

When the ventricles expand for some period of time due to an increase in full load, the ventricles become widened.

When the volume of the ventricles expands, the systolic pressure received by the ventricles causes an increase in the wall of the ventricles.

As the amount of pressure increases by the ventricles, it acts as a stimulus for hypertrophy of the ventricular myocardium resulting in a change in cell structure, a process referred to as restructuring of the ventricles.

Hypertrophy can increase systolic pressure but also decrease the compliance of the ventricles and thus result in more severe congestion as a result of increased diastolic filling pressure of cardiac dilatation.

Persistent stress, which is the cause of hypertension, is shown to cause apoptosis of cardiomyocytes and to gradually cause wall thinning, which gradually causes deterioration of heart function.

Thus, enlargement and enlargement of the ventricles preferentially complement or increase cardiac output, but the process eventually results in two dysfunctions, dilation and contraction.

The degree of ventricular structural alteration has been known to correlate with increased mortality in patients with congestive (CHF) heart failure.

Over the past several decades, numerous clinical trials have shown two drugs that significantly improve the overall survival of patients with signs of urgent heart failure (lower left ventricular discharge or increased ventricular hypertrophy). .

These drugs are beta blockers and ACE inhibitors. Beta-receptor blockers have been known to act to block the effects of adrenaline in the heart and have many effects on various types of heart disease.

Beta-receptor blockers reduce the risk of angina in patients with coronary artery disease, greatly increase the survival of patients with heart failure, greatly reduce the risk of sudden death of patients after a heart attack, and prevent or delay structural changes in the left ventricle that are predicted after a heart attack. It turns out that you can.

However, patients with asthma or other lung diseases cannot take this drug. ACE inhibitors have a beneficial effect on the cardiovascular system by blocking angiotensin-modifying enzymes produced in the blood.

These drugs significantly improve the duration of survival among survivors with acute myocardial infarction and, in addition, reduce the incidence of heart failure, suffocation and sudden heart attack, which occur regularly by preventing and delaying heart structure changes.

Although the use of drugs may be beneficial, areas of the intact heart that follow myocardial infarction need to work harder and tissues damaged by infarction remain unfixed.

Really useful is to selectively provide treatments after heart failure and myocardial infarction to reduce or prevent harmful structural alterations and to treat damaged tissues. This optional method is a reasonable mix of traditional and new tissue regeneration therapy.

The configuration of the present invention is to provide a method for cardiac treatment according to myocardial infarction (MI).

Electrical stimulation is provided for selected parts of the heart, whether or not the diagnosis is prescribed.

The stimulus is in the form of excitatory or non-exciting pulses using a cathodic, bipolar, biphasic waveform.

The part of the heart chosen for stimulation is selected based on the extent of damage to the heart tissue and the type of stimulus given.

In the configuration of the present invention, only healthy heart tissue is stimulated.

In another configuration of the invention, the peripheral marginal cardiac tissue may also be stimulated to make the heart more balanced.

In one configuration, the biphasic, ventricular stimulation is confined to the intact area to increase muscle contraction in healthy tissue.

Thus, it allows the heart to achieve normal or near normal function.

Enhanced muscle contraction of a part of the stimulated heart reduces imbalanced heart load and prevents or reduces adverse forms of structural changes in the heart following myocardial infarction.

The biphasic or biventricular stimulus of the present invention is configured such that the pulsation of the anode and the cathode continues to be applied simultaneously to the left and right ventricles through an electrode contacting an intact portion of the heart.

In the configuration of the present invention, unlike the heartbeat that has been controlling and controlling arrhythmia, non-exciting phase 2 stimulation does not apply to the heart responsive to heart signals indicative of arrhythmia.

Rather, non-exciting phase 2 stimulation is applied to ensure that the heart continues to compensate for heart tissue causing myocardial infarction (MI), while avoiding undesirable forms of restructuring.

Optionally, the application of the biphasic stimulus is timed to coincide with the initiation of the depolarized wave determined by the heart's sense.

Moreover, the stimulation of this configuration is associated with the transplantation of stem cells where the heart tissue is damaged. After the damaged heart tissue is regenerated by stem cell therapy and over time, stimulation therapy may end.

In this configuration of the present invention, prevention of harmful structural changes occurs through various mechanisms.

The effect of ventricular pulsation tends to reduce the contraction of the damaged part of the heart by providing a control over muscle contraction but at the same time reducing the consumption of the heart's oxygen demand, reducing the tension in the heart wall and equalizing it. .

In addition, stimulation for stem cell transplantation and correct bearing power depends on proper wall expansion and electrical movement of the damaged area.

Such conditions are appropriately achieved by the treatment.

In addition, the damaged heart tissue can be exposed to electrical current to treat the damaged area directly.

This is similar to treating other tissues, such as bone fragments or skin incisions, using an appropriate current with a polar polarity.

Description As will be appreciated by one of ordinary skill in the art, the description of the embodiment is endless.

While biphasic, biventricular stimulation is described herein, other waveforms and stimulation locations can be used to reduce overloading intact cardiac tissue, thereby reversing the heart or avoiding undesirable structural changes. do.

In addition, the therapy may utilize excitatory or non-exciting pulses. As mentioned previously, tissues damaged by a heart attack (heart failure) do not respond to an excited pulse or respond slower than normal.

Healthy tissue can stretch and stretch the tissue by placing increased stress on the marginal tissue.

It is desirable to minimize the ongoing structural changes that are detrimental to heart attack treatment.

This can be accomplished by reducing the contractile force of healthy heart tissue, increasing the contractile force of marginal heart tissue, or a combination of both methods.

Therefore, an aspect of the present invention is in treating heart tissue affected by myocardial infarction.

Another aspect of the present invention is to increase the output of heart tissue unaffected by myocardial infarction through more controlled heart contraction, leading to greater pulsation and less burden.

Another aspect of the present invention is to stimulate the marginal region of the heart tissue to contract to maintain the balance of the heart to some extent after myocardial infarction.

Another aspect of the invention is to apply a combination of tissue stimulation.

In other words, the tissues damaged by myocardial infarction and intact tissues are combined to activate the function of the heart tissue after the myocardial infarction.

Another aspect of the invention is to reduce the deleterious form of restructuring of the heart after myocardial infarction.

Another aspect of the present invention is the use of stimulation pulsations to continue stimulating the selection unaffected by myocardial infarction.

Another aspect of the invention is the use of stem cells to improve the treatment of heart muscle affected by myocardial infarction.

Another aspect of the invention is to maintain wall tensions sufficient to tolerate the heart of patients suffering from heart failure.

Another aspect of the present invention is to improve the transplantation of stem cells into damaged tissue by improving the normalization of wall stress.

These and other aspects of the invention are apparent as described in more detail generally below.

According to the configuration of the present invention, an apparatus for minimizing cardiac structural alteration of a non-arrhythmic patient includes a cardiac stimulator, a left ventricular electrode group and a right ventricular electrode group.

The electrode group of the left ventricle consists of a left ventricular (LV) electrode attached to the left ventricle at a distance far from the AV node.

The electrode group of the right ventricle consists of a right ventricular (RV) electrode attached to the right ventricle at a distance far from the atrioventricular node.

Cardiac stimulators are applied to stimulate healthy and compromised areas of heart tissue.

The cardiac stimulator is attached to the left and right ventricular electrodes and generates a coincidental temporal signal during infertility.

In response to the temporal signal, the cardiac stimulator beats the left and right ventricular electrodes.

The pulsation occurs simultaneously with the first beat reaching the left ventricular and right ventricular electrodes closest to the AV junction, and the next beat reaches the left ventricular and right ventricular electrodes more gradually away from the atrioventricular junction.

The heart electrode device sends a pulse to such continuous left and right ventricle electrodes. In the configuration of the present invention, the heartbeat is excitable.

In another configuration of the invention, the beat is non-exciting. In another configuration of the present invention, the pulse is biphasic.

According to the configuration of the present invention, the two-phase pulsation is composed of the first stimulator having one polarity, one amplitude, one shape, and one period, allowing the myocardium to accept the subsequent stimulus. Becomes

Furthermore, the two-phase pulsation consists of two poles having a second phase polarity, two phase amplitudes having an absolute value greater than one phase amplitude, two phase shapes, and two periods.

In the configuration of the present invention, group 1 polarity is positive and group 2 polarity is negative. According to another configuration of the present invention, the first stage amplitude has a sub-threshold amplitude.

In the configuration of the present invention, stem cells are placed in heart tissue. In one configuration of the present invention, the electrodes of the left ventricle and the right ventricle are positioned to electrically stimulate damaged areas of heart tissue with stem cells.

In the configuration of the present invention, the electrodes of the left ventricle and the right ventricle are positioned so as not to electrically stimulate the damaged heart tissue site where the stem cells are located.

According to the configuration of the present invention, a device for minimizing cardiac structural alteration of a non-arrhythmic patient is composed of a cardiac stimulator, an electrode group of the right ventricle, an electrode group of the left ventricle, and a sensor.

Sense senses the excitability of the heart room. The left ventricular electrode group consists of left ventricular electrodes attached to the left ventricle significantly away from the atrioventricular node.

The right ventricular electrode group consists of a right ventricular electrode attached to the right ventricle significantly away from the atrioventricular node.

Cardiac stimulators are adapted to stimulate healthy or damaged areas of heart tissue.

Cardiac stimulators are attached to the left and right ventricular electrodes and sensors. In response to the signal from the sense, the cardiac stimulator sends pulses to the left and right ventricular electrodes.

This pulsation coincides with the first beat that reaches the left ventricular and right ventricular electrodes near the atrioventricular junction, and the next beat reaches the left ventricle and the right ventricular electrode progressively further away from the atrioventricular junction.

According to the configuration of the present invention, the heartbeat is excitable.

According to another configuration of the invention, the beat is non-exciting. According to still another configuration of the present invention, the heartbeat is two-phase.

According to the configuration of the present invention, the two-phase pulsation is composed of the first stimulator having one polarity, one amplitude, one shape, and one period, which presupposes that the myocardium receives subsequent stimulation.

Furthermore, the two-phase pulsation consists of two poles having two polarities, two amplitudes having an absolute value greater than one amplitude, two shape and two periods.

In the embodiment of the present invention, group 1 polarity is positive and group 2 polarity is negative.

According to another configuration of the present invention, the first amplitude has an amplitude below the maximum threshold.

In the configuration of the present invention, stem cells are placed in heart tissue. In one configuration of the present invention, the left ventricular electrode and the right ventricular electrode are positioned to electrically stimulate damaged areas of heart tissue with stem cells.

In the configuration of the present invention, the left ventricular electrode and the right ventricular electrode are positioned so as not to electrically stimulate the damaged heart tissue site on which the stem cells are placed.

In a configuration of the present invention, a method of minimizing cardiac structural alteration in a non-arrhythmic patient is provided.

Stem cells are administered in the myocardial infarction area of the patient. Phase 2 and 2 ventricular stimuli are administered in cardiac tissue in areas other than myocardial infarction.

According to the configuration of the present invention, the two-phase pulsation is composed of the first stimulator having one polarity, one amplitude, one shape, and one period, which presupposes that the myocardium receives subsequent stimulation.

Furthermore, the two-phase pulsation consists of two poles having two phase polarities, two phase amplitudes having an absolute value greater than one phase amplitude, two phase shapes, and two periods.

In the embodiment of the present invention, group 1 polarity is positive and group 2 polarity is negative.

According to another configuration of the present invention, the first amplitude has an amplitude below the maximum threshold.

In the configuration of the present invention, stem cells are placed in heart tissue.

In one configuration of the present invention, the left ventricle and the right ventricular electrode are positioned to electrically stimulate damaged areas of heart tissue with stem cells.

In the configuration of the present invention, the electrodes of the left and right ventricle are positioned so as not to electrically stimulate the damaged heart tissue region in which the stem cells are placed.

According to the configuration of the present invention, a device for minimizing cardiac structural alteration of a non-arrhythmic patient is composed of a cardiac stimulator, a left ventricular electrode group, a right ventricular electrode group, and a sensor.

The sensor detects the excitability of the heart room. The electrode group of the left ventricle consists of left ventricular electrodes attached to the left ventricle significantly away from the atrioventricular node.

The electrode group of the right ventricle consists of electrodes of the right ventricle attached to the right ventricle significantly away from the atrioventricular node.

Cardiac stimulators are applied to stimulate healthy or damaged areas of heart tissue. The damaged part of the heart is where the stem cells are located.

Cardiac stimulators are attached to the sense and left and right ventricular electrodes. In response to the signal from the sense, the cardiac stimulator sends pulses to the left and right ventricular electrodes.

This pulsation occurs simultaneously with the first beat reaching the left ventricular and right ventricular electrodes near the atrioventricular junction, and the next beat reaches the left ventricular and right ventricular electrodes progressively further away from the atrioventricular junction.

In the configuration of the present invention, stem cells are placed in heart tissue.

In one configuration of the present invention, the left ventricular electrode and the right ventricular electrode are positioned to enable electrical stimulation of the damaged part of the heart tissue where the stem cells are located.

In another configuration of the present invention, the left ventricular electrode and the right ventricular electrode are positioned so as not to electrically stimulate the damaged heart tissue region on which the stem cells are placed.

1 illustrates a heart composed of electrodes of a composite ventricle connected to an outer surface of a ventricle, including electrodes separately attached to left and right ventricles according to the configuration of the present invention.

Figure 2 is a schematic diagram showing the generation of the two-phase magnetic pole of the cathode mainly in accordance with the configuration of the present invention.

3 is a schematic diagram illustrating the generation of a long term and low level of predominantly cathodic stimulation in accordance with the anodic stimulation in accordance with the inventive arrangements.

4 is a schematic diagram illustrating the generation of a prolonged and low level of inclined predominantly cathodic stimulation in accordance with the anodic stimulation in accordance with the inventive arrangements.

Figure 5 is a schematic diagram showing the generation of the predominantly negative pole stimulus of short duration and low levels of duration continuously managed according to the positive pole stimulation in accordance with the inventive arrangements.

The present invention provides a method for cardiac treatment according to myocardial infarction.

Electrical stimulation is provided to selected parts of the heart, whether or not they have had symptoms of arrhythmia.

The stimulus is in the form of an excitatory or non-exciting pulse that uses waves of the anode, cathode and two phases.

The portion of the heart selected for stimulation is selected based on the extent of damage to the heart tissue and the type of stimulus to be managed.

In this configuration, only healthy heart tissue is stimulated.

In the configuration of the present invention, two-phase, two-ventricular stimulation is performed on the intact area to increase muscle contraction of healthy tissue.

Thus, the heart achieves normal or near normal function.

Enhanced muscle contraction of a part of the stimulated heart reduces unbalanced heart load and reduces or prevents harmful forms of cardiac restructuring due to myocardial infarction.

The stimulation of the two phase, two ventricle is to continuously apply the pulses of the positive and negative pulses simultaneously applied to the right ventricle and the left ventricle through the electrodes in contact with the damaged part of the heart.

In the configuration of the present invention, unlike the heartbeat that has been controlled and controlled from the arrhythmia, the stimulation of the two phases is not applied to the heart as a sensing response to the heart signal indicating the arrhythmia.

Rather, phase 2 stimulation is applied to keep the heart compensated for heart tissue that caused myocardial infarction, while avoiding undesirable forms of restructuring.

Optionally, application of the biphasic stimulus is consistent with the initial onset of depolarization wave determined by cardiac sense.

Moreover, the two-phase stimulation of this configuration is associated with stem cell transplantation where the heart tissue is damaged.

After the damaged heart tissue has been regenerated by stem cell therapy, the irritating treatment is completed.

Referring to FIG. 1 showing the heart, the four atria are: right atrium (RA), left atrium (LA), right ventricle (RV), and left ventricle (LV).

An electrode lead 201 connected to an electrode group 201A of the right ventricle consisting of individual electrode lines 202, 204, 206, 208, and 210 is shown with individual electrode lines connected to a composite point of the outer surface of the right ventricle.

An electrode lead 301 connected to an electrode group 301A of the left ventricle consisting of individual electrode lines 302, 304, 306, 308, 310 is shown with individual electrode lines connected to a composite point of the outer surface of the left ventricle.

The electrode group 201A of the right ventricle and the electrode group 301A of the left ventricle display five electrode lines per group, but this is not limiting.

The other group electrodes do not depart from the scope of the present invention.

In another configuration, the positions 202, 204, 206, 208, 210, and 302, 304, 306, 310 of the individual electrodes of FIG. 1 are selected to avoid stimulation of heart tissue, eg, tissue damaged by myocardial infarction.

In another configuration of the present invention, a pulse (stimulation) is applied to the electrode to mimic the normal physiological flow of normal ventricular depolarization wavelengths.

In this configuration, the part closest to the atrioventricular node is first stimulated at a predetermined pulsation.

In the configuration of the present invention, atrial excitation is detected (PQ interval) or ventricular excitability is detected (QRS interval) and the external excitatory pulse (stimulation) is first applied to the electrode (after an appropriate delay) to match the initial of the ventricular depolarization wave. Apply.

Subsequent excitatory pulses (irritation) are directed towards the progressively distal segment of the atrioventricular node.

The middle region between the two extremes is stimulated at a planned time according to the normal conduction path that most easily facilitates cardiac contraction.

In the configuration of the present invention, the pulse (stimulation) is applied to healthy heart tissue that does not cause myocardial infarction.

Thus, the damaged tissue is treated and the stimulation voltage is low.

This gradual stimulation practice requires special knowledge of the placement of each electrode relative to the different electrodes as well as the placement associated with the electrical conduction pathways of the heart.

As such, it is appropriate to consider the classes of electrodes in which the electrodes are classified or identified as they pass.

For example, the electrodes are identified or categorized according to their timing of operation.

For example, with a five-electrode system, the first individual electrode line operates first (ie the electrode closest to the atrioventricular node), followed by the second, third, fourth, and fifth electrode lines (in normal conduction paths). Temporary and accordingly).

The fifth electrode wire lasts and the electrode position in the ventricles corresponds to the last region of depolarization during normal ventricular contraction and pulsation.

Simpler (ie 2, 3, 4) discrete electrode system schemes are used, and more complex composites (e.g., more corrosive schemes than five discrete electrodes, or pathologies known as periodicity, reentry, conduction, and contractility). Electrode bases in other locations, such as honeycomb arrays, may also be used in special areas.

Furthermore, the composite electrodes in the set electrodes can be counted or clearly identified, allowing the practitioner to experiment with the electrodes by knowing their placement in the heart, for example by circumventing or pre-treating the electrical barrier (blocking) area. do.

In the configuration of the present invention, the composite small electrode is pulsed with an excitatory pulse in a physiological continuous manner.

According to another configuration of the present invention, the above-described ventricular stimulation technique is also applied to the atria. In this embodiment, the electrode resembles the normal inherent conduction path of the atrium, moving progressively from a position close to the parietal nodule (first actuation) to a position close to the atrioventricular node (last actuation).

Bypassing of damaged tissue sites (passing by-passing bypass) is also contemplated by the present invention and may be affected by the first identification area that determines the myocardial resistance of the electrode.

The electrical pulsation then circulates in the myocardium with a moderately low resistance, as close as possible to the conduction of the normal inherent conduction path.

In addition to the development of bypass protocols for special patients, resistance measurements, resistance control and resistance transfer between electrodes can be influenced by external computers.

An external computer can interact with the pacemaker in the traditional way. Traditional methods are, for example, wireless telemetry, direct connection (connecting the external wires of the heart rate control device to the patient's skin surface).

2 to 5 show the range of the two-phase stimulation protocol. Such a protocol is disclosed in Moor US Pat. No. 5,871,506, which is incorporated herein by reference in its entirety.

2 shows the two-phase electrical stimulation of the first stimulator with bipolar stimulus 202 managing amplitude 204 and duration 206.

One stimulator immediately becomes a two stimulator, which consists of a negative stimulus having the same density and duration as the bipolar stimulus 202.

3 shows the electrical stimulation of two phases. One stimulator consists of a low level, long term bipolar stimulus 302 having an amplitude 304 and a period 306.

One stimulator, followed by two stimulators, consists of a negative pole 308 having a traditional density and duration.

According to another configuration of the invention, the bipolar stimulus 302 has an amplitude below the maximum threshold.

According to another configuration of the present invention, the bipolar stimulus 302 is 3 volts or less. According to another configuration of the present invention, the bipolar stimulus 302 is in a duration of approximately 2-8 milliseconds (ms).

According to another configuration of the invention, the negative pole 308 is in a short period of time. According to another configuration of the present invention, the negative pole 308 is in a duration of approximately 0.3-1.5 milliseconds (ms).

According to another embodiment of the present invention, the negative pole 308 has a high amplitude.

According to another configuration of the invention, the negative pole 308 is in the range of approximately 3-20 volts.

According to another configuration of the invention, the negative pole 308 is in a period less than 0.3 milliseconds (ms) and at a voltage greater than 20 volts.

According to another configuration of the present invention, the bipolar stimulus 302 is administered at 200 milliseconds or more after the heartbeat.

As will be apparent from the specification and reading of the present specification as described in the foregoing embodiments, the maximum cell membrane potential without activity is achieved with stage 1 stimulation.

4 shows the electrical stimulation of two phases. One stimulator, composed of bipolar stimulus 402, is managed over a period 404 with an elevated intensity level 406.

Ramps of increasing intensity level 406 may be linear or non-linear and the slope may vary.

The bipolar stimulus immediately becomes a bipolar stimulus consisting of the negative stimulus 408 with traditional strength and duration.

According to another embodiment of the present invention, the bipolar stimulus 402 rises to an amplitude below the maximum threshold.

According to another configuration of the invention, the bipolar stimulus 402 rises to a maximum amplitude of 3 volts or less.

According to another configuration of the invention, the bipolar stimulus 402 is in a period of about 2-8 milliseconds (ms).

According to another configuration of the invention, the negative pole 408 is in a short period of time. According to another embodiment of the present invention, the negative pole 408 is about 0.3-1.5 milliseconds (ms).

According to another configuration of the invention, the negative pole 408 has a high amplitude.

According to another embodiment of the present invention, the negative pole 308 is in the range of about 3-20 volts.

According to another configuration of the invention, the negative pole 408 is within a period of 0.3 milliseconds (ms) or less and has a voltage greater than 20 volts.

According to another configuration of the present invention, the bipolar stimulus 402 is administered at 200 milliseconds or more after the heartbeat.

As described in the above configuration and reading the present specification, the maximal cell membrane potential without activity as achieved by specific examples or modifications is achieved by stage 1 stimulation.

5 shows the electrical stimulation of two phases.

The monostimulus, consisting of bipolar rhythm series 502, is managed with amplitude 504.

In one embodiment, the remaining period 506 is the same period as the stimulator 508 and is managed at baseline amplitude.

In another embodiment, the residual period 506 is different in duration from the stimulator 508 and is managed at baseline amplitude.

Remaining period 506 occurs after each stimulator 508, with the exception of two stimuli consisting of a negative stimulus 510 having traditional strength and duration.

According to another embodiment of the present invention, the total charge changed through the bipolar stimulus 502 series is below the maximum stimulus threshold.

According to another embodiment of the present invention, the series 502 of bipolar stimulators is administered at 200 milliseconds (ms) or more after the heartbeat.

According to another embodiment of the invention, the negative pole 510 is in a short period of time.

According to another embodiment of the present invention, the negative pole 510 is about 0.3 to 1.5 milliseconds (ms).

According to another embodiment of the present invention, the negative pole 510 has a high amplitude.

According to another embodiment of the present invention, the negative pole 510 is in the range of about 3 to 20 volts.

According to another embodiment of the invention, the negative pole 510 is within a period of 0.3 milliseconds (ms) or less and has a voltage greater than 20 volts.

The individual beats of the pulsating series can be square waves or other types of beats, falling in a straight line or curve, falling to lower amplitudes at amplitudes below the initial threshold.

In the two-phase stimulation protocol embodying the present invention, the size of the bipolar device cannot exceed an amplitude below the maximum threshold.

Bipolars are a prerequisite for stimulated myocardium, which lowers the excitatory threshold, such as negative polar stimuli of less than normal yields depolarization leading to contraction.

Normalizing pacing and consequent Wall Stress promotes stem cell transplantation of damaged tissue and leads to proper positioning during cell maturation.

The value of duration and amplitude depends on such factors as the location of the particular electrode (ie, whether the electrode is pure muscle tissue or special facemaking tissue).

This depends on whether the injured wounded tissue is near the electrode, the depth of the electrode in the tissue, what is the local tissue resistance, whether or not a large range of local pathology is present or not.

However, typical periods of bipolarity are in the range of about 2 milliseconds (ms) to 8 milliseconds (ms) while typical periods of negative polarity are often in the range of about 0.3 milliseconds (ms) to 1.5 milliseconds (ms).

Typical anode amplitudes (often below the maximum threshold) are often in the range of about 0.5 volts to 3.5 volts, while typical cathode amplitudes are in the range of about 3 volts to about 20 volts.

The pacing beats work without the need for sensing, as the heart is constantly stimulated.

Furthermore, constant and consistent pacing reduces heart stress.

In an embodiment of the invention, the damaged tissue is found and treated with an insertion application of donor cells or stem cells.

Methods of inserting stem cells into damaged tissues are described in US Pat. No. 60 / 429,954 entitled "Methods and Devices for Surviving Tissue Cells and Electrotherapy."

This patent is a utility application filed November 25, 2003, which is incorporated by reference in its entirety.

In an embodiment of the invention, the damaged tissue is treated and the two ventricular pacing beats continue to apply to the functional part of the heart.

In one embodiment, the pacing site is found and where the tissue is treated with stem cells is not electrically stimulated.

In another embodiment, the pacing site is selected, which allows the site having the electrical stimulation pulsation to be selected such that the tissue treated with the stem cells is below the amplitude required to excite the heart tissue.

Systems and methods have been disclosed to manage deleterious structural alterations of the heart following myocardial infarction.

It is to be understood that the invention has been embodied in other specific forms so as not to depart from the scope of the disclosure, and it is to be understood that the specific examples disclosed herein are enumerated and not restrictive.

Those skilled in the art will recognize that other embodiments using the concepts described herein are also possible. Moreover, singular elements using articles such as "one", "one", "the", and the like are not necessarily limited to singular.

According to the present invention, a heart stimulator for minimizing cardiac structural changes (changes) according to a heart malfunction of a heart disease patient, and an artificial heart rate control device including an electrode group of left and right ventricles and a sense are provided. It will be used as a convenient means to efficiently perform heart rate control of disease patients.

Claims (28)

A device for minimizing cardiac structural alterations in non-arrhythmic patients, a cardiac stimulator designed to stimulate cardiac tissue, damaged areas of healthy or unhealthy tissue, and left ventricular electrodes with left ventricular electrode groups attached to the left ventricle away from the atrioventricular node Consisting of a right ventricular electrode attached to the right ventricle farther from the atrioventricular node, and a cardiac stimulator attached to the left ventricular electrode and the right ventricular electrode, sending a time signal consistent with the intractable period, And arrive at the left ventricular electrode and the right ventricular electrode gradually away from the atrioventricular junction in response to a time signal. The device of claim 1, wherein the heartbeat is excitatory. The device of claim 1, wherein the heartbeat is non-exciting. The device of claim 1, wherein the heartbeat is biphasic. 3. 5. The device of claim 4, wherein the two-phase pulsation is configured as follows. As a prerequisite for accommodating the stimulation accompanying the myocardium, phase 1 polarity, phase 1 amplitude, phase 1 waveform, phase 1 stimulus with phase 1 period, phase 2 polarity, phase 2 amplitude and phase 2 waveforms whose absolute value is greater than phase 1 amplitude. And two stimulators with two phase periods. 6. The device of claim 5, wherein stage 1 polarity is positive and stage 2 polarity is negative. 6. The device of claim 5, wherein the first phase amplitude is less than or equal to the maximum threshold. The device of claim 1, wherein the stem cells are placed in an injured region of the heart tissue. 9. The device of claim 8, wherein the electrodes of the left and right ventricles are positioned to electrically stimulate the damaged area of the heart tissue where the stem cells are located. The device of claim 8, wherein the left ventricular electrode and the right ventricular electrode are positioned to prevent electrical stimulation of the damaged area of the heart tissue in which the stem cells are placed. 10. A device for minimizing cardiac structural alterations in non-arrhythmic patients, a cardiac stimulator adapted to stimulate cardiac tissue, the cardiac tissue being a healthy, damaged area and a left ventricular electrode with a group of left ventricular electrodes attached to the left ventricle away from the atrioventricular node. And a right ventricular electrode group consisting of a right ventricular electrode attached to the left ventricle farther from the atrioventricular node, and one sensor, and the sensor adapted to detect excitability of the heart chamber, and the cardiac stimulator with the left ventricular electrode The heartbeat is attached to the right ventricle electrode, attached to the sensor, and in response to a signal from the sensor, the heartbeat sends a pulse to the left ventricle electrode and the right ventricle electrode in response to the first beat reaching the left ventricular electrode and the right ventricular electrode in close proximity to the atrioventricular junction. Before the left ventricle gradually away from the atrium junction Apparatus for minimizing cardiac arrhythmia structure change of patients with non being to arrive at the right ventricular electrode. 12. The device of claim 11, wherein the heartbeat is excitatory. The device of claim 11, wherein the heartbeat is non-exciting. 12. The device of claim 11, wherein the heartbeat is biphasic. 15. The method of claim 14, wherein the configuration of the two-phase stimulation is a precondition for accommodating the stimulation accompanying the myocardium, and the polarity of the first phase, the first amplitude, the first shape, the first period having the first period, and the second polarity, the absolute value A device for minimizing cardiac structural alteration in a non-arrhythmic patient, characterized by consisting of a bistimulus having a biphasic amplitude, biphasic shape, and biphasic periods greater than the first amplitude. 16. The device of claim 15, wherein the first phase polarity is positive and the second phase polarity is negative. 16. The device of claim 15, wherein the first phase amplitude is at or below a maximum threshold. 12. The device of claim 11, wherein the stem cells are placed in an injured region of the heart tissue. 19. The device of claim 18, wherein the left ventricle electrode and the right ventricle electrode are positioned to electrically stimulate the damaged area of the heart tissue where the stem cells are placed. 19. The device of claim 18, wherein the left ventricular electrode and the right ventricular electrode are positioned to prevent electrical stimulation of the damaged area of the heart tissue on which the stem cells are placed. As a method of minimizing cardiac structural changes in non-arrhythmic patients, the composition manages stem cells in the myocardial infarction region of the patient and continuously manages the two-phase two ventricular stimulation of heart tissue outside the myocardial infarction region. Consists of the following elements: It is composed of one stimulator having one polarity, one amplitude, one shape, and one period, which presupposes that the myocardium receives subsequent stimulation. And a cardiac structure change of a non-arrhythmic patient, comprising a second stimulus having a phase 2 polarity, a phase 2 amplitude having an absolute value greater than the phase 1 amplitude, and a 2 stimulus having a phase 2 shape and a period of 2 phases. How to minimize it. 22. The method of claim 21, wherein stage 1 polarity is positive and stage 2 polarity is negative. 22. The method of claim 21, wherein the first phase amplitude is at or below a maximum threshold. 22. The method of claim 21, wherein the phase 2 stimulation is administered to electrically stimulate the myocardial infarction area in which the stem cells are administered. 22. The method of claim 21, wherein the phase 2 stimulation is administered to prevent electrical stimulation of the managed myocardial infarction region of the stem cells. A device that minimizes cardiac structural alterations in non-arrhythmic patients is a cardiac stimulator whose configuration is adapted to stimulate cardiac tissue, where the heart tissue is a healthy and injured area, where the stem cells are placed, and the left ventricular electrode group is removed from the atrioventricular node. Consisting of a left ventricular electrode attached to a distant left ventricle, the right ventricular electrode group consisting of a right ventricular electrode attached to a left ventricle farther from the atrioventricular node, and one sensor and a sensor adapted to detect the excitability of the heart chamber And a cardiac stimulator is attached to the left and right ventricular electrodes, is attached to the sensor, and is adapted to arriving at the left ventricular and right ventricular electrodes gradually from the atrioventricular junction in response to a signal from the sensor, The two-phase stimulus consists of the following elements: It consists of one stimulus with one polarity, one amplitude, one shape, and one period, which presupposes the myocardium to accept the subsequent stimulus. And a cardiac structure change of a non-arrhythmic patient, comprising a second stimulus having a phase 2 polarity, a phase 2 amplitude having an absolute value greater than the phase 1 amplitude, and a 2 stimulus having a phase 2 shape and a period of 2 phases. To minimize the device. 27. The device of claim 26, wherein the left ventricular electrode and the right ventricular electrode are positioned to electrically stimulate damaged regions of the heart tissue in which the stem cells are placed. 27. The device of claim 26, wherein the left ventricular electrode and the right ventricular electrode are positioned to prevent electrical stimulation of the damaged area of the heart tissue in which the stem cells are placed.

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