Surgery – Means for introducing or removing material from body for... – Treating material introduced into or removed from body...
Reexamination Certificate
2001-08-24
2003-08-19
Mendez, Manuel (Department: 3763)
Surgery
Means for introducing or removing material from body for...
Treating material introduced into or removed from body...
C604S031000, C607S106000
Reexamination Certificate
active
06607517
ABSTRACT:
FIELD OF THE INVENTION
This invention relates generally to methods for medical treatment and more particularly to the application of hypothermia by various means including by endovascular heat exchange to treat chronic heart disease. These methods find particular usefulness in treating congestive heart failure.
BACKGROUND OF THE INVENTION
Chronic cardiac failure may occur over a long period of time and may result from many root causes: diabetes, high blood pressure, clogged coronary arteries, and even acute events such as heart attacks. Whenever a heart has inadequate output, the resultant problems are legion and often systemic. The diseases is progressive; because of the inadequate supply of oxygen-rich blood to fuel the body's needs, people with heart failure often experience shortness of breath and uncommon fatigue with daily activities. Then as the condition progresses, the chambers of the heart—particularly the ventricles —become increasingly enlarged as the heart tries to compensate for the inefficiencies. Ultimately a complex process of damaging structural and functional changes to the heart result. The enlarged heart looses the ability to pump efficiently. There may be inadequate ability to handle venous return, leading to congested liver, water retention in the extremities and other problems of edema. There may be inadequate output from the left heart leading to congested lungs. There may be inadequate supply of oxygenated blood to various organs including the heart itself, and areas including the brain, leading to all the problems associated with hypoxia. There may be inadequate removal toxic metabolic waste products from organs or failure to clear drugs or toxic substances via the liver, leading to
The condition of heart failure is complex and may be diagnosed by any one or a number of different criteria: the cardiac output may be low, generally consideredbelow 2.5 liters per minute; the stroke volume of the heart may be low, for example below 25 cc; the ejection fraction of the sick heart may be below 40%; there may be echocardiographic findings of enlarged or improperly pumping hear; physical examinations including x-rays and stress testing may indicate cardiac failure; there may be cardiomegally; there may be increased left ventricular wall thickness and chamber dilation indicative of cardiac failure; there may be pulmonary edema, which with other sympotoms and findings may indicate cardiac failure; there may be angiographic findings indicative of heart failure; and a diagnostic test of blood components, such as electrolytes or proteins may indicate heart failure. This lis is not exhaustive of the symptoms and findings that may help diagnose heart failure, but is offered to show the extent to which heart failure impacts the entire patient and may radically deteriorate the patient's life quality.
One common condition is congestive heart failure (CHF). CHF is one of the most serious health problems in the world. An estimated 4.8 million Americans alone have CHF. It is often the end stage of serious heart disease; half of those diagnosed with CHF will be dead within 5 years. An estimated 400,000 new case are diagnosed each year. It is the most common diagnosis in hospital patients age 65 years and older, with the disease affecting 10% of all those over the age of 70. The financial cost of treatment of CHF patients is over $17 billion a year. The human cost is beyond measure.
CHF is a complex clinical syndrome characterized by impaired ventricular performance, exercise intolerance, a high incidence of ventricular arrhythmias, and shortened life expectancy. It general, the heart is not pumping well enough to meet the body's metabolic demands and to provide adequate venous return. CHF is generally the result of a long clinical process. A general description of the downward spiral is: from normal heart function, to asymptomatic left ventricular (LV) dysfunction, to compensated CHF, to decompensated CHF and finally refractory CHF.
In the patient with asymptomatic left ventricular dysfunction, the abnormality in function is usually detectable by laboratory testing only. As the disease progresses, the patient develops symptoms such as mild exercise intolerance indicating inadequate cardiac output during stress. Milder forms of therapy are required at this point, such as diuretics, vasodilators and digoxin. The heart compensates by dilating to increase the volume of blood ejected per beat to increase cardiac output. Over time, the heart grows in size (myocardial hypertrophy) but also dilates to become more flaccid and less able to pump efficiently.
As the disease progresses, the structural changes become inadequate to successfully compensate, and the patient decompensates and becomes symptomatic at rest. Aggressive therapy is required at this point, consisting of diuretics,vasodilators and potent inotropic agents. These inotropic agents can lead to a transient improvement in hemodynamics, but may also accelerate the degenerative process in the heart, and increase mortality. Once the patient becomes unresponsive to inotropic therapy, a period of refractory CHF ensues. Treatment options are then generally limited to mechanical support (e.g. LV assist devices) or cardiac transplantation.
When the sufferer of CHF enters this final stage and the cardiac disease is so severe that he or she needs a heart transplant to survive for any length of time, the outlook is grim. According to the United Network for Organ Sharing (UNOS), more than 40,000 patients were waiting for a heart transplant as of February of 2000, and only 2,235 people received a donated heart in 2000. The vast majority of those needing a heart transplant will die waiting.
One method of increasing the likelihood that the patient will survive to receive a heart transplant is to treat the patient's heart with inotropic drugs or heart pacer to return it temporarily to an improved state and temporarily provide the patient's body with improved cardiac output. This treatment regime has the severe disadvantages set out below, and is not always available, but when available does provide a temporary improvement that might forestall death.
Inotropic drugs are drugs that increase muscle contractility, and in particular the contractility of the heart muscle. The drugs available include digitalis glycosides, available for almost 200 years to increase the force of contraction in both normal and failing heart muscles, but these have a very narrow therapeutic range and are limited by toxic side effects. The patient may develop tolerance and these drugs loose their effectiveness and the dose must be increased. Eventually they may not be effective at all.
Another treatment for those with decompensated congestive heart failure is the administration of the inotropic drugs milrinone or dobutamine. These drugs cause the heart to pump more vigorously and perhaps more effectively and to lead to improved overall condition of the patient, temporarily, However, chronic administration of these inotropic drugs generally leads to worsened long term prognosis and increased mortality rates. It has been postulated that the increase in metabolic activity leads to the buildup of potentially harmful metabolic by-products and perhaps also artificially overrides the auto protective effect of hibernation of heart tissue. In any event, the administration of these drugs may lead to long term heart muscle deterioration and long term increased mortality. There may also be more immediate dangers: patient's who receive inotropic drugs and show clinical improvement over the short term often have symptomatic and hemodynamic rebound leading to worsened heart failure during or shortly after being weaned from the inotropic drugs. As a result, these inotropic agents are only indicated for short-term intravenous administration in CHF patients who can be closely monitored and who have not responded well to digitalis, diuretics or vasodilators.
These intermittent periods of artificially increased heart output by drug therapy are sometimes
Dae Michael W.
Stull Paul M.
Buyan Robert D.
Mendez Manuel
Radiant Medical Inc.
Stout, Uxa Buyan & Mullins, LLP
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