Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Radical -xh acid – or anhydride – acid halide or salt thereof...
Reexamination Certificate
2001-03-16
2003-04-29
Cook, Rebecca (Department: 1624)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Radical -xh acid, or anhydride, acid halide or salt thereof...
Reexamination Certificate
active
06555579
ABSTRACT:
FIELD OF THE INVENTION
The invention relates to reducing deposits in arteries. In particular, the invention relates to reducing atherosclerotic plaques using fatty acids.
BACKGROUND OF THE INVENTION
Atherosclerosis is one of the major vascular diseases affecting people throughout the world and has been defined by the World Health Organization as a “variable combination of changes of the intima of arteries (as distinct from arterioles) consisting of the focal accumulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits, and associated with medial changes.” See “Classification of Atherosclerotic Lesions,” Report of a Study Group Definition of Terms, W. H. O. Tech. Rep. Ser., 143:4 (1958).
Atherosclerosis in mammals is characterized by formation of atherosclerotic plaques or atherosclerotic lesions in large and medium-sized arteries. See, e.g., Naito & Schwartz,
Nutrition and Heart Disease,
pp. 1-25, Ed. Naito, Spectrum Publications, Jamaica, N.Y. (1982). Atherosclerotic plaques reduce the arterial lumen thereby reducing, obstructing or, in severe cases, stopping blood flow through the artery. The irregular surface of atherosclerotic plaques can lead to intra-arterial thrombi. Detachment of all or a portion of a thrombus from an atherosclerotic plaque can lead to obstruction of an artery located downstream from the plaque, resulting in localized tissue ischemia and/or stroke.
Early stages of atherosclerotic plaque formation are manifested as “fatty or lipid streaks” on arterial walls. These fatty streaks contain lipid-laden foam cells located in the subendothelial layer of the arterial intima. Additional intracellular and extracellular lipids accumulate at the site of the plaque during later plaque formation stages causing raised lesions. In addition, smooth muscle and connective tissue cells may migrate into the plaque and/or proliferate within the plaque. Plaques (sometimes referred to as atheromata) damage the intimal surface of the artery weakening the artery and decreasing its elasticity. Intimal damage may also attract additional cells and extracellular materials to accumulate at or near the plaque. Over time, a plaque may calcify. As cells and extracellular materials accumulate, the intimal surface of the artery becomes irregular, which may lead to the accumulation of blood platelets and thrombus formation. The committee on lesions of the American Heart Association has recognized from 6 to 8 different stages of plaque formation starting from the basically invisible lipid streaks, through the visible raised lesions and ending in a fully occluded artery. As such, atherosclerotic plaque formation is really a continuum of events.
Current methods for preventing atherosclerosis target reducing known risk factors. These risk factors include hypercholesterolemia, hypertension, tobacco smoking, obesity, physical inactivity, familial history, and (possibly) personality type. Prevention methods include reducing cholesterol and other fat intake, exercise, weight control, cessation of smoking, and monitoring of blood lipid levels. For example, it has been suggested that administering cholesterol-lowering or cholesterol-sequestering compounds and/or drugs, including conjugated linoleic acids may prevent the formation of atherosclerotic plaques. Lee et al.,
Atherosclerosis,
108:19-25 (1994); and Nicolosi et al.,
Artery,
22:266-277 (1997).
Once an atherosclerotic plaque has formed, and particularly once the plaque has become fibrous or infiltrated by smooth muscle cells, treating atherosclerotic plaques is complicated especially when the plaques cause significant obstruction of an artery. In fact, obstruction of coronary arteries by atherosclerotic plaques is one reason numerous coronary bypass surgical procedures are performed each year.
Current methods for treating existing atherosclerotic plaques are limited. Pharmaceutical or surgical approaches to atherosclerotic plaque diminution have only inconsistently resulted in minimal plaque regression. See, e.g. Buchwald et al.,
New Eng. J. Med.,
232:946-55 (1990); Rodrigueza et al.,
Biochim. Biophys. Acta,
1368:306-320 (1998); and Wissler et al.,
Ann. N.Y. Acad. Sci.,
275:363 (1976). Known physical methods for removing or reducing atherosclerotic plaques include angioplastic flattening of the atherosclerotic lesions, insertion of arterial stents, surgical excision of the plaque, ablation of a portion of the plaque (e.g., laser angioplasty), and replacement of an occluded artery with another artery or a vein obtained from the same patient (e.g., cardiac bypass surgery or mammary artery grafting).
These current physical methods exhibit severe limitations, costs and risks. For example, expanding a plaque-occluded artery by balloon angioplasty or surgically removing occluding material from such an artery often provides only temporary relief from atherosclerosis because the expanded or surgically invaded artery often quickly returns to the pre-surgical reduced lumenal diameter. In fact, about 40% of the arteries subjected to angioplasty reocclude. Furthermore, removing lipid and other material adhering to an arterial wall can release particles that travel through the bloodstream and occlude cerebral blood vessels or reduce cerebral blood flow causing a stroke. Surgical or angioplastic intervention at the site of an atherosclerotic plaque may also further weaken already compromised vascular tissues, increasing the likelihood of hemorrhage or aneurysm. Surgical grafting of an artery or vein obtained from elsewhere in the patient's body do not tend to lengthen the life expectancy of patients relative to similarly afflicted patients who do not undergo such the surgery. Furthermore, grafted blood vessels are also likely to become re-occluded.
As such, despite advances in the preventing, detecting, and treating of atherosclerotic plaques, coronary artery disease, atherosclerotic heart disease and complications related to these disease states remain leading causes of death. Accordingly, there exists a need for non-invasive methods for treating existing atherosclerotic lesions in humans.
SUMMARY OF THE INVENTION
In one aspect, the invention features a method for reducing atherosclerotic plaques that includes administering an effective amount of at least one polyunsaturated fatty acid composition to a mammal such as a human. The fatty acid composition can have a carbon chain of at least 16 carbons in length and at least one pair of double bonds in a conjugated position. In one embodiment, the fatty acid composition is a mixture of different fatty acids with some of the fatty acids being at least C
16
fatty acids having one or more pairs of conjugated double bonds.
In some embodiments, the effective amount of the fatty acid composition can be altered. Useful effective amount concentrations include amounts ranging from about 0.01% to about 5% of a total diet on a weight by weight basis, from about 0.01% to about 1% of a total diet on a weight by weight basis, or from about 0.01% to about 0.5% of a total diet on a weight by weight basis. For example, the effective amount can be about 0.01%, about 0.025%, about 0.05%, about 0.1%, about 0.5%, or about 1.0% of a total diet on a weight by weight basis.
The effective amount may also be measured directly. The effective amount may be given daily or weekly or fractions thereof. For example, in some embodiments the effective amount is a fatty acid dose that ranges from about 1 milligram to about 25 grams of the fatty acid composition per day, about 50 milligrams to about 10 grams of the fatty acid composition per-day, from about 100 milligrams to about 5 grams of the fatty acid composition per day, about 1 gram of the fatty acid composition per day, about 1 milligram to about 25 grams of the fatty acid composition per week, about 50 milligrams to about 10 grams of the fatty acid composition per week, about 100 milligrams to about 5 grams of the fatty acid composition every other day, and about 1 gram of the fatty acid composition once a week.
In anoth
Cook Rebecca
Fish & Richardson P.C. P.A.
The Wistar Institute
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