Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...
Reexamination Certificate
2000-09-05
2002-07-23
Gitomer, Ralph (Department: 1623)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Having -c-, wherein x is chalcogen, bonded directly to...
C514S568000, C514S824000, C514S529000, C514S729000
Reexamination Certificate
active
06423742
ABSTRACT:
TECHNICAL FIELD AND INDUSTRIAL APPLICABILITY OF THE INVENTION
The present invention is related to novel, therapeutic pharmaceutical and nutraceutical compositions useful in treating stenotic vascular diseases and disorders, such as atherosclerosis (also known as arteriosclerosis) and coronary heart disease (also known as coronary artery disease and ischemic heart disease). More particularly, the present invention relates to dietary supplements comprised of gallic acid, or a derivative thereof, and limonene, or a derivative thereof, formulated with or without additives, excipients, and/or stabilizers. The invention further relates to the use of such therapeutic compositions to reduce vascular plaque formation, reverse plaque deposition and degenerative changes in the arterial walls, and/or remove or stabilize existing plaques from the vascular walls. Additionally, the invention relates to a non-invasive diagnostic test and method of using same to monitor a patient's potential for a heart attack.
BACKGROUND OF THE INVENTION
Stenotic vascular diseases and disorders constitute the primary cause of death in industrialized societies. Exemplary stenotic vascular diseases include coronary heart disease (CHD) and peripheral vascular disease (PVD). These diseases generally result from accumulation of “plaque”, often deposited slowly over time on vascular walls of arteries. “Plaque” is a generic term describing a heterogeneous sludge of hardened fat, cholesterol, white blood cells, calcium, decaying tissue, and other cellular “garbage.” Over time, wear and tear inside the blood vessel walls create rough spots on which plaque can “catch” and build up, eventually blocking blood flow through those vessels. This condition is called atherosclerosis, or “hardening of the arteries.”
Atherosclerosis, the underlying condition implicated in most myocardial infarctions and strokes, is a complex pathologic process involving the inner layer (intima) of the arteries. Theories relating to the etiology of atherosclerosis are many and vary from genetic and ecologic factors to levels of lipids in the bloodstream to injury of the arterial wall. While the normal intima serves as a barrier to the influx of serum cholesterol, during atherogenesis the arterial intima breaks down, permitting the entry of blood constituents. With this increase in permeability there is an uptake of particles normally excluded form the vessel wall.
In the early stages, the atherosclerotic lesion is comprised primarily of fatty substances, such as lipid-laden macrophages (white blood cells) and lipid-laden smooth muscle cells. Cholesterol crystals, necrotic debris and calcium deposits are also found in atherosclerotic lesions. As the disease progresses, a dense fibrous cap of smooth muscle and connective tissues develops over the lipid-rich plaque lesion. As the deposition of debris progresses, the lumen of the artery is narrowed and/or obstructed, thereby resulting in diminished or occluded blood flow.
These occluding atherosclerotic lesions ultimately result in ischemia and/or infarction of the affected organ or anatomical part (e.g., the brain, heart, intestine or extremities). In other cases, the plaque tears or ruptures, triggering the formation of a blood clot that can block the artery and lead to a heart attack. Such an event is sometimes called a coronary thrombosis or coronary occlusion. Alternatively, the plaque may cause the arterial wall to become so weakened that soft and/or brittle areas can become segmentally dilated (aneurysmal) and rupture or crack leading to hemorrhage. In any of these events, if the blood supply is cut off severely or for a long time, the result can be significant, often times irreversible, loss of function and cellular substance and may require requiring emergency medical and/or surgical procedures as well. Disability or death can result, depending on how much the tissue (such as the heart muscle) is damaged.
While the basic definitive cause (or causes) of atherosclerosis are not fully known or understood, most therapies are directed to means and methods for affecting deposition of plaque and/or improving arterial flow and function. Examples of the latter include the administration of beta blockers to function as governors on the heart, and aspirin therapy to thin and prevent clotting of the blood. While these may provide some benefit, more preferred therapies are directed at the former, i.e., reducing or preventing vascular plaque formation and removing or dissolving existing plaques.
In light of the empiric clinical observations of many investigators and medical practitioners, it has been hypothesized that plaque formation is related to the plasma cholesterol and lipid levels. Consequently, the most favored regimens for treating atherosclerosis consists of medication, dietary management, behavior modification and exercise aimed at controlling and reducing the plasma cholesterol levels. For examples of specific therapies, see de Feyter P J et al.,
Eur Heart J
(1995) 16 Suppl. 1:26-30 and Thompson G R,
Cardiology
(1990) 77 Suppl. 4:66-69.
Exemplary cholesterol-lowering agents include Atromid-S™ (clofibrate), Choloxin™ (dextrothyroxine sodium), Colestid™ (colestipol hydrochloride), Lopid™ (gemfibrozil), Lorelco™ (probucol), Nicolar™ (niacin
icotinic acid) and Questran™ (cholestyramine resin).
Flavonoids and polyphenols have also been described in the literature as “cardiovascular protecting agents” (see U.S. Pat. No. 5,648,377; U.S. Pat. No. 4,707,360; Bohr D.,
J Pharmacol. Exp. Ther
. (1949) 97: 243; Haeger K. Zbl.,
Phlebol
. (1967) 6:526; Allen S.,
Practioner
(1970) 205:221; Gugler R.,
Ces. Arch. Exp. Pathol. Pharm
. (1972) 247:45; Klurfeld,
Exp. Mol. Path
.(1981) 34:62; Lisunetz H.,
Polyphenols
, (1990) 764; Frankel E.,
Lancet
(1993) 341:454; Kontek A.,
Polyphenols
(1995) 94; Folts J., Circul (1995) 91: 1182; Yamakoshi et al. (1999)
Atherosclerosis
142(1):139-49).
However, these drugs, and the treatments in general are typically directed only at the cause, and not the result of, atherosclerosis, and have not been shown to be effective in reversing the plaque deposition and degenerative changes in the arterial walls. These pharmacologic agents have many other shortcomings such as, for example, adverse side effects (hypertension, cardiac arrhythmias, gastrointestinal disturbances, headache, hypersensitivity, etc.), substantial contraindications (heart, liver or kidney disease, pregnancy, etc.), requirement for lifelong conscientious administration, difficulty in maintaining consistent patient compliance, variable reliability and high cost.
Unfortunately, drug and diet therapies are frequently insufficient to control atherosclerosis. Once the disease has progressed to the stage of significant persistent symptoms and compromised function, more invasive procedures, such as angioplasty, atherectomy, arterial stenting and grafting, and by-pass surgery, are often required. Clearly, surgery is not the solution to the pathologic process since it has no arresting or reversing effect on the progress of the disease and only temporarily overcomes the most critically affected artery (or arteries) by bypassing them, if possible. Surgery is only effective in isolated symptomatic lesions and cannot affect the multitude of atherosclerotic lesions throughout the body. In fact, it is often only a temporary solution as lesion recurrence and restenosis occur in most cases. Moreover, there is a significant risk of morbidity and mortality associated with surgery which many patients are reluctant to accept. Indeed, the disease may continue to progress even as the operation is being performed, and the autogenous veins or arteries used to bypass the disease impaired arteries undergo atherosclerotic changes postoperatively generally at a faster rate than the original, affected arteries.
Thus, there is clearly a need for alternate compositions and methods for treating atherosclerosis and its underlying cause, i.e., vascular plaque formation. The present invention attempts to address the drawbacks an
Gitomer Ralph
Khare Devesh
Smith Chalin A.
Smith Patent Consulting
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