Drug – bio-affecting and body treating compositions – Lymphokine – Interferon
Patent
1991-05-17
1993-05-04
Wax, Robert A.
Drug, bio-affecting and body treating compositions
Lymphokine
Interferon
424 854, 530351, A61K 3766, C07K 1526
Patent
active
052080196
DESCRIPTION:
BRIEF SUMMARY
The present invention is directed to the use of gamma-interferon for the preparation of a pharmaceutical preparation for the treatment of vascular stenosis caused by e.g. intimal hyperplasia, including the treatment of restenosis following angioplasty and/or vascular surgery. The present invention is especially directed to the treatment of arterial stenosis following angioplasty and/or vascular surgery.
BACKGROUND OF THE INVENTION
Progress in cardiovascular research has made it possible to reduce the incidence of heart attacks in patients principally by reducing the risk factors for atherosclerosis, such as hypercholesterolemia, smoking, and hypertension. It is known that the development of a heart attack can be stopped by administering tissue-type plasminogen activator (t-PA), which dissolves the thrombus in the coronary artery. Recently, the cloning and production of t-PA by recombinant DNA techniques has made it possible to produce t-PA in unlimited quantities.
For prevention of heart attacks in patients who have developed coronary atherosclerosis, there are, however, only surgical methods available. Several important new techniques have been developed for surgical therapy. In particular, angioplastic procedures using balloon catheters, and more recently lasers, have made it possible to treat patients with less severe symptoms, where coronary bypass surgery is not warranted, and also patients whose general condition is too poor to permit major surgery.
All manipulations of major blood-vessels, be it conventional surgery or angioplastic procedures, are, however, hampered by the frequent occurrence of intimal hyperplasia leading to restenosis of the artery. For example, approximately 30% of all patients who undergo percutaneous transluminal coronary angioplasty at Sahlgren's Hospital, Gothenburg, Sweden, develop intimal lesions that give rise to ischemic symptoms.
The problem is also observed after conventional vascular surgery. Reconstructive surgery of the arteries, that supply the lower extremities with blood is followed by a recurrence of the ischemic symptoms, due to intimal lesions, in 50% of all cases. (See Rutherford R. (ed). Vascular Surgery. Ch. 58. 2nd ed., Saunders, 1984.) Similarly, approximately 20% of all patients who undergo carotid endarterectomy develop intimal hyperplasia. Similar results have been reported from several other treatment centers. Intimal hyperplasia is also often observed in connection with coronary bypass surgery. Postoperative and "postangioplastic" intimal hyperplasia is therefore today a major problem in clinical cardiology, heart surgery and vascular surgery.
For example, many patients with angina pectoris will have to undergo repeated angioplastic procedures, and coronary bypass surgery may eventually have to be performed. It is clear that if one could stop the development of intimal hyperplasia, it would be possible to save patients from muc pain and suffering and also to reduce the costs of treatment substantially.
The mechanisms underlying intimal cell proliferation have been meticulously studied by vascular biologists. It is known that mechanical injury to the artery results in migration-of medial smooth muscle cells into the intima. Once in the intima, the cells begin to proliferate, forming an intimal lesion that persists for months. (See Schwartz S. M., Campbell GR, Campbell J. H. Circ Res 58:427, 1986.) Reendothelialization of the surface seems to be important for regression of the lesion, and both the endothelial area involved and the amount of damage to subendothelial structures are important for the progression of the lesion.
The proliferation of vascular smooth muscle cells is probably controlled by growth factors that either circulate in the blood, such as insulin, or are released from cells, such as the platelet-derived growth factor. The latter factor is synthesized not only by megakaryocytes but also by monocytes and endothelial cells (see Ross R. New Engl J Med 314:488, 1986 and Ross R., Raines E. W., Bowen-Pope D. F. Cell 1986:46:155-169), and t
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Hansson Goran
Holm Jan
Jonasson Lena
Ekstrom Richard C.
Wax Robert A.
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