Antithrombotic treatment in stable coronary syndromes: long-term intermittent urokinase therapy in end-stage coronary artery disease and refractory angina pectoris.

Interventions that modify lipid metabolism and blood coagulation have been shown to favourably influence the natural course of coronary artery disease in terms of the primary prevention and treatment of acute cardiovascular events. Various findings suggest that such interventions may also preserve and enhance myocardial perfusion in the chronic stage of the disease. Long-term intermittent urokinase therapy was developed for patients with end-stage coronary artery disease and refractory angina pectoris. A dose of 500,000 IU of urokinase given intravenously as a bolus three times a week for of 12 weeks reduced symptoms by 70% and was accompanied by objective improvements in myocardial perfusion and an increase of ergometric exercise capacity. The possible therapeutic mechanisms of long-term intermittent urokinase therapy-improvement of rheological blood properties mediated by fibrinogen reduction, thrombolysis of non-occlusive subclinical thrombi, and regression of atherosclerotic plaques-are discussed in the context of other antithrombotic approaches.

[1]  A. Hamsten,et al.  Angiographic assessment of effects of bezafibrate on progression of coronary artery disease in young male postinfarction patients , 1996, The Lancet.

[2]  M. Leschke,et al.  Chronic‐intermittent urokinase therapy in patients with end‐stage coronary artery disease and refractory angina pectoris—A pilot study , 1996, Clinical cardiology.

[3]  M. Leschke,et al.  Chronic-intermittent urokinase therapy in refractory angina pectoris* , 1995 .

[4]  S. Miyazaki,et al.  Angioscopic prediction of successful dilatation and of restenosis in percutaneous transluminal coronary angioplasty. Significance of yellow plaque. , 1995, Circulation.

[5]  A. Yeung,et al.  The effect of cholesterol-lowering and antioxidant therapy on endothelium-dependent coronary vasomotion. , 1995, The New England journal of medicine.

[6]  V. Fuster,et al.  Antithrombotic therapy in coronary artery disease. , 1994, Current Opinion in Lipidology.

[7]  M. Sugimachi,et al.  Reduction in serum cholesterol with pravastatin improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia. , 1994, Circulation.

[8]  M. Pirisi,et al.  Fibrinogen Plasma Levels as a Marker of Thrombin Activation: New Insights on the Role of Fibrinogen as a Cardiovascular Risk Factor , 1994, Thrombosis and Haemostasis.

[9]  A. Branzi,et al.  Benefit of Adding Low Molecular Weight Heparin to the Conventional Treatment of Stable Angina Pectoris A Double‐Blind, Randomized, Placebo‐Controlled Trial , 1993, Circulation.

[10]  A. Quyyumi,et al.  Angiogenic effects of low molecular weight heparin in patients with stable coronary artery disease: a pilot study. , 1993, Journal of the American College of Cardiology.

[11]  H. Hecker,et al.  Dose‐Dependent Effect of Aspirin on Carotid Atherosclerosis , 1993, Circulation.

[12]  W. Koenig,et al.  The possible role of hemorheology in atherothrombogenesis. , 1992, Atherosclerosis.

[13]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.

[14]  V. Armstrong,et al.  The HELP‐LDL‐apheresis multicentre study, an angiographically assessed trial on the role of LDL‐apheresis in the secondary prevention of coronary heart disease , 1991, European journal of clinical investigation.

[15]  E. Raftery,et al.  Fibrinogen, factor VII clotting activity and coronary artery disease severity. , 1990, Atherosclerosis.

[16]  E. B. Smith,et al.  Fate of fibrinogen in human arterial intima. , 1990, Arteriosclerosis.

[17]  T. Meade,et al.  Arterial disease risk factors and angiographic evidence of atheroma of the carotid artery. , 1989, Stroke.

[18]  M. Davies,et al.  Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. , 1986, Circulation.

[19]  E. Falk.  Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. , 1985, Circulation.

[20]  V. Bertele',et al.  Antithrombotic therapy in coronary artery disease. , 1985, Arteriosclerosis.

[21]  V. Gurewich,et al.  The Effect of the Fibrinogen Concentration and the Leukocyte Count on Intravascular Fibrin Deposition from Soluble Fibrin Monomer Complexes , 1976, Thrombosis and Haemostasis.

[22]  J. Bigger,et al.  Observations on blood viscosity changes after acute myocardial infarction. , 1975, Circulation.

[23]  R. J. Gordon,et al.  Potential significance of plasma viscosity and hematocrit variations in myocardial ischemia. , 1974, American heart journal.

[24]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (1). , 1992, The New England journal of medicine.

[25]  Shu Chien,et al.  Physiological and pathophysiological significance of hemorheology , 1987 .

[26]  H. Schmid-schönbein.  Interaction of Vasomotion and Blood Rheology in Haemodynamics , 1981 .