[Chronic intermittent urokinase therapy in therapy-refractory angina pectoris]
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1Abteilung für Kardiologie, Pneumologie und Angiologie, Universität Düsseldorf.
Insights
Chronic intermittent urokinase infusion significantly reduced fibrinogen and plasma viscosity in patients with treatment-resistant angina. This improved myocardial perfusion and exercise capacity, offering a promising treatment alternative.
Area of Science:
- Cardiology
- Hematology
Background:
- Coronary heart disease (CHD) with treatment-resistant angina pectoris presents a significant clinical challenge.
- Myocardial perfusion deficits are a key factor in the pathophysiology of angina.
Purpose of the Study:
- To evaluate the impact of urokinase-induced fibrinogen reduction on myocardial perfusion in patients with end-stage CHD.
- To assess the efficacy of chronic intermittent urokinase infusion as a treatment for refractory angina.
Main Methods:
- 24 men with end-stage CHD and refractory angina received daily intravenous urokinase infusions, adjusted to achieve target fibrinogen levels (150-200 mg/dl).
- Treatment continued with 2-4 weekly infusions as outpatients for 12 weeks.
- Measurements included fibrinogen concentration, plasma viscosity, anginal attack frequency, exercise capacity, and thallium myocardial scintigraphy.
Main Results:
- Fibrinogen levels decreased from 348 +/- 88 to 211 +/- 52 mg/dl (P<0.01).
- Plasma viscosity reduced from 1.44 +/- 0.08 to 1.33 +/- 0.09 mPa.s (P<0.01).
- Anginal attacks decreased from 3.2 +/- 1.6 to 0.7 +/- 0.4 daily (P<0.01), and exercise capacity increased by 76%.
- Thallium scintigraphy showed improved myocardial perfusion in 16 of 19 patients.
Conclusions:
- Chronic intermittent urokinase infusion effectively reduces fibrinogen and plasma viscosity.
- This treatment leads to significant improvements in myocardial perfusion, angina symptoms, and exercise tolerance in patients with treatment-resistant coronary heart disease.
- Urokinase offers a potential therapeutic option for patients with refractory angina pectoris due to advanced coronary heart disease.
Abstract:
To assess the effect of urokinase-induced reduction of fibrinogen concentration on myocardial perfusion, urokinase infusions were administered for 3 months to 24 men (mean age 59 +/- 10 years) in the inoperable end-stage of coronary heart disease with treatment-resistant angina pectoris. Initially 500,000 IU urokinase were infused i.v. daily until a fibrinogen concentration of 150-200 mg/dl was reached. Treatment was then continued as out-patients at a dosage of 500,000 IU two to four times per week. After 12 weeks the fibrinogen concentration had fallen from 348 +/- 88 to 211 +/- 52 mg/dl and plasma viscosity from 1.44 +/- 0.08 to 1.33 +/- 0.09 mPa.s (P for each less than 0.01). Up to the end of 12 weeks after the end of treatment the frequency of anginal attacks fell significantly from 3.2 +/- 1.6 to 0.7 +/- 0.4 daily (P less than 0.01), while ergometric exercise capacity increased by 76%. Thallium myocardial scintigraphy demonstrated an increased perfusion in all but three of 19 patients, global in 10, regional in 6. These results indicate that in patients with treatment-resistant angina due to coronary heart disease chronic intermittent urokinase infusion provides a promising treatment alternative.