UAP is a frequent manifestation of ischaemic heart disease; it is intermediary between stable angina and myocardial infarction and sudden death resp. The hospitalization mortality is 5%, approximately 15% of the patients with UAP develop myocardial infarction. The aim of UAP treatment is: 1. prevention of ischaemic episodes, 2. prevention of infarction and 3. control or elimination of risk factors, to improve the long-term prognosis in these patients. As antianginal drugs in UAP as a routine calcium antagonists, beta-blockers and nitrates are used. A very important part in the treatment of UAP is played by antithrombotic and thrombolytic treatment as in this disease rupture or fissure of plaques and subsequent thrombus formation is important. Non-occlusive thrombi are present in 80% in UAP, while in infarctions they are present in 21%. Rupture of an atherosclerotic plaque leads to thrombocyte activation, release of tissue thromboplastin and activation of the coagulation system aspirin inhibits platelet function and thus reduces thromboxane A2 formation. Heparin affects the coagulation process in UAP, reduces the number of anginal attacks and protects from the development of infarction. Treatment of UAP with streptokinase and rt-PA has no great advantages, when compared with heparin. Surgical treatment of UAP has somewhat better results than conservative treatment. Coronary angioplasty is an ideal solution in UAP when one or two arteries are damaged.

Keywords: Angina, Unstable /therapy/; Humans