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The 4 widely available thrombolytic agents, alteplase (recombinant tissue plasminogen activator, rt-PA), anisoylated plasminogen streptokinase activator complex (APSAC; anistreplase), streptokinase and urokinase have revolutionised the treatment of acute myocardial infarction and are also effective in treating pulmonary embolism and peripheral arterial thrombosis. Therapeutic efficacy of the agents appears to be similar. Choice of a thrombolytic agent depends more on patient characteristics, availability and familiarity with the drug, cost and differences in tolerability. While overall thrombolytic therapy is relatively safe, these 4 agents differ in their tolerability profiles. Streptokinase has the lowest cerebral haemorrhage rate, anistreplase an intermediate and alteplase the highest rate. The incidence of total stroke is also higher with alteplase and anistreplase than with streptokinase, translating to an actual difference in patient risk of 4 extra strokes per 1000 patients treated. Risk of major bleeding is dependent on predisposing factors and seems to be similar with each agent. The incidence of hypotension with alteplase (4.3% in ISIS-3) is less than with streptokinase or anistreplase (6.8 and 7.2%, respectively in ISIS-3). The incidence of major anaphylactic reactions with streptokinase and anistreplase is low (< 1%). Urokinase and alteplase may be preferred for readministration of thrombolytic therapy and anistreplase is the agent of choice where rapid completion of therapy is desirable. The various agents may have different tolerability profiles with different adjunctive therapies and further data are therefore required.

The coronary flow reserve is abnormal in syndrome X, but the response to the cold pressor test, which in normals produces flow-mediated endothelium-dependent epicardial coronary dilation, has not been studied. In this study, in 12 patients with typical syndrome X and angiographically normal coronary arteries, the response to the cold pressor test was abnormal with a mean fall in diameter (10 ± 8%) in 6 patients, no change in 1, and a minimal increase (4 ± 2%) in 5 patients (normal increase 12 ± 1%). The coronary blood flow fell slightly during the cold pressor test, and the coronary vascular resistance increased significantly (from 2.4 ± 1.1 to 3.2 ± 1.7 mm Hg/cm-s^-1mm²; p = 0.05), both abnormal responses. This study confirms that in syndrome X patients there is coronary endothelial dysfunction which is apparent in response to physiological stimuli induced by the cold pressor test.

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