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OBJECTIVE: To examine the clinical characteristics and 30-day fatality rate among patients with electrocardiograms (ECGs) ineligible for fibrinolysis in a consecutive series in four general hospitals in the UK. METHODS: We studied 2439 consecutive patients who were identified from regular ward visits, surveillance of results from hospital laboratories, and hospital discharge coding. RESULTS: Thirty percent (732) of patients did not have ECGs eligible for fibrinolysis therapy, while indications were uncertain in 55 (2%). Within the ineligible group, patients presenting with ST depression (n = 294) had a higher 30-day fatality rate than those with ST elevation or left bundle branch block (26% versus 17%; P < 0.001); they represented 40% of the group ineligible for fibrinolysis therapy, or 12% of the total cohort. Thirty-day fatality rates in patients presenting with pathological Q waves and no diagnostic ST segment changes (n = 130), those with T wave changes but no other abnormality (n = 168) and those with a normal ECG (n = 128) were 10%, 5% and 3%, respectively. Despite their high fatality rate, fewer patients with ST depression were admitted to coronary care units than those with ECGs eligible for fibrinolysis therapy (61% versus 85%; P < 0.001) and 23% did not receive heparin. The coronary anatomy in a subset of patients with ST depression showed two- or three-vessel disease in 79% and left main stenosis in 9%. The rates of coronary revascularisation were low in all groups (< 10%). CONCLUSION: Patients with ECGs ineligible for fibrinolysis therapy are a disparate group, with a high rate of fatality occurring in patients who present with ST depression. The high prevalence of multiple vessel coronary disease in patients with ST depression suggests that a more active management strategy is required.

To investigate why approximately one third of patients thrombolysed with streptokinase fail to reperfuse, we assessed the lytic status, antistreptokinase antibody and non invasive parameters of reperfusion in 95 consecutive patients with acute myocardial infarction treated with streptokinase for the first time. The lytic status was assessed by Clauss fibrinogen assay and thrombin clotting time before and 2 h after streptokinase infusion. Antistreptokinase antibody was measured prior to the infusion. Reperfusion was assessed by measurement of the 24:96 h troponin-T ratio (a ratio1 indicating reperfusion) and ST segment resolution 2 h post streptokinase. Ninety-two (97%) patients achieved a systemic lytic state with a fibrinogen titre of less than 1.0 g/l and thrombin clotting time ratio of2.5. Despite this, 27% failed to reperfuse with a mean 24:96 h troponin-T of 0.9, SD 0.6 vs. 3.4 +/- 3.2 in the reperfused group, (P0.0001). 83% of the reperfused group but none of the non reperfused group had ST segment resolution. No difference was observed in the levels of fibrinogen and thrombin clotting time between the reperfused 0.25 +/- 0.3 g/l; 6.9 +/- 4, and the non reperfused group 0.4 +/- 0.6 g/l; 7.9 +/- 2.6. No difference was observed in the levels of antistreptokinase antibody between the reperfused (median = 168 U/ml and the non reperfused (median = 177 U/ml). Failure to reperfuse with Streptokinase is not due to failure to achieve a lytic state. Therefore increased or accelerated dosages of streptokinase are unlikely to increase the rate of reperfusion.

Intravenous hydrocortisone in high doses is often prescribed when immunosuppression is required urgently, such as in the treatment of acute asthma. It is also sometimes used when patients are unable to take oral prednisolone. This practice is potentially dangerous, however, as high dose hydrocortisone may precipitate clinically significant hypokalaemia in susceptible patients. The importance of this effect is emphasised by the following report. A 63 year old man with a history of alcohol abuse presented with a two day history of haematemesis, melaena, and blackouts. He admitted drinking 3.4 litres of beer a day but denied drinking in the week before admission because of indigestion. On examination he was pale with a generalised purpuric rash. The liver was enlarged to 5 cm below the costal margin, and he had a small retinal haemorrhage. A full blood count showed a haemoglobin concentration of 51 g/l, a white cell count of 8.8x109/l, and a platelet count of 4x109/l. Electrolyte analysis showed the following plasma concentrations: sodium 131 mmol/l (normal 133-144 mmol/l), potassium 3.7 mmol/l (normal 3.4-5.2 mmol/l), total calcium 1.92 mmol/l (normal 2.26-2.60 mmol/l), urea 9 mmol/l (normal 2.5-7.5 mmol/l), and creatinine 91 μmol/l (normal 50-100 μmol/l). A coagulation screen gave a thrombin time of 12.5 s (control 13.0 s), a prothrombin time of 14.2 s (control 13.7 s), a kaolin cephalin clotting time of 39.3 s (control 40.8 s), and a reduced thrombotest result of 60%. (The thrombotest is a combined assay of the activities of factors II, VII, IX, and X.) Liver function tests showed the following serum bilirubin concentrations: 11 μmol/l (normal 1-17 μmol/l), albumin 24g/l (normal 35-50 g/l), and (gamma)-glutamyltrans-ferase 60 IU/l (normal

AIMS: To investigate the current use of thrombolytic therapy in the management of patients with acute myocardial infarction and to determine the potential for an increased use of thrombolysis or percutaneous transluminal coronary angioplasty (PTCA). METHODS AND RESULTS: All hospitalised cases of acute myocardial infarction were identified in three health districts in the UK (population of 960,000) in patients under the age of 76 years during a 2-year period; 2439 patients had acute myocardial infarction, of whom 1264 (52%) received thrombolytic therapy. Failure to administer thrombolytic therapy was a result of the absence of diagnostic electrocardiograms in 712 (29.2%) patients, late presentation in 127 (5.2%), therapeutic error in 112 (4.6%), presence of a bleeding risk in 139 (5.7%) and other miscellaneous reasons in 80 (3.3%) patients. Thirty-eight of the 139 patients in whom bleeding risk was reported as a contra-indication could, in retrospect, have received thrombolytic therapy and a further 76 would have been suitable for primary PTCA. CONCLUSIONS: The potential for increasing the use of thrombolytic therapy seems to be limited and is unlikely to make a major impact on the in-hospital mortality from acute myocardial infarction. However, primary PTCA should be considered in those who are ineligible for thrombolysis because of bleeding risk as a contra-indication.