Within four hours of the onset of acute myocardial infarction 57 consecutive patients were randomised blindly to infusion of 150 mg recombinant tissue plasminogen activator (rt-PA) (group 1) over five hours or placebo (group 2) when they were first seen outside hospital or in the accident and emergency department. When they were admitted to the coronary care unit patients in group 1 also had placebo infused and those in group 2 were treated with rt-PA as well as placebo. Treatment with rt-PA started at a mean of 119 minutes (range 38-235) after the onset of pain in group 1 and 187 minutes (range 80-285) after the onset of pain in group. In 19 (79%) of 24 in group 1 and 16 of 25 (64%) in group 2 cardiac catheterisation 10-14 days after infarction showed thrombolysis in myocardial infarction grades 2 or 3. There was mean percentage shortening of the infarct related segments (Leighton method) of 16% in group 1 and 10.3% in group 2. For patients with anterior infarction mean percentage shortening was 20.5% in group 1 and 12.2% in group 2. Although there was no significant difference in global ejection fraction as assessed by contrast ventriculography or radionuclide ventriculography the infarct related regional third ejection fraction (a measure of the function of the territory of the affected coronary artery) was significantly improved by early treatment (41% group 1 and 28% group 2). Assessment of infarct size by the QRS scoring method of Palmeri showed QRS score less than or equal to 15/25 patients in group 1 and 8/27 in group 2. Nine patients developed 11 episodes of ventricular fibrillation; all patients in whom ventricular fibrillation developed during treatment with rt-PA were successfully resuscitated. There was no clinically significant bleeding. In seven (12%) patients clinical and electrocardiographic criteria suggested reocclusion. Five patients died from cardiac causes. Prehospital administration of rt-PA was feasible and significantly reduced the delay before thrombolysis was started. Earlier treatment improved myocardial function in the the infarct area and reduced the infarct size.

To assess the thrombolytic efficacy and the effect on the systemic fibrinolytic system of recombinant tissue plasminogen activator doses of 20 mg, 50 mg, and 100 mg were compared in a randomised study. Tissue plasminogen activator was infused intravenously over 90 minutes in 50 consecutive patients with acute myocardial infarction of four hours' duration or less; on average the infusion was started 135 minutes (range 20 to 240) after the onset of pain. The affected artery was patent at the end of the 90 minute infusion in 14/17 (82%) of those who received 100 mg, 12/17 (71%) of those who received 50 mg, and 8/16 (50%) of those who received 20 mg. Regardless of dose, reperfusion rates were significantly better for patients treated within two hours of the onset of symptoms (81%) than for those treated in the third and fourth hours (54%). At the end of the infusion serum fibrinogen concentrations fell to 86% of the preinfusion value after 20 mg, 75% after 50 mg, and 63% after 100 mg, and similar dose dependent changes occurred in plasminogen, (alpha 2 anti-plasmin, and fibrinogen and fibrin degradation products. The mean infarct related regional third ejection fraction was 46% for patients with grade 2 or 3 reperfusion and 35% for those with grade 0 or 1. Ventricular fibrillation occurred in six (12%) patients during the infusion of tissue plasminogen activator, but no late ventricular fibrillation occurred. Bleeding was minimal, reocclusion occurred in three patients, and four patients died from cardiac causes. Recombinant tissue plasminogen activator is an effective thrombolytic agent which produces better reperfusion rates after a 50 or 100 mg dose than after a 20 mg dose. The effect on the systemic fibrinolytic system is dose dependent. Successful reperfusion results in improvement of left ventricular function.

The safety and efficacy of a device allowing the trans-telephonic control of defibrillation have been assessed in 32 attempted defibrillations performed in 29 patients. The initial rhythm was atrial fibrillation in 27; ventricular tachycardia in 4; and ventricular flutter in 1. Satisfactory voice and ECG transmission were established in all cases. The mean time taken by the patient unit to dial and activate the base station was 20·3 seconds. The mean defibrillator charge time was 5·5 seconds to 50 joules and 9·3 seconds to 360 joules. A total of 84 synchronised and 5 unsynchronised shocks were delivered satisfactorily. Lay persons were trained to use the patient unit, and were able to operate the device at home. This device has the potential for rapid defibrillation of patients who develop ventricular fibrillation outside hospital.

Une observation: garcon de 16 ans fortement drogue (4 a 6 l par semaine d'une colle contenant du toluene), presentant un infarctus anterieur du myocarde et une fibrillation ventriculaire

Despite extensive experimental use of t-PA in patients with acute myocardial infarction (AMI) a randomised dose ranging study has not yet been published. Fifty-five patients were randomised to BW t-PA 20 mg, 50 mg or 100 mg administered over 90 minutes. They received the drug 2.3 hours (range 0.3-4.3 hours) after the onset of AMI and underwent coronary arteriography to determine perfusion grade of the infarct related artery at 90 minutes. Responders were defined by TIMI perfusion grades 2 or 3. Response rates were: A logistic model fitted to the data showed the probability of reperfusion to increase in a dose related manner to 70%. Fibrinogen concentrations were measured in 30 patients and decreased to 83.6% of the preinfusion value at 90 minutes after 20 mg, to 76.2% after 50 mg and to 67.1% after 100 mg. There was a significant correlation between the dose of BW t-PA in megaunits/kg and consumption of fibrinogen at 90 minutes (p<0.05). This study indicates that thrombolysis with double chain t-PA proceeds in a dose related manner and that systemic fibrinogenolysis appears to be mild.

The single greatest cause of death in these islands is coronary artery disease. Over 60% of premature deaths from acute myocardial infarction occur within the first hour of the onset of symptoms and are thus termed "sudden". Ventricular fibrillation is the cause of sudden death in over 90% of patients with myocardial infarction who usually collapse at home. Rapid detection and correction are major determinants of the outcome of ventricular fibrillation.

There are many causes of pericardial effusion. After excluding lymphoma and leukaemia, cardiac, metabolic, infective or immunological disorders take precedence to malignancies in the differential diagnosis. Clinical pericardial effusions are uncommon in patients with carcinoma of the bronchus, and cardiac tamponade as a presenting symptom is very rare. We report three such patients and relate them to the spectrum of bronchial carcinoma.