SUMMARY The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS <0-12 s) adenosine (2-5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS > 0 12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses ofover 2 s in 16% of patients, the longest pause being 6*1 s.Adenosine is ofvalue in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence of arrhythmia.Adenosine is a naturally occurring, rapidly metabolised compound that produces transient atrioventricular nodal block in humans when injected intravenously.' It can terminate reentrant supraventricular tachycardias that involve the atrioventricular node,' while in tachycardias of atrial origin it may be of diagnostic value, because adenosine induced atrioventricular block slows the ventricular rate and reveals the unaffected atrial arrhythmia.2 Such diagnostic and therapeutic effects of adenosine should be of most value in broad complex Requests for reprints to Dr A C Rankin,

SUMMARY The effects of different types of adrenoreceptor blocking agents on portal venous pressure were studied in patients with cirrhosis and portal hypertension. Oral atenolol (selective P1 blocker), propranolol (non-selective 13I and 12 blocker), and prazosin (aX blocker) were compared in three groups of eight patients. Haemodynamic measurements were made before and after two or three and eight weeks of therapy. The dose of beta blockers was sufficient to reduce the exercise heart rate by more than 25%. Propranolol and prazosin produced a sustained reduction in the mean portohepatic venous pressure gradient of the order of 25% and 18% respectively. The cardiac index was significantly reduced by propranolol but not altered by prazosin. Atenolol produced an early reduction in portohepatic venous pressure which, although not sustained, showed a good correlation with reduction in cardiac index. No such relationship was found with propranolol. All three drugs were well tolerated by these patients with advanced cirrhosis. Therefore propranolol and prazosin have proved to be effective agents for the reduction of portal venous pressure.Lebrec and colleagues have suggested that propranolol can be used in patients with cirrhosis to lower portal venous pressure and thereby reduce the incidence of further variceal haemorrhage.1 2 Portal venous pressure is determined by the product of the outflow resistance and the portal venous blood flow. Outflow resistance is increased in cirrhosis because of the mechanical compression of portal venous radicles and thereafter somewhat reduced by the development of portal-systemic collateral venous flow. Animal studies have shown that the portal vein contains a adrenoreceptors only and no ,3 receptors and its tone is partly maintained by adrenoreceptor stimulation.3 Normally the portal vein shows a linear pressure-blood flow relationship with no evidence of autoregulation, such as is seen in the heart or kidney, whereby blood flow is maintained over a range of pressure changes.3 Propranolol is thought to act by a 1,3 blocking effect reducing cardiac output, hence reducing splanchnic blood

SummaryBRL 26921 is the p-anisoyl derivative of the primary streptokinase-human plasminogen complex in which the acyl group is specifically located at the catalytic centre of the enzyme. Doses of BRL 26921 ranging from 5 mg to 25 mg were given intravenously or into a coronary artery to 12 patients with acute myocardial infarction. The complex was well tolerated and produced no serious bleeding. Coronary artery reperfusion was demonstrated angiographically in three patients.In most patients, fibrinogen, plasminogen, α2 antiplasmin and a2 macroglobulin levels fell and the level of fibrinogen degradation products increased acutely post treatment indicating systemic fibrinolytic activation. The degree of this activation was variable but was profound in some. It appeared to be dose related and modified by the presence of streptokinase antibodies. BRL 26921 appears less “selectively” thrombolytic in patients than had been expected from animal models.

Adenosine may be of therapeutic and diagnostic value in the emergency management of arrhythmias. It causes transient atrioventricular nodal block and thus ends paroxysmal supraventricular tachycardias that involve the atrioventricular node. Also, it may uncover underlying atrial arrhythmias by slowing the ventricular response. Its duration of action is brief and serious adverse effects have not been reported. A 12 year old patient with atrial flutter is presented, in whom intravenous adenosine was followed by acceleration of the heart rate to a potentially dangerous arrhythmia. (Br Heart J 1993;69:263-265) Adenosine is an endogenous purine nucleoside that causes atrioventricular nodal block when injected intravenously.' 2 It is effective, therefore, to end paroxysmal supraventricular tachycardias that have a re-entrant circuit that includes the atrioventricular node.Y4 With atrial arrhythmias, such as atrial flutter, adenosine induced atrioventricular nodal block may be of diagnostic value by slowing the ventricular response to show the underlying atrial tachyarrhythmia.3-5 Transient side effects, including chest discomfort, flushing, and dyspnoea, are common, but serious adverse effects of adenosine have not been reported. This may be attributable to its extreme brevity of action because of rapid metabolism and removal from blood.7 We report a case where intravenous administration of adenosine was followed by an increase in the ventricular response to atrial flutter, with a resultant potentially life threatening arrhythmia. Case report A 12 year old boy was admitted to hospital after an episode of syncope. He had a history of Mustard repair of transposition of the great arteries at the age of 10 months. After the repair of an atrial baffle leak one year before the present admission, he had undergone implantation of a permanent ventricular pacemaker (Medtronic "Activitrax II", VVI-R) for symptomatic sinus node dysfunction. He had continued to complain of episodes of dizziness, the aetiology of which was not identified.On admission he was well with no evidence of heart failure. Heart rate was 120 beats/min and he was normotensive, with a blood pressure of 109/58 mm Hg. An electrocardiogram showed a narrow complex tachycardia. To clarify the diagnosis of the tachycardia, and possibly restore normal rhythm, adenosine was given intravenously with incremental boluses of 0 1, 02, and 0-4 mg/kg (4, 8, and 16 mg). Transient symptoms of increasing severity (flushing, non-specific malaise) were reported with each dose. After the 8 mg dose of adenosine, the ventricular rate briefly slowed to 86 beats/min (for four seconds) but then increased to 235 beats/min. This rapid rate persisted for three minutes before settling to 120 beats/min. A further dose (16 mg) was given. This slowed the ventricular rate so that the pacemaker paced the ventricle at 60 beats/min for 10 seconds ( fig IA). During this period of ventricular slowing, underlying atrial flutter waves at 280 beats/min were apparent. The ventricular respons...

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