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The members of the Task Force on Sudden Death dedicate this paper to the memory of our former friend and colleague, Professor Ronald W. F. Campbell. Ronnie spent his life working in the field of sudden cardiac death; he contributed much and helped many. But his own life fell victim to this very problem, sadly illustrating its unexpected nature. With Ronnie’s memory in mind the Task Force has worked diligently to describe the extent of our expanding knowledge in this field, hoping that our small contribution might help to appease his sad and sudden death.

Atrial fibrillation, a commonly encountered arrhythmia, has in recent years, been the subject of increased interest and intensive clinical research. There is also increasing awareness that atrial fibrillation is a major cause of embolic events which in 75% of cases are complicated by cerebrovascular accidents[1,2]. Atrial fibrillation is often associated with heart disease but a significant proportion of patients (about 30%) have no detectable heart disease[3]. Symptoms, occasionally disabling, haemo-dynamic impairment and a decrease in life expectancy are among the untoward effects of atrial fibrillation, resulting in an important morbidity, mortality and an increased cost for the health care provider[4]. The Working Group of Arrhythmias of the European Society of Cardiology created a Study Group on Atrial Fibrillation in order to establish recommen-dations for the better management of this arrhythmia and to promote multicentre studies. The purpose of this paper is to briefly outline the state of our knowledge on the clinical presentation, the causes, the mechanisms and therapeutic approaches currently available and to propose recommendations for management. Although atrial flutter can coexist with atrial fibrillation, it is considered a different arrhythmia and will not be covered in the present paper.

Indoramin is a selective post-synaptic alpha blocker. Animal experiments had shown that it has antiarrhythmic effects, but whether this is due to its alpha blocking effect or some other mechanism is not known. Fifteen patients (10 males) underwent electrophysiological investigations before and 15 minutes after intravenous indoramin injection (0.2-0.5 mg kg-1). The plasma level of indoramin was measured and the patients were divided into two groups: group 1 (8 patients) whose plasma level was less than 100 micrograms ml-1 (average 72 micrograms ml-1) and group 2 (7 patients) whose plasma level was more than 100 micrograms ml-1 (average 151 micrograms ml-1). In both groups there was a significant drop in the systolic blood pressure after indoramin (129 +/- 22 to 111 +/- 23 mmHg, P less than 0.001). There was a marked improvement in the sinus node recovery time in group 1 only (253 +/- 92 to 163 +/- 40 ms, P less than 0.01). Similarly there was a decrease in AH interval during fixed rate atrial pacing in group 1 only (128 +/- 33 to 100 +/- 37 ms, P less than 0.05) and a significant decrease in the Wenckebach cycle length after indoramin in group 1 only (372 +/- 85 to 347 +/- 74 ms, P less than 0.05). At the atrial level there were no significant effects in either group but there was a significant increase in the ventricular effective refractory period in group 2 (231 +/- 35 to 264 +/- 64 ms, P less than 0.05) but no change in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)