After exposure to hepatitis B (HB) virus, passive immunisation with HB immune globulin is widely used for protection while active immunity is induced by conventional vaccination regimens. Protective antibody titres can be achieved much more quickly with accelerated vaccination, and the role of passive immunisation may need to be reconsidered.

Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process of mechanoelectric feedback. Moreover, when changes in cardiac loading similar to those seen in heart failure are produced experimentally in normal heart, there is a greater tendency to arrhythmogenesis. The intimate relation between changes in mechanical function and arrhythmia in heart failure could account for the lack of effect of most conventional antiarrhythmic drugs on arrhythmogenesis, and the beneficial effect of peripheral vasodilators. This paper argues that mechanically induced changes in electrophysiology are very important in the development of arrhythmia in cardiac failure; there may be no need to implicate other mechanisms, such as relative ischaemia, metabolic changes, or changes in sympathetic tone.