Familial sinuatrial disorder.

Greenwood and Finkelstein (I964), in a review of 223 patients including their own and those reported by other authors in the preceding 50 years, listed the aetiological factors resulting in sinuatrial block as increased vagal tone, infections in childhood, including rheumatic carditis, diphtheria, and influenza and, in adults, ischaemic heart disease and digitalis intoxication. However, in their series 20 per cent of the patients were reputed to be otherwise normal. It can be very difficult clinically to differentiate between sinuatrial block due to increased vagal tone, from that which is thought to be due to disease affecting the sinuatrial node and the specialized conducting tissue. Many patients with sinuatrial block present with symptoms associated with a severe bradycardia or transient cardiac asystole. In these the junctional atrioventricular specialized conducting tissue does not usually add its own rhythmic activity to maintain cardiac function. This suggests that during attacks of pronounced bradycardia the activity of the entire specialized conducting tissue is depressed. Since such attacks are commonly associated with intermittent bouts of tachycardia of all types originating from foci within this same conducting tissue, terms which have been used such as sinuatrial block and 'lazy sinus syndrome' (Ginks, I970) are not satisfactory. We suggest that a more suitable description of this syndrome is sinuatrial disorder. It is known that the vagus controls the electrical activity of the specialized conducting tissue in the dog (Brockman, I965). In man, the effect of vagal activity can vary in degree and, in our experience, is not the sole determinant of the depression of activity of the specialized