[Torsades de pointe with spiramycine and metiquazine therapy. Apropos of a case]. / Torsades de pointes sous traitement par spiramycine et méquitazine. A propos d'un cas.

The authors report the case of a 21 year old woman with a congenital long Q7 syndrome who had several syncopal attacks at least one of which was caused by torsades de pointe. This sudden complication was attributed to the simultaneous prescription of Spiramycine and Mequitazine over a 48 hour period. These two drugs are not considered to be predisposing factors for torsades de pointe despite the fact that they belong to two families of drugs which can trigger this type of arrhythmia. The withdrawal of this treatment led to the complete regression of the syncopal episodes with a follow-up of two years and a significant shortening of the initial QTc interval which remained, nevertheless, longer than normal. This case underlines the potential risks of drug associations of these two families of drugs, especially in patients with the congenital long Qt syndrome.

Atrial natriuretic factor release during exercise in patients successively paced in DDD and rate matched ventricular pacing.

Dual chamber pacemakers were implanted in nine patients with permanent second or third degree AV block (eight had complete retrograde block). Two identical exercise tests were performed after at least 1 month after implantation. During the first test (T1) the pacemaker was programmed to the DDD mode and heart rates were recorded every 15 to 30 seconds during exercise and 30 minutes after exercise. Following 30 minutes of rest, the implanted pacemaker was programmed to the VVT mode and driven by an external pacemaker via a skin electrode. The second exercise test (T2) was then performed and the rate of the external pacemaker was progressively changed to reproduce exactly the rate observed during T1 at the same exercise stress. Atrial natriuretic factor (ANF) levels were determined at rest, at regular intervals during exercise, and 30 minutes after exercise. ANF levels and release were statistically higher during rate matched ventricular, than DDD pacing. It is concluded that preservation of AV synchrony reduces ANF release induced by heart rate acceleration during exercise.