The mechanism of the occurrence of this conductive disorder is due to the fact that the nucleus of the vagus nerve is rapidly and completely inhibited by exposure to TNFa because thalidomide inhibits the expression and activity of TNF-a, thus inducing hyperactivity of the parasympathetic system and bradycardia [1].

Clinical trials have shown that thalidomide induces mild bradycardia (in 25 to 50% cases) and in some cases it can trigger severe bradycardia causing syncope or hypotension, only 1 to 3% of these patients needs a pacemaker [2].

Treatment with thalidomide should be started at a dose of 100-200 mg / day and increased weekly by 50-100 mg / day until the final dose of 400-800 mg / day is reached. The maximum tolerated dose should be administered. Patients receiving daily doses of 200 mg or less appear to tolerate treatment well with few side effects. However, almost all patients taking more than 400 mg / day have thalidomide-related toxicity. The latter is usually given at bedtime to minimize drowsiness and fatigue [1,3].

In our patient case, the maximum dose of thalidomide was 50 mg / day, the heart rate decreased sharply to 35 beats/min, resulting in dizziness, physical asthenia and dyspnea, the electrocardiogram performed, was in favor of sinus dysfunction. This latter could be mild, moderate or severe.

In severe cases, temporary stimulation is indicated [3]. In some patients, the sinus dysfunction would require a permanent pacemaker like in our patient whereas some patient could just be managed by discontinuing the thalidomide.

In a Spanish series carried out on patients suffering from hematological pathologies who were put on thalidomide 15.1% presented a sinus bradycardia under a daily dose going from 100 to 300 mg / day with a duration varying from 1 to 18 months. In all affected cases, the electrocardiogram showed sinus bradycardia with a heart rate between 32 and 48 beats per minute. The recovery time from normal heart rate ranged from 12 to 21 days after stopping thalidomide [4].

Our patient received thalidomide only for 20 days and at a dose of 50 mg / day, however, he presented with poorly tolerated persistent sinus dysfunction which ultimately required the implantation of a pacemaker. In the literature, at least a daily dose of 100 mg of thalidomide was required to cause bradycardia when our patient was only on 50 mg. Would this low threshold in our patient be accentuated by moderate aortic stenosis?

It should be noted that the prescription of thalidomide in patients suffering from cardiovascular disease whatever the etiology must be done with caution [5].

So, if patients are on thalidomide treatment, concomitant use of beta- blockers should be avoided and the EKG should be monitored regularly. Atropine helps improve the clinical signs associated with thalidomide-induced bradycardia.