DOMINANT LEFT VAGAL CONTROL OF THE HEART INDUCES HEART RATE IRREGULARITIES

In a pilot study on the effect of decreased baroreflex sensitivity in well-trained long distance speedskaters we showed that directly after the contest period the sensitivity was significantly decreased. One month later, the sensitivity increased to almost normal values. In the first week after the contest period, 4 of the 9 speedskaters showed (pre)syncope behavior in a tilt table experiment. This was seen several minutes after tilting, in ongoing decrease of bloodpressure even until 50 mmHg, while heart rate was paradoxically further decreased. After 2 weeks, this behavior disappeared. We attributed this decreased sensitivity and syncope incidents to the increased vagal activity in rest as found in these athletes. It is well known that the right vagal nerve mainly influences the rhythmogenesis of the SA-node, while the left branch predominantly influences the conductivity of the AV-node. These effects will be amplified in the case of well-trained physical condition. In a study on the changes in baroreflex sensitivity, we compared the effect of acute increase in arterial bloodpressure in rats by phenylephrine infusion in cases of unilateral vagotomy. We showed that in cases of right vagotomy, with only the left vagal branch intact, the PQ interval increases 5 to 10 times more than in cases of left vagotomy. Also, in the right vagotomy cases, much more AV-blocking was found. These results suggest that in cases of predominantly left vagal nerve activity on heart rate control, increased vagal activity induces heart rate irregularities, while under normal conditions no irregularities were observed. The acute increase in pressure only increases vagal activity acutely, so after ten to twenty seconds the heart rate is normal again. Therefore we studied the effect of right vagotomy in endurance trained rats. For this study we used 20 rats with both vagal nerves intact: 10 sedentary for control and 10 were trained at 80% of maximal VO2 during 6 months, (BV-rats), and 20 rats in which the right vagal nerve was cut: 10 sedentary and 10 trained (RV-rats). Weekly ECG's were recorded about 5 hours after training. In the BV-rats, heart rate decreased significantly compared to control after 2 weeks, stabilizing at about 20% lower after 5 weeks. In the RV-rats, it took 5 weeks before they had a significantly lower heart rate, and after 7 weeks they stabilized at about 10% lower heart rate. All rats except one, had PQ intervals between 40 and 55 ms during the experiment. In several RV-rats, irregularities in AV conduction were seen. In one RV-rat, the PQ interval was increased directly after vagotomy from 45 to 65 ms. In the fourth week this rat died suddenly during a recording session. The AV conduction changed from first degree block to complete block. Ventricular rate was decreased progressively from 300 beats/min to about 150. After 1 minutes the rat was reanimated. In the period hereafter no other "sudden death" was observed, although it is well possible that in the absence of the investigator also this sudden death pattern occurs, which than was interrupted by life saving activity of the sympathatic nerves system. This study showed that in case of predominantly control of the heart by the left vagal branch, under increased vagal activity due to training or acute increase in arterial pressure, sudden death can occur under normal physiological conditions, due to the decreased sensitivity of the baroreflex.