Increased AAI mode pacing threshold after termination of atrial fibrillation by acute administration of disopyramide phosphate.

AIMS: We studied changes in atrial pacing threshold after termination of atrial fibrillation (AF) by acute administration of disopyramide phosphate (DP) to elucidate the suitable setting for atrial pacing output before AF termination. METHODS AND RESULTS: Four patients with sick sinus syndrome implanted with AAI mode pacemakers were examined. Disopyramide phosphate (2 mg/kg body weight) was injected intravenously for termination of a total of eight AF episodes. The maximal pacing threshold after AF termination (5.2+/-0.8 V at 0.45 ms) was significantly higher than that at baseline (1.3+/-0.2 V at 0.45 ms; P<0.01) and the average increment was 433+/-68%. During a period free from AF, an acute administration of DP did not increase the atrial pacing threshold and serum disopyramide levels were not toxic. CONCLUSION: The increased atrial pacing threshold observed after AF termination cannot be explained by the action of DP alone. However, our results suggest that atrial pacing output should be set at the maximum value before DP is administered to induce AF termination in patients with AAI pacemaker-dependent bradyarrhythmias.

Intracellular sodium increase and susceptibility to ischaemia in hearts from type 2 diabetic db/db mice.

AIMS/HYPOTHESIS: An important determinant of sensitivity to ischaemia is altered ion homeostasis, especially disturbances in intracellular Na(+) (Na(i)(+)) handling. As no study has so far investigated this in type 2 diabetes, we examined susceptibility to ischaemia-reperfusion in isolated hearts from diabetic db/db and control db/+ mice and determined whether and to what extent the amount of (Na(i)(+)) increase during a transient period of ischaemia could contribute to functional alterations upon reperfusion. METHODS: Isovolumic hearts were exposed to 30-min global ischaemia and then reperfused. (23)Na nuclear magnetic resonance (NMR) spectroscopy was used to monitor[Formula: see text] and (31)P NMR spectroscopy to monitor intracellular pH (pH(i)). RESULTS: A higher duration of ventricular tachycardia and the degeneration of ventricular tachycardia into ventricular fibrillation were observed upon reperfusion in db/db hearts. The recovery of left ventricular developed pressure was reduced. The increase in[Formula: see text] induced by ischaemia was higher in db/db hearts than in control hearts, and the rate of pH(i) recovery was increased during reperfusion. The inhibition of Na(+)/H(+) exchange by cariporide significantly reduced (Na(i)(+)) gain at the end of ischaemia. This was associated with a lower incidence of ventricular tachycardia in both heart groups, and with an inhibition of the degeneration of ventricular tachycardia into ventricular fibrillation in db/db hearts. CONCLUSIONS/INTERPRETATION: These findings strongly support the hypothesis that increased (Na(i)(+)) plays a causative role in the enhanced sensitivity to ischaemia observed in db/db diabetic hearts.

[Effects of oral amezinium metilsulfate in patients with sick sinus syndrome].

The effects of amezinium metilsulfate (Risumic) were studied in patients with sick sinus syndrome. Four males and 11 females with clinical symptoms were treated with 0.5 mg/kg for 1 to 40 weeks. In all patients, the length of sinus pause observed during 24-hour Holter monitoring was longer than 2.0 sec, and/or the sinus node recovery time in the electrophysiologic study was longer than 2.0 sec. The effects were evaluated by Holter monitoring and standard electrocardiography. The total number of heart beats every 24 hours by Holter monitoring were significantly increased from 78,917 +/- 15,983 (mean +/- SD) to 85,753 +/- 17,849 beats after the treatment. The length of the sinus pause was significantly decreased from 3.89 +/- 1.24 to 2.36 +/- 1.45 sec. Patients with sinus node recovery time of less than 5.0 sec showed the effects especially clearly. The total number of premature ventricular contractions was decreased from 530 +/- 767 to 123 +/- 182 beats. The PQ, QRS and QTc intervals did not change. Only diastolic pressure was slightly increased. Clinical symptoms disappeared in almost all patients and the clinical courses were favorable. Amezinium metilsulfate, which stimulates the intrinsic sympathetic nervous system, increased total heart beat and shortened sinus pause in patients with sick sinus syndrome. Few side effects, such as arrhythmogenecity or increase of blood pressure were observed. These results show that amezinium metilsulfate is useful in the treatment of patients with sick sinus syndrome, if the disease is not so severe as to require implantation of a cardiac pacemaker.