The occurrence of paradoxical bradycardia was a rare finding during isoprenaline infusion (7%); sinus or junctional bradycardia was a sign of hypervagotonia, but was without clinical significance in 35% of these patients. The development of second-degree AV block was always pathological and associated with AV conduction disturbances, which occurred spontaneously during exercise. Isoprenaline infusion appeared to be a simple means to detect organic AV conduction disturbance in patients complaining of exercise or stress-related dizziness/syncope and unable to perform exercise test.

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Flecainide is an effective antiarrhythmic drug, but when administered orally in patients with left ventricular (LV) dysfunction, its effect on LV function is unknown. To assess the effects of flecainide on cardiac function, LV ejection fraction (LVEF) was measured by radionuclide ventriculography in 36 patients with LV dysfunction (LVEF less than or equal to 40%), prior to, and 7 days after, drug therapy was initiated. To analyse the possibility of a dose-dependent effect on LVEF, 18 patients received 200 mg day-1 of flecainide and 18 patients with an identical initial LVEF (27 +/- 8 vs 27 +/- 9) (NS) received 300 mg day-1. The study was stopped in 7 patients because of severe cardiac adverse effects; in these patients the LVEF was significantly lower (15 +/- 7) than that of the 29 patients who completed the protocol (27 +/- 8) (P less than 0.01). In patients who completed the protocol, there was no significant change in LVEF either with a daily dosage of flecainide of 200 mg day-1 (27 +/- 8 vs 27 +/- 8) or with 300 mg day-1 (27 +/- 9 vs 28 +/- 13). Thus, in the patients with LV dysfunction studied, oral flecainide did not significantly affect LV function either with a low or with the usual daily dosage. However, in patients with severe impairment of LV function (LVEF less than 30%) flecainide must be used carefully owing to a higher incidence of adverse effects on cardiac rhythm.

Rapid ventricular pacing (VP) reproduces neurohumoral variations associated with ventricular tachycardia. This study was set up to analyse the mechanisms that cause changes in sinus heart rate after rapid VP and to find the clinical factors that adapt sinus heart rate to VP, and the clinical value of the method. Rapid VP was performed in 356 patients aged 15 to 86 years, in increments of 10 beats, at progressively faster rates every 10 s up to 200 beats.min-1. Group I comprised 122 patients with no underlying heart disease; group II comprised 234 patients with an underlying heart disease. The sinus heart rate (HR) was initially accelerated (SR1), in comparison with the basal sinus HR, for 2 to 5 s (90.5 beats.min +/- 21 vs 71 +/- 19 in group I, 89.5 +/- 26 vs 76 +/- 16 in group II). Five seconds later, there was a decrease in HR (SR2) which was slower than the basal HR (62 beats.min +/- 22 in group I, 75 +/- 15 in group II). The variations in HR, defined as SR1-SR2/SR1, were significantly higher in group I than group II: 31 +/- 18% vs 19 +/- 15%, (P < 0.001). With the injection of 2 mg atropine in 14 group I patients the variations in HR were suppressed after ventricular pacing. When oral beta-blockers were administered to 21 group I patients, there were still significant changes in HR. The changes in HR were reproducible during electrophysiological study.(ABSTRACT TRUNCATED AT 250 WORDS)

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