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To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2-8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (-40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 +/- 3 to 14 +/- 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 +/- 18 to 65 +/- 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 +/- 16 and 42 +/- 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5-10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias.

The objective of this study was to examine the antiarrhythmic mechanisms of magnesium (Mg). The 12 patients who were selected for the study were given 12 mmol Mg sulphate followed by an infusion of 8 mmol/h. Ventricular effective refractory period (VERP). monophasic action potential duration at 50% and 90% repolarization during spontaneous rhythm (MAPD50, MAPD90) and atrial pacing at a cycle length of 600 ms (MAPD(50)600, MAPD(90)600) were measured before and after the intervention. Plasma magnesium concentration rose from 0.83 +/- 0.05 to 1.85 +/- 0.24 mmol/l (p < 0.001). Shortening of MAPD(50) (250 +/- 45 vs 240 +/- 46 ms; p < 0.05), MAPD(90) (294 +/- 42 vs 283 +/- 41 ms; p < 0.05) and shortening of sinus cycle length (SCL) (783 +/- 153 vs 742 +/- 160 ms; p < 0.01) were detected. During controlled cycle length, magnesium decreased MAPD(50)600 (230 +/- 28 vs 221 +/- 28 ms; p < 0.01), MAPD(90)600 (274 +/- 25 vs 261 +/- 29 ms; p < 0.01) and VERP (247 +/- 25 vs 241 +/- 21 ms: p < 0.05). QRS duration, QT interval and blood pressure remained unchanged. The change in SCL correlated with the change in MAPD(50) (r = 0.58; p < 0.05) and MAPD(90) (r = 0.55; p = 0.06 ) but not with MAPD(50)600, MAPD(90)600 or VERP. Magnesium acutely shortens ventricular monophasic action potential duration and refractoriness. This effect is partly mediated by mechanisms that increase heart rate. The reductions might bring salutary effects in arrhythmias evoked by prolonged repolarization.