Electrode for recording direction of activation, conduction velocity, and monophasic action potential of myocardium.

Conduction velocity and recovery of excitability are central facets of reentry arrhythmias, and yet there are no satisfactory techniques for the simultaneous measurement of both from the same area of myocardium. We have developed an electrode arrangement that allows the simultaneous recording of conduction velocity, repolarization of the myocardium together with an index of dispersion, and direction of activation of the myocardium. Three silver/silver chloride electrodes were arranged in an equilateral triangle with a reference electrode at the center. From this arrangement three monophasic action potentials were recorded. From the time of arrival of the wavefront of activation at each electrode the direction of activation and conduction velocity were calculated in real time by a computer. There was a good correlation for the in vivo signals from the circular electrode and the new electrode both for conduction velocity (r = 0.99, P < 0.001) and for direction of activation (r = 0.99, P < 0.001). This new mathematical method and electrode design allows the simultaneous measurement of conduction velocity and direction and monophasic action potential, and this can give a beat-by-beat indication of wavelength and dispersion of action potential duration.

Contribution to heart rate variability by mechanoelectric feedback. Stretch of the sinoatrial node reduces heart rate variability.

BACKGROUND: Heart rate variability is an important prognostic indicator for sudden death. An increased risk of sudden death and arrhythmia is associated with reduced heart rate variability in heart failure. In heart failure, there is also dilatation of the atria, which raises the prospect that there could be some physiological basis to possibly link heart rate variability with atrial dilatation. We therefore investigated whether sustained atrial stretch could modulate heart rate variability directly. METHODS AND RESULTS: Pigs were anesthetized and their hearts exposed. A specially built device stretched the sinoatrial node before and after vagal section and then after administration of propranolol. Stretch of the sinoatrial node decreases heart rate variability in the following ways: The standard deviation of the beat-to-beat interval decreases (4.2 to 2.6 ms; P = .004), and the high-frequency components are reduced (control, 6.5 +/- 2.2 ms2, during stretch, 1.4 +/- 0.3 ms2, P = .003). After section of both vagi, the high-frequency components are reduced by stretch of the sinoatrial node (2.8 +/- 0.9 ms2 for control versus 1.2 +/- 0.3 ms2 during stretch; P = .05). Similarly, after both vagal section and beta-blockade, stretch of the sinoatrial node reduces the high-frequency components (10.6 +/- 3.5 ms2 for control verses 3.0 +/- 1.5 ms2 during stretch; P = .01). CONCLUSIONS: We conclude that stretch of the sinoatrial node reduces high-frequency heart rate variability. This may account in part for the reduced heart rate variability seen in clinical conditions in which the right atrium is dilated, such as congestive cardiac failure.