Key result
Single short-coupled beat drives ~60% of the ventricular refractory shortening seen with eight beats.
Why the study?
The relationship between cycle length and refractory periods in human atrium, AV node, and ventricle and the effect of sudden cycle length changes on refractoriness require clarification.
Does a single beat at a shorter cycle length produce the same change in refractory periods as eight beats at a shorter cycle length in human cardiac tissue?
Does a single beat at a shorter cycle length produce the same change in refractory periods as eight beats at a shorter cycle length in human cardiac tissue?
Answers are grounded in this paper and cite their sources.
A single premature beat produces significant but incomplete adaptation of ventricular refractoriness compared to steady-state changes, providing insight into the mechanisms of tachycardia initiation.
In the steady state, the refractory periods of the human atrium, atrioventricular (AV) node, and ventricle are a function of cycle length.We compared the change in refractoriness that occurred when these refractory periods were measured after eight beats at a shorter cycle length with the change that occurred when these refractory periods were measured after a single beat at the shorter cycle length.For a decrease in cycle length of 235 ± 63 msec, the atrial effective refractory period shortened 31 ± 24 msec (p < 0.01) when measured after eight beats at the shorter cycle length and 26 ± 24 msec (p < 0.01) when measured after a single beat at the shorter cycle length.Similar changes were seen in atrial functional refractory period.For a decrease in cycle length of 214 ± 63 msec, the AV nodal effective refractory period increased 30 ± 39 msec (p < 0.05) when measured after eight beats and 31 ± 34 msec (p < 0.05) when measured after a single beat.The AV nodal functional refractory period showed moderate shortening with decreases in cycle length, both when measured after eight beats and when measured after a single beat (p = NS).For both the atrium and AV node, there was no significant difference between the change in refractoriness after a single beat at the shorter cycle length and after eight beats at the shorter cycle length.For a decrease in cycle length of 175 ± 52 msec, the ventricular effective refractory period shortened 26 ± 10 msec (p < 0.01) when measured after eight beats and 16 ± 12 msec (p < 0.01) when measured after a single beat at the shorter cycle length.Thus, a single beat at the shorter interval produced 60% of the shortening of refractoriness produced by eight beats at the shorter interval (p < 0.01).These findings have implications for the performance and interpretation of stimula- tion studies and provide insight into the mechanism of initiation of tachycardia by premature beats.REFRACTORINESS of cardiac tissue is a function of cycle length.This relationship, first recognized in isolated heart tissue, has subsequently been shown in both the canine and human atrium, atrioventricular (AV) node and ventricles.'-"There is some con- troversy as to whether changes in refractory periods in the canine heart occur after a single beat at the new
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Wiener et al. (1981) studied this question. Single beat at a shorter cycle length vs. Eight beats at a shorter cycle length was evaluated on Change in ventricular effective refractory period (msec) (p=<0.01). A single beat at a shorter cycle length produced 60% of the ventricular refractoriness shortening produced by eight beats (16 vs 26 msec; p<0.01), with no significant difference in the atrium or AV node.
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