The relationship between HRV and parasympathetic effect is best described by a function in which there is an ascending limb where HRV increases as parasympathetic effect increases until it reaches a plateau level; HRV then decreases as parasympathetic effect increases. Because there is marked interindividual variation in this relationship, differences in HRV between individuals may reflect differences in this relationship and/or differences in autonomic effects.

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Within the acceptable noise range for SAECG, lower noise results in longer QRSd and larger variance, suggesting that more accurate recordings may have less reproducibility. The random timing of noise relative to signal results in the distribution/variance of repeated measurements. Statistical strategies may be used to reduce some of this variance and may enhance the diagnostic utility of SAECG.

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These data confirm that HRV reflects the character of parasympathetic modulation of the heart rate rather than parasympathetic tone per se. Furthermore, this study identifies two distinct physiologic explanations for the finding of low HRV, namely, diminished vagal discharge and resistance of cardiac muscarinic receptors to vagal discharge. Further delineation of the relationships between parasympathetic tone and HRV will allow for better understanding of the pathophysiologic derangements associated with low HRV.

Background: Although gender differences in the corrected QT interval (QT,) have been described, gender differences in QT dispersion (QTd) have not been carefully evaluated. This study was designed to measure QTd in 22 young healthy women and in 20 healthy men.Methods and Results: Twelve-lead ECGs were recorded at rest and following double autonomic blockade with atropine 0.04 mg/kg and propranolol 0.2 mg/kg during the menstrual, follicular, and luteal phases of the menstrual cycle, which was confirmed by hormone levels. Men were studied during three separate visits as controls. In women, there was no difference in QTd among the three phases of the menstrual cycle, and thus all three visits were pooled for comparison with men. The 12-lead QT dispersion (maximumminimum QT) was larger in men than in women at baseline (41 t 17 ms vs 35 5 16 ms), and this difference tended to decrease after double autonomic blockade (35 t 14 ms vs 32 2 11 ms). The standard deviation of the QT interval across the 12 leads was larger in men than in women at baseline (12.6 ? 4.5 vs 10.8 2 4.1), and this difference was no longer significant after double autonomic blockade (10.4 2 4.4 vs 10.1 ? 3.5). QT dispersion was significantly reduced by autonomic blockade (P < 0.05). Conclusions:(1) Double autonomic blockade slightly reduces QTd. (2) QTd is higher in men than in women at baseline but more similar after autonomic blockade. These findings may contribute to the gender difference in the corrected QT interval. (3) Increased female QTd is not the mechanism of increased female susceptibility to torsade de pointes. The clinical implications of gender differences in QTd and QT, remain to be defined.

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