Neurally mediated cardiac syncope: autonomic modulation after normal saline infusion.

OBJECTIVES: This study assessed the heart variability response to orthostatic stress during tilt table testing before and after normal saline administration. BACKGROUND: The efficacy of sodium chloride and mineralocortoid in the treatment of neurally mediated cardiac syncope is attributed to intravascular volume expansion; however, their modulation of autonomic nervous system activity has not been evaluated. METHODS: Heart rate variability analysis was performed on 12 adolescents with a history of syncope or presyncope (mean age 15.2+/-0.7 years) during tilt table testing. Subjects were upright 80 degrees for 30 min or until syncope. After normal saline administration, the patient was returned upright for 30 min. Heart rate variability analysis data were analyzed by an autoregression model (Burg method). RESULTS: All subjects reproducibly developed syncope during control tilt table testing; median time to syncope was 9.4+/-2.1 min. After normal saline infusion, none of the subjects developed syncope after 30 min upright. In the control tilt, there was an initial increase followed by a progressive decrease in low frequency power until syncope. Repeat tilt after normal saline administration demonstrates that low frequency power increased but the magnitude of initial change was blunted when compared with control. In addition, low frequency power increased during normal saline tilt sequence compared with the control tilt, during which it decreased. CONCLUSIONS: Normal saline blunted low frequency power stimulation and prevented paradoxical low frequency power (sympathetic) withdrawal. Increasing intravascular volume with normal saline alters autonomic responses that may trigger neurally mediated syncope reflexes.

Sex hormones prolong the QT interval and downregulate potassium channel expression in the rabbit heart.

BACKGROUND: Sex hormones are known to exert direct and indirect effects on cardiovascular function, but their effects on cardiac repolarization have not been elucidated. The repolarization phase of the cardiac action potential or QT interval of the ECG is regulated largely by potassium channels such as the delayed rectifier currents HK2 and IsK. METHODS AND RESULTS: The effects of ovariectomy (OVX) and estradiol (E2) or dihydrotestosterone (DHT) treatment were evaluated on HK2, HERG, and IsK mRNA levels, QT duration, and quinidine-induced changes in QT interval in isolated rabbit hearts. HK2 and 0.7-kilobase IsK mRNA were downregulated in cardiac ventricular tissue from OVX rabbits treated with either E2 or DHT. The QT interval was prolonged in E2- and DHT-treated animals (OVX + vehicle, 223 +/- 6 ms; OVX + DHT, 236 +/- 10 ms; and OVX + DHT, 245 +/- 6 ms; P < .05). CONCLUSIONS: The association between hormone-induced changes in baseline QT interval and the mRNA level for these channels suggests that sex hormones may play a critical role in regulating cardiac repolarization. However, the changes in baseline QT and potassium channel mRNA after hormone treatment were not concordant with the changes in QT interval after the infusion of quinidine, after which E2-treated animals responded similarly to controls (18.4 +/- 4.6% and 19.3 +/- 4.6% increase in QT interval, respectively) and DHT-treated animals exhibited less QT prolongation (11.4 +/- 3.8% increase; P < .03).