Effects of head-up tilt-table test on the QT interval.

BACKGROUND: The QT interval shortens in response to sympathetic stimulation and its response to epinephrine infusion (in healthy individuals and patients with long QT syndrome) has been thoroughly studied. Head-up tilt-table (HUT) testing is an easy way to achieve brisk sympathetic stimulation. Yet, little is known about the response of the QT interval to HUT. METHODS: We reviewed the electrocardiograms of HUT tests performed at our institution and compare the heart rate, QT, and QTc obtained immediately after HUT with the rest values. RESULTS: The study group consisted of 41 patients (27 females and 14 males) aged 23.9 +/- 8.4 years. Head-up tilting led to a significant shortening of the RR interval (from 825 +/- 128 msec at rest phase to 712 +/- 130 msec in the upward tilt phase, P < 0.001) but only to a moderate shortening of the QT interval (from 363.7 +/- 27.9 msec during rest to 355 +/- 30.3 msec during upward tilt, P = 0.001). Since the RR interval shortened more than the QT interval, the QTc actually increased (from 403 +/- 21.5 msec during rest phase to 423.2 +/- 27.4 msec during upward tilt, P < 0.001). The QTc value measured for the upward tilt position was longer than the resting QTc value in 33 of 41 patients. Of those, 4 male patients and 2 female patients developed upward-tilt QTc values above what would be considered abnormal at rest. CONCLUSIONS: During HUT the QT shortens less than the RR interval. Consequently, the QTc increases during head-up tilt.

Calcium channel blockers and beta-blockers versus beta-blockers alone for preventing exercise-induced arrhythmias in catecholaminergic polymorphic ventricular tachycardia.

BACKGROUND: The mainstay of therapy for catecholaminergic polymorphic ventricular tachycardia (CPVT) is maximal doses of beta-blockers. However, although beta-blockers prevent exercise-induced ventricular tachycardia (VT), most patients continue to have ventricular ectopy during exercise, and some studies report high mortality rates despite beta-blockade. OBJECTIVE: The purpose of this study was to investigate whether combining a calcium channel blocker with beta-blockers would prevent ventricular arrhythmias during exercise better than beta-blockers alone since the mutations causing CPVT lead to intracellular calcium overload. METHODS: Five patients with CPVT and one with polymorphic VT (PVT) and hypertrophic cardiomyopathy who had exercise-induced ventricular ectopy despite beta-blocker therapy were studied. Symptom-limited exercise was first performed during maximal beta-blocker therapy and repeated after addition of oral verapamil. RESULTS: When comparing exercise during beta-blockers with exercise during beta-blockers + verapamil, exercise-induced arrhythmias were reduced: (1) Three patients had nonsustained VT on beta-blockers, and none of them had VT on combination therapy. (2) The number of ventricular ectopics during the whole exercise test went down from 78 +/- 59 beats to 6 +/- 8 beats; the ratio of ventricular ectopic to sinus beats during the 10-second period recorded at the time of the worst ventricular arrhythmia went down from 0.9 +/- 0.4 to 0.2 +/- 0.2. One patient with recurrent spontaneous VT leading to multiple shocks from her implanted cardioverter-defibrillator (ICD) despite maximal beta-blocker therapy (14 ICD shocks over 6 months while on beta-blockers) has remained free of arrhythmias (for 7 months) since the addition of verapamil therapy. CONCLUSIONS: This preliminary evidence suggests that beta-blockers and calcium blockers could be better than beta-blockers alone for preventing exercise-induced arrhythmias in CPVT.

Indomethacin-induced early patent ductus arteriosus closure cannot be predicted by a decrease in pulse pressure.

Wide pulse pressure is considered to be a sign of patent ductus arteriosus (PDA). We tested the hypothesis that, following indomethacin therapy, PDA closure is associated with a significant decrease in pulse pressure. Thirty-two ventilated preterm infants were echocardiographically diagnosed within the first 24 hours of life with PDA. Systolic, diastolic, and mean arterial blood pressures were measured prior to indomethacin treatment and after echocardiographically confirmed PDA closure. Following PDA closure, systolic and diastolic blood pressures and mean arterial pressure increased significantly without a significant change of pulse pressure (17 +/- 7 to 20 +/- 12 torr). We conclude that in preterm infants with PDA, systolic, diastolic, and mean arterial blood pressures increase significantly within first few days of life. Pulse pressure does not appear to be affected by early PDA closure. We speculate that high pulmonary resistance in the first days of life prevents significant diastolic aortic runoff and leaves pulse pressure unaffected by PDA, as well as by its closure.