View clinical trials related to Cardiac Repolarization.
Filter by:This will be a Phase 1, single-center, 2-part study in healthy subjects. Parts 1 and 2 need to be conducted in sequential order.
For many years droperidol has been used in prophylaxis and therapy of PONV. Information that it can provoke disorders of cardiac ventricular rhythm reduced its popularity. However those data didn't base on solid examinations confirming torsadogenic action of droperidol. It is known that droperidol prolongs time of repolarisation, but there wasn't any data confirming its impact on transmural dispersion of repolarisation. Only estimation both of those actions in one time allows to define for sure arrhythmogenic role of droperidol. The aim of this study was to answer the questions: 6. Does droperidol make an significant prolongation of heart repolarisation, expressed as corrected QT interval? 1. Does droperidol cause increase of transmural dispersion of repolarisation? 2. Does possible torsadogenic acting of droperidol depend on dose of drug? 3. Does ondansetron cause changes of electrical heart function, suggesting its possibilities to induce TdP tachycardia? 4. What is torsadogenic potential of droperidol and ondansetron used in prophylaxis PONV in people not suffering from cardiovascular diseases?
The purpose of this study is to evaluate the effect of EVP-6124 at therapeutic and supratherapeutic concentrations on cardiac repolarization in healthy subjects.
The objective of this study is to evaluate the effect of repeat oral dosing of ASP1941 on electrocardiogram (ECG) measurements.
Background. In congenital long QT syndrome type 1 (LQT1), episodes of ventricular tachycardia are usually triggered by exercise and can be prevented in most patients by beta-blocker therapy. In addition, LQT1 associated with a normal resting QT interval can be unmasked by the abnormal QT response to exercise testing (failure of the QT interval to shorten normally). Preliminary data from our laboratory show that the exercise QT intervals of patients with LQT1 are partially normalized by beta-blocker therapy. It is still currently not known if beta-blockers modify the QT/heart rate relationship (a primary effect on repolarization) or if the "normalizing" effect is due to the inability of subjects on beta-blockers to attain sufficiently high workloads (due to reduced heart rate) for prolongation to occur. Moreover, the physiologic response of the exercise QT interval to beta-blockers in healthy control subjects is not known. Objective. The objective of this study is to define the impact of beta-blocker therapy on the QT response to exercise and recovery in normal subjects. Methods. Approximately 36 healthy adult subjects age-matched to previously studied LQT1 subjects will undergo 1) screening history, 2) two weeks of beta-blocker therapy ending in an exercise test, and 3) two weeks of placebo therapy ending in an exercise test. Beta blocker and placebo will be given in random order in a double-blind fashion. The QT response to exercise and recovery will be compared between drug-free and beta-blocker-treated states. These data will be compared to those previously collected for LQT1 subjects. Implications. These results will provide new information about the effect of beta-blocker therapy on repolarization parameters in normal subjects, and will provide a context in which to interpret the previous findings that beta-blocker administration modifies the QT response to exercise in LQT1 subjects.