| The precise relationship between test substance-induced delay of ventricular repolarization and risk of proarrhythmia is not known. |
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| The assessment of the effects of pharmaceuticals on ventricular repolarization and proarrhythmic risk is the subject of active investigation. |
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| Ventricular repolarization abnormalities may have been contributory factors. |
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| Dolasetron appears to prolong both depolarization and, to a lesser extent, repolarization time. |
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| An abnormality of cardiac muscle repolarization, defined as the time from Q wave deflection to the end of T wave on an electrocardiogram. |
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| Potassium nitrate inhibits repolarization of sensory nerve endings, thereby reducing the pain response to stimulation. |
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| Ion exchange is required for depolarization, reestablishing intracellular homeostasis, and cell repolarization. |
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| Ventricular repolarization, determined by the duration of the cardiac action potential, is a complex physiological process. |
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| There are, therefore, both depolarization and repolarization waves represented in the electrocardiogram. |
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| Time intervals of depolarization and repolarization were measured using optical action potentials. |
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| Paramyotonia congenita with an SCN4A mutation affecting cardiac repolarization. |
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| After repolarization there is a period during which a second action potential cannot be initiated, no matter how large a stimulus current is applied to the neuron. |
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| The cycle of depolarization and repolarization in the heart is known as the cardiac action potential and occurs approximately 60 times every minute. |
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| Intact animal models allow investigation of ventricular repolarization or associated arrhythmias where integrated effects on the full complement of ion channel and cell types are assessed. |
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| This guidance document describes a non-clinical testing strategy for assessing the potential of a test substance to delay ventricular repolarization. |
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| Species differences in terms of which cardiac ion channels contribute to cardiac repolarization and to the duration of the action potential should be considered in selecting a test system. |
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| Evidence of risk is the overall conclusion from the integrated risk assessment for a test substance to delay ventricular repolarization and prolong QT interval in humans. |
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| This document provides recommendations to sponsors concerning the design, conduct, analysis, and interpretation of clinical studies to assess the potential of a drug to delay cardiac repolarization. |
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| Dispersion of QT interval was studied as an index of repolarization heterogeneity in hypertensive men. |
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| A prolonged QT interval reflects abnormal repolarization and may lead to torsades de pointes and sudden cardiac death. |
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| Changes in this subunit or Klf15 can affect the potassium current that governs repolarization of the cardiac myocyte. |
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| By preventing repolarization of the nerve ending, the postsynaptic ending becomes refractory and unexcitable, resulting in flaccid muscles. |
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| In order to reliably assess the duration of ventricular repolarization and to minimize the influence of changing heart rate on the QT interval, it is necessary to carry out frequency correction of the QT interval. |
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| Atrial repolarization was not present as Ta wave in the PR segment. |
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| The electrocardiogram showed diffuse repolarization abnormalities. |
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| Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade de pointes in LQT2 and LQJ3 models of the long-QT syndrome. |
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| Outcomes in athletes with marked ECG repolarization abnormalities. |
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