
Ventricular repolarisation is the period that depolarised cells require to become polarised, that is to say excitable. In general cardiological practice, the duration of repolarisation is assessed by measuring the QT interval on the surface electrocardiogram. This measurement may be difficult because of the lack of precision in defining the end of the T wave. Automatic systems are becoming available and should circumvent these difficulties of manual measurements. Interpretation of a change in the QT interval during drug administration or related to cardiac pathology should take the many sources of physiological variation of ventricular repolarisation into account. One of the main causes of this variation is the heart rate which influences the duration of repolarisation in a complex manner. Analysis of the duration of repolarisation has many implications in pathology and pharmacology. Prolongation of the QT interval and its failure to adapt to the heart rate are trigger factors for torsades de pointe. Many drugs prolonging the duration of repolarisation and of the ventricular refractory period are being developed. Their effects are partially dependent on the heart rate. Finally, prolongation of the QT interval is associated with a poor prognosis after myocardial infarction.
Electrocardiography, Heart Conduction System, Heart Rate, Action Potentials, Humans, Arrhythmias, Cardiac, Blood Pressure, Autonomic Nervous System, Anti-Arrhythmia Agents
Electrocardiography, Heart Conduction System, Heart Rate, Action Potentials, Humans, Arrhythmias, Cardiac, Blood Pressure, Autonomic Nervous System, Anti-Arrhythmia Agents
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