Prolonged if it is more than 450 msec in men or more than 460 msec in women, correcting for heart rate.
Prolongation most frequently from delayed ventricular repolarization which is mediated by efflux of intracellular potassium.
Prolongation associated with excess risk for coronary artery disease.
Prolongation of the QT interval is accepted as a warning sign of life-threatening arrhythmia.
The duration of the QT interval, naturally varies, inversely with heart rate and a corrected QT (QTc) that adjusted for heart rate is most predictive of proarrhythmic potential.
QTc is widely used in clinical practice.
Prolongation can predict for sudden death in chronic ischemic disease, hypertension, sickle cell anemia, and healthy individuals.
Hypokalemia, hypomagnesemia, and hypocalcemia are all associated with prolonged QT interval which may have it increase relation to sudden cardiac death.
Increased variability, or QT dispersion, noted to be present in sudden deaths associated with congestive heart failure, acute myocardial infarction and hypertrophic cardiomyopathy.
Dispersion is an electrocardiographic measure of ventricular repolarization and a marker for ventricular tachyarrhythmias
Increased QT dispersion on an EKG found in hypertensive patients with severe disease and with the greatest left ventricle mass index and blood pressure.
Hereditary long QT syndrome associated with a prolonged ventricular repolarization and increased risk for ventricular tachyarrhythmias (torsades de pointes) and sudden cardiac death.
In approximately 75% of patients with LQTS have mutations in three major genes encoding ion channel subunits that control the action potential of the heart (Keating MT, Sanguinetti MC).
Long QT syndrome influenced by gender, congenital deafness, previous cardiac events, family history, QT interval length and genotype.
Majority of cases of long QT syndrome inheritance is autosomal dominant, but can be recessive.
Long QT syndrome characterized by abnormal QT-interval prolongation on EKG and increased risk of sudden death, usually related to ventricular fibrillation.
Long QT syndrome consists of a number of cardiac channelopathies with delayed repolarization of the myocardium.
Long-QT syndrome is most often related to an inherited potassium channelopathy, and there is an increased likelihood of electroencephalogram abnormalities in long-QT patients vs healthy controls, perhaps pointing toward an important link between the two conditions.
Long QT syndrome occurs in a structurally normal heart and is associated with increased risk of seizures, syncope, and sudden cardiac death, and these manifestations occur after a precipitating event such as extreme exertion, a motion or even an auditory trigger (Rodem DM).
Emotional and physical stress common causes for syncope or sudden death in long QT syndrome.
Cardiovascular events can be precipitated by loud noises or at rest in the long QT interval syndrome.
Cardiovascular events may occur with the congenital long QT syndrome with a familial gene mutation or due to an acquired long QT syndrome secondary to QT prolonging diseases or conditions that include ischemic heart disease, medications, electrolyte disturbances or bradycardia.
Patients with a prolonged QT interval may present with syncope, sudden cardiac death due to polymorphic ventricular tachycardia, also known Torsades de pointes, and ventricular fibrillation.
Long-QT syndrome associated with hundreds of mutations in 10 genes.
Mutations in the potassium channel genes KCNQ1 and KCNH2 cause the most frequent forms types 1 and 2, respectively of the long QT syndrome.
Female predominance in long QT syndrome.
Abnormal prolongation and shortening of QT-interval duration are associated with increased risk for ventricular arrhythmias and sudden cardiac death.
prolongation of the QT interval is a common adverse event associated with many chemotherapeutic agents, and can lead to life-threatening arrhythmias such as Torsades de pointes.
The prognosis of the congenital long QT syndrome if properly and promptly diagnosed and treated.
The mortality associated with acquired long QT syndrome in patients with cardiovascular disease and stroke is high.
The acquired long QT syndrome is often observed in patients with drug exposure, and in combination with other risk factors such as female gender, bradycardias, renal dysfunction, and electrolyte abnormalities fatal of ventricular arrhythmias may manifest.
A QT interval of more than 500 ms is used as a threshold for the risk of develping Torsades de pointes.
QTc interval refers to the QT interval corrected for the heart rate.
In a retrospective analysis of a QT alert system 86,107 ECGs on 52,579 patients compared the survival rate of those between those with a QTc interval of 500 ms or greater and those with QTc interval less than 500 ms:all cause mortality rate for patients with QTc interval of 500 ms or greater was 19% compared With 5% in patients with QTc interval less than 500 ms (Haugaa KH et al).
A number perioperative drugs prolonged QT interval and include volatile anesthetics, anti-emetics, muscle relaxants, and some opioids.
Droperidol may be associated with prolonged QT interval.