The fallacies of QT correction

Abstract

Not to correct QT, but how to, that is the question”. The QT interval is a reflection of the action potential in the cardiac cells. Homogenous or heterogenous changes in the action potential duration lead to alteration of QT interval (in addition to morphological changes of T & U waves) 1. Such changes can be due to change in heart rate & autonomic tone. They can also be markers of abnormal repolarization, depolarization or both as a result of electrolyte disturbances, cardiac diseases, drugs and congenital long QT syndromes 2. Repolarization disorders are responsible for life threatening arrhythmias like torsades de pointes2. The purpose of heart rate correction is to obtain a standardized value that would have been measured in the same subject if the heart rate was 60 beats per minute (QTc). Thus this QTc value will now become independent of the heart rate and measure replarization changes. It will thus be a surrogate marker of the risk of torsade de pointes. The concept of QTc appeared in 1920, when Bazett introduced his square root formula 3. This formula obtained from data on 39 young men has been questioned because it overcorrects QT at fast heart rate and undercorrects at low heart rate (4). Thus at slow heart rate, which is one of the predisposing factors of torsade initiation, Bazett correction can easily mask substantial QT prolongation by under correcting. This can hide the proarrhythmic toxicity of drugs slowing heart rate. An alternative, cube root correction of Fridericia, corrects better than Bazett but again is not reliable at fast heart rates. Compared to these non linear correction formulae, linear regression correction obtained from large population data, like the Framingham heart study linear correction are still better 4.