The fallacies
of QT correction
Yash Lokhandwala,
MD, DM* and Toal SC, MD, DM,**
*Consultant
Electrophysiologist PD Hinduja National Hospital, Mumbai; Arrhythmia
Associates, Mumbai; Lead Cardiologist, Quintiles ECG Services.
**Fellow Arrhythmia Associates, Mumbai; Medical Director, Quintiles
ECG Services.
Address for correspondence: Dr.Yash Lokhandwala, MD, DM, Consultant
Electrophysiologist, Arrhythmia Associates, Mumbai, India. Email:
yashlokhandwala@hotmail.com
“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.
However
the QT does not adapt to changes in heart rate immediately. It takes more
than 2 minutes for the QT to adapt (QT/RR hysteresis). Hence correction
needs to be done at steady heart rates 1. The concept of heart rate correction ignores the dynamicity
of QT/RR relationship6. The QT interval is also under autonomic control.
Therefore different modes of heart rate changes, e.g. fast heart rate
due to parasympathetic withdrawal versus sympathetic overactivity, lead
to different direct and reflex effects on QT prolongation. Hence the standard
QTc correction formula will not be representative of the actual repolarization
milleu. Ideally each individual should have his own correction derived
from multiple ECGs at different heart rates and conditions to get the ideal
correction constant. Since this is not feasible a compromise can be made
by using formula which have been developed and validated in a large population
based cohort like the Framingham study 1.
Alternatively,
a table of lower and upper limits of QT interval for different RR cycle
lengths can be used by clinicians for references purpose 4. This method obviates the need of using any QT correction
formula. The reliability of this model results from its derivation in
a large population based sample. Inspite of all the fallacies of Bazett’s
correction, it is still being used clinically. The reason probably lies
in its simplicity and the fact that all clinical data signaling risk of
torsade are derived from this formula only. But in the near future we feel
that the Bazett’s correction will be replaced by a better formula like Fridericia.
We also need to be aware that in addition to prolonged QT, an abnormally
short QT can also carry dangerous implications of arrhythmogenecity 5. The QT also represents depolarization events
and hence in the presence of depolarization abnormalities like Left Bundle
Branch Blocks (LBBB) and Preexcitation syndromes, QTc will not be representative
of repolarization abnormalities and should not be commented upon. An alternative
interval, the “JT” has been proposed in such cases 6.
In light
of all the above fallacies a well designed study looking at different correction
formulae and defining one which clinically can risk stratify patients
at risk of torsade best, is the need of the hour. There are limitations
not only in correcting QT, but also in how it is measured and the reproducibility
of these measurements. Therefore, it is possible that in the future the
measurement of QT interval may just become an adjunctive, being replaced
by more objective and reproducible signs of repolarization abnormalities.
Till than ask not why QT, but how to correct QT.
References
1.
Malik M, Camm AJ. Evaluation of Drug-Induced QT Interval
Prolongation Implications for Drug Approval and Labeling. Drug Safety 2001;
24 (5): 323-351
2. Roden DM. A Practical Approach to Torsade
de Pointes. Clin Cardiol 20; 1997: 285-290
3.
Bazett HC. An analysis of the time relations of electrocardiogram.
Heart 7; 1970: 353-370
4.
Sagie A,
Larson MG, Goldberg RJ, Bengtson JR, Levy D. An Improved Method for Adjusting
the QT Interval for Heart Rate (the Framingham Heart Study). Am J Cardiol
70; 1992: 797-801
5.
Gaita F Giustetto C, Bianchi F, Wolpert C, Schimpf
R, Riccardi R, Grossi S et al. Short QT Syndrome: A Familial Cause of Sudden
Death. Circulation 2003;108:965-970
6.
Zhou SH, Wong S, Rautaharju PM, Karnik
N, Calhoun HP. Should the JT rather than the QT interval be used to detect
prolongation of ventricular repolarization? An assessment in normal conduction
and in ventricular conduction defects. J Electrocardiol 1992; 25: Suppl:
131-6
