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The QT interval, its origin and importance of the knowledge of formulas for its measurement in different clinical circumstances

Authors:
  • Universidad de Ciencias Médicas. Villa Clara. Cuba. Cardiocentro Ernesto Guevara

Abstract

The long QT syndrome is an arrhythmogenic channelopathy characterized by severe alterations in ventricular repolari-zation, electrocardiographically translated as a QT interval prolongation. The involvement of various ion channels in the genesis of cardiac action potential causes that altera-tions in their structure and function lead to the so-called syndrome and to the presence of malignant ventricular arrhythmias. In 1920, Bazett adapted the formula of the cardiac electrical systole duration to the QT interval of the electrocardiogram, and proposed normal values of QT for a given heart rate. After Bazett’s description, several formulas were described in different clinical situations to calculate the corrected QT interval. The knowledge about how to measure the QT interval and about its correction as a tool for the diagnosis of arrhythmogenic conditions and preven-tion of primary or secondary malignant ventricular arrhyth-mias is of vital importance for its clinical use.
CorSalud 2014 Jan-Mar;6(1):79-85
RNPS 2235-145 © 2009-2013 Cardiocentro Ernesto Che Guevara, Villa Clara, Cuba. All rights reserved.
79
Cuban Society of Cardiology
______________________
Special Article
The QT interval, its origin and importance of the knowledge of
formulas for its measurement in different clinical circumstances
El intervalo QT, su origen e importancia del conocimiento de fórmulas para su medición
en diferentes circunstancias clínicas
Elibet Chávez González
, MD, MSc.
Service of Clinical Cardiac Electrophysiology and Pacing. Cardiocentro Ernesto Che Guevara. Villa Clara, Cuba,
Este artículo también está disponible en español
ARTICLE INFORMATION
Key words: QT interval, QT interval measurement
Palabras clave: Intervalo QT, Fórmulas de medición
ABSTRACT
The long QT syndrome is an arrhythmogenic channelopathy
characterized by severe alterations in ventricular repolari-
zation, electrocardiographically translated as a QT interval
prolongation. The involvement of various ion channels in
the genesis of cardiac action potential causes that altera-
tions in their structure and function lead to the so-called
syndrome and to the presence of malignant ventricular
arrhythmias. In 1920, Bazett adapted the formula of the
cardiac electrical systole duration to the QT interval of the
electrocardiogram, and proposed normal values of QT for a
given heart rate. After Bazett’s description, several formulas
were described in different clinical situations to calculate
the corrected QT interval. The knowledge about how to
measure the QT interval and about its correction as a tool
for the diagnosis of arrhythmogenic conditions and preven-
tion of primary or secondary malignant ventricular arrhyth-
mias is of vital importance for its clinical use.
RESUMEN
El síndrome de QT largo es una canalopatía arritmogénica
caracterizada por una grave alteración en la repolarización
ventricular, traducida electrocardiográficamente por una
prolongación del intervalo QT. La implicación de varios ca-
nales iónicos en la génesis del potencial de acción cardíaco
hace que las alteraciones de estructura y función de ellos
conlleven al llamado síndrome y a la presencia de arritmias
ventriculares malignas. En 1920, Bazett adaptó la fórmula
de la duración de la sístole eléctrica del corazón al intervalo
QT del electrocardiograma, y propuso valores normales del
QT para una determinada frecuencia cardíaca. Después de
esta descripción, varias fueron las fórmulas descritas en di-
ferentes situaciones clínicas para el cálculo del intervalo QT
corregido. Es de vital importancia, para el uso clínico, el co-
nocimiento sobre cómo medir el intervalo QT y de su co-
rrección, como herramienta para el diagnóstico de afeccio-
nes arritmogénicas y la prevención de arritmias ventricula-
res malignas primarias o secundarias.
INTRODUCTION
The long QT syndrome (LQTS) is an arrhythmogenic
channelopathy characterized by severe alterations in
E Chávez González
Calle 1ra, e/ Unión y Río, Reparto
Ramón Ruiz del Sol. Santa Clara, CP 50200
Villa Clara, Cuba
E-mail address: elibet@capiro.vcl.sld.cu
The QT interval, its origin and importance of the knowledge of formulas for its measurement
CorSalud 2014 Jan-Mar;6(1):79-85
80
ventricular repolarization, and is electrocardiogra-
phically translated by aprolongation of the QT1 inter-
val, predisposing to sudden death from malignant
ventricular arrhythmias, of the helicoidal tachycardia
type (torsades de pointe in its original language).
11 years after identifying the main channels
affected in this disease, hundreds of mutations distri-
buted in 10 genes so far associated with the syndrome
have been described. Genetic research conducted
since then has shown that while the severe form of
the disease is sporadic, there are common polymor-
phisms in genes related to this condition, which may
confer susceptibility to the development of helicoidal
tachycardia, particularly with the use of certain drugs,
moreover, polymorphisms with regulatory properties
that may also enhance or still the severity of a mu-
tation have been identified. The understanding of the
molecular processes of the disease has allowed
optimizing treatment, improving survival of those
affected, and generating a significant genotype-
phenotype-treatment correlation.
Despite the progress, a quarter of the cases do not
have mutations in the genes described so far, so LQTS
continues to be object of research1. This paper aims to
summarize the foundations of ventricular repolariza-
tion (QT interval) and the importance of its measure-
ment in different clinical situations.
Márquez2 states that in his opinion the term
channelopathy can be strong. He would rather call it
"disease of ion channels", considering that the basis of
this disease is the presence of disturbances in ion
channels responsible for the balance between the in-
put and output of these during ventricular depolariza-
tion and repolarization. As to the latter concept,
Márquez2 himself suggests that from the electro-
cardiographic point of view, normal ventricular repo-
larization is represented by the ST segment and the T
wave. However, the electrocardiographic parameter
that is taken into account to assess the duration of
repolarization is the QT interval. It is important to
remember that this interval comprises not only
repolarization, but also the ventricular depolarization,
and that the QRS complex is included. This is funda-
mental to understanding why it can be prolonged in
the presence of conduction disturbances, and not just
for repolarization disturbances.
Some ionic basis of ventricular repolarization
Normal ventricular repolarization is caused by the
balance between inward currents of sodium (Na +)
and calcium (Ca +) and the outward currents of
potassium (K +). The latter are various but can be
grouped into two, those responsible for repolarization
in the initial phase of the action potential, called
transient outward (ITO) and those in charge of the rest
of repolarization known as “late rectifier”currents (Ikr,
Iks, IKur). There are several mutations that may affect
the ion channels and their effect can be grouped into
three: disorder of the channel permeability, changeof
its activation and dysfunction in its inactivation.
Anton Jervell and Fred Lange-Nielsen3 in 1957
described for the first time a family with 6 children, 4
of whom had congenital deafness and syncopal epi-
sodes, 3 of them had sudden death. The electrocardio-
gram (ECG) of the cases showed an unusually long QT
interval. Both parents were asymptomatic, had a
normal ECG and had no hearing problems. In 1963,
Romano4 and Ward independently published a familiar
cardiac syndrome characterized by recurrent syncope,
family history of sudden death and QT prolongation
without neuronal deafness. From these findings des-
cribed above,the classification of homozygous and
heterozygous LQTS arose, however, the molecular
complexity of ion channels and genetic study have
allowed a classification with emphasis on genetic dis-
orders.
Ion channels are transmembrane proteins that
transport ions across the cell membrane. Channels
involved in LQTS are selective or specialized in the
transport of a single ion and are voltage-dependent,
that is, its activation occurs at a specific intracellular
voltage that varies according to the channel subtype.
The electrical and contractile phenomena occurring in
cardiomyocytes are controlled by these structures. Ion
channels develop macromolecular complexes, there is
a main unit forming the channel pore and auxiliary
proteins that regulate it. The disorder on thechannel
function in LQTS can occur in two places: in the main
protein or in regulatory proteins.
The disorder in the pore forming unit, known as
alpha, generates the 3 most common subtypes of
LQTS: LQTS1(involving the potassium channel IKs)
LQTS2 (involvingthe potassium channel IKr) and LQTS3
(involvingthe channel sodium INa). Since they are the
most common, they have been characterized better
from both a clinical and genetic point of view. The so-
called Jervell-Lange-Nielsen syndrome currently corres-
ponds to the varieties of LQTS 1 and 5. Characteris-
Chávez González E.
CorSalud 2014 Jan-Mar;6(1):79-85
tically, these patients present congenital deafness and
have compound homozygous or heterozygous muta-
tions affecting IKs current. Romano Ward syndrome
ranges from LQTS 1 to 10 and is not manifested with
deafness1. To clinically describe the 10 genotypes of
LQTS is not the purpose of this article; the reader is
referred to the work of Medeiros et al.1, where each of
them is detailed.
Origin of formulas for measuring the QT
It is important to ask ourselves: how is the QT interval
measured and when is it normal?
The duration of mechanical systole was a topic of
much interest among the pioneers of cardiovascular
physiology of the nineteenth century. According to
Cobos and García5, A. D. Waller, now famous for his
contribution to the birth of electrocardiography,
proposed in 1891 the following expression for the
normal duration of systole: Mechanical systole= K
xRR1/2, where K has a value of 0.343. In 1920, Bazett
did nothing but to adapt this formula to the duration
of the electrical systole of the heart, the QT interval,
and suggested that the normal value for a given heart
rate isKx RR ½, where K is 0.37 for males and 0.4 for
females5. Thus, to determine whether a particular
patient has a normal QT interval, their QT should be
compared with the ideal QT derived from Bazett’s
formula. This ideal QT is one that can be read in the
popular electrocardiograms rules. Subsequently, to
the Bazett’s expression, the forgotten L.M.Taran and
N. Szilagyi, according Cobos García5, proposed a for-
mula from which the concept QT corrected arose,
which is the QT interval that a particular patient would
have, theoretically, at a frequency of 60 beats per
minute. Therefore, the expression used today, which is
erroneously attributed to Bazett, belongs to L.M. Ta-
ran and N. Szilagyi5. In classical texts of the sixties, the
role of these authors is clearly recognized and the
statement: "Taran and Szilagyi corrected QT interval or
Bazett’s formula modified by Taran and Szilagyi5” is
heard.
With the formula considered as corrected QT (QTc)
= QT measured / RR1/2, it is interesting to know that
only with it, the QTc for different clinical situations
found in medical practice cannot be calculated. There
are different mathematical models describing the
relationship between QT interval and the heart rate.
The relationship between the HR and QT interval is
curvilinear. There are different mathematical forms
that model the relationship between QT and HR. There
are models of different types: parabolic, polynomial,
linear, hyperbolic, exponential, tables and nomo-
grams6:
a) Linear: QTc = QT + x (1 − RR)
b) Hyperbolic: QTc = QT + x (1/RR − 1)
c) Parabolic: QTc = QT/RRx
d) Logarithmic: QTc = QT − x Nl(RR)
e) Logarithmic modified: QTc = Nl(exp(QT) + x (1 −
RR))
f) Exponential: QTc = QT + x (eRR − 1/e)
g) Arc-tangent: QTc = QT + x (arctg(1.0) - arctg(RR))
h) Arc-hyperbolic cosine QTc = QT + x (ln(2+30,5) −
arccosh(RR+1))
Nl is Napierian logarithm, "exp" is the exponential
function based on the number e = 2,718.
To optimize each formula the "x" parameter must
be found by solving the r ratio equation (RR, QTc(x)) =
0.
From these models different formulas were derived:
Bazett 1920, Fridericia 1920, Mayeda 1934, Adams
1936, Larsen and Skulason 1941, Ashman 1942 Schla-
mowitz 1946, Ljung 1949, Simonson 1962, Boudolas
1981, Rickards 1981, Hodges 1983, Kawataki 1984,
Sarma 1984 Kovacs 1985, Van de Water 1989, Lecocq
1989, Rautaharju 1990, Todt 1992, Sagie (Framing-
ham) 1992, Arrowood 1993, Yoshinaga 1993, Wohlfart
1994, Klingield 1995, Hodges 1997 and Matsunaga
19976.
The presentation of the mathematical models and
formulas of QTc is not intended to cram the reader
with the knowledge of their origins, or the formulas
themselves, but it is intended to present the com-
plexity of the issue. QT measurement is very often
overlooked or poorly performed; however, LQTS is
known by clinicians and cardiologists, who may evade
the measure and correction of this interval because
sometimes it is not simple. Viskinet al.7 reported that
less than 40% of physicians that are not cardiologists,
less than 50% of cardiologists and over 80% of
electrophysiologists, knew how to measure it correct-
ly.
Some formulas for calculating QTc6 are shown in
the table.
The QT interval, its origin and importance of the knowledge of formulas for its measurement
CorSalud 2014 Jan-Mar;6(1):79-85
82
Table. Formulas for calculating QTc.
Denomination Formula
Bazett modified by
Taran and Szilagyi
5
QTc = QT / (RR)½
Fridericia QTc = QT / (RR)
(0,33)
Framingham QTc = QT + 0,154 (1−RR)
Hodges QTc = QT + 1,75 (FC − 60)
Sarma
QTc = QT - B1 Exp (-k1 . RR)
QTc = QT [1-Exp (-k2 . RR)]
QTc = QT (RR)½ + B3
QTc = QT (RR)
½
*
Strength equation QTc = 453,65 × RR1/3.02 (R2 = 0,41)
Van de Water QTc = QT 0,087 (RR 1000)
Matsunaga QTc = log (600) QT / (log RR)
Kawataki QTc = QT/RR
(0,25)
Mayeda QTc = QT/RR x 0,604
Larsen and Skulason QTc = QT + 0,125 (1 RR)
Schlamowitz QTc = QT + 0,205 (1 RR)
Wohlfart QTc = QT + 1,23 (FC 60)
Boudolas QTc = QT + 2,0 (FC 60)
Sagie QTc = QT + 0.154 (1 RR)
Malik QTc = QT/RR x 0,371
Lecocq QTc = QT/RR
(0.314)
B and k: are regression parameters.
Exp: exponential function with base e = 2,718.
FC: heart rate.
RR: RR distance.
* It is stated that this formula is better than Bazett’s
The usefulness of many formulas is given by their
use in different clinical circumstances. The sympathe-
tic and parasympathetic nerve block can be performed
with propranolol and atropine. The standing + atro-
pine combination is purely an activity of the sympa-
thetic nervous system, the supine position + proprano-
lol combination is purely an activity of the parasym-
pathetic nervous system8. For these postural changes,
Hodges correction showed QTc increases and de-
creases for the supply of atropine and propranolol,
respectively. Individual correction would better adapt
to the dynamic changes of the RR, which inevitably
affect when correcting the QT interval in the right
form9. Regarding the autonomic nervous system it is
important to remember the usefulness of adrenaline
to unmask the presence of LQTS, primarily for types 1
and 2. It is particularly effective to detect asympto-
matic forms of LQTS1 (sensitivity, specificity, positive
and negative predictive value of 92.5, 86, 76 and 96%,
respectively). It may also be useful in diagnosing
LQTS2 with lower sensitivity and specificity. It is not
useful for LQTS3 or other forms of LQTS. Under normal
conditions, sympathetic stimulation induces phospho-
rylation of the IKs potassium channel, and optimizes
its function resulting in a shortening of the action
potential. In LQTS patients, especially type 1, a para-
doxical response to administration of low-dose epi-
nephrine (0.025-0,2µg/kg/min) is observed which
lengthen the QT interval more than 30 ms10-13.
Fridericia and Framingham formulas have proven
to be more useful for determining the QTc at one
minute after peak exercise, with which it has been
possible to prove that they are superior in establishing
LQTS when compared with Bazett and Hodges for-
mulas14.
During sleep, in young patients, since they have a
high heart rate, Hodges and Bazett formulas over-
correct the QTc, and Framingham and Fridericia for-
mulas underestimate it. However, Hodges has the best
approximation during sleep15.
The nomogram method for correcting the QT inter-
val is more accurate than the other three methods:
Bazett, Fridericia and Framingham. With heart rates
between 60 and 100 beats/min, the linear regression
equation is:
QT = 237 + 0.158 x RR (P < 0,001)16
When a 24-hour Holter is used in healthy subjects
no significant difference inQTc values among the
different formulas are found 17.
Considerations for the measurement of QT interval6
1. Record the ECG at baseline and at rest, and avoid
postprandial period.
2. Keep a few minutes of rest before performing the
ECG, to allow the QT interval to adapt to the heart
rate (it takes 1-3 minutes).
3. The QT interval should be measured:
a) Manually, preferably using the limb leads which
show betterthe end of the T wave.
Chávez González E.
CorSalud 2014 Jan-Mar;6(1):79-85
b) From the beginning of the QRS complex to the
end of the T wave, measuring in 3-5 beats. The
U wave probably corresponds to the late repo-
larization of medium myocardial cells and should
be included in the measurement, if it is wide
enough to be attached to the T wave. When
measuring, it is often found that the end of the
T wave is not clear, in such cases the end of this
wave should be determined by extrapolation
using the tangent method18.
4. The measurement of the QT interval should be ad-
justed to the heart rate, which is called QTc inter-
val. This correction is useful to make it independent
of the heart rate of each individual and transform it
into a comparable measure of the electrical activity
between healthy and ill patients.
5. The best way to determine the QTc has not yet
been achieved because studies are not prospective.
Some authors argue that the Framingham formula
is the most suitable mode from the epidemiological
point of view, based on empirical data obtained
from large population samples.
6. Avoid measuring the QT interval in cardiac cycles
with large variation in the sinus interval or in those
preceded by arrhythmias.
7. A stress test can be performed to rule out a marked
QT prolongation during the recovery phase.
8. QT measurement is particularly changeable if the
patient is in atrial fibrillation, because the QT inter-
val varies from beat to beat depending on different
RR intervals.
9. The QTc lengthens with age, it is longer in adult wo-
men than in men of the same age, and the longest
QTc is found shortly after awakening.
When can the QTc interval be considered normal?
It has been suggested that the QT interval should be
measured preferably in the Dll and V5 leads, where it
has been registered to have greater predictive power.
It reflects the duration of ventricular repolarization
and is measured from the start of the Q wave to the
end of the T wave. Conventionally, Bazett's formula is
used to correct the length of the interval according to
the heart rate (QTc = QT / RR1/2, expressed in seconds).
It is advisable that the physician performs a manual
measurement and should not rely on automated
measurements that, while useful for other intervals,
are usually imprecise in the calculation of the QT inter-
val; this is a dynamic range and normal limits depend
on several factors. While a QTc interval ≥ 440 ms in
men and ≥ 460 ms in women has been considered
abnormal, in this range we can find both carriers of
mutationsand healthy subjects. In families with LQTS1,
no case with positive genotype has a QTc < 410 ms,
and none with a negative genotype has a QTc > 470
ms. A QTc > 440 ms is effective for detecting patients
with mutations associated with LQTS, a QTc > 470 ms
is useful for detecting patients at risk of developing
symptoms and a QTc > 500 ms has been found in
symptomatic patients with treatment6.
As mentioned, the QT measurement includes QRS
duration, thus in the presence of branch blocks,
wherein the values of QRS duration are increased with
respect to its normal value, an increase in QT occurs.
Sometimes the measurement of QT is left out if QRS
duration 120 ms. In these circumstances the JT
interval (measured from the point J to the end of the T
wave) is more appropriate than QT as a measure of
ventricular repolarization19. The JT interval is indepen-
dent of QRS duration and represents a better index of
ventricular repolarization20.
Finally, it should be mentioned that observing
variations of T wave (macro and microalternans) is as
important as measuring the QT. These variations are
related to alterations in repolarization, which vary
from beat to beat, and cause its successive changes. In
LQTS patients, there has been increased presence of T
macroalternans prior to episodes of helicoidal tachy-
cardia21-23, although other studies have not shown this
relation24. In LQTS patients, during the day, it is easier
to observe the T wave macroalternans, perhaps re-
lated to the regional variations in the circadian
rhythm. Despite having described the presence of this
macroalternans prior to helicoidal tachycardia epi-
sodes, which may be a warning sign, no significant
differences in T macroalternans in patients with symp-
tomatic and asymptomatic LQTS, nor among patients
under treatment with beta-blockers or without them
have been reported. The beat-to-beat variations of T-
wave are related to changes in the action potential in
its ionic currents25,26.
CONCLUSIONS
The measurement and calculation of the QTc interval
can be challenging for daily clinical practice. The
knowledge about how to measure the QT interval and
The QT interval, its origin and importance of the knowledge of formulas for its measurement
CorSalud 2014 Jan-Mar;6(1):79-85
84
its correctionis vital for clinical use, as a tool for the
diagnosis of arrhythmogenic conditions and preven-
tion of primary or secondary malignant ventricular
arrhythmias.
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... Many other authors set the upper limit of QTc in men at 450 ms, whereas in women the normal QTc value is considered to be Taken from MSc. Dr. Elibet Chávez González [5]. ...
Article
Full-text available
For many authors, the electrical cardiac systole includes from the beginning of the Q wave (or beginning of the R wave if there is no Q wave) to the ending of the T wave, wherever the descending branch of the T wave reaches the isoelectric line of the ECG. For many others, to which we belong, the electrical cardiac systole must also include the P wave. In any case, it is imperative to measure waves, intervals and electrocardiographic segments in all cases.
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