Context Of the several factors implicated in causing QT interval prolongation
and torsades de pointes, errors in the use of medications that may prolong
this interval deserve special attention.
Objective To systematically summarize the available clinical data on the QT interval
and to offer improved recommendations for the use of QT-prolonging medications.
Data Sources We searched MEDLINE from 1966 through 2002 for all English-language
articles related to the QT interval. Additional data sources included bibliographies
of articles identified on MEDLINE, a survey of experts, and data presented
at a meeting of experts on long QT syndrome.
Study Selection We selected for review registries and case series examining clinical
outcomes of patients with prolonged QT interval and the effect of different
methods of measurement of the QT interval on patient outcomes. Ten studies
were identified, of which 6 were included in the analysis.
Data Extraction Data quality was determined by publication in the peer-reviewed literature.
Data Synthesis Optimal measurement of the QT interval is problematic because of lack
of standardization and lack of data regarding the best way to adjust for heart
rate. Reliable information on the proper use of QT-prolonging medications
is scarce. Although a QT interval of at least 500 milliseconds generally has
been shown to correlate with a higher risk of torsades de pointes, there is
no established threshold below which prolongation of the QT interval is considered
free of proarrhythmic risk. The risk of torsades de pointes should be assessed
in patients who are about to begin taking a QT-prolonging medication. Although
inadequate clinical studies preclude prediction of absolute risk for individual
patients, particularly high-risk situations can be defined based on clinical
variables. We propose recommendations on proper monitoring of the QT interval
in patients receiving QT-prolonging medications.
Conclusion Although the use of QT-prolonging medications can predispose to torsades
de pointes, there is a relative paucity of information that can help clinicians
and patients make optimal informed decisions about how best to minimize the
risk of this serious complication.
The QT interval on the electrocardiogram (ECG) has gained clinical importance,
primarily because prolongation of this interval can predispose to a potentially
fatal ventricular arrhythmia known as torsades de pointes. Multiple factors
have been implicated in causing QT prolongation and torsades de pointes. Among
these, improper use of QT interval–prolonging medications deserves special
attention. Recently, cisapride and grepafloxacin were removed from the US
drug market because of the risk for QT prolongation and fatal arrhythmias.1,2 The need to remove these agents from
the market was related not just to the inherent properties of the drugs but
also to the demonstrated failure of government-mandated black box warnings
and "Dear Doctor" letters to mitigate inappropriate prescribing by physicians.3
To reduce the risk of torsades de pointes, health care providers must
understand what is known about the QT interval. In this article, we address
the meaning and measurement of the QT interval, describe factors that affect
the QT interval, and assess the balance of risks and benefits of QT-prolonging
medications. We also evaluate the steps that have been taken to enhance proper
management of risk emanating from the use of QT interval–prolonging
Literature for this review was systematically identified by searching
MEDLINE for all English-language articles published from 1966 through 2002
related to the QT interval (search terms: long QT syndrome, death, outcomes, registries, case series, QT interval, and measurement),
reviewing bibliographies of articles identified on MEDLINE, surveying experts,
and reviewing data presented at a meeting of experts on long QT syndrome (LQTS).
We selected for review registries and case series examining clinical outcomes
of patients with prolonged QT interval and the effect of different methods
of measurement of the QT interval on patient outcomes. Ten studies were identified
by the search, of which 6 were included in the analysis.4-9 Data
quality was determined by publication in the peer-reviewed literature.
What is the qt interval and how should it be measured?
The QT interval on the surface ECG is measured from the beginning of
the QRS complex to the end of the T wave. Thus, it is the electrocardiographic
manifestation of ventricular depolarization and repolarization. This electrical
activity of the heart is mediated through channels, complex molecular structures
within the myocardial cell membrane that regulate the flow of ions in and
out of cardiac cells. The rapid inflow of positively charged ions (sodium
and calcium) results in normal myocardial depolarization. When this inflow
is exceeded by outflow of potassium ions, myocardial repolarization occurs.
Malfunction of ion channels leads to an intracellular excess of positively
charged ions by way of an inadequate outflow of potassium ions or excess inflow
of sodium ions. This intracellular excess of positively charged ions extends
ventricular repolarization and results in QT interval prolongation.10
In the clinical setting, it is now widely recognized that typical measurement
of the QT interval is subject to substantial variability, which can cloud
interpretation.11,12 This variability
in QT interval measurement results from biological factors, such as diurnal
effects, differences in autonomic tone, electrolytes, and drugs; technical
factors, including the environment, the processing of the recording, and the
acquisition of the ECG recording; and intraobserver and interobserver variability,
resulting from variations in T-wave morphology, noisy baseline, and the presence
of U waves. Interobserver variability also results from the lack of agreement
among experts about standardizing approaches to measure the QT interval.11,12 Although experts on the QT interval
argue that intraobserver and interobserver variability and measurement error
are higher when the corrected QT (QTc) interval is taken from computerized
ECG algorithms rather than from careful high-resolution manual measurements,
automated readings may be useful for rapid assessment of patient safety.13 Unfortunately, there is no credible empirical evidence
to support this view. In addition, as demonstrated by a recent survey of health
care practitioners, many clinicians simply do not know how to measure the
QT interval. Whereas 61% of respondents were able to identify what the QT
interval represented on an ECG, only 36% correctly measured it.14
Although it is standard practice to measure the QT interval from the
beginning of the QRS complex to the end of the T wave, the actual methods
of measurement have not been standardized. Because the QT interval is prolonged
at slower heart rates and shortened at faster heart rates, many formulas have
been proposed to adjust for these variations. Yet differences of opinion exist
regarding the most useful correction for heart rate.15-18 One
of the commonly used formulas is the Bazett formula, in which the QT interval
is adjusted for heart rate by dividing it by the square root of the R-R interval
(Figure 1, A). However, this formula
has been criticized for being inaccurate at fast heart rates.19 Other
formulas are the Fridericia cube-root correction (QT interval divided by the
cube root of the R-R interval) and the Framingham linear regression equation.16,17 From an epidemiological perspective,
the Framingham approach is the most sound because it is based on empirical
data from a large population sample rather than on hypothetical reasoning.
Unfortunately, none of these corrections has been examined comparatively to
determine the most effective formula in predicting which patients are at greatest
risk for torsades de pointes.
A group of experts on LQTS recently acknowledged the lack of empirical
data in determining the best approach to measuring the QT interval. This group
convened in August 2000 to discuss the current knowledge of LQTS (see Acknowledgment).
As a result of this meeting, the panel proposed the following 4 guidelines13 for measuring the QT interval, based on expert opinion:
The QT interval should be measured manually, preferably
by using one of the limb leads that best shows the end of the T wave on a
The QT interval should be measured from the beginning
of the QRS complex to the end of the T wave and averaged over 3 to 5 beats.
U waves possibly corresponding to the late repolarization of cells in the
mid myocardium should be included in the measurement only if they are large
enough to seem to merge with the T wave.
The QT interval should be measured during peak
plasma concentration of a QT-prolonging medication.
The QT interval should be adjusted for heart rate.
Because the best way to adjust for heart rate has not been determined by prospective
studies, the panel could not make a definitive recommendation in this regard.
Measurement of the QT interval is particularly challenging if the patient
is in atrial fibrillation because the QT interval varies from beat to beat
depending on the interval between successive R waves. Unfortunately, there
is no consensus on how to measure the QT interval in this circumstance. Some
clinicians suggest using the same steps in the aforementioned recommendations
but further advise averaging the measured QT interval over 10 beats. Others
prefer to measure the QT intervals that follow the shortest and longest R-R
intervals and divide each by the square root of the R-R interval preceding
it. The average of these intervals would then be used as the adjusted QT interval
(Figure 1, B).
Measurement of the QT interval is also difficult in the setting of a
wide QRS complex related to either ventricular conduction defects or a paced
QRS complex. This is primarily because of the lack of a standard method to
measure the QT interval in this setting; data on the best way to make this
measurement do not exist. The Pfizer Tikosyn program specifies that while
the QTc should be no more than 440 milliseconds (ms) to start dofetilide in
the setting of a narrow QRS complex, the QTc should be no more than 500 ms
in the setting of ventricular conduction abnormality.20 This
guidance may be used with other QT-prolonging medications until a standard
method to measure the QT interval in the setting of ventricular conduction
abnormality is identified.
Some argue that the QT interval should be measured only by cardiologists,
but this suggestion is impractical. In light of the number of medications
that could prolong the QT interval, other health care practitioners, especially
internists, family practitioners, and psychiatrists, should either learn how
to measure the QT interval or develop systematic approaches to ensuring that
accurate measurements are being made at the appropriate time by specialists.
Indeed, nurses, physician assistants, and clinical pharmacists may play an
important role in this regard; if properly trained, it is likely that they
can be relied on to measure the QT interval. However, the use of multiple
health care practitioners in measuring the QT interval for clinical decision
making needs to be tested in prospective studies.
It is important to realize that the methods proposed to correct the
QT interval have primarily been evaluated for their correlation with heart
rate. The formula with the best correlation with heart rate is believed to
be the most accurate. It would be of great clinical importance if these formulas
were validated prospectively and then compared with each other in adequately
sized prospective studies. In this way, it could be determined which one most
strongly correlates with an increased risk of adverse clinical events (especially
death). However, this endeavor would be challenging because it might be difficult
to identify a patient population with an event rate high enough to provide
adequate statistical power. In the absence of such studies, practitioners
must be aware of the ongoing uncertainty about the best way to adjust the
Factors that affect the qt interval
Although it is convenient to think of QT prolongation as occurring because
of either congenital or acquired abnormalities, the phenomenon probably most
often involves a gene-environment interaction. Pure congenital prolongation
characterized by lifelong, ambient QT prolongation is rare but does carry
a high risk of sudden death. Several forms of congenital LQTS have been reported,
and 3 forms (LQT1, LQT2,
and LQT3) have been well characterized in previous
studies.21 These forms have been found to have
distinctly different clinical outcomes and clinical manifestations, including
factors that trigger clinical events and ECG features.6,22 For
example, physical activity tends to trigger events in LQT1, auditory stimuli in LQT2, and rest or sleep
in LQT3.7,23,24 Each
form has also been characterized electrocardiographically by a specific pattern
of T waves.25 The T wave is of long duration
in LQT1, is small and/or notched in LQT2, and has an unusually long onset in LQT3.22 More important, the genotype of LQTS seems to have
a significant impact on outcome.4 In a study
using a large international registry of LQTS, it was noted that although the
risk of cardiac events was significantly higher among patients with LQT1 and LQT2 than with LQT3, the frequency of lethal cardiac events was significantly
higher in the LQT3 group.6
When exposed to QT-prolonging medications, individuals without lifelong
QT prolongation may develop QT prolongation with or without torsades de pointes
or may not develop QT prolongation at all. Even after adjustment for other
factors that could prolong QT interval, some patients seem to be more likely
than others to have QT prolongation at a given dose of a drug. This observation
led researchers to hypothesize that patients with acquired QT prolongation
may have a genetic predisposition for it.8,10,26 Recent
investigations suggest that such patients may have clinically silent gene
mutations that lead to overt QT prolongation only with exposure to QT-prolonging
It is important to note that the majority of patients with documented
acquired LQTS never experience torsades de pointes, and many patients with
torsades de pointes have a normal QT interval shortly before the event. It
appears that a variety of coincident circumstances, including genetic predisposition
and a prolonged QT interval (which may occur precipitously and transiently),
are required to precipitate torsades de pointes.
Factors that predispose to QT prolongation and higher risk of torsades
de pointes include older age, female sex, low left ventricular ejection fraction,
left ventricular hypertrophy, ischemia, slow heart rate, and electrolyte abnormalities
including hypokalemia and hypomagnesemia.5,27-34 Certain
drugs also predispose to QT prolongation (broach basic end-of-life issues
and to clarify goals of treatment (Box). An extensive list of these drugs can be found at http://www.torsades.org. Regarding antiarrhythmic QT-prolonging drugs, the risk of torsades
de pointes seems to be highest within the first few days of initiating therapy.35-37 For this reason,
physicians should consider admitting patients to the hospital when starting
such drugs, a practice most warranted among patients with structural heart
disease. Hospitalized patients can be better monitored for the warning signs
that precede torsades de pointes. In a rigorous study of patients with supraventricular
tachycardias, investigators reported that a 72-hour hospitalization for initiation
of antiarrhythmic therapy appeared to be cost-effective.38
Box Section Ref ID
Box. Potential of Selected Medications for Causing QT Prolongation
Based on a Survey of Expert Opinion*
POSSIBLE IN HIGH-RISK PATIENTS
*"Very probable" indicates more than 50% of respondents stated they
would always check an electrocardiogram (ECG) when starting this medication;
"probable," 40%-49% of respondents stated they would always check an ECG when
starting this medication; "possible in high-risk patients," more than 40%
of respondents stated they would always check an ECG in high-risk patients;
"improbable," 40%-49% of respondents stated they would never check an ECG
when starting this medication; "very improbable," more than 50% of respondents
stated they would never check an ECG when starting this medication; and "unknown,"
survey responses did not fit any of the other categories.
Several noncardiac medications can cause torsades de pointes, either
by directly blocking potassium currents or by interacting with other medications
(Table 1). These interactions
could be purely pharmacodynamic (both drugs block outward potassium currents),
purely pharmacokinetic (one drug interferes with the clearance of another),
or of mixed pharmacodynamic and pharmacokinetic origin. An example of a purely
pharmacodynamic interaction is that of quinidine and sotalol—both block
outward potassium currents. The interaction between cisapride and ketoconazole
provides an example of a purely pharmacokinetic interaction. Ketoconazole
inhibits the cytochrome P-450 3A4 isoenzyme that metabolizes cisapride, and
this inhibition results in increased cisapride levels that may augment QT
prolongation and result in torsades de pointes. An example of a mixed interaction
is that of erythromycin and cisapride. Not only do both drugs block potassium
currents, but erythromycin also inhibits cytochrome P-450 3A4.
Assessing the balance of risk and benefit of interval–prolonging
When drugs that can prolong the QT interval are used, physicians should
ensure that the potential benefits are clinically important and the risks
are minimized. Specifically, they should determine whether the likely benefit
justifies the potential risk and should do so in light of the treated condition,
the specific circumstances of the patient, and other available therapeutic
options. For example, a QT interval–prolonging medication is the appropriate
choice if it has a proven salutary effect on survival. However, the majority
of these medications have not been proven to improve survival. Another strong
reason to use such a medication is if it will significantly improve symptoms
and morbidity relative to other treatment options. In this regard, medications
that commonly cause significant QT prolongation must be used only if no other
medications have a comparable beneficial effect in treating the same condition,
if they are known to be or are potentially superior to other available medications,
or if other medications carry other more significant risks.
The benefit of antiarrhythmic therapy, for example, is clearest when
it results in the immediate termination of a sustained ventricular arrhythmia.
When antiarrhythmic therapy is used for patients with symptoms of chronic
arrhythmias, the risk may outweigh the benefit because few studies have shown
a significant effect of antiarrhythmic therapy in this situation.43 The risks are particularly disconcerting with antiarrhythmic
medications that have been shown to worsen survival.44-46
The risk of torsades de pointes should be assessed for patients who
are about to begin taking a QT-prolonging medication. Although inadequate
clinical studies preclude prediction of absolute risk for individual patients,
particularly high-risk situations can be defined based on clinical variables.
This estimate requires knowledge of the drug's properties, including route
of elimination and drug interactions, familiarity with factors that predispose
to torsades de pointes, and baseline measurement of the QT interval. For example,
sotalol and dofetilide are renally cleared; thus, it is important to monitor
the renal function of patients starting these medications and to reduce the
dose if renal function is impaired. To avoid risk of torsades de pointes,
physicians should be aware that dofetilide has significant interactions with
commonly used drugs such as verapamil and trimethoprim-sulfamethoxazole.
Among the factors that could predispose to torsades de pointes, hypokalemia
and hypomagnesemia are particularly significant and remediable. Physicians
should monitor potassium and magnesium levels in patients who start antiarrhythmic
QT-prolonging medications and supplement them as needed, especially in patients
taking other medications that can cause hypokalemia or hypomagnesemia.
Measurement of the baseline QT interval may also be of critical importance
when assessing the risk of torsades de pointes in a particular patient. However,
with many drugs that can cause QT interval prolongation, the risk of torsades
de pointes is so low that the majority of experts do not consider measurement
of the QT interval to be cost-effective. For some of these drugs, the QT interval
must be measured in thousands of patients to identify 1 person at risk of
significant QT prolongation. The cost of this practice, in our opinion, outweighs
the benefits. In a survey completed by LQTS experts, the majority would always
check an ECG before and after starting an antiarrhythmic medication, one third
to half would always check an ECG before and after starting an antipsychotic
drug, and less than one third would always check an ECG before and after starting
an anti-infective or antidepressant (Box). Based on the results of this survey,
we propose the following recommendations on the proper monitoring of the QT
interval in patients receiving QT-prolonging medications. First, an ECG should
be routinely checked before and after starting an antiarrhythmic agent that
can prolong the QT interval (Table 1).
If the patient has a prolonged QTc at baseline (>450 ms in men and >460 ms
in women in the absence of interventricular conduction defects), it is important
to try to avoid all QT-prolonging medications.47 Although
this is not an absolute contraindication to starting QT-prolonging drugs,
expert opinion should be sought before such drugs are started. If the patient
is already taking an antiarrhythmic agent with this potential and another
drug needs to be added, it is important to know whether the new drug may also
prolong the QT interval (Box) or can interact with the antiarrhythmic medication
(Table 1). If one of these events
is a possibility, an alternative agent should be considered. If no alternative
is available and the drug being added is necessary, an ECG should be performed
to monitor the QT interval before and after starting the new drug. Indeed,
concurrent prescribing of QT-prolonging drugs is common in the outpatient
setting; however, the clinical consequences of this practice are not known.48
Second, an ECG should be checked before and after starting a drug if
the drug is one that has been deemed by the LQTS experts to have very probable,
probable, or possible potential for causing QT prolongation
(Box). If the
drug was deemed by the LQTS experts to have improbable or very improbable
potential for causing QT prolongation, checking an ECG before and after starting
the drug, especially in low-risk patients, may not be necessary
Despite these recommendations, uncertainty remains regarding the specific
relationship between the degree of QT prolongation and the risk of life-threatening
arrhythmias with each individual drug. A QT interval of at least 500 ms generally
has been shown to correlate with a higher risk of torsades de pointes, but
there is no established threshold below which prolongation of the QT interval
is considered free of proarrhythmic risk.9,49 Thus,
physicians are left with great uncertainty regarding when to stop a QT-prolonging
medication. Respondents to the survey on LQTS were more likely to stop a QT-prolonging
medication for a QT of 520 ms than for a QT of 500 ms. However, it should
be emphasized that there is no clear-cut consensus on the degree of drug-induced
QT prolongation that should require drug discontinuation.
Despite the clinical importance of the QT interval, definitive information
on the clinical epidemiology of the QT interval and its prolongation by medications
is surprisingly lacking. Few studies have evaluated the relationship between
the QT interval and patient outcomes. Even for commonly used antiarrhythmic
drugs like sotalol and amiodarone, this relationship has not been adequately
explored. The newly marketed compound dofetilide is the only medication for
which such a relationship has been extensively explored and reported.20,50 It has been demonstrated that a linear
relationship exists between the plasma concentration of dofetilide and the
mean change from baseline QTc. It has also been shown that a relationship
exists between the dose and concentration of dofetilide and its efficacy as
well as the risk of torsades de pointes associated with its use.20 A
direct correlation between rate of torsades de pointes and increase from baseline
QTc has also been proven for dofetilide.20 Knowledge
of these relationships should enable an astute clinician to make a semiquantitative
decision about the use and dosing of dofetilide by weighing the risks and
the proposed benefits of preventing recurrent atrial fibrillation or flutter.
Likewise, detailed dosing and monitoring recommendations are part of the product
labeling for the 2 most recently approved antiarrhythmic agents, dofetilide
and sotalol. The product labeling for medications that could prolong the QT
interval contains warnings regarding their effect on the QT interval that
clinicians who prescribe these drugs should be aware of.
Some antipsychotic drugs have been shown to prolong the QT interval.51,52 A recent clinical epidemiological
study has demonstrated a direct relationship between the dose of the older
antipsychotic drugs and the risk of sudden death, but the QT interval was
not measured in this study to examine its correlation with sudden death.53 More recently, a population-based study confirmed
that antipsychotic drugs known to produce greater QT prolongation than other
antipsychotic drugs were associated with a higher risk of cardiovascular death.54 Of note, no consensus exists about the relative likelihood
of torsades de pointes among patients treated with different antipsychotic
drugs, nor is there a prospective study delineating the absolute risk of arrhythmia.
This paucity of data leaves the practitioner in a lurch concerning therapeutics:
the need for antipsychotic therapy cannot be ignored, and the patients with
the most severe psychoses may need the highest doses of drugs. These same
patients are also at higher risk of nonadherence to prescribed therapies (including
omitting and taking excessive amounts of needed therapies) and to the development
of other conditions, such as electrolyte depletion or sympathetic overactivity,
that may predispose to torsades de pointes.
Furthermore, no data exist on how and when to monitor the QT interval
when various antipsychotic drugs are used. Until more data are obtained, the
Box should provide some guidance in this regard. Of note, because of the concern
raised about risk of QT prolongation with ziprasidone, a trial has been launched
that will randomly assign more than 15 000 patients with schizophrenia
to ziprasidone and olanzapine. This trial's primary end point is all-cause
mortality (Brian Strom, MD, unpublished data, 2002).
Quinolone antibiotics also pose a difficult dilemma. They are used on
a wide scale for common infections without checking the ECG, an approach generally
agreed on by the aforementioned LQTS experts (Box). Yet, sporadic episodes
of torsades de pointes have been reported in association with quinolones,55 and there is evidence that quinolones are commonly
coprescribed with other QT-prolonging drugs.48 Because
of the immense uncertainly surrounding the effects of concurrent use of QT-prolonging
drugs, no preventive approach is currently recommended other than trying to
avoid quinolones in patients taking other QT-prolonging drugs or with other
Risk management of qt interval–prolonging medications
We have thus far discussed the role of health care practitioners in
management of the risk of QT-prolonging medications in treating individual
patients. The scope of risk management, however, extends beyond health care
practitioners and includes regulators, pharmaceutical companies, and investigators.
For example, regulators came to realize the potential of noncardiovascular
drugs to prolong the QT interval and potentially result in life-threatening
arrhythmias. Thus, regulatory guidances on drug development advise that all
new drugs be evaluated for possible effects on cardiac repolarization.56
Guidance in that regard had until recently been sketchy. The US Food
and Drug Administration's (FDA's) International Conference on Harmonization
(ICH) S7A guidance included only a general mention of cardiovascular testing
of new drugs, which led to a lack of standardization of preclinical and clinical
cardiovascular drug testing.57 For example,
it was not specified whether drug testing should explore the effect of the
drug on the QTc or the uncorrected QT interval. The label for dofetilide relies
on the QTc (using the Bazett formula), whereas the label for sotalol uses
the uncorrected QT interval.
In February 2002, the ICHS7B guidance was proposed and, although it
has not been finalized, provides more specific direction for cardiac safety
testing of new drugs.56 The ICHS7B specifies
that new drugs should be tested in 3 preclinical assays: the human ether-a-go-go–related
gene channel assay to check for blockade of the IKr channel, the action potential
duration (APD) assay that uses canine Purkinje fibers to check for significant
APD prolongation, and an in vivo rodent ECG with a detailed description of
test methods. The guidance also suggests that if the tested drug is shown
in preclinical assays to cause some blockade of the IKr channel or prolongation
of the APD, its potential clinical risks should be evaluated in carefully
designed clinical trials. Those studies must have adequate sample sizes and
should ensure frequent recording of ECGs.
Although the preliminary ICHS7B guidance lacks data on the standards
of clinical evaluation, it is hoped that the final version will provide specific
information on the clinical evaluation standards for compounds with and without
hazardous QT signals in preclinical testing. It is well known that many companies
are screening compounds and discontinuing those in which a flag is raised
at the preclinical level. The potential advantage of this approach is obvious:
it prompts stopping the drug's development before the complex clinical manifestations
become an issue. However, the list of QT-prolonging drugs includes several
that provide substantial health benefits, and it would be unfortunate if drugs
with the potential for a highly positive overall impact were dropped early
The ICHS7B is one of many initiatives recently developed to improve
the cardiac safety of new drugs. In November 2001, the FDA announced that
as of the fall of 2002, sponsors must submit ECG raw data in digital format
with annotations to enable the FDA to independently assess the cardiac safety
profile of new drugs.58 The FDA is also working
with Health Canada to develop guidance on the assessment of QT prolongation
during clinical trials.47 The final guidance
is still pending. Through these initiatives, regulators are hoping to standardize
preclinical and clinical cardiovascular testing of all drugs, an important
endeavor in enhancing efforts at risk management of QT-prolonging medications.
Equally important, however, is the clear dissemination of these guidelines
and clear labeling of drugs with QT-prolonging potential, specifically as
they relate to interactions that could augment prolongation.
In this article, we present an update of the current knowledge of the
QT interval and proposed ways to enhance risk management of QT-prolonging
medications. As more knowledge about this important topic is gained, it is
critical that this knowledge be disseminated in a timely fashion and in a
style that is easily comprehended by clinicians. Perhaps the most surprising
finding of our review is the relative paucity of information that can help
clinicians and patients make informed decisions about drugs that can prolong
the QT interval.
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