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    QTc

    QTc

    QTc: heart-rate corrected QT interval, correction formulas, normal values and the risks of long and short QT.

    QTc is the QT interval of the electrocardiogram corrected for heart rate. The QT interval reflects the total time the heart ventricles need to depolarise and then recover (repolarise) before the next beat. A QTc that is too long — or, much more rarely, too short — increases the risk of dangerous ventricular arrhythmias, including torsade de pointes and sudden cardiac death.

    ECGRepolarisationLong QT syndromeDrug safety
    Normal, men≈ 350–450 ms
    Normal, women≈ 360–460 ms
    High arrhythmia risk> 500 ms
    Short QT suspected≤ 360 ms

    What the QT interval is

    The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The QRS complex corresponds to electrical activation (depolarisation) of the ventricles; the ST segment and T wave correspond to their recovery (repolarisation). At the cellular level the QT interval mirrors the duration of the ventricular action potential, which is shaped mainly by sodium and calcium currents flowing into the cell and potassium currents (IKr, IKs) flowing out.

    When the outward potassium currents are weakened — by a gene mutation, a medicine or low potassium — repolarisation is delayed, the QT interval lengthens and the heart muscle becomes electrically unstable. Early afterdepolarisations can then trigger a polymorphic ventricular tachycardia called torsade de pointes, which may stop on its own (causing fainting) or degenerate into ventricular fibrillation.

    ECG cycle with P wave, QRS complex, ST segment and T wave; QT interval measured from QRS onset to end of T wave; RR interval between two R waves PRQST QT interval RR interval (one cardiac cycle)
    Figure 1. The QT interval runs from the start of the Q wave (or R wave if there is no Q) to the end of the T wave. The RR interval — the time between beats — is used to correct QT for heart rate.

    Why QT must be corrected for heart rate

    QT shortens when the heart beats faster and lengthens when it beats slower. To compare ECGs recorded at different heart rates, QT is converted to the value expected at 60 beats per minute (RR = 1 second). This is QTc. Several formulas exist (QT and RR in seconds; Hodges uses heart rate in beats per minute):

    Bazett: QTc = QT / √RR   |   Fridericia: QTc = QT / ∛RR
    Framingham: QTc = QT + 0.154 × (1 − RR)   |   Hodges: QTc = QT + 0.00175 × (HR − 60)

    Bazett's formula is the oldest and still the most used by ECG machines, but it over-corrects at fast heart rates (falsely long QTc) and under-corrects at slow ones. In a study of 6609 patients, the Fridericia and Framingham formulas gave the best rate correction and better predicted 30-day and 1-year mortality; Bazett performed worst. Fridericia is preferred when heart rate is above about 90 or below 60 beats per minute and in drug-safety monitoring.

    QTc calculated by Bazett and Fridericia formulas for a QT of 360 ms at different heart rates; Bazett rises steeply at high heart rates 507090110 Heart rate, beats/min (measured QT kept at 360 ms) 300400460520 Bazett Fridericia prolonged zone
    Figure 2. The same measured QT (360 ms) gives very different QTc values at high heart rates: Bazett crosses the prolonged zone at about 100 beats/min, whereas Fridericia rises much less. Red zone: QTc ≥ 460 ms; orange: 440–460 ms.

    Reference values

    QTc (ms)MenWomenInterpretation
    ≤ 340ShortShort QT syndrome possible — evaluate
    341–360Borderline shortSignificant only with symptoms or family history
    Normal≤ 440–450≤ 450–460Normal
    Prolonged≥ 450≥ 460Prolonged — look for causes, review medicines
    ≥ 480Markedly prolongedMajor criterion for long QT syndrome when repeated
    > 500, or rise > 60 ms from baselineHigh riskSubstantially increased risk of torsade de pointes
    Thresholds follow AHA/ACCF/HRS recommendations (Rautaharju 2009) and the AHA/ACCF statement on torsade de pointes prevention (Drew 2010). Women have a longer QTc than men after puberty.

    Long QTc

    Congenital long QT syndrome (LQTS)

    Congenital LQTS affects about 1 in 2000 people. It is caused by mutations in ion-channel genes; the three most common types account for most genotyped cases:

    TypeGene / currentTypical trigger of arrhythmia
    LQT1KCNQ1 — reduced IKsExercise, especially swimming
    LQT2KCNH2 (hERG) — reduced IKrSudden noise (alarm clock, phone), emotion, postpartum period
    LQT3SCN5A — persistent late sodium currentRest and sleep, slow heart rate

    Acquired QT prolongation

    Much more common is QT prolongation caused by external factors, often several at once:

    • Medicines that block the hERG (IKr) potassium channel: antiarrhythmics (sotalol, amiodarone, dofetilide, quinidine), some antibiotics (macrolides such as erythromycin and clarithromycin, fluoroquinolones), antifungals, antipsychotics (haloperidol, some atypical agents), antidepressants (citalopram, escitalopram, tricyclics), methadone, ondansetron, domperidone, hydroxychloroquine and others. An up-to-date list is maintained at CredibleMeds.org.
    • Electrolyte disorders: low potassium, low magnesium, low calcium.
    • Slow heart rate: sinus bradycardia, AV block.
    • Heart disease: heart failure, left ventricular hypertrophy, myocardial ischaemia.
    • Other: female sex, older age, hypothyroidism, hypothermia, kidney or liver failure (higher drug levels), anorexia and starvation, stroke or intracranial bleeding.

    Possible symptoms

    • Often none — QT prolongation is usually found on a routine ECG
    • Sudden fainting, especially during exercise, emotion or a loud noise
    • Seizure-like episodes (sometimes misdiagnosed as epilepsy)
    • Palpitations, near-fainting
    • Cardiac arrest or sudden death, sometimes as the first event

    What reduces the risk

    • Avoid QT-prolonging medicines and combinations of them
    • Keep potassium and magnesium normal (especially with diuretics, vomiting or diarrhoea)
    • Repeat the ECG after starting a QT-prolonging drug
    • In congenital LQTS: beta-blockers, lifestyle measures, sometimes an implantable cardioverter-defibrillator
    • Screen first-degree relatives of a person with LQTS

    Short QTc

    A short QTc is rare. It may be caused by high calcium or potassium levels, digoxin, fever, acidosis or increased vagal tone. Short QT syndrome is an inherited channelopathy (gain of function in potassium channels such as KCNH2, KCNQ1, KCNJ2) associated with atrial fibrillation, fainting and sudden cardiac death, sometimes at a young age. The diagnosis uses a scoring system that combines QTc, the J-point–to–T-peak interval, symptoms, family history and genetic testing.

    Measurement pitfalls

    • The end of the T wave is often hard to define; a U wave merged with the T wave can falsely lengthen QT. The tangent method (where the steepest slope of the descending T wave crosses the baseline) improves consistency.
    • Use the lead with the longest QT, usually II or V5, and average several beats.
    • In atrial fibrillation, RR changes constantly; QTc should be averaged over 10 or more beats.
    • A wide QRS (bundle branch block, pacing) lengthens QT without the same arrhythmic meaning; the JT interval or special corrections are used instead.
    • Automatic machine values are a good start but should be checked manually when they are abnormal.

    When to see a doctor

    Call emergency services if

    someone with a known long QT faints, has a seizure-like episode or suddenly collapses. Start cardiopulmonary resuscitation and use an automated external defibrillator if the person is not breathing normally.

    Arrange an assessment if

    QTc is ≥ 460–470 ms (men) or ≥ 470–480 ms (women) on more than one ECG, if QTc is over 500 ms or has risen by more than 60 ms since a medicine was started, if it is ≤ 360 ms with symptoms, or if a relative died suddenly before the age of 40. Tell every doctor and pharmacist about a long QT before you take a new medicine.

    References

    1. Rautaharju PM, Surawicz B, Gettes LS. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval. Circulation. 2009;119(10):e241–e250. doi:10.1161/CIRCULATIONAHA.108.191096
    2. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047–1060. doi:10.1161/CIRCULATIONAHA.109.192704
    3. Vandenberk B, Vandael E, Robyns T, et al. Which QT correction formulae to use for QT monitoring? J Am Heart Assoc. 2016;5(6):e003264. doi:10.1161/JAHA.116.003264
    4. Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013–1022. doi:10.1056/NEJMra032426
    5. Schwartz PJ, Stramba-Badiale M, Crotti L, et al. Prevalence of the congenital long-QT syndrome. Circulation. 2009;120(18):1761–1767. doi:10.1161/CIRCULATIONAHA.109.863209
    6. Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic criteria. J Am Coll Cardiol. 2011;57(7):802–812. doi:10.1016/j.jacc.2010.09.048

    This article is for general information and does not replace a consultation with a doctor. Never stop or change a prescribed medicine on your own because of a QTc value — discuss it with the prescribing doctor.

    Published on 7 July 2019