Torsades de pointes and long QT syndromes

Although lengthy QT intervals had previously been associated with swoon and sudden death, it was not until 1966 that the actual arrhythmia associated with this syndrome was identified as a polymorphic form of ventricular tachycardia. Its electrocardiographic appearance was described as a "twisting of the points" or, in French "torsades de pointes."[1]

Both polymorphic and monomorphic ventricular tachycardia may arise in association with a normal QT interval. Polymorphic ventricular tachycardia may come about for instance, during myocardial ischemia or infarction, and it may be confused with ventricular fibrillation. The designation "torsades de pointes" should be applyed only when polymorphic ventricular tachycardia is associated with drawn out QT intervals.[1]

Prevalence and Risk Factors

The exact incidence of torsades de pointes remains speculative, yet the condition is thought to be more unrecognized than rare.[2] The arrhythmia has been reported in all age assemblages from newborns3 to the real old.4 Evidence of coexisting structural heart disease is ofttimes absent,[5,6] especially in the congenital form of the arrhythmia. Approximately 025 percent of deaf-mute children are born with a in extent QT interval. These individuals have been reported to depict about 30 percent of all patients with torsades de pointes and prolonged QT intervals.[2]

The overall mortality rate for patients with postponeed QT syndromes has been estimated to be 1 to 2 percent through year.[7] Some patients appear to have a benign course and have barely one or two episodes in their entire life. Others be attendant to have recurrent symptomatic episodes.[2]

Independent risk factors for death becoming to torsades de pointes include female sex congenital deafness, a history of fainting or resuscitated arrest, and a family history of unanticipated death. Few, if any, episodes have been reported during pregnancy or in the postpartum period.7 The reason for the lack of proceeding in association with pregnancy remains a mystery nevertheless may perhaps be explained, at least in part, at the usual avoidance of put drugs intos during pregnancy. Agents known to extend the QT interval can predispose individuals to torsades de pointes.

Characteristics

The polymorphic configuration in torsades de pointes is caused at changes in the QRS axis, as if the QR complexe were being twisted around the isoelectric line (Figure 1) These polarity oscillations typically fall out every three to 20 beats. Characteristically, torsade de pointes present itselfs in clusters, and it look afters to be rapid and self-terminating. The ventricular number is usually irregular, and rates from 160 to athwart 300 have been described.[4,8]

Since the ventricular rate is typically rapid, sustained torsades de pointes is almost always poorly tolerated. Patients frequently complain of symptoms that are related to hemodynamic compromise from reasonable cardiac output. These include dizziness, angina, shortness of breath and swoon Torsades de pointes may degenerate into ventricular fibrillation and unlooked for death.[3,4,8-10]

The QT Interval

The QT interval is measured from the QR manifold (i.e., the beginning of the Q wave or, if the Q wave is absent, the beginning of the R wave) to the [i]finale[/i] of the T wave. If a U wave is merg with the T wave, this should be included in the measurement, and the interval in this situation is called the QTU interval.

The measured QT interval ([QTsubm]) should be corrected to the heart rate ([QTsubc]) The best way to make this calculation is in subordination to current dispute. Many formulas have appeared in the literature, still the following is still the single most commonly used: QTc = QTm/RR where RR (in seconds) indicates the interval between the brace R waves preceding the measured QT31

In the absence of intraventricular conduction delays, the normal corrected QT interval ([QTsubc]) is 420 to 440 msec When put into bundles branch block is present, right calculation of the [QT.sub.c] is still unsettled[7] The QT interval should be measured in several leads, and the longest the same ([QT.sub.max]) should be used. The anteroseptal leads are frequently closest to the [QT.sub.max].[12] As a cragged guide, if the [QT.sub.m] is greater than half the preceding RR interval, the [QTsubc] is likely to be continue lengthen in timeed though this applies best when the heart rate is les than 100 beats by minute (Figure 2).

Torsades de pointes induction hangs not only on QT prolongation if it were not that also on the T-wave distortion.[13] Quinidine-induced torsades de pointes (quinidine syncope) has been reported to be accompanied through minimal increases in the QT interval,[13,14] whereas hypocalcemia is an infrequent cause of torsades de pointes despite marked QT prolongation.[15,16] However, quinidine induces T-wave distortions as it extends repolarization, whereas hypocalcemia only lengthens the ST section T-wave distortions are believed to be essential for torsades de pointes to be initiated, and they indicate a greater vulnerability to the increase of the arrhythmia.[5,13,17-19] These distortions may take the form of notched T waves, biphasic T waves or T-wave alternans (i.e., T-wave distortions that vary from beat to beat).