Postgrad Med J: first published as 10.1136/pgmj.61.715.379 on 1 May 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 379-386 Review Article The prolonged QT interval - a frequently unrecognized abnormality R.A. Kenny and R. Sutton Department ofCardiology, Westminster Hospital, Horseferry Road, London SW] 2AP, UK. Introduction The clinical importance of the long QT interval slowing heart rate (Browne et al., 1983a; Lown et al., syndrome lies in its association with malignant ven- 1973). tricular dysrhythmias which are usually amenable to The physiological control of the QT interval has treatment with either drugs or cardiac pacing. been used to construct a cardiac pacemaker which The QT interval extends from the beginning of the senses the interval between the delivered stimulus and QRS complex (whether the initial component is a Q or the evoked T wave and uses this interval to set the an R wave) to the end of the T wave. It therefore subsequent pacemaker escape interval (Rickards & represents the algebraic sum of the individual action Norman, 1981; Donaldson et al., 1983). potentials of the ventricular myocytes, including both depolarization (the QRS complex or QJ interval) and repolarization (the T wave or JT interval). The rapid Measurement of the QT interval copyright. process of depolarization is rarely sufficiently prolon- ged to make any clinically significant difference to the Measurement of the QT interval on the surface QT interval duration and the term effectively refers to electrocardiogram (ECG) can present technical changes in the duration ofrepolarization, that is the JT problems because the end of the T wave may be interval. difficult to define. The point at which the line of maximal downslope ofthe T wave crosses the baseline is therefore often used to identify the end of the T Physiological variations in the QT interval wave. The surface ECG leads chosen for QT interval http://pmj.bmj.com/ measurement are those which show the greatest T It is well known that the QT interval alters with heart wave amplitude and duration. The QT interval should rate (Bazett, 1920). However, heart rate is only one of be measured in at least three consecutive cardiac cycles the determinants of the QT interval duration (Rick- and the time values averaged. Although tables that list ards & Norman, 1981) and other factors, particularly normal values for a specific cardiac rate, age and sex changes in autonomic activity, also contribute to QT are available, Bazett's formula (1920) for calculating interval shortening during exercise (Browne et al., the QT interval corrected for heart rate is commonly 1983b). By comparing QT interval changes during used: on September 24, 2021 by guest. Protected atrial synchronized and asynchronous ventricular pacing, Fanazapazir et al. (1983) determined that the QT calculated (QT,) = QT (measured) contribution of the intrinsic effect of the heart rate to k QT interval shortening during exercise varied from 26 /RR interval (s) to 75%. where k is 0.37 for men and 0.40 for women. The upper Sleep represents a naturally occurring period of limit is 0.39 s for men and 0.44 s for women (Braun- increased parasympathetic tone or sympathetic tone wald, 1984). Because ofvariations in the measured QT withdrawal (Kleinman, 1963; Baust & Bohnert, 1969) interval as a result of influences other than heart rate, and prolongs the QT interval independently of the such as sympathetic and parasympathetic activity, drugs, electrolyte changes, ventricular hypertrophy, Correspondence: R.A. Kenny, MB., M.R.C.P.I. Depart- ischaemia, and acid-base disturbances, different ran- ment of Cardiology, Westminster Hospital, Horseferry ges of normality are accepted by different inves- Road, London SWI 2AP tigators. For practical purposes therefore, minor Accepted: 9 October 1984 deviations from the expected QT, interval should be © The Fellowship of Postgraduate Medicine, 1985 380 R.A. KENNY & R. SUTTON Postgrad Med J: first published as 10.1136/pgmj.61.715.379 on 1 May 1985. Downloaded from disregarded as being of questionable clinical sig- sion of repolarization which involves premature re- nificance. polarization will not be reflected by prolongation of The use of QT, is at times misleading when interval the QT interval and, unless the mass of cells is large, changes are examined in association with rapid chan- may not even cause an alteration of T wave mor- ges in heart rate (Camm et al., 1984). The biophysical phology. Such patients are, however, just as likely to effect of heart rate on QT interval develops slowly be at risk from ventricular dysrhythmias as those in (Arnold et al., 1982) and therefore the use of formulae whom temporal dispersion of ventricular repolariza- such as that described by Bazett may result in gross tion is the result of abnormally delayed repolarization overcorrection (Milne et al., 1980). (Han & Moe, 1964; Han & Goel, 1972; El-Sherifet al., 1977). These concepts can explain the apparently paradoxical effects of different drugs. Thus, anti-arr- Repolarization, the vulnerable period and the long QT hythmic agents which prolong repolarization may act interval by normalizing premature depolarization in abnormal myocardium, while in other situations, such as tor- Myocardial repolarization is complex, poorly under- sades de pointes in the acquired LQTS, drugs which stood and even more difficult to study than de- shorten abnormally prolonged depolarization, such as polarization. It is also, possibly because of its slower isoprenaline, are effective when many standard agents time course, more obviously affected by disease, are not or may even exacerbate the dysrhythmia drugs, and biochemical abnormalities. It is normally a (Bennett, 1982; Soffer et al., 1982). well coordinated but non-uniform process, as is Long term treatment ofrabbits with beta adrenergic evident from the consistent asymmetry of the normal antagonists induces several adaptive changes in the T wave. myocardium which persist long after the drugs have The vulnerable period is that part of the cardiac been eliminated from the body (Vaughan Williams, cycle during which ventricular tachycardia or fibrilla- 1977). This 'adaptive syndrome' includes prolonga- tion can be most easily provoked and this is always the tion of the action potential duration and the QT relative refractory period of the ventricular myocar- interval and both these effects have been shown to dium, corresponding to the declining limb of the T occur in man although the full clinical implication of wave from peak to iso-electric line. Increased vul- the findings are unclear (Edvaardssonn & Olsson,copyright. nerability to the provocation ofventricular fibrillation 1981; Vaughan Williams et al., 1980; Milne et al., can be induced by many means which have in common 1980). the effects ofcausing temporal dispersal ofrepolariza- tion often combined with increased excitability. Tem- poral dispersal of the repolarization process may Torsades de pointes occur as a result of premature repolarization of some myocardial cells or as abnormally delayed repolariza- Torsades de pointes is virtually always associated with http://pmj.bmj.com/ tion of other cells. The latter may be reflected in the prolongation of the QTc interval (Smith & Gallagher, surface electrocardiogram as prolongation of T wave 1980) and is the most important and singular arrhyth- with corresponding lengthening of the QT interval. mia complicating both acquired and congenital long Marked lengthening of the QT interval of the order QT interval syndromes (Bonatti et al., 1983; Montro, which can be measured on the surface ECG is almost 1981). Torsades de pointes is characterized by short inevitably associated with increased temporal disper- intervals of ventricular tachycardia which consist of sion of repolarization and thus increases the duration bursts of ventricular waves occurring at a high rate of the vulnerable period as well as decreasing the (from 150 to 250 beats/min) and showing progressive- on September 24, 2021 by guest. Protected threshold for ventricular fibrillation. ly varying amplitude and polarity (Figure 1). Attacks The severe prolongation of repolarization found in may be brief or prolonged, when syncope may occur. the long QT syndrome (LQTS) decreases the degree of Attacks most often stop spontaneously but on some prematurity required for an ectopic beat to occur occasions they progress to ventricular fibrillation and within the vulnerable period and therefore enhances death (Krikler, 1976; Krikler et al., 1976). The distinc- the likelihood of ventricular arrhythmias (Lipman et tion between torsades de pointes and those polymor- al., 1979; Montro, 1981). These hypotheses account phous ventricular tachycardias occurring in patients for the frequent association of arrhythmias and the with a normal QT interval has important therapeutic prolonged QT syndrome. They may also explain why implications. The former requires strict avoidance of some patients with abnormally prolonged QT in- all drugs that may potentially further delay repolariza- tervals run a trouble free course. tion, including class I antiarrhythmic agents such as Conventional electrocardiography only reflects the quinidine, disopyramide and lignocaine. Immediately, net resultant of the repolarization of all ventricular the initiation of cardiac pacing is often necessary for myocardial cells. Thus any abnormal temporal disper- arrhythmia control and, on a long term basis, sym- Postgrad Med J: first published as 10.1136/pgmj.61.715.379