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Lidocain Mexiletin

Chinidin Ajmalin Disopyramid

Fig. 7. Antiarrhythmic drug effects on the ventricular action potential. Effects of various antiar-rhythmic drugs on the ventricular action potential. The unbroken line (a) represents the control state. The circles indicate the level of repolarization at which the fiber becomes reexcitable (ERP = effective refractory period). Action potential duration and the QT-interval are prolonged in b under the effect of Quinidine or Procainamide and shortened when exposed to Lidocain (c)

whereas Dirk Durrer and Henrick JJ Wellens were the first who executed programmed stimulation in men (Fig. 6) (65,66). The programmed stimulation technique has in firstline been used to induce ventricular tachycardia and to elucidate the mechanisms of tachycardias in the Wolff-Parkinson-White-Syndrome (67). Electrophysiologic testing was then more and more used to guide pharmacological therapy and to delineate the electrophysiologic effects of drugs on the normal and diseased myocardium (68). The registration of the action potential in the experimental laboratory and in the intact human heart via catheter technique did substantially change our mechanisms in cellular de- and repolarization (69-71), antiarrhythmic drug effects (Fig. 7) (72-75), and arrhythmo-genesis (76,77).

In the late 18th century the Italian scientist Felice Fontana described a phenomenon later called the refractory period while he was investigating irregular impulses of the heart (78). Subsequently, Moritz Schiff, a German physiologist (Fig. 8), reported in 1850 that a strong electrical stimulus that has been delivered during the late refractory period of cardiac muscle could induce a contraction. Confirmation of these findings was achieved by Hugo Kronecker and the French physiologist Etienne Jules Marey, who performed a first documentation of phenomenons like premature ventricular beats using a polygraph recording of the radial and apical impulse simultaneously (79). Schiff's, Kroneckers's, and Marey's experiments have been completed by the work of Anton Carlson, an American physiologist, who established the still accepted concept of absolute and relative

History of Repolarization

Fig. 8. Moritz Schiff (1823-1896).

refractory periods in cardiac tissue (80). In 1920 Bazett described the relationship between rate and the duration of the QT-interval in 39 normal subjects (81). He summarized, that the QT interval varies with the square root of the cycle length:

constant

The constant k has been fixed to 0.37 in men and 0.4 in women by Bazett. Later on Shipley and coworkers changed these values to 0.397 and 0.415 respectively after investigating 200 normal subjects (82). Today, the Bazett calculation is generally used as QTc = QT^R-R. Thus the QTc-interval is corrected or normalized to the QT interval at a heart rate of 60 beats/min. Several attempts have been made since to modify or substitute the Bazett calculation to gain a still better expression of the cardiac physiology. Fridericia for example proposed a cube root formula in 1920 after analyzing 50 normal subjects where QT = k(constant) x ^R-R (82). However, comparing the cube root formula to the normal range of the QT interval, this calculation gives too short intervals at low rates and too long intervals at high rates. Subsequently, Ashman proposed a logarithmic formula in 1942 with QT = k1 x log (10 x [R-R + k2]) with the disadvantage of this type of calculation again exhibiting too low intervals at low heart rates (83). A straight-line formula has also been discussed by various investigators (84-88), however the Bazett calculation is still the most widely accepted. It has also been Ashman who investigated the relationship of heart rate and the refractory period; he described first that aberration can be induced by prolongation of the preceding cycle, an observation which is commonly referred to as the Ashman phenomenon (89).

flu. 1.—T<Kmod J. (ul ECC: Julï H). 1013. during rm. Uu<l( I, II, III. Iv Ft. Q-T u.ftu ««. :: H - 11 g stir. (6) bcci ■ 1Î0. :i.onila i, II. iii. iv li. Q-T -0.(10 iiw. K-TC - 0 N/i ■■

Fig. 9. Jervell and Lange-Nielsen syndrome. A combination of deaf-mutism and a peculiar heart disease has been observed in 4 children in a family of 6. The parents were not related, and were, as the other 2 children, who otherwise seemed quite healthy and had normal hearing. The deaf-mute children, who otherwise seemed quite healthy, suffered from fainting attacks "occurring from the age to 3 to years. By clinical and roentgen examination, which was performed in 3 of the children, no signs of heart disease could be discovered. The electrocardiograms, however, revealed a pronounced prolongation of the QT interval in all cases. Three of the deaf-mute children died suddenly at the ages of 4, 5, and 9 years respectively."

Reproduced from Jervell A, Lange-Nielsen F: Congenital deaf mutism, functional heart disease with prolongation of the QT interval, and sudden death. Am Heart J 1957;54:59-68 with permission.

flu. 1.—T<Kmod J. (ul ECC: Julï H). 1013. during rm. Uu<l( I, II, III. Iv Ft. Q-T u.ftu ««. :: H - 11 g stir. (6) bcci ■ 1Î0. :i.onila i, II. iii. iv li. Q-T -0.(10 iiw. K-TC - 0 N/i ■■

Fig. 9. Jervell and Lange-Nielsen syndrome. A combination of deaf-mutism and a peculiar heart disease has been observed in 4 children in a family of 6. The parents were not related, and were, as the other 2 children, who otherwise seemed quite healthy and had normal hearing. The deaf-mute children, who otherwise seemed quite healthy, suffered from fainting attacks "occurring from the age to 3 to years. By clinical and roentgen examination, which was performed in 3 of the children, no signs of heart disease could be discovered. The electrocardiograms, however, revealed a pronounced prolongation of the QT interval in all cases. Three of the deaf-mute children died suddenly at the ages of 4, 5, and 9 years respectively."

Reproduced from Jervell A, Lange-Nielsen F: Congenital deaf mutism, functional heart disease with prolongation of the QT interval, and sudden death. Am Heart J 1957;54:59-68 with permission.

Lepeschkin and Surawicz described in 1952 QT interval differences among the 12 leads of the surface ECG as a possible expression of spatial inhomogeneity of ventricular repolarization (90). However, it lasted until the mid-80s until systematic investigations of the spatial inhomogeneity of repolarization were performed: Mirvis and colleagues studied the difference between the longest and shortest QT interval using body surface mapping in normals and patients after myocardial infarction (91). The term "QT dispersion" as an expression of regional differences in myocardial repolarization has been established in clinical cardiology by Ronald WF Campbell and coworkers (92). Even if in our days the relevance of the QT dispersion for clinical decision making is very limited owing to methodological problems and contradicting study results, it served as an important step for a better understanding of the spatial aspects of repolarization.

history of the "long qt syndrome" and "torsades de pointes" tachycardia

The long QT syndrome is characterized by QT interval prolongation and syncope or sudden cardiac death owing to ventricular tachyarrhythmias. The congenital form can either be familial or idiopathic (93,94). The familial type consists of two subgroups:

Fig. 10. Torsades de pointes tachycardia. Dessertenne first described this form of polymorphic tachycardia in 1966 when he observed this rhythm disorder in an 80-year old female patient with complete AV block (46).

1. The Jervell and Lange-Nielsen which is associated with deafness.

2. The Romano-Ward syndrome with normal hearing. Two classical descriptions of these functional, hereditary syncopal cardiac disorders exist (95-98).

Jervell and Lange-Nielsen Syndrome. In 1957 Anton Jervell and Fred Lange-Nielsen described a case of syncopal arrhythmia and QT prolongation combined with a profound congenital deafness in a Norwegian family with six children (95). Four of the children were deaf-mutes, suffered from syncopal episodes with loss of consciousness and demonstrated a clear QT interval prolongation on their surface electrocardiograms (Fig. 9). Three of the four children with the disease died suddenly. Interestingly the parents of those children were healthy as an indicator for the recessive genetics in the Jervell and Lange-Nielsen syndrome.

Romano-Ward Syndrome. Cesarino Romano was born in Voghera, Italy in 1924. After his study of medicine at the University of Pavia, he worked in pediatrics at the University of Genoa. In 1961 he became a professor for pediatrics and later he served as the director of the First Pediatric Department and the Scientific Institute of the Pediatric Clinics at the University of Genoa. Among numerous publications dealing with hereditary hypothyroidism, cystic fibrosis, and cardiac disorders, he described in 1963 an inherited functional syncopal heart disorder with prolonged QT interval in a 3-mo-old female patient

("Aritmie cardiache rare dell'eta'pediatrica") (96). Two brothers of his patient had exhibited the same symptoms and died suddenly at a young age. Independently of Romano, Owen Conor Ward, professor for clinical pediatrics at the University of Dublin, published one year later a work in Ireland entitled "A New Familial Cardiac Syndrome in Children." He also described syncopal attacks and a prolonged QT interval in both a young female patient and her brother (97). Ward was born in Monaghan, Ireland on August 27, 1923. After completing St. Macarten's College in Monaghan, Ward studied medicine at the University College of Dublin where he passed his examinations in 1947. After his internship in various Irish hospitals, Ward specialized in pediatric medicine in 1949 and earned his doctorate in 1951 with a thesis on hypoglycemia in neonates. After that, Ward worked for a few years in a Dublin pediatric clinic. In 1972, he was made a professor of clinical pediatrics at the University of Dublin, where he has served as first professor for pediatrics since 1983.

The typical arrhythmia of patients with congenital or acquired long QT syndrome is the torsades de pointes tachycardia. This specific form of a dangerous polymorphic ventricular tachyarrhythmia is characterized by a repetitive change of the main QRS vector during tachycardia in the presence of a prolonged repolarization. Dessertenne first described the torsades de pointes morphology in an 80-yr-old female patient with intermittent AV block (Fig. 10) (99). The cause of her recurring syncopal episodes was the torsades de pointes tachycardia rather than the bradycardia, as it has primarily been suspected. Dessertenne himself suggested in his description that two competing foci were responsible for the typical torsades de pointes morphology. This hypothesis has been tested in experimental animal studies, one using a porcine Langendorff heart technique by Christoph Naumann d'Alnoncourt and Berndt Lüderitz and in a canine heart in situ experiment from Gust H Bardy and Raymond E Idecker (100,101). In both studies pacing from the left and right ventricular site at a similar but periodically changing rate resulted in an electrocardiogram with torsades de pointes configuration.

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