Die verlängerte QT-Dauer im Elektrokardigoramm

Hegglin, R

doi:10.1007/bf02119125

Cited by 20 publications

(2 citation statements)

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“…Now the aortic valve closes before the T wave ends, 28 , 29 resulting in abnormal ventricular deformation, due to ventricular loading, when repolarization is still progressing ( Figure 1A ). Although this reversed electromechanical relation was first reported in acquired QT prolongation 30 and in the seminal paper by Jervell and Lange-Nielsen ( Figure 1B ), 31 its arrhythmogenic potential for patients with congenital LQTS was only recognized decades later. 28 , 29 , 32 …”

Section: Introductionmentioning

confidence: 84%

Electromechanical reciprocity and arrhythmogenesis in long-QT syndrome and beyond

Odening

Linde

Ackerman

et al. 2022

European Heart Journal

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An abundance of literature describes physiological and pathological determinants of cardiac performance, building on the principles of excitation–contraction coupling. However, the mutual influencing of excitation–contraction and mechano-electrical feedback in the beating heart, here designated ‘electromechanical reciprocity’, remains poorly recognized clinically, despite the awareness that external and cardiac-internal mechanical stimuli can trigger electrical responses and arrhythmia. This review focuses on electromechanical reciprocity in the long-QT syndrome (LQTS), historically considered a purely electrical disease, but now appreciated as paradigmatic for the understanding of mechano-electrical contributions to arrhythmogenesis in this and other cardiac conditions. Electromechanical dispersion in LQTS is characterized by heterogeneously prolonged ventricular repolarization, besides altered contraction duration and relaxation. Mechanical alterations may deviate from what would be expected from global and regional repolarization abnormalities. Pathological repolarization prolongation outlasts mechanical systole in patients with LQTS, yielding a negative electromechanical window (EMW), which is most pronounced in symptomatic patients. The electromechanical window is a superior and independent arrhythmia-risk predictor compared with the heart rate-corrected QT. A negative EMW implies that the ventricle is deformed—by volume loading during the rapid filling phase—when repolarization is still ongoing. This creates a ‘sensitized’ electromechanical substrate, in which inadvertent electrical or mechanical stimuli such as local after-depolarizations, after-contractions, or dyssynchrony can trigger abnormal impulses. Increased sympathetic-nerve activity and pause-dependent potentiation further exaggerate electromechanical heterogeneities, promoting arrhythmogenesis. Unraveling electromechanical reciprocity advances the understanding of arrhythmia formation in various conditions. Real-time image integration of cardiac electrophysiology and mechanics offers new opportunities to address challenges in arrhythmia management.

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Section: Introductionmentioning

confidence: 84%

Electromechanical reciprocity and arrhythmogenesis in long-QT syndrome and beyond

Odening

Linde

Ackerman

et al. 2022

European Heart Journal

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“…The following questions arose: (1) \iVIi:it was the n;iture of the heart tlisease in these chiltfrcn? a t i d (2) b\;as there an).…”

Section: )Isclrsslonmentioning

confidence: 99%

Congenital Deaf‐mutism, Functional Heart Disease With Prolongation of the Q‐t Interval, and Sudden Death

A¹,

Nielsen²

1999

Noninvasive Electrocardiol

194

230

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COMBINATION of deaf-mutism and a peculiar heart disease has been A observed in 4 children in a family of 6. The parents were not related, and were, as the other 2 children, quite healthy and had normal hearing.The deaf-mute children, who otherwise seemed quite healthy, suffered from "fainting attacks'' occurring from the age of 3 t o 5 years. By clinical and roeiitgen 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 Q-T interval in all cases.Three of the deaf-mute children died suddenly a t the ages of 4, 5 , and 9 years, respectively. CASE REPORTSCase 1. Tormod J., born 1944-This boy had suffered from repeated "fainting attacks" since the age of 3 years. The attacks occurred a t intervals of up to 6 months, and they never lasted for more than 2 to 3 minutes. The attacks usually occurred following efforts. His relatives stated that the attacks were associated partly with pallor and partly with cyanosis, but never with convulsions or biting of the tongue. Involuntary emptying of the bladder, howe\er, had been observed. Occasionally the boy had complained of palpitations and precordial pains.In July, 1953, he was examined at Aust-Agder and Arendal Central Hospital (Dr. Kloster). The only pathologic finding was a prolongation of the Q-T interval in the electrocardiogram.On the assumption that he might be suffering from epilepsy, the patient was treated with barbiturates and phenantoin, without effect, however.Since 1952, the boy attended a boarding school for deaf-mute children. On Oct. 10, 1953, he suddenly fainted without apparent cause. He remained unconscious for about 5 minutes with cyanosis of the face and with convulsive movements of the fingers. Afterwards he was somewhat exhausted, but after a few hours in bed, he was just as lively as usual and wanted to go out playing.The boy was admitted to the Medical Department of Vestfold Central Hospital where he was observed from Oct. 13, to Nov. 10, 1953. Apart from the deaf-mutism, no evidence of congenital defects could be discovered. He had a healthy appearance. Height: 142.5 cm.; weight 34.6 kilograms. His deaf-mutism to some extent prevented adequate contact, but he appeared normally developed and was cooperative when examined.The pulse was 72, with regular rhythm, blood pressure 100/60 mm. Hg. The temperature was normal and there was no cyanosis or congestion. A weak systolic murmur (Grade 1) was heard in the second left intercostal space.The physical examination revealed no essential abnormality.Neurological examination revealed nothing abnormal. w e k after his cliscli;irge, hr h:id ;inother attack. Hc suddenly bcc'amc pale and fell iincoiisvioiis. On the (lortor's arrival the pat icwt was pulseless with cold skin and with inarkrtl cyinosis. I7c \\':IS t;ikrn t o t.hr hospital ;is soon as possiblc, but on arrival hc presented t1efiiiit.c siaiis o f tlr;itli with ninrltcti hypost asis. 'I'hcre wiis no frothy discharge from the nose ...

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