Self-terminating ventricular tachyarrhythmias—a diagnostic dilemma?

Clayton, Richard H.; Murray, Alan; Higham, P D; Campbell, R. W. F.

doi:10.1016/0140-6736(93)92567-d

Cited by 46 publications

(24 citation statements)

References 6 publications

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“…If the core of the re-entrant wave moves to the boundary of excitable tissue, for example to the inexcitable tissue connecting the atria and ventricles, then the re-entrant wave is extinguished and the arrhythmia stops. Self-terminating arrhythmias have been observed experimentally (Jalife et al, 1998) and clinically (Clayton et al, 1993), and often occur in the LQTS . Striking di!erences in the lethality of ventricular arrhythmias in the di!erent LQTS phenotypes have also been reported (Zareba et al, 1998).…”

Section: Introductionmentioning

confidence: 98%

Re-entrant Cardiac Arrhythmias in Computational Models of Long QT Myocardium

Clayton

Bailey

Biktashev

et al. 2001

Journal of Theoretical Biology

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Section: Introductionmentioning

confidence: 98%

Re-entrant Cardiac Arrhythmias in Computational Models of Long QT Myocardium

Clayton

Bailey

Biktashev

et al. 2001

Journal of Theoretical Biology

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“…During the last two decades, it has been established that spontaneous ventricular defibrillation appears in various mammals [1] and in humans [2] and that different drugs experimentally transform sustained VF (SVF) into a transient form (TVF) [3][4][5]. TVF exhibits slow and well organized electrical fibrillating activity, with a large part of the ventricular mass acting in synchrony, while SVF exhibits unorganized, less synchronized electrical activity, at a higher rate and with small, local fibrillating areas [6].…”

Section: Introductionmentioning

confidence: 99%

The Protective effect ofd-sotalol against hypoxia-induced myocardial uncoupling

1996

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The effects of D-sotalol on intercellular electrical coupling and ultrastructure under hypoxic conditions were investigated in myocardial samples from eight young (1-2 months) and four older (10-12 months) guinea pigs. A right ventricular muscle strip was kept simultaneously in two divided chambers and superfused with normoxic and/or hypoxic (97% N2+ 3% Co2) Krebs solution. Hypoxia caused shortening of action potential duration (APD) and electrical cell-to-cell uncoupling. If the uncoupling appeared after short-term hypoxia (less than 30 min), administration of 3.10(-7)M of D-sotalol to the hypoxic perfusate led to a recovery of electrical coupling. Transmission electron microscopy revealed moderate reversible ultrastructural alterations of the cardiomyocytes. No apparent changes in intercellular junctions were observed. The recoupling effect of sotalol decreased with the time of hypoxia as the ultrastructural damage progressed. After prolonged hypoxia (more than 30 min), cardiomyocytes were markedly injured, intercellular junctions were severely affected, and gap junctions occurred less frequently. In these cases, administration of D-sotalol caused only transient recoupling. After 1 h of hypoxia, no recoupling was observed. Pretreatment with D-sotalol prevented hypoxia-induced electrical uncoupling and markedly attenuated ultrastructural damage, although shortening of APD still persisted. Our results indicate that the cardioprotective effect of D-sotalol on electrical intercellular coupling is closely associated with sotalol-induced prevention of the ultrastructural damage. Considering previous results, we suggest that this protective effect of D-sotalol may be related to its ability to increase intracellular cyclic adenosine monophosphate and, thereby, to decrease cytosolic free Ca. These effects can explain the antiarrhythmic and defibrillating properties of D-sotalol.

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“…Clinical experience provides such strong evidence that a trial for this potentially lethal indication would hardly be justified 39. Torsades de pointes may be mistaken for VF even by experienced cardiologists,40 a fact that may be partly responsible for the impression that magnesium may control recurrent VF. Hypokalaemia predisposes to malignant arrhythmias and is frequently associated with hypomagnesaemia.…”

Section: Specific Drugs For Special Situationsmentioning

confidence: 99%

Antiarrhythmic drugs in resuscitation

Chamberlain

1998

Heart

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Self-terminating ventricular tachyarrhythmias—a diagnostic dilemma?

Cited by 46 publications

References 6 publications

Re-entrant Cardiac Arrhythmias in Computational Models of Long QT Myocardium

Re-entrant Cardiac Arrhythmias in Computational Models of Long QT Myocardium

The Protective effect ofd-sotalol against hypoxia-induced myocardial uncoupling

Antiarrhythmic drugs in resuscitation

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