ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01319.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Antidromic Conduction.During entrainment or resetting of ventricular tachycardia, the distance a stimulated antidromic wave front propagates determines the degree of QRS fusion observed. Determinants of antidromic wave front propagation distance during stimulation at reentry circuit sites were studied in computer simulations of figure eight reentry circuits. When not limited by refractory tissue, antidromic propagation distance depended on the stimulus timing, the conduction velocity in the antidromic direction away from the stimulus site, and the time available for propagation before collision with a returning orthodromic wave front. The latter was determined by the conduction time through the circuit in the orthodromic direction from the stimulus site. Faster conduction from the stimulus site in the orthodromic direction relative to the antidromic direction diminished antidromic wave front propagation distance. Consequently, in circuits with heterogeneous conduction velocities, antidromic propagation distance was dependent on the location of the stimulus site. Stimulation in slow areas limited antidromic propagation distance, although increasing stimulus prematurity increased antidromic propagation distance markedly if the antidromic wave front reached faster tissue. These findings explain the ability of rapid or premature stimuli to entrain or reset tachycardia without producing detectable antidromic wave front effects (QRS fusion) on the surface electrocardiogram when the stimulation site is located centrally within slowly conducting areas in the reentry circuit. However, greater antidromic propagation occurs with stimulation at or near more rapidly conducting sites increasing the likelihood that antidromic effects will be seen on the surface electrocardiogram.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01320.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Mechanism of Torsade de Pointes.A computer model that simulated propagation, nonuniform cycle length dependent recovery of excitability, and slow propagation during incomplete recovery in cardiac muscle has been shown to exhibit behavior similar to torsade de pointes. The conditions required in the model resembled those in long QT syndromes with regionally prolonged ventricular repolarization. In the model, premature excitation of a path with relatively short refractory periods resulted in sequential reentry of that path from a region with longer refractory periods. Sites of reentry become progressively more distal to the site of initiation. The episodes terminated spontaneously when reentrant excitation reached the end of unclosed paths or collided in closed paths. Each reentry site moved away from its initial position in the short recovery path because the distance traversed by propagation in that path exceeded the distance at which reentry occurred via the longer recovery region. The migrating sites of reentry resulted in changing QRS waveform in calculated electrocardiograms including changing QRS polarity when calculated from appropriate sites. Variations of the basic behavior occurred with nonuniform distribution of refractory periods within relatively short and long refractory period regions and included unidirectional progression of reentry sites and multiple circuits of reentry in closed paths. Termination of serial reentry at times other than those when activation reached the end of unclosed paths or collided in closed paths also occurred with nonuniform distribution of refractory periods. Findings provide a plausible explanation for the changing QRS waveform, spontaneous termination, and association of torsade de pointes with long QT syndromes but do not elucidate the mechanism of initiation of the tachyarrhythmia.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01321.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Suppression of Sustained VT by Left Stellectomy.Holter monitoring and ventricular pacing were used to examine control, right stellate ganglionectomy, and left stellate ganglionectomy treatment groups, 6‐24 hours after left anterior descending coronary artery ligation in dogs. In nine of 27 controls (33%), spontaneous ventricular triplets (358 ± 8 beats/min) initiated sustained monomorphic ventricular tachycardia (386 ± 16 beats/min), followed by ventricular fibrillation at 12.6 ± 1.4 hours. Ventricular pacing produced sustained monomorphic ventricular tachycardia in 13 of 18 survivors (73%) at 24 hours. Left but not right stellectomy performed 15 minutes before coronary artery ligation reduced the incidence of spontaneous sustained monomorphic ventricular tachycardia (2 of 27, 7%, P = 0.06; 7 of 27, 26%, P = 0.50, respectively) and reduced the maximal ventricular triplet rate (332 ± 12, P<0.05 and 358 ± 10 beats/min, respectively, P = NS vs control). Neither left nor right stellectomy altered the incidence of ventricular triplets during the 6‐24 hour period (153 ± 58 and 222 ± 55/hour, respectively, vs control, 177 ± 59/hour, P = NS) nor prevented pacing‐induced sustained monomorphic ventricular tachycardia in the survivors at 24 hours (20 of 24, 75%; and 16 of 20, 80%, P = NS). The data demonstrate that left but not right stellectomy reduces spontaneous sustained ventricular tachycardia and ventricular fibrillation during the 6‐24 hour period following coronary artery ligation in the dog. Left stellectomy reduces the triggers for sustained monomorphic ventricular tachycardia (rapid ventricular triplets) without altering the underlying reentrant substrate for sustained ventricu

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01322.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Mechanisms of Arrhythmias in Ventricular Hypertrophy.Cardiac hypertrophy is an adaptative process by which the heart accommodates to abnormal pressure and volume overloads. However, hypertrophy of the left ventricle is associated with a high incidence of ventricular arrhythmias and sudden death. The cellular mechanisms responsible for the abnormal rhythmic activity in hypertrophied myocardium has not been clearly defined, but left ventricular hypertrophy is associated with characteristic electrical abnormalities in experimental models and in hypertrophied human tissue. The most consistent electrical alteration is prolonged duration of the action potential in hypertrophied myocardium. The prolonged duration of depolarization predisposes hypertrophied tissue to develop early afterdepolarizations, which can encourage the development of arrhythmias by a variety of mechanisms. Early afterdepolarizations interrupt repolarization and can lead directly to sustained triggered activity. Early afterdepolarizations can depolarize adjacent excitable fibers and thereby induce triggered activity. The prolonged duration of repolarization can enhance influx of calcium, which can in turn lead to delayed afterdepolarizations that can give rise to triggered activity. Early afterdepolarizations can also produce conduction block or delay, which could contribute to the development of reentrant arrhythmias. Early afterdepolarizations are the most likely electrical abnormality to arise from the prolonged time course of repolarization in hypertrophied myocardium. Therefore, therapeutic measures aimed at preventing the development of early afterdepolarizations in hypertrophied myocardium could prove to be a fruitful approach to inhibiting the development of arrhythmias. The development of agents that selectively reduce the duration of the action potential requires a better understanding of the ionic mechanisms responsible for prolonging the action potential in hypertrophied myocardium. In the meantime, avoiding factors known to favor the development of afterpotentials (e.g., extremes of heart rate, electrolyte abnormalities, certain antiarrhythmic drugs) in patients with left ventricular hypertrophy seems prudent.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01323.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

“For the best and safest method of philosophizing seems to be, first diligently to investigate the properties of things and establish them by experiments, and then later seek hypotheses to explain them… For hypotheses ought to be fitted merely to explain the properties of things and not attempt to predetermine them except so far as they can be an aid to experiments.” (I. Newton, Opera, Vol. IV, p. 314; FromThe Metaphysical Foundation of Modern Science.E.A. Burtt, Doubleday&Company, Inc., Garden City, New York, 1932; p

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01324.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Book Review in This Article:Cardiac Catheterization, Angiography and Intervention, Fourth Edition. Edited by William Grossman arul Donald S. Baim, Lea&Febiger.McDonald's Blood Flow in Arteries. Edited by Wilmer W. Nichols arid Micheal F. O'Rourke, Lea arui Febiger.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01325.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY