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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Effect of amiodarone on the extrasystolic and post-extrasystolic contractions of the isolated myocardium of rats and of patients with chronic ischemic heart disease].

Peculiarities in the extrasystolic and post-extrasystolic contractility of the isolated myocardium of patients suffering from chronic ischemic heart disease (IHD), in comparison to that of intact rats, were studied in the presence of the antiarrhythmic drug amiodarone. The contractility was measured in an isometric mode at an electric stimulation frequency of 0.5 Hz, a temperature of 37 degrees C, and a perfusion rate of 10 ml/min. The extrasystolic action was produced by additional electric pulses generated 25 sec after the base stimulation signal. Amiodarone (1 microgram/ml) reduced the inotropic response of intact rat myocardium to the extrasystolic action, but increased the post-extrasystolic contractility. In the myocardium of IHD patients, the drug also suppressed manifestations of the spontaneous abnormal contractility, while not decreasing the inotropic response to the extrasystolic action. An increase in the post-extrasystolic contractility reached on the average 24% (against 6% in the control). The effect of amiodarone on the post-extrasystolic contractility can be related to a change in the functional state of sarcoplasmic reticulum (SR) and in the content of deposited Ca2+ ions. SR is an important factor of intracellular homeostasis of cardiomyocytes during IHD and can probably influence the antiarrhythmic efficacy of amidarone in IHD patients.

Amiodarone↗
PubMed1990

Mechanism of ventricular extrasystoles with fixed coupling. A theoretical model derived from the concept of longitudinal dissociation in the reentrant pathway of extrasystoles.

An electrocardiogram taken from a 29-year-old man with old myocardial infarction is presented as an exemplary case of ventricular extrasystoles with fixed coupling. To explain the mechanism of ventricular extrasystoles with fixed coupling, a theoretical model is derived from the concept of longitudinal dissociation in the reentrant pathway. In the model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When a sinus impulse is blocked in pathway F and passes only through pathway S, it becomes a manifest reentrant extrasystole because of marked conduction delay in pathway S. When the sinus rate does not exceed a certain value, such an impulse always becomes a manifest extrasystole with fixed coupling. Part of the impulse passing through pathway S enters pathway. F retrogradely. In some cases, thereafter, it reenters pathway S and initiates ventricular reentrant tachycardia. When, on the other hand, a sinus impulse passes through both of pathways F and S, it becomes a concealed reentrant extrasystole because of insufficient conduction delay in the pathways.

Adult↗
PubMed2002

Effect of class III antiarrhythmic preparation nibentan on extrasystolic and post-extrasystolic contraction of rat papillary muscle.

The effect of nibentan (2.5 and 25 muM) on extrasystolic and post-extrasystolic contraction of isolated and perfused papillary muscle was studied. The muscle contracted in an isometric regimen at a rate of external electrical stimulation of 0.5 Hz in a temperature-stabilized chamber (36.0+0.5 degrees C). The extrasystolic contraction was induced with an extra electrical pulse applied 0.25 sec after the regular stimulus. Nibentan decreased the amplitude of extrasystolic contraction in a dose-dependent manner. At the same time, the effect of nibentan on extrasystolic contraction practically did not depend on its concentration. It is concluded that nibentan produces a dose-dependent effect on excitability of rat ventricular myocardium, and in parallel improves calcium-accumulating capacity of the sarcoplasmic reticulum in cardiomyocytes.

Animals↗
PubMed1992

Mechanism of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy. A theoretical model derived from the concepts of longitudinal dissociation and multilevel block in the reentrant pathway of extrasystoles.

A case of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy is presented. To explain the mechanism of such bradycardia-dependent appearance, a theoretical model is derived from the concepts of "longitudinal dissociation" and "multilevel block" in the reentrant pathway of extrasystoles. In the theoretical model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When manifest extrasystoles are not found for a long time, alternate sinus impulses pass through both pathways F and S, but become concealed extrasystoles because of insufficient conduction delay in the pathways. The other alternate sinus impulses are blocked in the pathways; in pathway F, the impulses are blocked at the entrance, while in pathway S, the impulses are blocked at a more distal level. When sinus cycles gradually lengthen, one of such alternate sinus impulses passes through the entrance of pathway F and, traveling very slowly, is blocked at a more distal level. The next sinus impulse is blocked at the entrance of pathway F; namely, 3:2 Wenckebach block occurs at the entrance of pathway F. Thus this sinus impulse enters only pathway S and passes through pathway S with enough conduction delay to become a manifest reentrant extrasystole.

Bradycardia↗
PubMedDate not supplied

Bigeminal rhythm due to reentrant ventricular extrasystoles coupled to ventricular and A-V junctional escapes: comparison with ventricular parasystole associated with ventricular extrasystoles of bundle branch reentry.

Bigeminal rhythm due to reentrant ventricular extrasystoles coupled to either ventricular escape of varying aberrant conduction or atrio-ventricular (A-V) junctional escape in association with coexisting idioventricular rhythm and A-V junctional rhythm is presented (Case 1). Dual A-V pathways with longitudinal dissociation in the left bundle branch was presumed to be the mechanism. Generally, both ventricular and A-V junctional escapes were discharged and reset as a result of the retrograde concealed conduction of the reentrant ventricular extrasystoles and the arrhythmia was thought to represent a variant of parasystole. Ventricular parasystole associated with ventricular bigeminy of bundle branch reentry, which was precipitated by hypokalemia during administration of a thiazide diuretic, was added for comparison (Case 2). In the latter, a reentrant ventricular extrasystole arising from the left anterior fascicle brought on and terminated ventricular parasystolic trigeminy and hexageminy of left posterior fascicular origin. Longitudinal dissociation with unidirectional block in the left posterior fascicle was presumed to be the mechanism. At times intermittent ventricular extrasystoles with broad and notched QRS in leads II and III initiated recurrent runs of ventricular bigeminy of varying bundle branch reentry.

Aged↗
PubMed1990

[The significance of spontaneous variability in ventricular extrasystole in the evaluation of the effectiveness of therapy of ventricular extrasystole].

In a mixed population of 104 ambulatory patients the authors assessed, based on 24-hour Holter monitoring, the spontaneous variability of ventricular extrasystoles within one-, two-, three-, four-, six-, eight- and twelve-hour intervals. As significant they evaluated a decline of the frequency of ventricular extrasystoles by more than 90% during the subsequent period of time. The magnitude of variability is influenced substantially more by the frequency of extrasystoles than by the period of monitoring. This fact is not generally accepted so far, although it was already described in 1978. It is probable that this fact participates in a significant way in the difference of values of spontaneous variability reported by different departments.

Adult↗
PubMed1991

Ventricular extrasystoles masquerading as aberrantly conducted atrial extrasystoles because of postectopic T wave change.

This presentation reflects a case where broad and bizarre premature QRS complexes are preceded by sinus beats whose T wave is "abnormal," and seems to contain a premature P wave. A diagnosis of atrial extrasystoles with aberrancy thus could be entertained. The extrasystoles, however, are ventricular in origin. The pattern is explained on the basis of postectopic T wave change, that is, the change in configuration of the T wave that occurs in the sinus beat after an extrasystole.

Cardiac Complexes, Premature↗
PubMed1979

Initial vector rates in differentiation between supraventricular extrasystoles with aberration and ventricular extrasystoles.

A computer method was constructed for analysing vector rates. Initial vector rates of QRS of ventricular extrasystoles (VES) and of aberrant supraventricular extrasystoles were compared. Bundle branch block (BBB) was used as a model for aberration. Spontaneous VES during heart catheterization and VES found by His-bundle recording represented the VES group. The VES were found to contain a longer average "activation time," i.e. the duration from the onset to the spatial amplitude maximum, than the BBB. The maximum amplitudes were similar. A method for calculating initial vector rate distribution was also developed. This showed a significantly higher proportion of fast rate components in BBB than in VES. The calculation of vector rate distribution gave advantages over the calculation of the mean initial vector rate, when considering electrocardiographic abnormalities such as preexcitation QRS or post-infarction Q waves. With a simple discriminatory analysis using initial vector rate distribution values, a 95% precision was obtained in differentiating between VES and BBB. It is concluded that a QRS from a supraventricular impulse focus with aberration has faster initial vector rates than a QRS from a ventricular focus and that this difference is useful in distinguishing between them.

Bundle-Branch Block↗
PubMed1976

Intervention ventriculography. Comparative value of nitroglycerin, post-extrasystolic potentiation and nitroglycerin plus post-extrasystolic potentiation.

The comparative value of nitroglycerin (TNG), post-extrasystolic potentiation (PESP) and their combination (TNG + PESP) to unmask asynergic residual contraction was examined, each patient serving as his own control. Twelve of 13 hypokinetic zones improved both with TNG and PESP. One remained unchanged with either. Of 15 akinetic zones, four improved with both TNG and PESP, while ten remained unchanged. One akinetic zone, although improved with TNG, remained unchanged with PESP. Four dyskinetic zones did not change with either. Six asynergic zones responding to TNG alone demonstrated further augmentation with TNG + PESP. However, none of 13 TNG unresponsive zones improved with TNG + PESP. Thus, TNG, PESP, and TNG + PESP are each equally capable of unmasking asynergic residual contractile ability.

Cardiac Output↗