Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias
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Dilated Cardiomyopathy
Sudden Death
Fibrillation
Ventricular fibrillation in humans is generally sustained (SVF), but it can be also transient (TVF), reverting spontaneously to sinus rhythm. In previous studies we have shown that: a) TVF appears in all young mammals and varies according to age and species; b) it requires synchronization of myocardial cell activity; c) infusion of certain drugs may change the type of ventricular fibrillation from sustained into transient. We hypothesize that the synchronization required for TVF depends on the electrical conductivity of intercellular structures. These intercellular couplings differ among species and decrease with age. Comparison between the inter- and intra-specific variations of intercellular connective structure described in the literature with the type of ventricular fibrillation found in our previous studies on various animals of different ages showed a clear relationship between these histological variations and the changes in the type of ventricular fibrillation. In this study we examined intercellular connective structures ultrastructurally in 3 groups of cats: a. control, untreated cats exhibiting sustained ventricular fibrillation; b. untreated cats exhibiting transient ventricular fibrillation; c. treated cats exhibiting sustained ventricular fibrillation before infusion of a defibrillating drug and transient ventricular fibrillation thereafter. It was found that the intercellular connective structure in cats exhibiting sustained ventricular fibrillation differs significantly from that in cats exhibiting transient fibrillation. In hearts exhibiting sustained ventricular fibrillation, many intercellular connective structures are widened and the degree of widening is pronounced, forming a continuous line, while in hearts exhibiting transient ventricular fibrillation the widened junctions are rare and isolated and the widening is relatively small. These preliminary results strongly support our above-mentioned hypothesis, providing an explanation for the origin of transient ventricular fibrillation and a tool for the development of new defibrillating drugs.
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Ventricular fibrillation has been studied by driving the ventricles of the isolated rabbit heart electrically and observing whether fibrillation persisted after stimulation was stopped. The hearts were perfused by solutions of different ionic composition and the proportion of hearts in which persistent fibrillation was seen was determined for each solution. The proportion was controlled from 0 to 100 per cent according to the amount of K + , hearts fibrillating spontaneously in .25 N K + . A similar study was made by varying Ca ++ . Fibrillation was arrested by ATP and prolonged by dinitrophenol. Fibrillating hearts lost more K + than when they were not fibrillating. Fibrillation appeared to depend on disturbances of the metabolic processes concerned with ion movements.
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Development of ventricular fibrillation or pulseless ventricular tachycardia after an initial rhythm of pulseless electrical activity or asystole is associated with significantly increased cardiac arrest mortality.To examine differences in epinephrine administration during cardiac arrest between patients who had a secondary ventricular fibrillation or ventricular tachycardia develop and patients who did not.Data were collected for 2 groups of patients with in-hospital cardiac arrest and an initial rhythm of pulseless electrical activity or asystole: those who had a secondary ventricular fibrillation or ventricular tachycardia develop (cases) and those who did not (controls). Dosing of epinephrine during cardiac arrest and other variables were compared between cases and controls.Of the 215 patients identified with an initial rhythm of pulseless electrical activity or asystole, 51 (23.7%) had a secondary ventricular fibrillation or ventricular tachycardia develop. Throughout the total duration of arrest, including periods of return of spontaneous circulation, the dosing interval for epinephrine in patients who had a secondary ventricular fibrillation or ventricular tachycardia develop was 1 mg every 3.4 minutes compared with 1 mg every 5 minutes in controls (P= .001). For the total duration of pulselessness, excluding periods of return of spontaneous circulation during the arrest, the dosing interval for epinephrine in patients who had a secondary ventricular fibrillation or ventricular tachycardia develop was 1 mg every 3.1 minutes versus 1 mg every 4.3 minutes in controls (P= .001).More frequent administration of epinephrine during cardiac arrest is associated with development of secondary ventricular fibrillation or ventricular tachycardia.
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Recent studies have been performed on feature selection for diagnostics between non-ventricular rhythms and ventricular arrhythmias, or between non-ventricular fibrillation and ventricular fibrillation. However they did not assess classification directly between non-ventricular rhythms, ventricular tachycardia and ventricular fibrillation, which is important in both a clinical setting and preclinical drug discovery. In this study it is shown that in a direct multiclass setting, the selected features from these studies are not capable at differentiating between ventricular tachycardia and ventricular fibrillation. A high dimensional feature space, Fourier magnitude spectra, is proposed for classification, in combination with the structured prediction method conditional random fields. An improvement in overall accuracy, and sensitivity of every category under investigation is achieved.
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In a clinical study of 49 patients with acute ischemie heart disease poor success rates from ventricular defubrillation were associated with a low dominant frequency of ventricular fibrillation (generally < 5 Hz) as determined by Fast Fourier Transform analysis of the body surface ECG. Experimental studies in the dog and pig are in accord with these observations, and indicate that the dominant frequency of ventricular fibrillation is reduced both by a long duration of fibrillation in a normal heart, and by some causes of ventricular fibrillation (ouabain or potassium toxicity in the dog, secondary fibrillation in man).
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The mechanisms responsible for the initiation and maintenance of ventricular fibrillation (VF) remain largely unknown. Most of the tools traditionally used to map the activation sequence of more stable arrhythmias cannot be used with fibrillation because of its unstable, chaotic behaviour. In the absence of traditional markers such as local activation time determination, novel techniques had to be developed to describe the electrical organisation or disorganization during VF. In this chapter we describe a technique known as phase mapping that was first used by basic scientists to study VF in cell cultures and isolated animal heart preparations. The chapter provides a brief overview of the technique and application to human VF. We present results obtained from clinical and experimental data demonstrating that both rotors and wave breaks coexist during VF. We conclude with a discussion on the limitations of the technique and potential clinical applications.
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Implantable cardioverter defibrillators (ICD) are usually implanted in patients with malignant ventricular tachyarrhytmias. Aim of this study was to investigate the recurrence of minor ventricular arrhythmias to predict the occurrence of ventricular fibrillation episodes in patients with ICD. The study design was a retrospective analysis of 237 patients, whose ICD was programmed to deliver electrical therapy only for ventricular fibrillation (VF) but not for ventricular tachycardia (VT). We calculated the number, the mean duration and the mean ventricular cycle of the non-sustained ventricular tachyarrhythmias (NST) and of the sustained ventricular tachyarrhythmias (ST). We found that VF patients had a significant higher incidence of ventricular tachycardia compared to the no-VF patients.In addition, the mean VT episodes duration was higher in patients of the VF group than in patients free from ventricular fibrillation and the ventricular cycle length resulted to be significantly shorter in VF patients.
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The implications of ventricular fibrillation induced during elect rophysiologic testing are unclear. To determine the profile of patients in whom this arrhythmia occurs and to determine whether it has any prognostic value, follow‐up data were obtained on all patients in whom this arrhythmia was in duced in our laboratory during a ventricular stimulation protocol over an 18‐month period. Of 836 patients tested, 29 (27 men and 2 women) had inducible ventricular fibrillation. Most (52%) had coronary disease and 12 (41%) had suffered a prior myocardial infarction. All but 3 had some form of heart disease. Sixteen (55%) had abnormal left ventricular function. Eleven (38%) presented with spontaneous sustained ventricular tachycardia or ventricular fibrillation. Eight others had a history of nonsustained ventricular tachycardia.Follow‐up was obtained for a mean of 12 months. In spite of therapy, 2 patients died an arrhythmic death, 1 was resuscitated from ventricular fibrillation, 1 had spontaneous sustained ventricular tachycardia, 4 had inducible sustained ventricular tachycardia, 2 continued to have inducible ventricular fibrillation at second study, and 1 had recurrent syncope. Five patients had ventricular fibrillation induced on multiple occasions. Ventricular fibrillation induced during electraphysiologic study was found primarily in patients with structural heart disease and appeared reasonably reproducible. When reproducible, ventricular fibrillation appears to indicate a poor prognosis rather than an aspecific finding. The clinical profile of our poor prognosis group includes a history of prior ventricular tachycardia or ventricular fibrillation and the presence of coronary artery disease.
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