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Computerized mapping of ventricular fibrillation.

Ventricular fibrillation (VF) is a complicated rhythm disorder. To study the mechanisms of VF, we used computerized mapping techniques with up to 512 channels of simultaneous multisite recordings for data acquisition. The data were then processed for dynamic display of the activation patterns and for mathematical analyses of the activation intervals. The results show that VF can be initiated by a single strong premature stimulus given during the vulnerable period of the cardiac cycle. The initial activations form figure-eight patterns. Afterwards, VF perpetuates itself without any outside help. The ability to perpetuate itself is, in part, due to the ability to generate new reentry by wavebreak. When two wavelets intersected perpendicular to each other, the second wavelet was broken by the residual refractoriness left over from the first wavelet. In diseased hearts, such as in hearts with dilated cardiomyopathy, the generation of reentry is facilitated by tissue inhomogeneity and anisotropy. We conclude that VF is a form of reentrant cardiac arrhythmia. Strong electrical stimulus initiated single or dual reentrant wavefronts that broke up into multiple wavelets. Sometimes short-lived organized reentry is also generated during the course of VF. These organized reentry and broken wavelets serve as the source of activations that sustain VF.

Electric Stimulation↗

Significance of inwardly directed transmembrane current in determination of local myocardial electrical activation during ventricular fibrillation.

Ventricular fibrillation (VF) is the principle cardiac rhythm disorder responsible for sudden cardiac death in humans. The accurate determination of local cardiac activation during VF is essential for its mechanistic elucidation. This has been hampered by the rapidly changing and markedly heterogeneous electrophysiological nature of VF. These difficulties are manifested when attempting to differentiate true propagating electrical activity from electrotonic signals and when identifying local activation from complex and possibly fractionated electrograms. The purpose of this investigation was to test the hypothesis that the presence of a balanced inwardly and outwardly directed transmembrane charge, obtained from the ratio of the inward to outward area under the cardiac transmembrane current curve (-/+ Im area), could reliably differentiate propagating from electrotonic deflections during VF. To test this hypothesis, we applied a recently described technique for the in vivo estimation of the transmembrane current (Im) during cardiac activation. A 17-element orthogonal epicardial electrode array was combined with an immediately adjacent optical fiber array to record electrical and optically coupled transmembrane potential signals during VF. Recordings were obtained during electrically induced VF in six dogs to determine the Im associated with activation and the time course of repolarization, as well as unipolar electrograms and bipolar electrograms recorded at multiple center-to-center interelectrode distances from 0.2 to 3 mm. Propagating local activations were associated with the presence of an easily identified inwardly directed Im, with a balanced inward and outward charge (-/+ Im area approximately 1.0). Electrotonic wave-forms lacked this inward Im (-/+ Im area approximately 0.0). Normal Na(+)-mediated inward currents were directly demonstrated to be responsible for some activations during VF.

Animals↗

Multifractal analysis of ventricular fibrillation and ventricular tachycardia.

A study of ventricular fibrillation and ventricular tachycardia was undertaken using multifractal analysis. By applying the method of direct determination of the f(alpha) singularity spectrum, the value of the area of the VF and VT singularity spectrum was calculated. The comparison between the results showed that the value of the area of the VF singularity spectrum tended to be larger than that of the value of the area of the VT singularity spectrum. This makes the multifractal singularity spectrum a powerful criterion for discriminating between VF and VT.

Algorithms↗

Computational framework for simulating the mechanisms and ECG of re-entrant ventricular fibrillation.

Ventricular arrhythmias remain an important cause of morbidity and mortality in the Western world. Although the underlying mechanisms of these arrhythmias can be studied experimentally, these investigations are in general limited to mapping electrical activity on the heart surface. Computational models of action potential propagation offer a potentially powerful way to study electrical activation and arrhythmias, but current models are not easy to link to the clinical environment. In this paper, we describe a framework for computing action potential propagation in which the geometry, electrophysiology and regional properties of ventricular myocardium can be specified so that, for example, different models for cardiac cellular electrophysiology can be used. We have computed action potential propagation during both normal beats and re-entry in an anatomically accurate model of ventricular geometry. By computing the resultant electric current flow in the torso we have also generated simulated ECG signals that result from specific activation patterns in the ventricular model. Models can be powerful tools for explaining observations, and this approach is able to provide a direct link between the different configurations of re-entry observed in computational and experimental studies, and the ECG signals observed in patients.

Action Potentials↗

Comparison of arrhythmia recurrence in patients presenting with ventricular fibrillation versus ventricular tachycardia in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial.

Because many episodes of ventricular fibrillation (VF) are believed to be triggered by ventricular tachycardia (VT), patients who present with VT or VF are usually grouped together in discussions of natural history and treatment. However, there are significant differences in the clinical profiles of these 2 patient groups, and some studies have suggested differences in their response to therapy. We examined arrhythmias occurring spontaneously in 449 patients assigned to implantable cardioverter-defibrillator (ICD) therapy in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial to determine whether patients who receive an ICD after VT have arrhythmias during follow-up that are different from patients who present with VF. ICD printouts were analyzed both by a committee blinded to the patients' original presenting arrhythmia and by the local investigator. During 31 +/- 14 months of follow-up, 2,673 therapies were reported. Patients who were enrolled in the AVID trial after an episode of VT were more likely to have an episode of VT (73.5% vs 30.1%, p <0.001), and were less likely to have an episode of VF (18.3% vs 28.0%, p = 0.013) than patients enrolled after an episode of VF. Adjustment for differences in ejection fraction, previous infarction, and beta-blocker and antiarrhythmic therapy did not appreciably change the results. Ventricular arrhythmia recurrence during follow-up is different in patients who originally present with VT than in those who originally present with VF. These findings suggest there are important differences in the electrophysiologic characteristics of these 2 patient populations.

Adrenergic beta-Antagonists↗

Idiopathic left ventricular aneurysm: an unusual substrate of ventricular fibrillation and ventricular tachycardia.

Idiopathic left ventricular aneurysm (LVA) is a very rare clinical condition. This article describes a patient with idiopathic LVA associated with episodes of ventricular tachycardia and ventricular fibrillation. Clinical and instrumental examinations did not reveal the pathogenesis of the aneurysm. The malignant clinical course suggests that an aggressive antiarrhythmic treatment, including ICD implantation, may be warranted.

Anti-Arrhythmia Agents↗

A chronically implanted system for automatic defibrillation in active conscious dogs. Experimental model for treatment of sudden death from ventricular fibrillation.

Ventricular defibrillation was acheived in active conscious dogs with a chronically implanted automatic system composed of a defibrillator and an alternating current fibrillator. The hermetically sealed defibrillator is encased in titanium, weighs 250 g and has a volume of 145 ml. The sensor continuously monitors ventricular electircal activity and recognizes fibrillation by the absence of isoelectric potential segments. Fibrillation is induced by placing a magnet over the implanted fibrillator. The resulting syncope closely resembles the clinical entity of sudden death, while the defibrillator automatically restores normal rhythm with a truncated exponential pulse of 30 J, 15 seconds after the onset of the arrhythmia. The operational status of the defibrillator can be tested in vitro and noninvasively in vivo with an external analyzer. This experimental model allows for the first time a long-term study of the automatic implantable defibrillator approach to prevent sudden death from ventricular fibrillation under a variety of physiopathologic conditions.

Animals↗

Signal-averaged electrocardiographic late potentials in patients with ventricular fibrillation or ventricular tachycardia: correlation with clinical arrhythmia and electrophysiologic study.

High-frequency potentials measured in the terminal 40 ms of the signal-averaged QRS complex during sinus rhythm are of abnormally low amplitude in most patients with ventricular tachycardia (VT). However, less is known about high-frequency late potentials in patients with ventricular fibrillation (VF), and the relation between late potentials and arrhythmia inducibility during electrophysiologic study has not been established. Signal-averaged electrocardiography was used to measure high-frequency (more than 25 Hz) late potentials in 24 patients with spontaneous VF, 27 patients with spontaneous sustained VT, and 19 normal subjects, none of whom were receiving antiarrhythmic drugs. Late-potential amplitude in patients with VT was significantly lower than that in patients with VF (p less than 0.02). Late-potential amplitude in patients with VF was not significantly different from that in normal subjects. Ventricular arrhythmia induction was attempted during electrophysiologic study in 46 of the patients with VF or VT. Late-potential amplitude was significantly lower in 26 patients with reproducibly inducible sustained ventricular arrhythmias than in 20 without (p less than 0.001). The correlation between late-potential amplitude and arrhythmia inducibility was independent of that between late-potential amplitude and clinical arrhythmia (VT vs VF).

Action Potentials↗

Effect of beta blockade on ventricular fibrillation- and ventricular tachycardia-induced circulatory arrest in acute myocardial infarction.

The risk of developing circulatory arrest secondary to ventricular fibrillation or tachycardia in acute myocardial infarction (AMI) is greatly increased in patients with hypokalemia, whether diuretic induced or not. In a retrospective study of 5,877 infarctions during an 8-year period, hypokalemia was more common (22.5%) in diuretic-treated AMI patients than in those not treated with diuretics (12.9%). Thus, hypokalemia should be avoided in diuretic-treated patients with increased risk of myocardial infarction. Circulatory arrest occurred in 13% of hypokalemic patients treated with nonselective beta blockers on admission compared with 26% in those treated with selective beta blockers. No difference was found in normokalemic patients. The mean serum potassium value was 4.07 mM/liter in the patients treated with nonselective beta blockers compared with 4.0 and 4.01 in those treated with selective and no beta blockade, respectively. In a separate study, adrenaline infusion in healthy volunteers produced a decrease not only in serum potassium but also in serum magnesium, although the latter occurred later. Pretreatment with verapamil exaggerated the decrease in serum potassium. When starting beta-blocker treatment in patients at risk of developing AMI, consideration should be given to commencing with a nonselective instead of a selective beta blocker.

Adrenergic beta-Antagonists↗

Transition from ventricular fibrillation to ventricular tachycardia: a simulation study on the role of Ca(2+)-channel blockers in human ventricular tissue.

We study the effect of blocking the L-type Ca(2+)-channel on fibrillation in simulations in two-dimensional (2D) isotropic sheets of ventricular tissue and in a three-dimensional anisotropic anatomical model of human ventricles, using a previously developed model of human ventricular cells. Ventricular fibrillation (VF) was obtained as a result of spiral wave breakup and consisted of a varying number of chaotically wandering wavelets activating tissue at a frequency of about 6.0 Hz. We show that blocking the Ca(2+)-current by 75% can convert ventricular fibrillation into a periodic regime with a small number of stable spiral waves, ranging from six in 2D sheets of 25 x 25 cm to a single spiral in the anatomical model of human ventricles. The dominant frequency during this process changed to about 10.0 Hz in the 2D simulations, but to only 5.0 Hz in the whole heart simulations where a single spiral wave anchored around an anatomical obstacle. We show that the observed effects were due to a flattening of the electrical restitution curve, which prevented the generation of wave breaks and stabilized the activation patterns.

Calcium↗

The effects of lidocaine on the ventricular fibrillation threshold and primary ventricular fibrillation following acute experimental coronary occlusion.

Experiments were performed on 39 anaesthetized open-chest dogs (BW 16-33 kg) to examine the effect of lidocaine on the frequency of primary ventricular fibrillation (VF) and the time course of the ventricular fibrillation threshold (VFT) (train of stimuli-method) following acute coronary artery occlusion, and also to study the effects of lidocaine on the VFT of non-ischaemic heart at different therapeutic and high non-therapeutic doses. At effective plasma levels of lidocaine usually reached in clinical therapy (130-480 micrograms/l) there was no measurable increase in VFT compared to control values. The drop in VFT following acute ligation of the left anterior descending coronary artery (LAD) was neither eliminated nor even merely diminished. After occlusion of the left circumflex coronary artery (CIR), the incidence of spontaneous VF was not reduced in comparison to a control group. With regard to the doses administered and the plasma levels of lidocaine achieved, only the application of clinically extremely high or toxic doses resulted in increases in VFT in the non-ischaemic heart.

Acute Disease↗

The impact of catecholamines in patients with or without beta-blockers on the ventricular fibrillation cycle length and ventricular fibrillation cycle length variability.

OBJECTIVES: To evaluate the impact of epinephrine, norepinephrine, or placebo on the ventricular fibrillation cycle length (VFCL) and the variability of VFCL (cvVFCL) measurements in implantable cardioverter defibrillator (ICD) patients with or without beta-blockers. METHODS: Forty-three patients scheduled for their 6-week post-ICD placement noninvasive electrophysiologic study were included in the study at the Arrhythmia Procedure Laboratory at Hartford Hospital, Hartford, CT. This randomized, double-blind, placebo-controlled evaluation was approved by the Hartford Hospital Institutional Review Board. RESULTS: After 2 seconds of continuous VF, 7 consecutive VFCLs were measured from the ICD device recording printout using a 0.5 mm scale ruler under magnification at baseline and after the infusion of catecholamines (epinephrine or norepinephrine at 2 mcg/min) or matching placebo at steady state. The average VFCL and the cvVFCL were determined for each study phase. Subgroup analysis based on chronic beta-blocker use was performed. No between-group differences were noted for epinephrine, norepinephrine, or placebo group for baseline (P=0.538) or postinfusion VFCL (P=0.749) or for baseline (P=0.561) or postinfusion cvVFCL (P=0.623) Regardless of catecholamine group randomization, longer pre- and postinfusion VFCL were noted in those receiving beta-blockers (P=0.157, P=0.019) but no differences in cvVFCL were noted (P=0.216, P=0.474) versus those without beta-blockers, respectively. CONCLUSION: Moderately dosed epinephrine or norepinephrine does not affect either VFCL or the variability of VFCL after short duration of ventricular fibrillation. Chronic cardioselective beta-blockade prolongs VFCL without any impact on coefficient of variation of VFCL.

Adrenergic alpha-Agonists↗

Bortner type A scores and eight basic emotions for survivors of ventricular fibrillation and left ventricular failure during acute myocardial infarction.

We examined Bortner scores for behavioral patterns and eight basic emotional dimensions named by Plutchik for patients with acute myocardial infarction who survived ventricular fibrillation and left ventricular failure. There were 70 patients, 48 men and 22 women ages 26 to 69 yr. (M = 54, SD = 8), admitted to the coronary care unit within 24 hours of the onset of a long-lasting chest pain. Six patients survived an episode of ventricular fibrillation that occurred within 24 to 48 hours after their admission. 15 patients developed left ventricular failure and were in Killip Classes II and III. Patients with acute myocardial infarction and left ventricular failure had mean Bortner scores significantly lower than others with acute myocardial infarction and were classed as Type B behavior. There was no difference in Bortner scores between patients with ventricular fibrillation and others with acute myocardial infarction. Patients with acute myocardial infarction and left ventricular failure scored significantly higher on Timid than others with acute myocardial infarction. Patients with acute myocardial infarction and ventricular fibrillation scored significantly lower on Depressed and higher on Distrust than other patients with acute myocardial infarction. Our findings suggest that patients with ventricular fibrillation and low scores on Depressed have good hospital prognosis. They are more critical and tend to reject people and ideas more than patients with acute myocardial infarction. This study suggests that the way in which patients with acute myocardial infarction react to their infarction, in terms of eight basic emotions and test patterns, is dependent on the complications of myocardial infarction.

Adult↗

Ventricular fibrillation and polymorphic ventricular tachycardia with critical coronary artery stenosis: does bypass surgery suffice?

INTRODUCTION: Previous studies have suggested that coronary artery bypass surgery is sufficient to prevent recurrence of sudden death in patients with critical coronary artery stenosis presenting with ventricular fibrillation or polymorphic ventricular tachycardia. We present our experience in patients with one or more episodes of sudden death associated with documented ventricular fibrillation or polymorphic ventricular tachycardia and severe operable coronary artery disease who underwent defibrillator implant at the time of bypass surgery. METHODS AND RESULTS: Fifty-eight consecutive patients (age 63 +/- 8 years) were included in this study. Eighteen of the 58 patients had no evidence of previous myocardial infarction. The mean ejection fraction was 37 +/- 13%. All patients underwent electrophysiologic study before and after revascularization. At the time of first defibrillator discharge, each patient was reevaluated to exclude the presence of ischemia. The benefits of defibrillator implant were estimated comparing the projected survival based upon defibrillator discharge preceded by syncope or presyncope with survival curves generated including total death and sudden plus cardiac death. After a mean follow-up of 4.6 +/- 2 years, 22 patients received appropriate shocks preceded by syncope or presyncope, and an additional 19 patients received asymptomatic shocks. At 4 years, survival free of total death was 71.2%, and the projected survival was 58.8% (P < 0.05). Multivariate analysis showed that ejection fraction lower than 30% and induction of arrhythmia with one or two extrastimuli (S2, S3) were independent predictors for defibrillator discharge. None of the remaining variables including age, gender, number of bypasses, history of myocardial infarction, and type of arrhythmias induced were predictive for death and occurrence of shocks. CONCLUSIONS: In patients with ventricular fibrillation and polymorphic ventricular tachycardia, bypass surgery does not protect from recurrence of life-threatening arrhythmias, and, as in our population, defibrillator implant may have significant impact on survival.

Adult↗

Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy.

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.

Animals↗

Ventricular fibrillation during programmed ventricular stimulation: incidence and clinical implications.

Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.

Adolescent↗