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At least 73 records · Page 4Linked to original sources
PubMed1997

Automatic arrhythmia identification using analysis of the atrioventricular association. Application to a new generation of implantable defibrillators. Participating Centers of the Automatic Recognition of Arrhythmia Study Group.

BACKGROUND: Atrioventricular association is a key criterion for arrhythmia diagnosis. Its use in a defibrillator should significantly reduce the incidence of inappropriate shocks. Therefore, we evaluated the diagnostic accuracy of an algorithm that uses dual-chamber sensing and analysis of atrioventricular association to discriminate ventricular from supraventricular arrhythmias in a prototype of an implantable defibrillator. METHODS AND RESULTS: The algorithm performed a stepwise analysis of arrhythmias. The rhythm was first classified on the basis of cycle lengths. Each episode was then classified as supraventricular or ventricular in origin on the basis of the stability of cycle lengths and atrioventricular association. This algorithm was evaluated in 156 episodes of induced sustained tachycardias. Eighty-nine tachycardias were taken from the Ann Arbor electrogram library; the others were recorded in 50 patients during electrophysiological studies. The atrial and ventricular signals were stored on an external recorder and then injected into an external prototype of a defibrillator system. The algorithm correctly diagnosed 96% of ventricular tachycardia episodes, 100% of ventricular fibrillation episodes, and 92% of double-tachycardia episodes. The mean detection time for ventricular tachycardia was 2.6 +/- 0.8 seconds, and for ventricular fibrillation, it was 2.1 +/- 0.4 seconds. The positive predictive values for the diagnoses of atrial fibrillation and atrial flutter were 92% and 86%, respectively. For ventricular tachycardia and ventricular fibrillation, the values were 95% and 100%, respectively. CONCLUSIONS: Analysis of atrioventricular association promotes reliable differentiation between ventricular and supraventricular tachycardias and should enhance the diagnostic capabilities of implantable defibrillators.

Algorithms↗
PubMed1991

[Arrhythmia and anti-arrhythmia therapy as prognostic risks].

The incidence of sudden death is estimated to be 0.25%/year in the industrialized world. 30 to 40% of patients are known to be at major risk before they succumb sudden death. Etiology is usually coronary heart disease (75%), dilated and hypertensive cardiomyopathy as well as valvular disease. 75% of patients dying suddenly die from ventricular fibrillation. The most common mechanism of sudden cardiac death in heart failure is sustained ventricular tachycardia deteriorating into ventricular fibrillation, the initiating factors being single ventricular beats, ventricular pairs or nonsustained ventricular tachycardia (trigger mechanism). At least 50% of patients dying during Holter monitoring have been on antiarrhythmic treatment during the time of sudden death and this percentage is increased to 70% in patients dying from torsade de pointes ventricular tachycardia. The question that has arisen is whether suppression of such arrhythmias by antiarrhythmic agents will reduce the incidence of sudden cardiac death. Unfortunately, the patient group at highest risk - low ventricular ejection fraction and high incidence of nonsustained ventricular tachycardia episodes during 24 hour-monitoring and thus, the group most in need of arrhythmia suppression - has the lowest responder rate as well as the highest incidence of serious toxicity. Until the suppression of those arrhythmias by antiarrhythmic agents is demonstrated to improve prognosis in this patient group, routine use of antiarrhythmic agents cannot be recommended in this patient population.

Anti-Arrhythmia Agents↗
PubMed1990

[High-dosage oral magnesium therapy in arrhythmias. Results of an observational study in 1.160 patients with arrhythmia].

In the treatment of cardiac arrhythmias of varying genesis, an "observational study" in 1,160 patients showed that a high-dose oral magnesium preparation (Magnesium-Diasporal N 300 Granulat) was effective. In 82% of the patients observed, a dose of at least 300 mg magnesium/day produced good to very good results. Adverse effects of the drug were observed in only 1.6% of the patients. For all groups, the "success parameters" improved significantly. High-rate arrhythmias showed a better response to magnesium treatment than did low-rate arrhythmias, with a close correlation being found with the heart rate at the start of treatment. High-dose oral magnesium had a positive effect on concomitant hypertension. At a dosage of 300 mg treatment should be continued for at least 6 weeks.

Adult↗
PubMed1984

[Programmed stimulation in patients with malignant ventricular arrhythmia. II: Individual optimization of anti-arrhythmia therapy].

The major purpose of programmed ventricular stimulation in patients with malignant ventricular arrhythmias (sustained ventricular tachycardia/ventricular fibrillation) is not the diagnostic or prognostic evaluation but the individual optimization of antiarrhythmic therapy. For successful antiarrhythmic treatment, the choice of an adequate parameter of efficacy is of outstanding relevance: in patients with frequent daily episodes of malignant ventricular arrhythmias, proper treatment can be based on Holter monitoring; however, in patients with infrequent but life-threatening attacks, Holter monitory appears to be inadequate and programmed stimulation is the method of choice for proper treatment decisions. A total of 394 serial pharmaco-electrophysiological studies was performed in 82 patients with inducible sustained ventricular tachycardia or ventricular fibrillation. During the acute serial studies, one drug was tested each subsequent day using short-term intravenous infusions. The only criterion for drug efficacy was prevention of inducible sustained ventricular tachycardia or ventricular fibrillation that had been reproducibly initiated under control conditions before antiarrhythmic treatment. At least one preventive drug was found in approximately 2/3rd of the patients. Following serial acute studies using intravenous administration, an effective agent was selected and given orally. Programmed stimulation was repeated usually after three days demonstrating reproducibility of preventive efficacy in 90% of the trials. During a subsequent follow-up period of an average of 15 months, the number of acute events (9%) including sudden death or life-threatening recurrences of malignant ventricular arrhythmias was significantly reduced as compared to patients with non-optimized therapy (54%; p less than 0.05). The number of cardiac deaths due to progressive heart failures was not significantly different in patients placed on optimized or non-optimized antiarrhythmic treatment.

Administration, Oral↗
PubMed1994

[Anti-arrhythmia agents in the therapy of ventricular arrhythmias in the post-CAST era].

This review provides a 20-year perspective on the most significant reports on antiarrhythmic drug therapy of ventricular arrhythmias, with particular reference to the CAST trials. The following conclusions are drawn: 1. Based on the CAST trials and other studies investigating the effectiveness of antiarrhythmic agents during the last 20 years, prophylactic treatment with antiarrhythmic class I, III and IV drugs after myocardial infarctions is not indicated. 2. Betablockers without intrinsic sympathomimetic activity are effective in the prevention of reinfarction and sudden cardiac death. 3. The effectiveness of amiodarone as secondary prophylaxis is currently under investigation in several multicenter trials. 4. Antiarrhythmic intervention is indicated in patients with hemodynamically compromising ventricular tachycardia or ventricular fibrillation, irrespective of spontaneous ventricular arrhythmias. Effective treatment with arrhythmic agents can be achieved in approximately half of the patients. Arrhythmia surgery, implantable cardioverters/defibrillators, or heart transplantation are possible alternative treatment modalities.

Adrenergic beta-Antagonists↗
PubMed1985

Dialysis-induced cardiac arrhythmias: fact or fiction? Importance of preexisting cardiac disease in the induction of arrhythmias during renal replacement therapy.

Frequency and grade of premature ventricular depolarizations were assessed in 10 patients on maintenance renal replacement therapy. All medication was withdrawn prior to the study. Each patient was treated sequentially by 8 different methods [acetate and bicarbonate hemodialysis (HD), hemofiltration, hemodiafiltration, ultrafiltration, use of 5 different membranes]. Despite marked changes in serum electrolyte concentrations there was no difference in frequency or grade of premature ventricular beats between the periods before, during, and after renal replacement therapy. Comparison of the 8 methods tested revealed no superiority of 1 method during the observation period of 192 h for each patient. In a second group of 8 patients with confirmed coronary artery disease, acetate HD had no effect on grade and frequency of ventricular arrhythmias, although arrhythmias occurred more often (p less than 0.05) and were more dangerous. We therefore conclude that the incidence of ventricular arrhythmias is primarily dependant on the presence of preexisting coronary artery disease and that HD or related methods do not increase the risk of ventricular ectopies in patients without digitalis medication.

Adult↗
PubMed1980

Cardiac arrhythmias: mechanisms and management: II. Electrocardiographic analysis of cardiac arrhythmias.

Optimal diagnosis may require continuous monitoring, intracardiac studies, or provocative electrophysiologic testing, in addition to the standard 12-lead ECG. One must keep in mind that clinical significance is largely a function of the patient's clinical condition and of the arrhythmia's site of origin. In general, supraventricular arrhythmias are less threatening than ventricular.

Adolescent↗
PubMed2004

Inherited cardiac arrhythmia syndromes: what have they taught us about arrhythmias and anti-arrhythmic therapy?

1. In recent years, the identification of the gene defects in a vast array of monogenic disorders has revolutionized our understanding of the basic mechanisms underlying numerous disease processes. 2. Mutations in cardiac ion channels have been identified as the basis of a wide range of inherited arrhythmia syndromes, including the congenital long QT syndromes, Brugada syndrome, Lenegre syndrome, Andersen's disease and familial atrial fibrillation. 3. Identification of mutations in the human-ether-a-go-go-related gene (HERG) K(+) channel as the molecular basis of congenital long QT syndrome type 2 also led to the discovery that HERG is the molecular target for the vast majority of drugs (both cardiac and non-cardiac) that cause drug-induced arrhythmias. This has had profound implications not only for the development of anti-arrhythmic agents, but also for drug development in general. 4. The sequencing of the human genome in a sense represents the pinnacle of the reductionist era of molecular medicine. The great challenge now is to re-integrate the information gathered during the 'reductionist era' to provide a better understanding of the intact organism. Computer modelling is likely to be a key component of that re-integration process.

Animals↗
PubMed2002

Management of common arrhythmias: Part I. Supraventricular arrhythmias.

Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.

Amiodarone↗
PubMed1992

[Comparative anti-arrhythmia effectiveness of activators of body stress-limiting systems in patients with arrhythmia].

The antiarrhythmic effects produced by activators of the body's stress-limiting systems were comparatively evaluated in patients with cardiac arrhythmias of ischemic and non-ischemic etiology. Acediprol, gidazepam, and befol were found to be beneficial in ventricular premature contraction when psychoemotional stress was simulated, as evidenced by 24-hour monitoring. The most pronounced protective therapeutical effect of the drugs was observed in patients with arrhythmias of extracoronary origin and in individuals with a marked arrhythmogenic effect of stress. Gidazepam was shown to suppress the provocative arrhythmogenic effect of the stress test.

Adult↗
PubMed1979

[Quantitative evaluation of the efficacy of anti-arrhythmia agents in chronic ventricular arrhythmia].

The authors describe a computer system for the analysis of ventricular arrhythmias and its use in the evaluation of anti-arrhythmic drugs. Provided the arrhythmia is stable, this method allows an estimation of the onset and duration of action of the drug and gives guidelines for the choice of an appropriate drug regimen. Using this system, a comparison can be made between different drugs based on quantification of their efficacy.

Amiodarone↗
PubMed1993

Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after myocardial infarction. The original design concept of the Cardiac Arrhythmia Suppression Trial (CAST).

OBJECTIVE: To test the hypothesis that in survivors of myocardial infarction, the suppression of ventricular premature depolarizations improves survival free of cardiac arrest and arrhythmic death. DESIGN: International, prospective, multicenter, randomized, placebo-controlled trial. SETTING: University and community hospitals. PATIENTS: A total of 3549 patients with myocardial infarction and left ventricular dysfunction. INTERVENTION: Administration of encainide, flecainide, moricizine, or placebo to suppress ventricular premature depolarizations. MAIN OUTCOME MEASURES: Overall survival and survival free of cardiac arrest or arrhythmic death were compared in patients randomized to long-term, active antiarrhythmic drug therapy vs corresponding placebo, using the stratified log rank statistic. RESULTS: At 1 year from the time of randomization to blinded therapy, 95% of placebo-treated patients vs 90% of active drug-treated patients remained alive (P = .0006). Similarly, at 1 year, 96% of placebo-treated patients vs 93% of active drug-treated patients remained free of cardiac arrest or arrhythmic death (P = .003). CONCLUSIONS: The suppression of asymptomatic or mildly symptomatic ventricular arrhythmias after myocardial infarction does not improve survival and can increase mortality. Treatment strategies designed solely to suppress these arrhythmias should no longer be followed.

Aged↗
PubMedDate not supplied

[The anti-arrhythmia action of low-molecular polyvinylpyrrolidone in experimental arrhythmias].

The experiments on 258 albino rats and on 74 albino mice have established that low molecular polyvinylpyrrolidone (PVP) has antiarrhythmic effects. When administered intravenously on a adrenaline model of arrhythmia, PVP and ethmozine showed a very close activity, but PVP resulted in a lower incidence of mortality and proarrhythmia. The action of PVP was weaker than that of ethmozine when they were used in an aconitine model. Oral PVP acted on aconitine-induced arrhythmia stronger and longer than did ethmozine. It is advisable to study the mechanisms of antiarrhythmic activity of PVP.

Aconitine↗
PubMed2000

[Cardiac arrhythmias in targeted connexin deficient mice: significance for the arrhythmia field].

Intercellular communication can be mediated by gap junction channels. One channel is composed of two hexameric hemichannels which consist of six polypeptide subunits called connexines (Cx). Three different connexines were documented in the cardiac myocytes: Cx40, Cx43 and Cx45. The labeling by number represents the rounded, molecular mass of the amino acid sequences given in kD. Identical connexons form homotypic channels different connexons can form heterotypic channels. Each channel type has specific properties regarding permeability and electrical conductance. Beside a typical age-dependent alignment of gap junction channels on the surface of the cardiac myocytes, regional distribution of the different connexins is different at distinct parts of the mouse heart. The ventricular working myocardium is characterized by Cx43, whereas Cx40 and Cx45 were not found in this region. In the atria as well as in the conduction system, Cx40 is the most frequently expressed. Cx45 appears to form a border zone between conductive and the surrounding working myocardium. In line with the localization and the conduction properties of distinct homotypic gap junction channels, the Cx43 deficient mouse is suitable for analysis of ventricular arrhythmias and the Cx40 deficient mouse primarily for studies of atrial arrhythmias. Increased ventricular conduction velocity and increased ventricular vulnerability were observed in the presence of a decreased number and density of Cx43 gap junction channels. This observation, however, is controversially discussed. Cx40 deficiency induces an impairment of the sinuatrial, intraatrial and atrioventricular conduction properties and is associated with an increased atrial vulnerability. Transgenic mouse models and new mapping techniques for detection of the electrical wavefront propagation provide new insights into the mechanisms of arrhythmogenesis. Geneticists, clinicians and basic researchers need to collaborate in order to explore the clinical relevance of the new mouse models and their use for molecular medicine.

Animals↗
PubMed2006

Comparison of 1-year effects of left ventricular and biventricular pacing in patients with heart failure who have ventricular arrhythmias and left bundle-branch block: the Bi vs Left Ventricular Pacing: an International Pilot Evaluation on Heart Failure Patients with Ventricular Arrhythmias (BELIEVE) multicenter prospective randomized pilot study.

BACKGROUND: Little is known on the chronic effects of left ventricular pacing (LV) in heart failure. METHODS: Seventy-four patients with LBBB, QRS >130 milliseconds, New York Heart Association class (Bradley DJ, Bradley EA, Braughman KL, et al. Cardiac resynchronization and death from progressive heart failure: a meta-analysis of randomized controlled trials. JAMA 2003;289:730-40.) II, LV ejection fraction (LVEF) <35%, and a class I cardioverter/defibrillator indication were implanted with CRT-D devices and were randomized to either LV or biventricular (BiV) pacing. Response (defined as increases of >5 points increase of LVEF and/or > or = 10% 6-minute walking test [6MWT]) between LV and BiV pacing were compared in an attempt to define the number of patients needed to claim noninferiority of LV pacing. In addition, absolute change in LVEF at 12 months in heart failure patients treated with LV pacing was evaluated. The safety of LV pacing was assessed comparing the total number of ventricular arrhythmia episodes, of hospitalizations, and of deaths between the two pacing modes. RESULTS: The percentage of responders was comparable for both groups (LV = 75%, BiV = 70%, P = .788); based on the 95% CI of the difference between the groups, 1100 patients would be needed to claim noninferiority of LV pacing (with a 5% CI lower limit). LV pacing induced siginificant LVEF increase (5.2%, P = .002). These results remained unchanged after performing adjustment analyses. There were no differences in the numbers of ventricular arrhythmias, hospitalizations, and death events between the 2 pacing modes. CONCLUSIONS: At 12 months, percentage of responders to LV pacing was similar to BIV pacing. Furthermore, LV pacing achieved a significant increase of ejection fraction. LV pacing is both safe and feasible.

Aged↗
PubMed1993

The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology.

Radiofrequency (RF) catheter ablation has developed into a new non-pharmacological therapy for the definitive treatment of patients with cardiac arrhythmias. Although an increasing number of recent reports have indicated the widespread use of the procedure, no data are available to estimate the number of procedures performed in Europe. Furthermore, currently no data on a large series of patients are available that provide information on the risk of procedure-related complications. This report presents the results of the Multicentre European Radiofrequency Survey (MERFS) that was conducted by the Working Group on Arrhythmias of the European Society of Cardiology. The objectives of this voluntary retrospective survey were to assess the number of radiofrequency catheter ablation procedures performed in 86 European institutions from January 1987 until March 1992 and the incidence of procedure-related complications with respect to the different types of ablative procedures. A total of 4398 patients were reported on from 68 out of 86 institutions (79%) from 15 European countries that agreed to participate in MERFS. From 1987 to 1991, the number of patients who underwent RF ablation per year increased from 45 to 2000. In the first 3 months of 1992, a total of 1640 patients were reported on. The number of patients reported on in relation to the different types of ablative procedures were: ablation of atrial tachycardialatrial flutter: n = 141 (3.2%); ablation of the atrioventricular junction: n = 900 (20.5%); modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: n = 815 (18.5%); ablation of accessory pathway: n = 2222 (50.5%); ablation of ventricular tachycardia: n = 320 (7.3%). Procedure-related complications occurred in 223 patients (5.1%). The incidence of complications in relation to the ablative procedure was: ablation of atrial tachycardia/atrial flutter: 5.0%; ablation of the atrioventricular junction: 3.2%; modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: 8.0%; ablation of accessory pathway: 4.4%; ablation of ventricular tachycardia: 7.5%. Complications occurred significantly more often in patients who underwent modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia, when compared to ablation of the atrioventricular junction (P < 0.001) or ablation of accessory pathway (P < 0.001), and in patients who underwent ablation of ventricular tachycardia, when compared to ablation of the atrioventricular junction (P < 0.002) or ablation of accessory pathway (P < 0.02). The highest incidence of complications was reported after modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Effects of amiodarone on cardiac electrophysiology and inducibility of arrhythmias in chronically infarcted dogs: late arrhythmias, haemodynamics, and sympatholytic actions.

The electrophysiological and antiarrhythmic effects of acute (2 and 10 mg/kg i.v.) and chronic (400 mg/day p.o. for 28 days) amiodarone (AM) treatment were compared in anaesthetised dogs with 5-6-day-old myocardial infarcts. Intravenous AM prolonged the RR interval, sinus node recovery time, the PR interval, and atrial to His conduction time by 36, 33, 25, and 36%, respectively. Corresponding increases after oral amiodarone were 50, 57, 12, and 26%. Atrial and His-Purkinje conduction times were unchanged. Atrial and ventricular refractory periods were increased especially after oral treatment. Oral AM additionally prolonged QRS, QT, and paced QT (by 4, 34, and 19%, respectively). Effects of oral AM on ventricular repolarisation and on the fast inward sodium current were confirmed in vitro. Both modes of AM administration protected against inducible arrhythmias, an effect that was more marked during normal sinus rhythm than during pacing in orally treated dogs. Oral amiodarone failed to protect against spontaneous late arrhythmias 24 h after infarction whilst both modes of administration noncompetitively inhibited isoprenaline-induced tachycardia. Oral AM reduced blood pressure (13%) and LV dP/dt/P (24%) whereas cardiac output was maintained by an increase in stroke volume. It was concluded that oral AM is haemodynamically well tolerated and that prolonged ventricular repolarisation enhanced by bradycardia together with sympatholytic actions may be important mechanisms for antiarrhythmic efficacy, whereas the mechanisms involved in i.v. efficacy are less clear but may depend, at least partly, on sympatholytic actions and perhaps (tentatively) on sodium channel block in Purkinje tissue.

Action Potentials↗
PubMed2006

Recommendations for participation in leisure-time physical activity and competitive sports of patients with arrhythmias and potentially arrhythmogenic conditions. Part II: ventricular arrhythmias, channelopathies and implantable defibrillators.

This consensus paper on behalf of the Study Group on Sports Cardiology of the European Society of Cardiology follows a previous one on guidelines for sports participation in competitive and recreational athletes with supraventricular arrhythmias and pacemakers. The question of imminent life-threatening arrhythmias is especially relevant when some form of ventricular rhythm disorder is documented, or when the patient is diagnosed to have inherited a pro-arrhythmogenic disorder. Frequent ventricular premature beats or nonsustained ventricular tachycardia may be a hallmark of underlying pathology and increased risk. Their finding should prompt a thorough cardiac evaluation, including both imaging modalities and electrophysiological techniques. This should allow distinguishing idiopathic rhythm disorders from underlying disease that carries a more ominous prognosis. Recommendations on sports participation in inherited arrhythmogenic conditions and asymptomatic gene carriers are also discussed: congenital and acquired long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular cardiomyopathy and other familial electrical disease of unknown origin. If an implantable cardioverter defibrillator is indicated, it is no substitute for the guidelines relating to the underlying pathology. Moreover, some particular recommendations for patients/athletes with an implantable cardioverter defibrillator are to be observed.

Arrhythmias, Cardiac↗