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Transcoronary chemical ablation of arrhythmias.

BACKGROUND: Chemical or electrical ablation of an arrhythmogenic ventricular area and the atrioventricular (AV) node is still an experimental technique. After we introduced alcohol ablation in the clinical situation we conducted this study to develop the catheter technique for delivering alcohol in patients with incessant ventricular tachycardia after myocardial infarction and patients with atrial fibrillation and flutter with uncontrollable ventricular rates. METHODS: In patients with incessant ventricular tachycardia, the coronary artery supplying blood to the site of origin of the tachycardia could be identified by the combined information from coronary and left ventricular angiography and from programmed electrical stimulation, including endocardial mapping and pace mapping. In the 12 patients with incessant ventricular tachycardia we selected, the coronary artery supplying blood to the site of origin of the tachycardia could be identified and catheterized in ten patients. Ethanol ablation was successful in all of them. With a follow-up from 2 to 44 months, seven of the ten treated patients are still alive and six remain free of tachycardia. In patients with atrial fibrillation or flutter and uncontrollable ventricular rates, the AV artery could be catheterized and ethanol injected in 13 of the 19 patients. Complete block was produced in ten patients and AV conduction was sufficiently modified to control symptoms in three patients. Long-term results with ethanol ablation have remained excellent in this setting. CONCLUSION: Chemical ablation is a technique that may be of enormous value and even lifesaving for patients with an incessant form of tachycardia not responding to any form of medical therapy. Transcoronary ablation of AV conduction should be considered in patients with a right dominant coronary circulation in whom radiofrequency ablation has failed.

Adult↗

Current trends in transcatheter treatment of cardiac arrhythmias.

Catheter ablation has become established as a gold standard therapy for patients suffering from many supraventricular and ventricular arrhythmias, offering a curative alternative to these patients by way of destroying or isolating the arrhythmia substrate. Radiofrequency has been used as a primary source of energy for transcatheter ablation due to its safety and efficacy. Another technique is transcoronary chemical ablation, consisting of the infusion of ethanol through the coronary blood supply to the site of origin of the arrhythmia. Most supraventricular arrhythmias like atrial tachycardia, atrioventricular nodal reentrant tachycardia and arrhythmias related to atrioventricular accessory pathways can be managed with radiofrequency catheter ablation. However, some concerns exist regarding the value of this technique for the treatment of atrial flutter and ventricular tachycardia. In this review we discuss the state-of-the-art in catheter ablation of cardiac arrhythmias and its future perspectives.

Catheter Ablation↗

Atropine-induced ventricular fibrillation: case report and review of the literature.

A bradycardic and mildly hypotensive acute myocardial infarction patient developed sinus tachycardia, ventricular tachycardia, flutter, and fibrillation following intravenous atropine. Previous case reports are reviewed and the literature regarding the advisability of this mode of therapy is discussed. In the light of conflicting opinion as to the necessity of atropine in the mildly hypotensive and bradycardic acute myocardial infarction patient, and in view of its potentially deliterious effects on ischemic myocardium, a cautious and selective application of this drug is advised.

Atropine↗

Mechanisms of regular, wide QRS tachycardia in infants and children.

A regular wide QRS tachycardia was electrocardiographically documented in 32 patients aged 1 month to 18 years. The mechanisms of the tachycardia were evaluated using standard multicatheter electrophysiologic techniques. These mechanisms included (1) orthodromic reciprocating tachycardia with bundle branch aberration (seven patients), (2) antidromic reciprocating tachycardia using single (three patients), or multiple (three patients) atrioventricular connections (Kent bundles), (3) atrial flutter with ventricular preexcitation over accessory connections (eight patients), (4) reciprocating tachycardia using a nodoventricular connection (Mahaim fiber) (five patients), and (5) ventricular tachycardia (six patients). Regular side QRS tachycardias are not rare in pediatric patients. Their mechanisms can be quite complex, and electrocardiographic analysis with respect to QRS configuration, heart rate, or the presence or absence of ventriculoatrial dissociation is not sufficient for diagnostic purposes. Our results show that considerable understanding of the mechanism of regular, wide QRS tachycardias can be obtained by multicatheter electrophysiologic study. Understanding the mechanism is essential in order to make rational use of available therapeutic options.

Adolescent↗

Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues.

The Wolff-Parkinson-White syndrome (WPW), estimated to occur in approximately 0.1% to 3% of the general population, is a form of ventricular preexcitation involving an accessory conduction pathway. The definition of WPW relies on the following electrocardiographic features: (1) a PR interval less than 0.12 seconds (2) with a slurring of the initial segment of the QRS complex, known as a delta wave, (3) a QRS complex widening with a total duration greater than 0.12 seconds, and (4) secondary repolarization changes reflected in ST segment-T wave changes that are generally directed opposite (discordant) to the major delta wave and QRS complex changes. The accessory pathway bypasses the atrioventricular (AV) node, creating a direct electrical connection between the atria and ventricles. The majority of patients with preexcitation syndromes remain asymptomatic throughout their lives. When symptoms do occur they are usually secondary to tachyarrhythmias; the importance of recognizing this syndrome is that these patients may be at risk to develop a variety of supraventricular tachyarrhythmias which cause disabling symptoms and, in the extreme, sudden cardiac death. The tachyarrhythmias encountered in the WPW patient include paroxysmal supraventricular tachycardia (both the narrow QRS and wide QRS complex varieties), atrial fibrillation, atrial flutter, and ventricular fibrillation. Diagnostic and urgent, initial therapeutic issues based on initial electrocardiographic information are presented via 5 illustrative cases.

Adult↗

The mechanism of flutter interval alternans.

The mechanism of atrial flutter alternans was investigated by observing the effects of ventricular systole on flutter intervals in a patient with atrioventricular dissociation. Interval measurements were made both from atrial electrograms recorded from an esophageal electrode, and from surface ECG recordings. Flutter cycle intervals that occurred during a well-defined period subsequent to ventricular systole were consistently prolonged by up to 30 msec relative to the baseline flutter cycle interval. This prolongation was observed in two vastly different electrode configurations, implying that motion artifact was not predominantly responsible. We concluded that, by altering the characteristics of the flutter reentry circuit, transient increases in atrial volume and/or pressure arising during ventricular systole were responsible for the lengthening of the flutter cycle intervals.

Adult↗

[Electrocardiography changes in patients with acute cerebrovascular insufficiency].

In patients with an acute cerebrovascular insufficiency a great number of disturbances of the cardiac rhythm is existing. In our investigations the absolute arrhythmia with auricular fibrillation and flutter (21%), ventricular and supraventricular extrasystoles (22%), atrioventricular blocks (13%) and patterns of bundle-branch block (25%) are concerned. Disturbances of the repolarisation of different size were present in 74% of all patients. A pathological QT-interval was to be stated in 31% of the patients examined. In the decreased patients a greater number of the disturbances of rhythm proved was to be observed. There were significant differences in disturbances of repolarisation. We stated a tendency to significance in the tachyarrhythmia. Apart from the sinus tachycardia the atrioventricular blocks were particularly distinct in the cerebral haemorrhage. The tachyarrhythmia was characteristic in patients with cerebral embolism. The mixed form of the cerebrovascular insufficiency was associated with a sinus bradycardia - above all as an expression of the cerebral pressure.

Arrhythmias, Cardiac↗

Verapamil plasma levels and ventricular rate response in patients with atrial fibrillation and flutter.

The acute effect of verapamil on the ventricular rate in atrial fibrillation and flutter was studied in 15 patients, 13 of whom had heart rate inadequately controlled with digitalis. Plasma concentrations were measured 5 and 10 min after intravenous doses of 0.075 mg/kg and 0.15 mg/kg verapamil. In 9 patients who were clinically compensated, the 0.075-mg dose alone decreased the ventricular rate to under 100/min (responders); in the remaining 6, who had acute congestive heart failure manifested by orthopnea, rales, and pulmonary congestion, ventricular rates were above 100/min after the 0.075-mg dose (nonresponders). The 6 nonresponders received the 0.15-mg dose 30 min later. In all, the response was greater when plasma drug concentration rose after the high dose, although the rate decrease was smaller than in the 9 compensated patients who received the low dose. These results can be explained by assuming an antagonism of the verapamil effect by sympathetic stimulation in nonresponders.

Adult↗

[Propafenon therapy of arrhythmias in infancy and childhood (author's transl)].

The therapeutic dose range of propafenon was studied in 28 infants and children aged 5 days to 15.2 years (mean 8.8 years) with the following cardiac arrhythmias: paroxysmal tachycardia (20) atrial flutter (5) ventricular extrasystoles (2) and junctional tachycardia (1). With the intravenous administration of the drug in a dosage of 1.03-3.2 mg/kg/d (mean 2.28 mg/kg/d) in patients less than 15 kg and of 0.71-2.06 mg/kg/d (mean 1.26 mg/kg/d) in patients more than 15 kg body weight arrhythmias abolished. In the same patients the oral dosage was 12.2-22.6 mg/kg/d (mean 16.03 mg/kg/d) and 7.2-16.6 (mean 11.12 mg/kg/d). After 10 to 14 days a therapeutic serum level above 150 ng/ml could be maintained by a reduced oral dosage of 5.7-13.3 mg/kg/d) mean 8.5 mg/kg/d) and 3.6-11.1 mg/kg/d (mean 6.33 mg/kg/d) respectively. There were no side effects except for transitory by elevated gamma-GT in 8 patients. During a follow-up period of 1 month to 2.2 years (mean 1.6 years) 20 patients had no more arrhythmias, in 7 the number of arrhythmic attacks was reduced, and in 1 therapy failed.

Adolescent↗

Acute treatment of recent-onset atrial fibrillation and flutter with a tailored dosing regimen of intravenous amiodarone. A randomized, digoxin-controlled study.

A 24 h intravenous dosing regimen of amiodarone was designed to reach a peak plasma concentration at 1 h and to maintain the concentration above a certain level during the infusion period. A randomized, open-label, digoxin-controlled study was undertaken to observe the efficacy and safety of the dosing regimen of amiodarone in treating recent-onset, persistent, atrial fibrillation and flutter with ventricular rates above 130 beats.min-1. Fifty patients with a mean age of 70 +/- 7 (SD) years were enrolled and randomly assigned to receive either amiodarone intravenously (n = 26) or digoxin (n = 24). Amiodarone HCl was infused over 24 h according to the following regimen: 5 mg.min-1, 3 mg.min-1, 1 mg.min-1 and 0.5 mg.min-1 for 1, 3, 6 and 14 h, respectively, for a 70-kg subject. Digoxin (0.013 mg.kg-1) was infused in three divided doses, each dose 2 h apart and infused over 30 min. The mean heart rates in the amiodarone group decreased significantly from 157 +/- 20 beats.min-1 to 122 +/- 25 beats.min-1 after 1 h (P < 0.05 vs baseline), and then decreased further to stabilize at 96 +/- 25 beats.min-1 after 6 h (P < 0.05). The digoxin group had fewer dramatic alterations in heart rates, compared to the amiodarone group, in the first 8 h (P < 0.05, respectively). Maximum reduction was reached only after 8 h. The amiodarone infusion was prematurely aborted in two patients due to severe bradycardia and death after conversion in one patient and aggravation of heart failure in the other.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Entrainment techniques for mapping atrial and ventricular tachycardias.

Many atrial tachycardias, atrial flutter, and postmyocardial infarction ventricular tachycardias are due to reentry through large "macroreentrant" circuits. These circuits can be difficult to define by catheter mapping of the activation sequence. Entrainment techniques allow the relation of a mapping site to the reentrant circuit to be assessed on a site-by-site basis during catheter mapping. Regions of abnormal conduction that are in the reentrant circuit can be distinguished from bystander sites outside the circuit. A mapping site classification to guide catheter ablation is reviewed.

Atrial Flutter↗

Echocardiographic manifestations of flail aortic valve leaflets.

Six patients with aortic regurgitation secondary to flail aortic valve leaflet syndrome were studied echocardiographically, angiographically, surgically, and pathologically. The etiology of flail aortic leaflet was myxomatous degeneration in four patients and bacterial endocarditis in two. The echocardiographic manifestations of flail aortic valve leaflet are diastolic fluttering of the aortic cusp echoes, abnormal systolic aortic leaflet movement, and abnormal diastolic fluttering echoes in the left ventricular outflow tract. Diastolic fluttering of the aortic valve leaflets is specific echocardiographic evidence of aortic regurgitation due to flail aortic leaflets, and demonstration of diastolic fluttering of the aortic leaflets and diastolic fluttering echoes in the left ventricular outflow tracts is direct evidence of flail and prolapsed aortic leaflets.

Adult↗

Familial sinus node disease and degenerative myopia--a new hereditary syndrome?

A family is reported in which the father and both offspring suffered from sick sinus syndrome (SSS) accompanied by degenerative myopia in the two elder of the three family members. In all three individuals, the basic manifestations of the SSS were total sinus arrest with secondary AV junctional rhythm at a normal rate. Only the 7-year-old boy also exhibited paroxysmal atrial flutter and ventricular asystole lasting up to almost 7 s. Since he had, furthermore, recently sustained a left hemiparesis, a ventricular demand pacemaker was implanted. Chronic atrial fibrillation was eventually established in the father in whom observations were available for 16 years. Myopia of -11 D and -4.5 D, respectively, existed in the father and his 14-year-old daughter. The familial association of this defect with SSS suggests a hitherto undescribed genetic syndrome, presumably with underlying autosomal dominant transmission of the two traits.

Adolescent↗

Differential effects of superoxide dismutase on high energy phosphates, creatine kinase release, and arrhythmias during post-ischaemic reperfusion in isolated rat hearts.

In isolated rat hearts, 25 min of global ischaemia led to significant decreases in the ATP, creatine phosphate (CP), and glycogen contents and increased glucose-6-phosphate (G-6-P) and lactate in the myocardium. During a subsequent reperfusion for 15 min only the CP level, but not ATP and glycogen were restored. G-6-P and lactate were reduced, but remained still elevated in comparison with non-ischaemic hearts. The post-ischaemic coronary flow volume and creatine kinase (CK) release increased significantly compared with preischaemic values. Arrhythmias such as extrasystoles, ventricular tachycardia, flutter and fibrillation, occurred, especially during the first few minutes of reperfusion. Application of the oxygen radical scavenger, superoxide dismutase (SOD), enhanced the myocardial creatine phosphate content during reperfusion. In fibrillating hearts, SOD also increased the ATP content in comparison with non-treated hearts. Superoxide dismutase was effective only during reperfusion and not during the preceding ischaemia. Neither the CK release nor reperfusion arrhythmias were decreased by the radical scavenger. The results suggest that the superoxide radical is involved in the reduction of high energy phosphates during post-ischaemic reperfusion and that this effect can be antagonised by the superoxide anion scavenger superoxide dismutase.

Animals↗

Flecainide acetate for treatment of tachyarrhythmias in children: review of world literature on efficacy, safety, and dosing.

A review of all published experience with flecainide in infants, children, and fetuses was performed to evaluate the appropriate place of the drug in pediatric practice and to determine dosing guidelines. A total of 704 case references was generated. Flecainide appeared to be safe (no deaths with usual oral dosing, < 1% serious proarrhythmia) and effective (73% to 100% control, depending on mechanism) in children with supraventricular tachycardia. The drug was very effective for treatment of fetal tachyarrhythmias. Flecainide may not be safe for children who have structurally abnormal hearts and atrial flutter or ventricular arrhythmias. The safety of flecainide for patients with ventricular arrhythmias and normal hearts requires further investigation. Pharmacokinetic data reveal an age-dependent change in elimination half-life. Patients younger than 1 year of age have a plasma elimination half-life that is similar to that in children older than 12 years (i.e., 11 to 12 hours). Children aged 1 to 12 years have a mean elimination half-life of 8 hours. The effective flecainide dose is 100 to 200 mg/m2/day or 1 to 8 mg/kg/day. Toxicity may occur with doses in excess of these ranges, especially when high doses are accompanied by low serum trough levels. Milk blocks flecainide absorption, and toxicity may become manifest when milk products are removed from the diet.

Arrhythmias, Cardiac↗

Catheter ablation for cardiac arrhythmias.

The safety and efficacy of catheter ablation for treatment of most types of cardiac arrhythmias are well established. These arrhythmias and arrhythmia substrates include AVNRT, accessory pathways, focal atrial tachycardia, atrial flutter, idiopathic ventricular tachycardia, and bundle-branch re-entry. Catheter ablation is considered as an alternative to pharmacologic therapy in the treatment of these cardiac arrhythmias.

Arrhythmias, Cardiac↗