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PubMed1994

The "automatic mode switch" function in successive generations of minute ventilation sensing dual chamber rate responsive pacemakers.

Automatic mode switch (AMS) from DDDR to VVIR pacing is a new algorithm, in response to paroxysmal atrial tachyarrhythmias. With the 5603 Programmer, the AMS in the Meta DDDR 1250 and 1250H (Telectronics Pacings Systems, Inc.) operates when VA is shorter than the adaptable PVARP. With the 9600 Programmer, an atrial protection interval can be defined after the PVARP. The latest generation, Meta DDDR 1254, initiates AMS when 5 or 11 heart cycles are > 150, 175, or 200 beats/min. From 1990 to 1993, 61 patients, mean age 61 years, received a Meta DDDR: in 24 a 1250, in 12 a 1250H and in the remaining 25 a 1254 model. Indication for pacing was heart block in 39, sick sinus syndrome in 15, the combination in 6, and hypertrophic obstructive cardiomyopathy in 1. Paroxysmal atrial tachyarrhythmias were present in 43. All patients had routine pacemaker surveillance, including 52 Holter recordings. In 32 patients, periods of atrial tachyarrhythmias were observed, with proper AMS to VVIR, except during short periods of 2:1 block for atrial flutter in 4. In two others, undersensing of the atrial arrhythmia disturbed correct AMS. With the 1250 and 1250H model, AMS was observed on several occasions during sinus rate accelerations in ten patients. This was never seen with the 1254 devices. Final programmation was VVIR in 2 (chronic atrial fibrillation), AAI in 1 (fracture of the ventricular lead), VDDR in 1 (atrial pacing during atrial fibrillation), DDD in 5, and DDDR in 53, 48 of whom had AMS programmed on.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2003

Time course for resolution of left atrial appendage stunning after catheter ablation of chronic atrial flutter.

OBJECTIVES: This study assessed the time course of resolution of left atrial appendage (LAA) stunning after catheter ablation of chronic atrial flutter (AFL). BACKGROUND: Although the presence of LAA stunning after ablation of chronic AFL calls for anticoagulation in the post-cardioversion period, limited information has been obtained, particularly regarding its duration. METHODS: Sixteen patients who underwent ablation of chronic, pure AFL were studied, only five of whom had structural heart disease and one of whom had a reduced left ventricular ejection fraction. The LAA emptying velocities (LAAEV) and left atrial spontaneous echo contrast (SEC) were assessed using transesophageal echocardiography before, within 24 h after, one week after, and two weeks after ablation. RESULTS: Within 24 h after ablation, the LAAEV decreased from 39 +/- 10 cm/s during AFL to 21 +/- 10 cm/s during sinus rhythm (p < 0.01), with eight patients (50%) having documented SEC. After one week, the LAAEV increased (39 +/- 17 cm/s, p < 0.01 vs. within 24 h) and SEC resolved in five of eight patients. After two weeks, the increase in LAAEV persisted (54 +/- 14 cm/s, p < 0.01 vs. 1 week) and SEC was no longer present in any of the patients. The numbers of patients with LAAEV >30 cm/s and absence of SEC were three within 24 h, 11 at one week, and 16 at two weeks after ablation. CONCLUSIONS: Patients with chronic, pure AFL and preserved left ventricular function who will undergo catheter ablation may not require anticoagulation therapy for more than two weeks after the procedure because of the presence of forceful mechanical LAA contractions and the absence of SEC.

Aged↗
PubMed1986

The mechanism of action of the optical enantiomers of verapamil against ischaemia-induced arrhythmias in the conscious rat.

The actions of (-)-verapamil (0.2-6 mg kg-1) and (+)-verapamil (0.4-12 mg kg-1) against arrhythmias induced by coronary artery occlusion were studied in conscious rats. Intravenously administered (-)- and (+)-verapamil dose-dependently reduced ventricular arrhythmias. (-)-Verapamil was consistently 4 times more potent than (+)-verapamil. In the same animals, (-)-verapamil was approximately 4 times more potent than (+)-verapamil for effects on heart rate and blood pressure. Both enantiomers prolonged P-R interval, but had no effect on QRS interval. In separate groups of conscious rats, neither enantiomer influenced the threshold voltage and pulse width required to elicit fibrillo-flutter, or altered the maximum following frequency, during electrical stimulation of the left ventricle. In isolated, paced, Langendorff-perfused ventricles of the rat, both enantiomers dose-dependently reduced contractility, (-)-verapamil being 8-21 times more potent than (+)-verapamil; both absolute and relative potencies were dependent on potassium concentration. These results are compatible with the hypothesis that calcium antagonism in the ischaemic ventricular myocardium is antiarrhythmic during acute myocardial ischaemia.

Animals↗
PubMed1997

Essential pathway of reentry in the canine model of atrial flutter. Analysis using radiofrequency ablation.

In humans, the isthmus in the low right atrium between the tricuspid annulus and the inferior vena cava or the coronary sinus ostium is a well-established target of catheter ablation of common atrial flutter. In the canine model of atrial flutter with a Y-shaped incision, the tricuspid annulus was thought to constitute the essential reentrant pathway. The present study was designed to determine whether the supravalvular tissue around the tricuspid annulus is essential to atrial flutter in the canine model with an intercaval obstacle on the basis of the results of radiofrequency ablation. Epicardial approach of radiofrequency ablation was tested in 4 groups of dogs. Group A (5 dogs): Single application of radiofrequency energy (20 W) for 5 sec to the mid right atrial free wall. Group B (9 dogs): One to two applications to the tricuspid annulus. A ligature was also placed encircling the tricuspid annulus from the supravalvular atrial tissue to the subvalvular ventricular tissue. Group C (9 dogs): Linear transverse applications to the mid right atrial free wall between the tricuspid annulus and the intercaval obstacle. Group D (10 dogs): The isthmus between the inferior vena cava and the tricuspid annulus was ablated. After the experiment, the heart was excised for anatomical and histological studies. Atrial flutter was never abolished in all dogs in Groups A and B. A ligature encircling the tricuspid annulus also failed to terminate atrial flutter in 2 dogs tested. In contrast, atrial flutter was successfully abolished in 6 dogs (67%) of Group C and in 7 dogs (70%) of Group D. Total energy delivered was significantly higher in Group C than in Group D (364 +/- 133 versus 139 +/- 65 joules, p < 0.003). The total energy required for successful ablation was related to the cross sectional area of the ablation site (r = 0.55, p < 0.05). These results indicate that the tricuspid annulus is not an essential part of the reentrant pathway in the canine model of atrial flutter with an intercaval obstacle. The entire atrial tissue between the anatomical barriers could be involved in the reentrant pathway, and should therefore be ablated transmurally for successful ablation.

Animals↗
PubMed2005

Ibutilide for rapid conversion of atrial fibrillation or flutter in a mixed critically ill patient population.

INTRODUCTION: Ibutilide is an intravenous class III antiarrhythmic agent that has been shown to be effective in converting acute onset atrial fibrillation/flutter in stable medical and cardio-surgical patients. Data on its use in critically ill patients are rare. The aim of this open, non-randomized, prospective trial was to assess the potential role of ibutilide for conversion of recent onset atrial fibrillation/flutter in a mixed critically ill ICU-population. METHODS: Twenty cardiac-surgical and 17 medical patients with acute tachycardic atrial fibrillation or flutter received up to two 10-min intravenous infusions of 1.0 mg ibutilide. RESULTS: The cumulative conversion efficacy of ibutilide was 56.8% (21 of 37 patients). The mean time to termination of the arrhythmia was 17.7 +/- 12.5 min (range 4 to 45 min) after the start of the first infusion. Conversion success was significantly higher in medical compared to cardiac-surgical patients (82.4 versus 35.0%, p=.0063). In a multivariate binary stepwise logistic regression analysis adjusted for age, heart rate and reduced left ventricular function, cardiac surgery remained significantly associated with a lower conversion probability (RR, .14; 95%CI, 0.02 to 0.76; p=.0190). Serious, ibutilide-induced ventricular arrhythmias developed in 3/37 patients (8.1%). Two of these 3 patients had a left ventricular ejection fraction < 20%. CONCLUSION: Ibutilide is an effective treatment for conversion of acute tachycardic atrial fibrillation/flutter in critically ill patients. Higher efficacy can be expected in medical than cardiac-surgical patients. Ventricular proarrhythmia, especially in patients with severely depressed left ventricular function represents the most important limitation of ibutilide treatment.

Aged↗
PubMed1989

Efficacy, safety, and tolerance of d-sotalol in patients with refractory supraventricular tachyarrhythmias.

The efficacy, safety, and electrophysiologic effects of intravenous and oral d-sotalol, an investigational class III antiarrhythmic agent, are not yet well characterized. We evaluated the electrophysiologic, antiarrhythmic, and hemodynamic effects of d-sotalol infusion (1.5 to 2.75 mg/kg) and of chronic oral therapy (200 to 400 mg bid) in 10 patients with chronic, paroxysmal supraventricular tachyarrhythmias refractory to 5 +/- 2 standard agents. Four patients had paroxysmal supraventricular tachycardia (PSVT), four had paroxysmal atrial fibrillation, two had atrial flutter, and one had nonparoxysmal reciprocating junctional tachycardia (NPRJT). PSVT was inducible or spontaneously present in 4 of 4 before d-sotalol. After intravenous d-sotalol PSVT was noninducible in three patients and slowed by 40% in one. Atrial fibrillation was inducible or spontaneously present in 4 of 4 before therapy. After intravenous d-sotalol, one became noninducible, and three achieved rate-slowing (the mean falling from 69 to 61 bpm). In one patient, atrial flutter became noninducible; in another, d-sotalol slowed the rate of atrial flutter by 28%. D-sotalol restored sinus rhythm in the patient with NPRJT. Intravenous d-sotalol increased the sinus cycle length; the QTc, PR, and AH intervals; and the AV nodal functional refractory period, the AV nodal effective refractory period; and the right ventricular effective refractory period significantly. The atrial effective refractory period, sinoatrial conduction time, and corrected sinus recovery time tended to increase, but did not reach statistical significance. The QRS, PA, and HV intervals did not change. Mean BP fell 13.4 +/- 9.2% after intravenous d-sotalol, but no adverse symptoms developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMedDate not supplied

ECG interpretation: what is different in children?

While the electrical waveforms and basic approach to electrocardiogram (ECG) interpretation are similar for pediatric and adult patients, some important differences must be recognized to provide appropriate care for infants and children. Maturational changes that occur over the early childhood years result in differences in normal heart rates, interval durations, and ventricular dominance. Any arrhythmia seen in adults can occur in the pediatric patient; however, the most common variations from normal rhythms are sinus arrhythmia, bradycardia, and supraventricular tachycardia. Nurses caring for infants and children must recognize the important similarities and differences in rhythm strip interpretation between the adult and the pediatric patient.

Adolescent↗
PubMed2006

ST-segment abnormalities and premature complexes are predictors of new-onset atrial fibrillation: the Niigata preventive medicine study.

BACKGROUND: Left ventricular hypertrophy is a known risk factor for atrial fibrillation (AF). However, it is not well understood whether other electrocardiogram abnormalities are associated with development of AF. METHODS: This was a community-based cohort study based upon a database of annual health examinations. We included 63,386 subjects aged > or = 50 years, without baseline AF (including atrial flutter), structural heart disease, or heart failure, who completed the annual examination during a 10-year follow-up period (1991-2002). The electrocardiographic risk factors for AF were studied in the subjects. RESULTS: Atrial fibrillation developed in 873 subjects. Age, male sex, body mass index, hypertension, systolic and diastolic blood pressure, and diabetes were significant risk factors for the development of AF. In multivariable logistic regression analysis adjusted for these risk factors, electrocardiographic left ventricular hypertrophy (odds ratio [OR], 1.43), ST-segment abnormality without left ventricular hypertrophy (OR, 1.89), and the presence of premature complexes during a 10-second recording (OR, 2.89) were significantly associated with AF, whereas either right (OR, 0.84) or left bundle branch block (OR, 0.96) was unrelated. The risk for AF increased progressively with the severity of both ST-segment change and premature complexes. CONCLUSIONS: ST-segment abnormality and comparably high-frequency premature complexes were each associated with increased risk for the development of AF. These electrocardiographic findings may be useful to stratify high-risk subjects for new-onset AF.

Aged↗
PubMed1984

[Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases].

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.

Administration, Oral↗
PubMed1985

[Extrasystole in the neonatal period].

We investigated the clinical course in 35 healthy newborn with premature beats and studied the literature with regard to their frequency, pathogenesis, and therapy with the following results: Investigations with continuous monitoring or long-term ECG registration show a frequency of 7-25%. In literature, almost one-fourth, in our patients one-half of the newborn have ventricular premature beats. These will probably disappear later than atrial premature beats, but their prognosis is not worse. The premature beats of newborn are often complex (blocked or aberrant conduction, bigeminus, tachycardia). Atrial flutter is sometimes associated. In one-half of cases they disappear spontaneously during the first month of life. However, they lasted for longer than 4 months in 7 out of 35 infants. The disorder increased after birth in 2 children, which is unusual. Therapy was indicated if there were signs of heart failure, frequent or increasing rate of tachycardia or atrial flutter. Premature beats do not indicate primary operative delivery. Immaturity of the central and autonomous nervous system and of the conduction-tissue of the heart may be the reason for frequent perinatal premature beats.

Anti-Arrhythmia Agents↗
PubMed1982

M-mode echocardiographic features of endomyocardial fibrosis.

M-mode echocardiographic findings are described in 21 patients with endomyocardial fibrosis. Features associated with right ventricular endomyocardial fibrosis include: (i) exaggerated motion and thickening of the anterior right ventricular wall; (ii) increased right ventricular end-diastolic dimension; and (iii) paradoxical septal motion. Pericardial effusion (viz an echo-free space behind the posterior left ventricular wall) was shown in three patients. The tricuspid valve was easily recorded in all. Six patients with left ventricular endomyocardial fibrosis had diminished left ventricular end-diastolic dimension. Three had echo features of pulmonary hypertension (viz reduced e-f slope, absent a wave in sinus rhythm, and systolic notching of the pulmonary valve echogram). Fine fluttering of the anterior mitral valve and tricuspid valve echo was observed in two patients (one of whom was in sinus rhythm) with biventricular endomyocardial fibrosis, and no angiographic evidence of aortic regurgitation.

Adolescent↗
PubMed2004

Atrial tachycardia ablation in a patient with double outlet right ventricle corrected by surgery.

The development of surgical and percutaneous techniques for treatment or palliation of congenital heart disease has prolonged survival in these patients and has increased late complications, particularly arrhythmias. Such arrhythmias are more frequently refractory to medical therapy, requiring percutaneous ablation. We present the clinical case of a 14-year-old child with complex congenital heart disease (double outlet right ventricle) who underwent two corrective surgeries (Rastelli operation and subsequent replacement of the homograft in the conduit connecting the right ventricle to the pulmonary artery; ventricular septal defect closure and tricuspid valve repair). After the second surgery the patient presented with wide complex syncopal tachycardia, refractory to medical therapy. Electrophysiologic study (EPS) identified an isthmus-dependent atrial flutter that was successfully treated by radiofrequency (RF) ablation (a linear block was created along the cavo-tricuspid isthmus). Three months later a new episode of tachycardia occurred, but without syncope. The second EPS revealed an atrial tachycardia originating from the lateral wall of the right atrium, which was treated by ablation with focal application of RF energy. Four months after the last EPS the child remains free of arrhythmic symptoms, under no anti-arrhythmic therapy.

Adolescent↗
PubMed2005

[The use of auto mode switching in patients with sick sinus syndrome].

BACKGROUND: At present the dual chamber pacing, originally developed for patients with AV blockades, is widely used also for patients with Sick sinus syndrome (tachycardic-bradycardic type). But these patients often cause therapeutical problems to their physicians. In these cases either antiarrhythmic therapy is necessary to prevent recurrent supraventricular tachycardias (which are cause of rapid ventricular pacing) or in the case of failure of AA therapy the pacing mode has to be changed to DDI/R, which excludes physiological VAT pacing. The Auto Mode Switching (AMS) function ensures adequate ventricular pacing rate in the time of SV arrhythmias. METHODS AND RESULTS: Effects of dual chamber pacemakers equipped with AMS were studied in a group of patients with paroxysmal atrial fibrilation and/or atrial flutter. CONCLUSIONS: Therapy brings effects in lower of expenses due to less frequent visits at the physician, lower rate of rehospitalizations and lower need for powerful AA therapy.

Adult↗