[The diastolic rumble and fluttering of the ventricular wall after atrioventricular valve replacement with the Hancock xenograft (author's transl)].
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Adolescent↗
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A case of arrhythmogenic right ventricular dysplasia with atrial flutter.
A 57-year-old male who had arrhythmogenic right ventricular dysplasia (ARVD) with recurrent atrial flutter (AF) is reported. The patient had more frequent episodes of AF than of ventricular arrhythmias. Magnetic resonance imaging, echocardiography and right ventriculography revealed dilatation of the right ventricle and endomyocardial biopsy specimens from the right ventricle showed findings which were compatible with ARVD. The left ventricular specimen, however, also revealed a loss of myocytes and interstitial fibroelastic changes. The present case demonstrates an overlap of post-inflammatory or primary endomyocardial fibroelastic changes with ARVD.
Aged↗
Efficacy of the novel calcium antagonist R(+)-semotiadil in limiting the ventricular rate during atrial flutter in isolated guinea pig hearts.
Ca2+ antagonists slow the ventricular rate by blocking conduction in the anterograde direction through the atrioventricular (AV) node. The aim of this study was to investigate the efficacy of the novel Ca2+ antagonist semotiadil compared with verapamil and diltiazem on the filtering capacity of the AV node during simulated atrial flutter in isolated guinea-pig hearts perfused by the method of Langendorff. During sinus rhythm, semotiadil as well as verapamil and diltiazem induced comparable depressant effects on AV-nodal conduction time and, during tachycardia, a comparable enhancement of this effect. The time constant (tau-on) for the drug-specific rate-dependent effect on AV-nodal conduction slowing was longest in the presence of verapamil compared with the long tau-on of semotiadil and the short tau-on of diltiazem. Verapamil and semotiadil exhibited a significantly greater effect than diltiazem on the mean ventricular cycle length (VCLmeun), on the maximal ventricular cycle length (VCLmax) and on the standard deviation of the VCL (SD(VCL)) during atrial flutter. Therefore the kinetics of the rate adaptation of AV-nodal conduction time in the presence of Ca2+ antagonists predicts the filtering capacity of the AV node during atrial flutter. Semotiadil has a verapamil type of action on ventricular cycle length during atrial flutter, whereas the disadvantageous prolongation of maximal VCL as well as the dispersion of VCL with semotiadil was only about half those found with verapamil.
Animals↗
Acceleration of the ventricular response to atrial flutter by amiodarone in an infant with Wolff-Parkinson-White syndrome.
Amiodarone resulted in a rapid ventricular response to atrial flutter in an infant with Wolff-Parkinson-White syndrome.
Amiodarone↗
[Atrial flutter with 1/1 nodo-ventricular conduction with amiodarone. From physiopathology to diagnosis].
Atrial flutter with 1/1 nodo-ventricular conduction is a classical complication of Vaughan-Williams's Class I antiarrhythmic drugs. The increase of the flutter cycle and weak action of the antiarrhythmic on the atrioventricular node leads to 1/1 conduction of atrial depolarisation to the ventricles. In view of their marked action on the atrioventricular node, this type of pro-arrhythmic effect is very unexpected with Class III antiarrhythmics. The authors report 7 cases of 1/1 atrial flutter with oral amiodarone observed between 1994 and 2001. The patients were 6 men and 1 woman with an average age of 58 +/- 14 years. Four of them had underlying cardiac disease; none were hyperthyroid. The initial arrhythmia was 2/1 atrial flutter (n = 4), 1/1 atrial flutter (n = 2) and atrial fibrillation (n = 1). Treatment was preventive with doses of 400 mg/day associated with carvedilol in one patient and 200 mg/day in another. The other five patients all received loading doses of 9200 +/- 2400 mg over 10 +/- 4 days. The symptoms were palpitations (n = 2) associated in one patient with hypotension, one syncope, one near syncope and one cardiogenic shock. The ventricular cycle of the 1/1 flutter was 287 +/- 33 ms. The QRS duration was 136 +/- 35 ms with ventricular tachycardia-like appearances in 3 cases. An adrenergic trigger factor was noted in 5 patients. One patient required emergency cardioversion. The authors discuss the physiopathology of 1/1 flutter and theoretical diagnostic methods are proposed. In conclusion, amiodarone does not always prevent the occurrence of 1/1 nodo-ventricular conduction in atrial flutter.
Administration, Oral↗
Paroxysmal auricular flutter with 1:1 ventricular response.
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Atrial Flutter↗
EKG of the month. Atrial flutter with 2:1 ventricular response.
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Aged↗
Relation between atrioventricular pathways and ventricular response during atrial fibrillation and flutter.
We have analysed the ventricular response as seen on the surface electrocardiogram in patients with paroxysmal atrial fibrillation and flutter in relation to the electrophysiological properties of the corresponding atrioventricular pathways. In 15 patients who had atrial fibrillation with conduction solely through the atrioventricular node, there was a significant correlation between th shortest and mean RR intervals during atrial fibrillation and the functional refractory period, "pre-Wenckebach cycle length", and the shortest ventricular cycle length that resulted from 1:1 atrioventricular conduction. In 18 patients with conduction through an accessory atrioventricular pathway the only good correlation was between the shortest and mean ventricular rate during atrial fibrillation and the "pre-Wenckebach cycle length" and shortest ventricular cycle length during 1:1 atrioventricular conduction. In 12 patients with an atriofascicular bypass tract or rapidly conducting atrioventricular node there was no significant correlation between the RR intervals during atrial fibrillation and the electrophysiological indices; the same lack of correlation was evident in all 11 patients with atrial flutter, all of whom had atrioventricular nodal conduction. The response of atrioventricular pathways to electrophysiological testing, particularly the use of incremental atrial pacing, provides useful guidance in the further management of these atrial arrhythmias.
Adult↗
Apical hypertrophic cardiomyopathy associated with life-threatening paroxysmal atrial flutter with a slow ventricular response: a case report.
A 58-year-old male patient had apical hypertrophic cardiomyopathy (HCM) associated with a life-threatening tachycardia due to atrial flutter. Following palpitation and dyspnea for 2-3 h, he became unconscious because of circulatory catastrophe, but was fully resuscitated. An electrocardiogram recorded just before the loss of consciousness revealed atrial flutter at a rate of 260 beats/min with a 2:1 ventricular response. He was diagnosed as having apical HCM based on the echocardiographic and left ventriculographic findings. Atrial stimulation at a rate of 150 pacings/min for 1 min caused a marked drop in systemic systolic blood pressure from 170 to 120 mmHg. The patient was treated with 150 mg of cibenzoline per day to prevent supraventricular tachyarrhythmias and to improve left ventricular diastolic function. At the time of the recent follow-up at 2 and a half years, he felt quite well.
Atrial Flutter↗
Clinical decision making of critical care nurses managing computer-simulated tachydysrhythmias.
The purposes of this study were to describe the clinical decision making of critical care nurses managing computer-simulated tachydysrhythmias and to assess the major sources of error related to the management of two tachydysrhythmias: atrial flutter and ventricular tachycardia. In this descriptive study, 142 critical care nurses each completed four computerized clinical simulations (two atrial flutter and two ventricular tachycardia). Simulation performance was measured by proficiency score (comparison with expert performance), patient outcome (cure or die), and amount of data collected before the first intervention. Mean proficiency scores were 51% for atrial flutter and 35% for ventricular tachycardia. Thirteen percent of the atrial flutter and 35% of the ventricular tachycardia simulations ended in patient death. Failure to recognize ventricular tachycardia and unfamiliarity with second- and third-line treatments were major sources of error. Medication errors were the cause of death in 87% of the simulations ending in patient death. These results document the need for emphasis on dysrhythmia management in the critical care curriculum.
Arrhythmias, Cardiac↗
Ventricular tachycardia as a complication of atrial flutter ablation.
A 61-year-old woman with dilated cardiomyopathy, who previously underwent successful radiofrequency catheter ablation for atrial flutter, developed monomorphic ventricular tachycardia (VT). The site of VT origin was the inferobasal right ventricle adjacent to the previous atrial isthmus ablation area. The most likely mechanism for the VT was scar-related reentry, the scar being the result of previous radiofrequency lesions in the atrial isthmus. The VT was successfully ablated.
Atrial Flutter↗
Real-time arrhythmia identification from automated analysis of intraatrial and intraventricular electrograms.
Implantable cardioverter defibrillators have dramatically improved survival rates for patients at risk of sudden cardiac death, but the occurrence of inappropriate shocks remains an unresolved problem. Various means for better tachycardia detection, chiefly morphological analysis, have been proposed to address this problem. A new computerized scheme entitled Two-Channel Rate-Morphology (2CRM) was introduced. It is a real-time arrhythmia detection algorithm that combines timing and morphology information from intraatrial and intraventricular electrograms for arrhythmia diagnosis. The program 2CRM applies an initial cycle-by-cycle coding scheme followed by contextual diagnosis of underlying rhythm. The program was tested on 36 distinct passages of two-channel intracardiac signals from 30 patients. The distribution of the arrhythmias are as follows: 4 atrial fibrillation, 6 atrial flutter, 6 supraventricular tachycardia, 10 ventricular tachycardia, and 10 ventricular flutter-fibrillation. Of the analyzed 3,417 individual cardiac cycles 3,135 (91.7%) were correctly identified. Contextual diagnosis reversed 123 single-cycle errors to obtain a performance of 3,258 correct out of 3,417 (95.3%). Utilizing an uninterrupted continuous correct contextual diagnosis as indicator of successful arrhythmia detection, 2CRM obtained an accuracy of 34 out of 36 passages (94.4%).
Algorithms↗
Tricuspid valve fluttering; echocardiographic features of ventricular septal defect.
M-mode echocardiographic features are presented in four patients with membranous ventricular septal defect. The most consistent echo findings in all the patients were the presence of fuzzy, fluttering echoes of the tricuspid valve during systole. More careful echocardiographic evaluation of the tricuspid valve in ventricular septal defect is therefore recommended.
Adolescent↗
Effects of verapamil and diltiazem on the ventricular rate during simulated atrial flutter in isolated guinea pig hearts.
To compare the direct effects of verapamil and diltiazem on the ventricular rate during atrial flutter, we developed an atrial flutter model in guinea pig isolated hearts. Atrial flutter was simulated by rapid atrial pacing (cycle length = 50 ms). At this atrial pacing cycle length, the shape of the frequency of distribution of the ventricular cycle lengths was comparable to that during spontaneous atrial flutter. Verapamil (0.01, 0.03 microM) and diltiazem (0.03, 0.09 microM) caused a comparable prolongation of the atrioventricular conduction time and atrioventricular refractoriness. Also, the anterograde Wenckebach cycle length was increased to a comparable degree by both substances. The mean ventricular cycle length during atrial flutter was comparable prolonged by both substances. The prolongation of the maximal ventricular cycle length was significantly more pronounced in the presence of verapamil. The time dependence of drug-induced alterations in atrioventricular conduction time during abrupt changes of heart rate is significantly more pronounced in the presence of verapamil compared to diltiazem. In conclusion, the more pronounced effect of verapamil on the maximal ventricular cycle length compared to the action of diltiazem may be explained by the slow binding kinetic of this drug to the Ca2+ channel resulting in a longlasting blockade of the Ca2+ channel.
Animals↗
Atrial and ventricular pressures in atrial flutter.
The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 +/- 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Both the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 +/- 15 beats/min) or in those with variable conduction (heart rate 96 +/- 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.
Atrial Flutter↗
Acceleration of ventricular response to atrial flutter after intravenous adenosine.
Adenosine may be of therapeutic and diagnostic value in the emergency management of arrhythmias. It causes transient atrioventricular nodal block and thus ends paroxysmal supraventricular tachycardias that involve the atrioventricular node. Also, it may uncover underlying atrial arrhythmias by slowing the ventricular response. Its duration of action is brief and serious adverse effects have not been reported. A 12 year old patient with atrial flutter is presented, in whom intravenous adenosine was followed by acceleration of the heart rate to a potentially dangerous arrhythmia.
Adenosine↗
Safety of oral propafenone in the treatment of arrhythmias in infants and children (European retrospective multicenter study). Working Group on Pediatric Arrhythmias and Electrophysiology of the Association of European Pediatric Cardiologists.
This study was designed to assess adverse effects of oral propafenone in a large number of pediatric patients. Retrospective data from 27 European centers covering 772 patients treated with oral propafenone were analyzed. The following arrhythmias were treated: reentrant supraventricular tachycardia in 388 patients, atrial ectopic tachycardia in 66, junctional ectopic tachycardia in 39, atrial flutter in 21, ventricular premature complexes in 140, ventricular tachycardia in 78, and other arrhythmias in 39 patients. Two hundred forty-nine patients (32.3%) had structural heart disease. Significant electrophysiologic side effects and proarrhythmia were found in 15 of 772 patients (1.9%): sinus node dysfunction in 4, complete atrioventricular block in 2, aggravation of supraventricular tachycardia in 2, acceleration of ventricular rate during atrial flutter in 1, ventricular proarrhythmia in 5, and unexplained syncope in 1 patient. Cardiac arrest or sudden death occurred in 5 of 772 patients (0.6%): 2 patients had supraventricular tachycardia due to the Wolff-Parkinson-White syndrome and a normal heart; the remaining 3 patients had structural heart disease. Overall, adverse cardiac events were more common in the presence (12 of 249 patients, 4.8%) than in the absence (8 of 523 patients, 1.5%) of structural heart disease (p <0.01). There was no difference between patients treated for supraventricular and ventricular arrhythmias. Thus, propafenone is a relatively safe drug for the treatment of several pediatric tachyarrhythmias. Proarrhythmic effects seem to be less frequent than those reported for encainide or flecainide and occur predominantly in patients with structural heart disease.
Administration, Oral↗
Clinical implications of fetal magnetocardiography.
OBJECTIVES: To test the usefulness and reliability of fetal magnetocardiography as a diagnostic or screening tool, both for fetuses with arrhythmias as well as for fetuses with a congenital heart defect. METHODS: We describe 21 women with either a fetal arrhythmia or a congenital heart defect discovered during prenatal evaluation by sonography. Four fetuses showed a complete atrioventricular block, two an atrial flutter, nine ventricular extrasystole, and one a complete irregular heart rate. Five fetuses were suspected to have a congenital heart defect. In all cases magnetocardiograms were recorded. RESULTS: Nine fetuses with extrasystole showed a range of premature atrial contractions, premature junctional beats or premature ventricular contractions. Two fetuses with atrial flutter showed typical flutter waves and four fetuses with complete atrioventricular block showed an uncoupling of P-wave and QRS complex. One fetus showed a pattern suggestive of a bundle branch block. In three of four fetuses with confirmed congenital heart defects the magnetocardiogram showed abnormalities. CONCLUSION: Fetal magnetocardiography allows an insight into the electrophysiological aspects of the fetal heart, is accurate in the classification of fetal arrhythmias, and shows potential as a tool in defining a population at risk for congenital heart defects.
Adult↗