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PubMed1982

[Ventricular tachyarrhythmia in childhood. Syncope, differential diagnosis of epilepsy].

In recent years we have noticed an increased number of severe ventricular tachyarrhythmias in children with structurally normal hearts. It is necessary to search for this condition specifically. Fainting fits caused by ventricular fibrillation or flutter with or without lengthening of the QT interval in the electrocardiogram are triggered by shock, fear or physical exertion. Distinguishing the condition from epilepsy can sometimes be difficult. Diagnosis in the case of a 14 year old boy with no history of genetic disorder could only be established with the aid of a 24-hour-ECG. Extended QT-times were observed here only in the higher heart frequency area. A 7 year old boy, initially given anti-convulsion therapy, showed QT-lengthening with ventricular extrasystoles only after repeated ECGs. His mother died suddenly following acoustic trauma. A 10 year old girl with no history of genetic disorder exhibited similar symptoms. On the basis of our observations we are of the opinion that a clear distinction into a genetically homogenous group with long QT-times, and one with a normal QT-interval, is not possible. Investigation of presumed epileptic cases by means of 24-hour-EEG-ECG in combination and ergometrics is recommended. Our patients were treated successfully with beta-blockers (propranolol).

Adolescent↗
PubMed1987

[Reduction of auricular fibrillation and tachycardia using intravenous flecainide].

Fifty-one consecutive patients with atrial tachycardia [atrial fibrillation (FA) 37, atrial flutter (Fl) 10, tachycardia (TSA) 4] received a single 2 mg/kg dose of flecainide injected intravenously over 5 to 10 minutes. Patients over 75 years of age or presenting with heart failure or disorders of conduction were excluded from the study. Sinus rhythm was restored during the injection or within the following 5 minutes in 15 patients (FA 12, Fl 1, TSA 2). The most frequent side-effects were visual disorders (5 cases) and moderate prolongation of QRS (all cases). Five patients had more pronounced disorders of conduction, but none developed heart failure. Reduction was obtained in 12 of the 18 patients whose arrhythmia had lasted for less than 8 days, against only 3 of the patients whose arrhythmia was more than 8 days old. Drug-induced reduction always failed in patients with left atrial dilatation (greater than 45 mm at echocardiography). An increase in the ventricular rate of unreduced flutter was observed in only one patient. Plasma flecainide levels were high (1.5 and 5.5 mg/l) at the end of the injection, but they fell to the therapeutic range within less than 10 minutes. Flecainide therefore appears to be effective in reducing recent atrial fibrillation on a non-dilated atrium. In cases with disorders of conduction, altered ventricular function or flutter, the therapeutic risk is such that another method of conversion should be used.

Adult↗
PubMed1975

[Syncopal attacks and sudden death due to ventricular fibrillation -- a variant of the Jervell or Lange-Nielsen syndrome (author's transl)].

Syncopal attacks due to ventricular fibrillation or -- flutter with elongation of QT in the ECG and deafness are signs of a congenital condition described by Jervell and Lange-Nielsen 18 years ago. Since then we have learned that the range of variation of symptoms is very wide. There are differences genetically and in age-groups. A boy aged 15 years with supposedly cerebral fits is reported on. Since the right diagnosis was missed he had been treated with anticonvulsants for years. But these were syncopal attacks, Effort produced a tendency to bigeminus. -- A knee-bending exercise repeated 13 times lead to his death from ventricular fibrillation. Post-mortem examination showed no pathologic findings except mild left hypertrophy of the ventricle. His sister also had similar attacks without spasms after excitement or mild physical effort. She too had no extension of the QT interval. Their mother and grandmother also had syncopal attacks and died at the ages of 31 and 24 years. A girl-cousin died suddenly at the age of 15. In addition we have seen a neonate with a mild cardiac murmur on whom an ECG was done on the 16th day. The QT interval was significantly prolonged. There were numerous extrasystoles. He died suddenly 2 days later. Post mortem showed no cardiac pathology. One should now be able to explain some cases of unexpected natural death. But ignorance of the pathogenesis does not yet permit definition of the clinical pictures.

Adolescent↗
PubMed1976

[Plasma level studies of quinidine retard, their significance for dosage and onset of effect].

A new sustained-action preparation of quinidine-bisulfate (BM-Chinidin Retard) was investigated in 21 patients. After a single oral dose of 1 g peak plasma levels are reached within 3-4 hours with an unsubstantial decrease during the following 4 hours. After 2 g in three divided doses within 12 hours maximal plasma levels are found after 14-16 hours, but an effective level is reached as early as 4 hours after the first dose. With 1 g Chinidin retard given in two doses within 24 hours, varying plasma concentrations are reached after 24 hours, reaching a maximum after 48 hours and decreasing to a medium level thereafter. The minimal concentrations measured were 23 percent lower than the maximal concentrations suggesting that during longterm application rather stable plasma levels are achieved. The effectiveness of the preparation was demonstrated in patients with atrial fibrillation and flutter, supra-ventricular and ventricular premature beats. Longterm treatment was attempted in all patients. Quinidine effectiveness and plasma concentrations were constant throughout the observation period. Side effects were rare: inappetence, vertigo, and headache were observed transiently in 4 patients without necessitating a change in medication. ECG-alterations occurred as described for quinidine-prepartions in general.

Administration, Oral↗
PubMedDate not supplied

Efficacy of radiofrequency catheter ablation in treatment of elderly patients with supraventricular tachyarrhythmias and ventricular tachycardia.

Radiofrequency catheter ablation was performed in 100 men and 81 women, mean age 78 +/- 5 years, referred for ablation of atrial flutter, supraventricular tachycardia, and ventricular tachycardia, and for ablation of the atrioventricular junction with permanent pacemaker implantation in patients with atrial fibrillation and a rapid ventricular rate not controlled by drug therapy. A hematoma in 1 of 182 ablation procedures (<1%) was the only complication. Radiofrequency catheter ablation was successful in treating 63 of 70 patients (90%) with atrial flutter, in treating 60 of 66 patients (91%) with supraventricular tachycardia, in treating 2 of 2 patients (100%) with ventricular tachycardia, and in ablating the atrioventricular junction in 43 of 44 patients (98%) with atrial fibrillation and a rapid ventricular rate not controlled by drug therapy.

Aged↗
PubMed1976

[Effect of chronic stimulation of the negative and positive emotionogenic centers of the hypothalamus on development of cardiac arrhythmias].

Chronic experiments were conducted on 46 rabbits; a study was made of the changes in cardiac activity arising in prolonged (up to 1--2 weeks) electric stimulation of the ventro-median nuclei of the hypothalamus. Disturbances of the cardiac rhythm in the form of tachycardia, atrial flutter and fibrillation, ventricular extrasystole and paroxysmal ventricular tachysystole occurred mostly during the first days of stimulation and ceased after inderal infusion. Functional "weakness" of the cardiac pacemakers was revealed in the animals subjected to 1--2-week stimulation of the ventromedian nuclei. This was indicated by the post-stimulation suppression of the pacemaker automaticity and the appearance of Liciani's periods. Disturbances of the cardiac rhythm originating in stimulation of the ventromedian nuclei ceased in stimulation of the lateral hypothalamic field.

Animals↗
PubMed1988

Esmolol: safety and efficacy in postoperative cardiothoracic patients with supraventricular tachyarrhythmias.

Esmolol, an intravenous, ultrashort-acting beta-blocker, was studied for its ability to safely control supraventricular arrhythmias up to 24 hours in 15 postoperative cardiothoracic surgery patients with atrial fibrillation or flutter and rapid ventricular response. Esmolol obtained an initial therapeutic response in nine (60 percent) patients. Mean heart rate for the 15 patients was reduced from 139 +/- 12 beats/min before therapy to 106 +/- 21 beats/min during esmolol infusion (p less than 0.01). The mean time to a therapeutic response after initiation of therapy, using a multistep titration regimen (500 micrograms/kg/min loading infusions over one minute, prior to incremental titration steps from 50 to 300 micrograms/kg/min over 4 to 14 minutes), was 22 +/- 9 minutes, and therapy was continued for 17 +/- 9 hours in responders. Esmolol significantly lowered blood pressure in the group studied and resulted in mild supine or orthostatic hypotension in ten (67 percent) patients. Side effects, including hypotension (10/15 patients), gastrointestinal disturbances (2/15), and weakness or somnolence (6/15), were transient and were not associated with serious clinical sequelae. We conclude that esmolol is effective for rate control in a majority of postoperative cardiothoracic surgery patients with atrial fibrillation or flutter. Side effects, although mild, occur relatively frequently, limiting prolonged infusions and warranting close surveillance of patients.

Adrenergic beta-Antagonists↗
PubMed1980

[Paradoxic response to disopyramide and quinidine (author's transl)].

Until recently, severe paradoxic responses to disopyramide have been believed to occur only, if at all, at extremely high doses. This credo has been shaken by some recent reports on severe ventricular tachyarrhythmias occurring in some patients on disopyramide. A further case (62 years, female, mitral commissurotomy in 1966, combined mitral valve lesion) is presented in whom a normal oral regimen (100 mg disopyramide four times daily) induced syncope due to ventricular tachycardia and flutter. The patient exhibited a long QT time before medication without deafness. Indication for treatment was the preservation of sinus rhythm as intermittent atrial fibrillation or flutter has been documented before. The serum potassium level was in the range of normal. Similar side-effects occurred some days later when the patient received quinidine sulfate. A survey of the most recent literature reveals a total of 20 patients with proven or suspected paradoxic responses to disopyramide. Factors that might favour the occurrence of paradoxic effects were preexisting QT prolongation, hypokaliemia, or massive overdosage. Though the total incidence of these side-effects seems to be relatively low, disopyramide should be given to special subgroups of patients only under careful monitoring.

Adult↗
PubMed1981

Procainamide-induced polymorphous ventricular tachycardia.

Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.

Administration, Oral↗
PubMed2005

Impact of congestive heart failure and left ventricular systolic function on the prognostic significance of atrial fibrillation and atrial flutter following acute myocardial infarction.

BACKGROUND: Reports on the prognostic importance of atrial fibrillation following myocardial infarction have provided considerable variation in results. Thus, this study examined the impact of left ventricular systolic function and congestive heart failure on the prognostic importance of atrial fibrillation in acute myocardial infarction patients that might explain previous discrepancies. METHODS: The study population was 6676 patients consecutively admitted to hospital with acute myocardial infarction. Information on the presence of atrial fibrillation/flutter, left ventricular systolic function and congestive heart failure were prospectively collected. Mortality was followed for 5 years. RESULTS: In patients with left ventricular ejection fraction<0.25, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.8 (1.1-3.2); p<0.05) but not an increased 30-day mortality. In patients with 0.25 0.35. In patients with congestive heart failure, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.5 (1.2-1.9); p<0.001) and increased 30-day mortality (OR=1.4 (1.1-1.7); p<0.001) but not in patients without congestive heart failure. In hospital survivors, atrial fibrillation/atrial flutter was associated with an increased long-term mortality in all subgroups except those with left ventricular ejection fraction<0.25. CONCLUSIONS: Atrial fibrillation/atrial flutter is primarily associated with increased in-hospital mortality in heart failure patients. Long-term mortality is increased in all subgroups except those with left ventricular ejection fraction<25%.

Aged↗
PubMed1992

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension.

Sixty-two patients with recent-onset (less than or equal to 1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p less than 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p less than 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 +/- 147 minutes) than for amiodarone (705 +/- 418; p less than 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate less than or equal to 150 beats/min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Sonographic assessment of fetal cardiac arrhythmias.

The fetus with an arrhythmia may be at high risk both from the arrhythmia itself and from the condition that provoked it. Incorrect diagnosis and inappropriate or delayed treatment may further compound the hazard. Although echocardiography can specifically identify the arrhythmia, this technique requires very skilled and careful examination by a physician who fully understands how to differentiate optimally between similar-appearing but mechanistically different arrhythmias. Congenital heart disease may also be present and must be evaluated specifically. This report describes ultrasound recording techniques used to diagnose arrhythmias and includes a discussion of M-mode echocardiography, two-dimensional imaging, pulsed Doppler, and color-flow Doppler. It also differentiates specific arrhythmias--premature atrial contractions, ventricular tachycardia, atrial flutter, complete heart block, and supraventricular tachycardia--and presents the optimal diagnostic tools for each.

Arrhythmias, Cardiac↗
PubMed1999

Prospective clinical evaluation of a programmed atrial stimulation protocol for induction of sustained atrial fibrillation and flutter.

UNLABELLED: We sought to define a minimum standardized protocol for induction of atrial fibrillation [AF] and/or atrial flutter. In contrast to ventricular stimulation protocols, a stimulation protocol for induction of AF or atrial flutter has not been critically evaluated. Since suppression of inducible AF or atrial flutter is used as one of the endpoints of success of pharmacologic and ablation therapies, there is an obvious need to define a minimally appropriate electrical stimulation protocol for induction of AF or atrial flutter. We prospectively evaluated 70 patients, 44 with spontaneous atrial flutter or AF and 26 controls without documented atrial arrhythmias. A standardized programmed stimulation protocol, which employed up to three atrial extrastimuli delivered at two atrial sites at two atrial drive pacing lengths, was used in attempt to reproduce sustained AF and atrial flutter. The study endpoint was induction of sustained (> 30 s) AF or atrial flutter. Sustained AF or atrial flutter was induced in 39/44 (89%) patients and 2/26 (7%) of controls (p < 0.01). The arrhythmia induced was atrial flutter in 19/21 (91%) of atrial flutter patients, AF in 17/18 (94%) AF patients, both atrial flutter and AF in 5 AF/atrial flutter patients (100%). Two patients with atrial flutter had both AF/atrial flutter and 1 patient with AF had atrial flutter induced. The arrhythmia was induced from first stimulation site in 37 patients (85%) using a single extrastimuli in 9 (20%) patients, double extrastimuli 18 (41%) patients and triple extrastimuli in 10 (23%) patients. Two patients (5%) required stimulation from second site with two and three extrastimuli, respectively. The overall sensitivity and specificity of this stimulation protocol were 89% and 92%, respectively with a positive predictive accuracy of 95%. CONCLUSIONS: 1. Up to three atrial extrastimuli and two atrial sites are needed to increase yield of AF/atrial flutter induction at electrophysiologic study. 2. Induction of either AF or atrial flutter correlates well with the presence of a similar spontaneous arrhythmia. 3. A baseline determination of the induction mode may be desirable prior to evaluation of interventions directed at AF or atrial flutter.

Aged↗
PubMed2006

Effect of oligomer procyanidins on reperfusion arrhythmias and lactate dehydrogenase release in the isolated rat heart.

The antiarrhythmic effect of an oral 3-week-pretreatment with oligomer procyanidins derived from Vitis vinifera was investigated on the isolated perfused heart after global no-flow ischemia (procyanidin-treated group: n = 9, control group: n = 13). Hearts were perfused with a modified Krebs-Henseleit solution in which the K+ content was reduced to 3.0 mmol/l in order to lower the fibrillation threshold. Monophasic action potentials in addition to ECG were recorded. The durations of ischemia and reperfusion were 20 and 30 min, respectively. Arrhythmias including ventricular fibrillation (VF), ventricular tachycardia (VT), flutter (Fl) and bradycardia were evaluated. During the reperfusion, irreversible VF occurred in most of control hearts. The incidence of VF (percentage of the hearts in which VF occurred) was lowered by oligomer procyanidins from 84.6 to 55.6 %, and the duration of the episodes of VF (expressed as percentage relative to the total duration) was significantly shortened from 76.1 +/- 27.9 % to 36.6 +/- 40.6 % (p = 0.036). Simultaneously, the percentage of duration of normal sinus rhythm (NSR) increased from 19.5 +/- 30.3 % to 46.2 +/- 35.9 % (n.s.). VF occuring in the procyanidin-treated hearts could be reversed in two hearts within few minutes to a stage of "reversible arrhythmias" consisting of short episodes (1 to 60 s) of either Fl or VT or bradycardia or NSR alternating with each other. LDH (lactate dehydrogenase) release in the first drops appearing from the reperfused heart was significantly reduced in the procyanidin-treated rats (66.7 +/- 36.2 mU/min, n = 8) in comparison to controls (159.7 +/- 79.0 mU/min, n = 10; p = 0.010). These results demonstrate an antiarrhythmic and cytoprotective effect of oral pretreatment with oligomer procyanidins under the given experimental conditions.

Animals↗
PubMed2001

The use of diltiazem for treating rapid atrial fibrillation in the out-of-hospital setting.

STUDY OBJECTIVE: We sought to evaluate the use of intravenous diltiazem for treatment of rapid atrial fibrillation or flutter (RAF) in the out-of-hospital setting. METHODS: This study is a retrospective review of data with historical control subjects. Data were drawn from out-of-hospital patients reported to a statewide paramedic system who presented with atrial fibrillation or flutter and a ventricular response rate (VRR) of 150 beats/min or greater. The intervention (diltiazem) group included patients who received diltiazem during a 9-month period in 1999. The control group included patients from 1998 who did not receive diltiazem. Patients who were intubated or underwent cardioversion were omitted. Therapeutic response was defined as the occurrence of change to sinus rhythm, reduction of VRR to 100 beats/min or less, or reduction of baseline VRR by 20% or greater. Data were analyzed by using the chi(2) test, the Student's t test, and odds ratios (ORs). A Bonferroni adjusted P value of.005 was used to define statistical significance. RESULTS: Forty-three patients receiving diltiazem and 27 control subjects were included in the study. The mean total diltiazem dose was 19.8 mg (95% confidence interval 17.8 to 21.8). The diltiazem and control groups did not significantly differ with respect to age; sex; history of atrial fibrillation; prior use of digitalis, beta-blockers, or calcium channel blockers; concurrent out-of-hospital therapies; or baseline VRR or systolic blood pressure (P =.09 to 1.00). The difference in VRR reduction between the diltiazem and control groups was 38 beats/min (95% confidence interval 24 to 52); this difference was statistically significant (P <.001). The mean percentage reduction of VRR in the diltiazem group was -33.1%. The difference in systolic blood pressure change between the diltiazem and control groups was not statistically significant (P =.17). The diltiazem group had a higher prevalence of achieving VRR reduction to 100 beats/min or less than did the control group (OR 22.6; P <.001), of achieving a VRR reduction of 20% or greater (OR 19.3; P <.001), and of achieving overall therapeutic response (OR 19.3; P <.001). Few changed to sinus rhythm in either group (estimated OR 6.3; P =.15). No patients in the diltiazem group required treatment for hypotension, endotracheal intubation, resuscitation from cardiac arrest, or emergency treatment of unstable dysrhythmias. CONCLUSION: The effects of diltiazem on RAF can be appreciated within the constraints of the out-of-hospital environment. Diltiazem should be considered as a viable field therapy for rate control of RAF.

Aged↗
PubMed1984

Diagnosis and management of acute myocarditis aided by serial myocardial biopsy.

Two cases in which right ventricular endomyocardial biopsy established a definitive pathologic diagnosis of acute myocarditis are presented. Both patients presented with severe left ventricular dysfunction, atrial flutter and an intraventricular conduction defect. Immunofluorescent and immunoperoxidase examination of the biopsy specimens suggested a humoral immune mechanism in one case and a cell-mediated immune mechanism in the other. Substantial improvement in cardiac function followed treatment with prednisolone and azathioprine in both cases. Significant regression of the myocardial inflammatory changes was documented by a further endomyocardial biopsy in each case following clinical improvement.

Adult↗
PubMed2001

Pregnancy after fontan repair of complex congenital heart disease.

We describe four successful pregnancies in three women who had previously had a Fontan repair for congenital heart disease. Each pregnancy resulted in a live birth and there was no maternal mortality The infants were premature, being delivered at 26, 30 and 35 weeks, and weighing 1,020, 1,333 and 1,930 g respectively The fourth infant was born at 32 weeks and no birthweight is available. Maternal complications occurred and were those anticipated after a Fontan repair. Two mothers required treatment for supraventricular arrhythmias (atrial flutter and fibrillation). Ventricular failure was present in two mothers and required ongoing drug treatment. Raised systemic venous pressures caused peripheral oedema in two mothers and hepatomegaly and ascites in one mother. The physiology, potential complications, anaesthetic concerns and drug treatment in pregnancy after Fontan repair are discussed.

Adult↗
PubMed1980

Catecholamine induced double tachycardia: case report in a child.

A six-year-old girl with syncope in association with atrial flutter-fibrillation and ventricular tachycardia produced by exercise or emotion is presented. The tachycardias could be reproduced by low-dose isoproterenol infusion and were blocked by high dose propranolol therapy. Catecholamine-induced tachyarrhythmias should be suspected in children with unexplained syncope in association with exercise or emotion.

Atrial Fibrillation↗