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PubMed2004

Myotonic dystrophy presenting as atrial flutter in childhood.

A 12-year-old boy presented with tachycardia and cardiomegaly. An electrocardiogram showed atrial flutter with a ventricular rate of 170 beats/min. The echocardiogram showed left ventricular dilation, with decreased contractility. Electromyography confirmed the diagnosis of myotonic dystrophy. The atrial flutter was converted to sinus rhythm by electroversion, leading to restoration of normal cardiac function. Our case illustrates that atrial flutter can be an early sign of the cardiac complications of myotonic dystrophy in childhood.

Atrial Flutter↗
PubMed1998

Conversion of recent-onset atrial fibrillation to sinus rhythm: effects of different drug protocols.

UNLABELLED: In a population of 417 hospitalized patients, the efficacy and safety of different drug regimens administered to convert atrial fibrillation (AF) of recent onset (< or = 7 days duration) to sinus rhythm were evaluated. All patients were in NYHA Class < or = 2, and free of heart failure. They were randomly allocated to treatment with placebo in 121 patients; i.v. amiodarone, 5 mg/kg bolus, followed by 1.8 g/24 hours in 51 patients; i.v. propafenone, 2 mg/kg bolus, followed by 0.0078 mg/kg/min in 57 patients; p.o. propafenone, 600 mg p.o. in a single dose in 119 patients; and p.o. flecainide, 300 mg p.o. in a single dose in 69 patients. All patients were continuously monitored by Holter ECG, and the number of conversions to sinus rhythm was measured at 1, 3, and 8 hours. RESULTS: (1) I.v. propafenone resulted in a higher conversion rate within 1 hour compared with the oral loading regimens of propafenone or flecainide, but the conversion rates at 3 and 8 hours were comparable, approximately 75% at 8 hours; 2) i.v. amiodarone was not different from placebo until 8 hours when it was associated with 57% of conversions; (3) conversion to sinus rhythm at 8 hours was observed in 37% of the placebo treated patients. Serious adverse effects occurred in few patients: two patients treated with flecainide and one treated with i.v. propafenone experienced left ventricular decompensation; one patient treated with placebo and two treated with flecainide had atrial flutter with rapid ventricular response. In conclusion, single-dose, oral loading with propafenone or flecainide are acceptable alternatives to conventional drug regimens in selected hospitalized patients. In addition, the measure of a placebo effect is mandatory in studies of recent-onset AF.

Amiodarone↗
PubMed1997

Cardiac Arrhythmias Following Intravenous Nicotine: Experimental Study in Dogs.

BACKGROUND: Nicotine, the active agent in tobacco, is released into the circulation during cigarette smoking. It elevates plasma catecholamines, heart rate, and arterial blood pressure; produces coronary spasm; and increases myocardial work and oxygen demand with concomitant reduction in oxygen supply. This may generate cardiac arrhythmias that might contribute to an increased incidence of sudden death due to smoking. It is hypothesized that acute administration of nicotine will induce cardiac arrhythmias, and this experimental study was planned with an aim to assess arrhythmogenic activity as a result of acute administration of nicotine. METHODS: Nicotine was administered in different doses intravenously in 16 anesthesized dogs, and 52 experiments were carried out at weekly intervals. In each experiment, continuing anesthesia and after nicotine administration. They were scrutinized by two experienced electrocardiographers at intervals of 1, 2, 3, 4, 5, 10, 15, and 30 minutes. RESULTS: Data revealed nonsignificant arrhythmias with doses of 2.5, 5.0, and 10.0 mg/kg of intravenous nicotine. The dose of 50 µg/kg induced supraventricular arrhythmias, atrioventricular junctional arrhythmias, and ventricular arrhythmias. Supraventricular bradycardia in 30 (83%; P <.0001), supraventricular arrhythmia in 30 (83%; P <.0001), sinus arrest in 18 (50%; P <.003), atrial ectopics in 24 (67%; P <.0004), and atrial tachycardia in 98 experiments (25%; P <.021). These results were statistically significant. In 18 experiments, sinus arrest was observed to be missing P waves and QRS complexes for a period corresponding to 4:1-10:1 SA block, lasting 2-6 seconds, within 3 seconds of injection. Occurrence of wandering pacemaker was observed in 6 experiments, atrial flutter in 2, and atrial fibrillation in 2, but these incidents were not significant. Atrioventricular junctional arrhythmias consisted of escape beats in 9 subjects (25%; P <.02), premature contractions in 12 (33%; P <.005), first-degree heart block in 9 (25%; P <.02), second degree heart block in 9 (25%; P <.02) and atrioventricular dissociation in 9 (25%; P <.02). All arrhythmias in this category were significant. Ventricular arrhythmias consisted of ventricular premature contractions that were unifocal in 32 subjects (89%; P <.0001), multifocal in 30 (83%; P <.0001), bigeminy in 28 salvos in 18 (50%; P <.003). Sustained ventricular tachycardia (> 30 beats) in 12 experiments (33%; P <.005) proved significant. The dose of 100 µg/kg induced fatal ventricular flutter and ventricular fibrillation. The dog expired and experiments with that dose were not repeated. CONCLUSION: Data reveal dose-dependent arrhythmogenecity of nicotine in dogs. Smaller doses of nicotine did not produce significant arrhythmias. Higher doses, bioequivalent to smoking two standard cigarettes, may generate cardiac arrhythmias of simple to severe nature. Further work in human beings may confirm whether nicotine in cigarette smoke will generate similar cardiac arrhythmias especially in patients with autonomic imbalance and/or compromised and ischemic myocardium.

Journal Article↗
PubMed1983

Echocardiographic features of aortic valve endocarditis in a dog, a cow, and a horse.

A horse, a cow, and a dog with aortic valve vegetative endocarditis were studied by M-mode echocardiography. Echocardiographic abnormalities of the aortic valve, mitral valve, and left ventricle were observed. These features were identical to those reported in human beings with aortic valve endocarditis. Abnormalities associated with aortic valve endocarditis included irregular thickening of the valve, multiple linear echoes in the aortic root, diastolic prolapse of the aortic vegetation, and diastolic fluttering of a torn aortic valve. Some of these features were found in each animal. The consequences of aortic regurgitation observed by echocardiography were left ventricular dilation, diastolic fluttering of the mitral valve, premature closure of the mitral valve, and left ventricular hyperkinesia.

Animals↗
PubMed1988

Control of cardiac arrhythmias by calcium antagonism.

In recent years calcium channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil, and bepridil; the dihydropyridines are devoid of significant electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the chronic control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias due to coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young subjects developing tachycardia with a right bundle branch block with left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity. The role of calcium antagonists in reducing the incidence of sudden death in the survivors of acute myocardial infarction remains uncertain.

Adenosine↗
PubMed1989

Transesophageal low-energy cardioversion in an animal model of life-threatening tachyarrhythmias.

The purpose of this study was to determine the feasibility and efficacy of terminating life-threatening ventricular tachyarrhythmia by low-energy synchronous or asynchronous shocks delivered through a transesophageal catheter that had both an anode and a cathode. Forty-three episodes of ventricular fibrillation or flutter (Vf or VF) were provoked by transesophageal asynchronous random shocks occurring during the vulnerable period of the ventricular cycle in seven dogs and seven pigs that were healthy adults. The 43 episodes of Vf or VF were terminated by the transesophageal technique. The defibrillation energy thresholds were 23.11 +/- 6.28 J (range, 5-30 J). Seven episodes of ventricular tachycardia (VT) with a cycle length of 360 msec or less (330 +/- 27 msec) were provoked by ventricular pacing stimuli during acute myocardial ischemia resulting from delayed resuscitation in two dogs and three pigs. Five of the seven VTs had a duration of 31 seconds or more, and they were all terminated by transesophageal synchronous shocks, the cardioversion thresholds being 1.71 +/- 2.25 J (range, 0.25-5 J). Fourteen episodes of idioventricular tachycardia (IVT) with a cycle length of 400 msec or more (445 +/- 33.5 msec) spontaneously occurred after the use of adrenaline and after defibrillation in four dogs and five pigs. We also succeeded in terminating seven episodes of IVT with a duration of 34 seconds or more by the same means of treating VT, although IVT is not an indication for cardioversion in the clinical setting.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

[Efficacy of frequent electrostimulation of the left atrium via the esophagus to stop atrial flutter].

Trans-esophagus high-frequency electrostimulation (240-520 impulses/min) of the left atrium was performed in 36 patients in order to arrest the atrial flutter. Immediately after the stimulation, the sinus rhythm was restored in 15 patients (37.5%), and 16 patients (40%) developed atrial fibrillation, 5 patients (12.5%) developed atrial flutter with irregular ventricular rhythm, in 4 patients (10%) the stimulation was ineffective. Subsequently, atrial fibrillation in 3 cases and atrial flutter in 1 case assumed the sinus rhythm. On the whole, the sinus rhythm recovered in 19 (47.5%) cases. Impulses of 20 V proved to be the most effective. This method is effective in cases of an unsuccessful drug antiarrhythmic treatment and electroimpulse therapy. There are no contraindications to this method. It can be successfully employed in cases where electroimpulse therapy is contraindicated or dangerous.

Adult↗
PubMed1995

Atrial fibrillation and flutter: maintaining stability of sinus rhythm versus ventricular rate control.

Two major treatment strategies have emerged for managing atrial fibrillation: maintaining sinus rhythm by chronic administration of suppressive antiarrhythmic agents versus controlling the ventricular rate and chronic anticoagulation. Potential benefits of maintenance of sinus rhythm include improvement of the hemodynamic profile of the patient, a decreased risk of cerebrovascular accidents, reduced symptoms, and, if atrial fibrillation is successfully suppressed, possible elimination of the need for the chronic anticoagulation. When selecting long-term antiarrhythmic drug therapy for suppression of atrial fibrillation, it should be recalled that at least 50% of patients have a recurrence of the arrhythmia within the first year and the majority of other patients have a recurrence within the next 3 to 5 years. In addition, the risk of proarrhythmia and sudden cardiac death must be considered; this has stimulated interest in nonpharmacologic approaches to maintaining sinus rhythm. Large multicenter randomized trials are now under way to compare the benefits and risks of maintaining sinus rhythm versus controlling the ventricular rate and chronically anticoagulating patients in atrial fibrillation. Important endpoints of these trials include mortality, functional capacity, and quality of life.

Anti-Arrhythmia Agents↗
PubMed1983

Calcium antagonists. Clinical use in the treatment of arrhythmias.

Calcium antagonists have recently emerged as a class of drugs for the treatment of angina, hypertension and certain cardiac arrhythmias. Verapamil is the prototype calcium antagonist and has the most clearly defined antiarrhythmic properties. Other agents in the class include D-600 (gallopamil), tiapamil, nifedipine, and diltiazem. The antiarrhythmic effects of these compounds can be correlated with their electrophysiological properties which may differ significantly among different compounds and also between isolated tissues in intact animals and man. As a class they do not increase the effective refractory period of the atria, ventricle, His-Purkinje fibres or the accessory pathways in the heart. The dominant effect is slowing of conduction in the AV node with the prolongation of the AV nodal refractory period. The most marked changes are produced by verapamil, the least with nifedipine which is devoid of antiarrhythmic actions. Verapamil and its congeners as well as diltiazem terminate paroxysmal supraventricular tachycardia and slow the ventricular response in atrial flutter and fibrillation. They are also of prophylactic value in preventing recurrences of paroxysmal supraventricular tachycardia and controlling the ventricular response in atrial flutter and fibrillation during long term oral therapy. Their value in ventricular arrhythmias is uncertain but they are unlikely to be effective except in those complicating coronary artery spasms. The relative merits and potencies of various calcium antagonists in different arrhythmias need further studies.

Anti-Arrhythmia Agents↗
PubMed2005

Supraventricular tachycardia in children.

Several different mechanisms are responsible for paroxysmal supraventricular tachycardia in children. Different forms of tachycardia occur at different age. Atrio-ventricular reentry tachycardia results from the presence of congenital atrio-ventricular bypass tracts and is frequently encountered at all ages. Infants may present with ectopic atrial tachycardia or atrial flutter. Atrio-ventricular node reentry tachycardia becomes more frequent in adolescence. Atrial scarring resulting from open heart surgery predisposes to complex intra-atrial reentry. Certain forms of congenital and acquired heart disease are associated with specific types of arrhythmia. Many children with paroxysmal supraventricular tachycardia do not require any therapy. The decision to proceed with treatment should be based on the frequency and severity of symptoms and on the effect of arrhythmia on the quality of life. Infants require medical treatment because of the difficulty to recognize symptoms of tachycardia and a risk of heart failure. Patients with Wolff-Parkinson-White syndrome as well as those with significant heart disease are at risk of sudden death. Syncope in children with paroxysmal tachycardia may indicate a severe fall in cardiac output from extremely rapid heart rate. Patients with potentially life-threatening arrhythmia should not participate in competitive physical activities. Treatment options have undergone significant evolution over the past decade. Indications for the use of specific antiarrhythmic medications have been refined. Contemporary catheter ablation procedures employ different forms of energy allowing for safe and effective procedures. Catheter ablation is the treatment of choice for symptomatic paroxysmal tachycardia in school children and in some infants who failed medical treatment. Surgery is the preferred treatment in few selected cases. The goal of this review is to present the state of the art approach to the diagnosis and management of paroxysmal supraventricular tachycardia in infants, children and adolescents.

Adolescent↗
PubMed2001

Atrial and ventricular electromechanical function in 1-ventricle hearts: influence of atrial flutter and Fontan procedure.

OBJECTIVE: Echocardiography was used to study electromechanical atrial and ventricular function in adult patients with a 1-ventricle heart who were in sinus rhythm to better understand the recurrence of atrial flutter in these conditions. Patients who had recent atrial flutter, with and without the Fontan procedure, were compared with those who had no arrhythmia. METHODS: This was a prospective study that used M-mode and 2-dimensional Doppler echocardiography and electrocardiography. Conventional measurements were used to evaluate ventricular long-axis function. Basic data were drawn from case notes. The setting was a designated quaternary service for grown-up congenital heart patients (GUCH) in a tertiary referral center for cardiology and cardiac surgery. From January 1997 to February 1998, 26 consecutive adult patients (aged >16 years) with a heart with one functioning ventricle and a history of atrial flutter were studied: group 1, with non-Fontan palliative surgery or no surgery (10 patients), and group 2, with Fontan-type repair (16 patients). Also studied were 20 patients with a 1-ventricle heart but no history of atrial flutter. These 20 patients were divided into 2 groups: control 1, which comprised 14 patients with previous shunts or no surgery, and control 2, which consisted of 6 patients with Fontan repair. RESULTS: P-wave duration on the electrocardiogram was similar in the 4 patient groups, but the amplitude was reduced in group 2 and control 2 (patients with Fontan surgery) (P <.016). Bifid P wave was seen in 5 (50%) of 10 patients in group 1 and in 6 (43%) of 14 patients in control 1, but it was not seen in patients with Fontan (P <.01). Ventricular systolic and diastolic dimensions and fractional shortening were not different between patients and controls. Right atrial transverse dimensions were greater in group 2 patients compared with those in controls. Significant atrioventricular valve regurgitation was seen in 9 of 10 group 1 patients but in none of the others. Right-sided total long-axis excursion and atrial A-wave amplitude were depressed in group 2 patients compared with the values in the others. The onset of right atrial shortening was delayed by 50 ms in group 2 compared with control 2, whereas the left atrial shortening was delayed by 30 ms in group 1 compared with control 1. This particular disturbance remained 6 months after cardioversion. CONCLUSION: In 1-ventricle hearts, significant atrioventricular valve regurgitation is commonly associated with atrial flutter in patients who did not undergo the Fontan procedure, and with electromechanical disturbances in those who did. Recognition of disturbances in ventricular long-axis function may thus assist in the identification of patients with a 1-ventricle heart who are prone to atrial flutter.

Adolescent↗
PubMed1987

Use of calcium antagonists for cardiac arrhythmias.

Calcium antagonists have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, these agents are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle, most readily demonstrated in isolated tissue preparations. In vivo, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the noncompetitive adrenergic-blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil and bepridil; the dihydropyridines are devoid of electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the atrioventricular node but exert little or no effect on atrial, ventricular, His-Purkinje or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of the reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the long-term control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias caused by coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of ventricular premature complexes. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young patients who develop tachycardia with a right bundle branch block and left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity.

Arrhythmias, Cardiac↗