[Disorders of heart rhythms. Physiology and physiopathology].
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Arrhythmias, Cardiac↗
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[Electrocardiographic diagnosis and acute treatment of atrial fibrillation and flutter episodes].
Both atrial flutter and fibrillation are common arrhythmias in the clinical setting. Although we have been aware of them for decades, little has been known until recently about their triggering or maintenance mechanisms. The diagnosis of these arrhythmias lies largely in the electrocardiogram, which shows characteristic features of atrial electrical activity, leading to a correct diagnosis. Usually, some maneuvers such as adenosine infusion, carotidus sinus massage, etc., are required, in order to unmask the atrial activity, that are often obscured by the QRS complex or T wave. Several therapeutic options can be attempted for the acute termination of both atrial flutter and fibrillation episodes. The choice of one or another depends on some extent, on the clinical status of the patient during the arrhythmia, the presence of structural heart disease and the preceding arrhythmic history. Antiarrhythmic drugs are quite efficacious in the acute conversion of atrial fibrillation, but such an effect is not expected in atrial flutter. Drugs that depress AV nodal conduction can be used in both instances, as a therapeutic end-point or as a previous measure to the arrhythmia conversion. Direct current cardioversion is a good and efficacious option for both arrhythmias, however sedation is mandatory which, may be a contraindication in some patients. Rapid atrial pacing is an elegant and reliable method for the acute termination of atrial flutter of the common type, although a transvenous catheter insertion is needed.
Atrial Fibrillation↗
Prescribing trends and pharmacoeconomic considerations in the treatment of arrhythmias. Focus on atrial fibrillation and flutter.
Considerable progress has been made regarding the treatment of atrial fibrillation and atrial flutter. However, controversies still exist with respect to the therapy of choice for ventricular rate control, requirements for long term preventive therapy, and the place of surgical and ablation alternatives. Surrounding these controversies also lies a paucity of pharmacoeconomic studies, which limits delineation of the most cost-effective therapy for patients with atrial fibrillation and atrial flutter. This article reviews prescribing trends in the US for antiarrhythmic agents, and the available pharmacoeconomic studies that have specifically addressed the treatment of atrial fibrillation and atrial flutter.
Arrhythmias, Cardiac↗
Significance of supraventricular arrhythmias induced by electrophysiologic studies.
The clinical history and the findings on Holter monitoring of 767 patients (without evidence of ventricular pre-excitation on the ECG) were compared with the results of electrophysiological studies to assess the significance of supraventricular arrhythmias induced by intracardiac study. The studies were undertaken to determine the cause of syncope, conduction disturbances or tachycardia. In 570 patients (group 1) supraventricular arrhythmias were not induced. On Holter monitoring, 36 (6%) had evidence of supraventricular tachycardias, including atrial flutter, atrial fibrillation and paroxysmal junctional tachycardia. In 86 patients (group 2) one atrial extrastimulus induced a paroxysmal junctional tachycardia; 79 (82%) of these patients had had spontaneous supraventricular tachycardia (SVT). In 111 patients (group 3) another type of SVT was induced: The movement of the catheter induced atrial flutter or fibrillation in nine patients, eight (89%) of whom had spontaneous SVT. Atrial pacing at a rate less than 200 bpm induced atrial flutter or fibrillation in 14 patients of whom nine (64%) had SVT. Ventricular pacing induced SVT in 15 patients, of whom 14 (64%) had SVT. An atrial extrastimulus during sinus rhythm induced atrial echoes in 62 patients, 47 (76%) of whom had SVT. The atrial extrastimulus during sinus rhythm induced atrial tachycardia in 11 patients, nine (82%) of whom had SVT.
Adolescent↗
[Paroxysmal AV block induced by atrial flutter in acute inferior myocardial infarction].
Conduction disturbances in the acute phase of an inferior myocardial infarction are frequent. Paroxysmal AV block and ventricular standstill is, on the other hand, an unusual event. We describe a case of paroxysmal AV block precipitated by, and dependent on, the presence of atrial flutter. Concealed conduction of atrial impulses to the AV node is the likely cause of this form of AV block. The transient development, ischaemia related, of a longitudinal and transverse dissociation of the AV node, increased the concealed penetration of atrial impulses and its effect on subsequent impulse formation, given rise to a form of paroxysmal AV block.
Aged↗
A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia.
The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.
Atrioventricular Node↗
Acute reductions in ventricular myocardial tissue velocities after direct current cardioversion of atrial fibrillation.
BACKGROUND: Cardioversion by direct current (DC) and other methods can cause atrial "stunning." There are case reports of acute pulmonary edema after DC cardioversion, but whether acute ventricular dysfunction is a general consequence of DC cardioversion is unknown. We have investigated whether DC cardioversion acutely affects myocardial velocity assessed by Doppler tissue imaging. METHODS: 40 patients (30 with atrial fibrillation and 10 with atrial flutter) undergoing elective DC cardioversion underwent transthoracic echocardiography with Doppler tissue imaging before and immediately after cardioversion, and after follow-up. Peak systolic velocity was derived for 6 ventricular segments using Doppler tissue imaging. RESULTS: Immediately after DC cardioversion of atrial fibrillation, peak systolic velocity decreased in basal lateral (4.3 +/- 2.0-3.3 +/- 1.7 cm/s, P <.001), mitral annulus-septal (3.8 +/- 1.0-3.5 +/- 0.9, P <.05), mitral annulus-lateral (4.9 +/- 1.6-4.1 +/- 1.7, P <.001), and tricuspid annular (7.8 +/- 2.0-7.0 +/- 1.2, P <.03) segments, even though left ventricular ejection fraction was unchanged. In contrast, for the atrial flutter group there were no significant changes in peak systolic velocity in any segment post-DC cardioversion. Follow up studies were performed after sustained in sinus rhythm in both atrial fibrillation and atrial flutter groups. For both groups, increased peak systolic velocity was found in all 6 segments on follow-up (all P <.05). CONCLUSIONS: DC cardioversion causes subclinical, acute reversible reduction in left ventricular peak systolic velocity in patients with atrial fibrillation. The causes of this reduction in myocardial contractile velocity and the circumstances in which acute dysfunction become clinically significant warrant further investigation.
Aged↗
A CLINICAL TRIAL OF ANTAZOLINE IN THE TREATMENT OF ARRHYTHMIAS.
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Antazoline↗
Long-term follow-up of arrhythmias in pediatric orthotopic heart transplant recipients: incidence and correlation with rejection.
BACKGROUND: Arrhythmias in adult orthotopic heart transplant (OHT) recipients are common and have been used as predictors of rejection. Because of the paucity of information in pediatric OHT recipients, the purpose of this study was to determine the incidence and correlation of arrhythmias with rejection or with coronary artery disease (CAD) in children. METHODS: We retrospectively reviewed the records, electrocardiograms (ECGs), and 24-hour ambulatory ECGs of patients who underwent OHT from January 1984 to December 1999. We excluded arrhythmias occurring in the first 2 weeks after OHT. RESULTS: Sixty-nine patients underwent OHT, received triple-immunosuppression therapy, were discharged home, and have been followed for a mean of 4.7 years (0.3-13 years). Each patient had an average of 10 ECGs and three 24-hour ECGs. Twenty-six patients had 33 arrhythmias: sinus bradycardia (n = 9), atrial tachycardia (n = 9), ventricular tachycardia (n = 3), and Wenckebach periodicity (n = 6). Sinus bradycardia was treated with theophylline in 8 patients, and 2 required pacemakers. Atrial tachycardias (atrial flutter in 4 patients and atrial ectopic tachycardia in 5) were treated with digoxin, propranolol, or procainamide. Ventricular tachycardia was treated with mexiletine, lidocaine, and amiodarone. There were 65 episodes of rejection, 20 of which were moderate/severe (> or =3B). Only Wenckebach was associated with the presence of either rejection or CAD (p < 0.05). CONCLUSIONS: We noted clinically significant arrhythmias in 38% of the pediatric OHT recipients. Sinus bradycardia, atrial tachyarrhythmias, and ventricular tachycardia occurred with the same frequency. Only new-onset Wenckebach periodicity was noted in the presence of either CAD or rejection. No arrhythmia was of negative predictive value for rejection or CAD. From this data, we suggest that new-onset Wenckebach prompt evaluation for rejection or CAD.
Adolescent↗
Implantable dual-chamber defibrillator for the selective treatment of spontaneous atrial and ventricular arrhythmias: arrhythmia incidence and device performance.
INTRODUCTION: Atrial tachyarrhythmias are a common co-morbidity in patients with an ICD indication. Recently introduced ICD's are equipped to independently detect and treat atrial and ventricular tachyarrhythmias. The purpose of this prospective study was to evaluate the incidence and termination of spontaneous atrial and ventricular tachyarrythmias in patients with a history of atrial tachyarrhythmias. METHODS AND RESULTS: Ninety patients, 70% male with an ICD indication and history of atrial tachyarrhythmia (LVEF 45 +/- 6%, [AT/AF indication 55 +/- 10, AT/VT 45 +/- 16], 46% CAD) were enrolled and 89 were implanted with a VENTAK PRIZM AVT (Guidant). Spontaneous atrial and ventricular tachyarrhythmias were printed and evaluated during an average follow-up period of 272 +/- 72 days utilizing the stored intracardial electrogram function of the device. Nineteen patients (21%) presented had only atrial tachyarrhythmias, 32 patients (36%) had both atrial and ventricular tachyarrhythmias and 18 patients (20%) had only ventricular tachyarrhythmias. Patients with only atrial tachyarrhythmias had a total of 3274 atrial episodes; 2002 terminated spontaneously, 1264 were treated with ATP and 8 with shock therapy. ATP was successful in 735 (58%) of 1264 episodes. Patients with both atrial and ventricular tachyarrhythmias had 7277 documented atrial tachyarrhythmias, 5231 terminated spontaneously, 1153 of 2009 were terminated by ATP (57.4%) and 37 by shock therapy (20 patient controlled). Atrial tachyarrhythmias identified as atrial flutter (AT) by the atrial rhythm classification (ARC) algorithm had a higher ATP conversion success rate than episodes identified as atrial fibrillation (AF); 66.7% for AT and 26.4% for AF. Patients with only ventricular tachyarrhythmias had 690 documented episodes, 401 terminated spontaneously, 248 (85.8%) were terminated by ATP and 41 by shock. CONCLUSION: Seventy-seven percent of patients with an ICD indication had spontaneous atrial and/or ventricular tachyharrhythmias within the first 6 months after ICD implantation. ATP therapy terminated 58% of all atrial tachyarrhytmias and 66.7% of the atrial flutters. The dual chamber ICD detected, classified and terminated all ventricular tacharrhythmias appropriately.
Aged↗
Results of sotalol (Darob) therapy in supraventricular tachyarrhythmias.
UNLABELLED: The benefit of sotalol therapy in atrial flutter and in atrial fibrillation was considered, aiming as well the suppression of paroxysmal episodes and the prevention of their recurrencies and the control of the ventricular rhythm in chronic cases. The prospective study comprises 60 patients institutionalized in the Cardiology Clinic in which the supraventricular tachyarrhythmia range included: atrial flutter (20 cases) and atrial fibrillation (40 cases), from which atrial fibrillation of recent onset (20 cases) and chronic atrial fibrillation with fast ventricular response (20 cases). Sotalol was administered orally in doses of 80 to 320 mg daily, b.i.d. The conversion to sinus rhythm was obtained in 45% of cases of atrial fibrillation of recent onset and in 30% of cases of atrial flutter. The prophylactic administration of sotalol on long term (6 months), in medium dose of 160 mg daily, may protect against the recurrence of the supraventricular arrhythmias (63.85%). As adverse effect, a case of "torsade des pointes" was recorded. IN CONCLUSION: 1) a greater benefit was noticed by using sotalol prophylactically for the recurrence of the supraventricular arrhythmias (63.85%) compared to the positive results in the therapy of acute cases (37.5%); 2) the maximal efficiency in the prevention of arrhythmia recurrencies can be observed in patients that present underlying compensated ischemic cardiopathy; 3) a decrease of 30% of the ventricular rhythm in patients with atrial fibrillation was obtained.
Anti-Arrhythmia Agents↗
Inappropriate shocks in patients receiving internal cardioverter-defibrillators for malignant ventricular arrhythmias.
Implantation of internal cardioverter defibrillators (ICDs) for treatment of malignant ventricular arrhythmias is complicated by failure of therapy or inappropriate shocks. We studied 81 patients (age range 16-72 years; mean 48 +/- 13 years) who underwent ICD implantation for device therapy. The underlying aetiology was ischaemic heart disease (39%), cardiomyopathies (32%) and others (28%). Information regarding shocks was collected using Holter monitoring, telemetry or device memory (stored electrograms) and lastly by clinical follow-up. Fifty-eight patients completed 36 months of follow-up. Thirty-five patients experienced 337 spontaneous shocks, appropriate in 21, inappropriate in 12, and both in two patients. Of the 74 episodes of inappropriate discharges for rhythms other that ventricular tachycardia (VT) or ventricular fibrillation(VF), 55 percent were due to supraventricular arrhythmias (atrial flutter or fibrillation). Lead malfunction occurred in four and the device was replaced in two. Additional drugs controlled AF in one. There was no mortality in any of the 81 patients. The frequency of shocks was highest in the first six months after implantation and atrial fibrillation remains the main cause. In conclusion, inappropriate shocks are frequent in patients undergoing ICD implantation.
Adolescent↗
Atrial pacing for cardioversion of atrial flutter in digitalized patients.
To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.
Adult↗
Arrhythmia and survival in patients >18 years of age after the mustard procedure for complete transposition of the great arteries.
Increasing numbers of patients who underwent Mustard repair as children are now adults. Loss of sinus rhythm, supraventricular arrhythmias, and sudden death have been described in pediatric series. However, little is known about the clinical course of adult patients. This retrospective cohort study examined 86 consecutive adults (age >18 years) who had undergone the Mustard procedure and were referred to an adult congenital cardiac clinic for ongoing follow-up. The incidence and predictors of arrhythmia, congestive heart failure, and death were determined. The median follow-up period was 8 years after age 18 or 23 years after Mustard repair. There were 8 deaths (9%), 2 were sudden. Congestive heart failure (CHF) requiring hospital admission occurred in 9 patients (10%). Pulmonary hypertension and systemic ventricular dysfunction were independent risk factors for death or CHF. Only 29 patients (34%) remained arrhythmia-free. Forty-one patients (48%) had at least 1 episode of supraventricular tachycardia (SVT), with most patients (30, 73%) having atrial flutter. SVT after the age of 18 was associated with CHF. Pulmonary hypertension, systemic ventricular dysfunction, and junctional rhythm before age 18 were independent risk factors for SVT. Pacemakers were implanted in 19 patients (22%); 13 of those were beyond age 18. Thus, adult survivors of the Mustard procedure continue to be at risk for premature death, CHF and supraventricular tachyarrhythmia.
Adolescent↗
Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias.
Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.
Adult↗
Differentiation of arrhythmias in the dog by measurement of activation sequence using an atrial and two ventricular electrodes.
Timing of atrioventricular activation and ventricular dispersion identifies and discriminates between beats of different origin. In eight dogs, three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during arrhythmias induced by programmed electrical stimulation and coronary artery occlusion and release. The interval between the left atrial and left ventricular intrinsic deflections (A-V1) and between the left ventricular and right ventricular intrinsic deflections (V1-V2) of each beat was measured. Recordings were of normal sinus rhythm (NSR) (mean of five beats in 8/8 dogs), atrial flutter (AFL) (five beats of one episode), atrial fibrillation (AF) (144 beats in 29 episodes in 7/8), monomorphic ventricular tachycardia (MVT) (24 beats with six morphologies in 2/8), polymorphic ventricular tachycardia (PVT) (63 beats in 15 episodes in 5/8) and premature ventricular contractions (PVC) (29 beats with 29 morphologies in 5/8). Supraventricular rhythms can be differentiated from ventricular rhythms by V1-V2 timing. The mean difference in V1-V2 during AFL and AF vs NSR was 1 ms (range of 0-3 ms). The change from sinus during MVT ranged from 18 to 43 ms (m 31 ms) and during PVC 10 to 75 ms (m 38 ms). Thirty-five of 35 of these ectopic ventricular morphologies exhibited 10 ms or more timing difference compared to corresponding beats of NSR. PVT was consistently distinguished from supraventricular rhythms and MVT by the variability of V1-V2. A-V1 intervals can be used to distinguish supraventricular arrhythmias from sinus rhythm; a 32 ms difference existed for AFL. AF could be detected by the variability in AV1.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Metoprolol in acute myocardial infarction. Arrhythmias. The MIAMI Trial Research Group.
Forty-five patients in the placebo (1.5%) and 29 in the metoprolol (1%) groups, respectively, were receiving antiarrhythmic drugs on a long-term basis before entry into the trial. Before randomization, 2.2% (n = 64) of the placebo and 1.7% (n = 50) of the metoprolol patients developed ventricular fibrillation (VF) in the hospital. The corresponding figures for atrial fibrillation or flutter were 3% (n = 87) and 3.3% (n = 94). After randomization, there was no significant difference in the number of patients who developed VF in the placebo (n = 52) and the metoprolol (n = 48) groups. The total number of episodes of VF tended to be fewer in the metoprolol group (n = 67) compared with the placebo group (n = 96). The tendency was, however, not apparent until after 5 days. When the occurrence of VF was related to high- and low-mortality risk groups, any beneficial effect of metoprolol was confined mainly to the high-risk group. A similar proportion of patients underwent electric conversion for ventricular tachyarrhythmia in the 2 groups. Although antiarrhythmic drugs were intended to be given only for major ventricular tachyarrhythmias a large proportion of patients received such treatment. Significantly more patients were treated with antiarrhythmics in the placebo (21.5%) than in the metoprolol group (19.2%, p = 0.03) during the study period, but predominantly during the first 5 days. Atrial fibrillation or flutter and other supraventricular tachyarrhythmias were significantly less frequent in the metoprolol than in the placebo group, as was the use of cardiac glycosides.(ABSTRACT TRUNCATED AT 250 WORDS)
Anti-Arrhythmia Agents↗
Studies on the effect of physostigmine on experimental cardiac arrhythmias in dogs.
1. Experimental cardiac arrhythmias were produced in dogs anaesthetized with pentobarbitone. Ventricular arrhythmias were induced by strophanthin-K, light petroleum plus adrenaline or coronary ligation procedures. Atrial flutter was induced by an injury-stimulation technique. The acetylcholine and glycogen concentrations of the atria and ventricles were estimated.2. Physostigmine pretreatment (0.1 mg/kg) significantly reduced the incidence of ventricular arrhythmias after myocardial ischaemia but had no effect on any of the other arrhythmias.3. Physostigmine markedly increased the acetylcholine concentrations of atria and ventricles in control dogs, to nearly the same extent. Physostigmine had no effect on ventricular acetylcholine concentrations in dogs treated with strophanthin-K and light petroleum plus adrenaline but in the coronary ligation group it caused a significant increase in the acetylcholine concentrations of both atria and ventricles, and of atrial acetylcholine only in the injury-stimulation group.4. All the arrhythmias produced marked glycogenolysis of both the atria and the ventricles, to nearly the same extent. Although physostigmine produced marked glycogenolysis in the control dogs it significantly inhibited cardiac glycogenolysis after light petroleum plus adrenaline, atrial glycogenolysis after strophanthin-K-induced arrhythmias and ventricular glycogenolysis after myocardial ischaemia.5. There appears to be a possible correlation between the increase in the acetylcholine concentration of the ventricles and anti-arrhythmic actions of physostigmine, but there is a less clear correlation between changes in the glycogen concentration of ventricles and the anti-arrhythmic action.
Acetylcholine↗