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PubMed1985

[The laser and rhythm disorders].

Of the different types of laser, Nd-YAG radiation (neodymium-yttrium-aluminium-Garnett) is the most suitable for the treatment of arrhythmias. Research in animals has, in fact, made it possible to demonstrate that its properties (high power, creation of a coagulation necrosis without a sectioning effect) may thus be used for the surgical treatment of supra-ventricular tachycardias (Wolff-Parkinson-White syndrome, common flutter, auricular ectopic rhythm) or ventricular tachycardias, the origin of which may or may not be ischemic. Since 1984, it has been possible to treat 25 patients in this way, with good result. In 15 cases, it was a question of curative treatment for a refractory arrhythmia (common flutter: = 1 case, ischemic VT = 12 cases, VT with congenital aneurysm = 1 case). In the other 10 patients the laser was used to prevent an arrhythmia in the course of a CSD (prevention of flutter = 4 cases) or of an aneurysmectomy (6 cases). The excellent results in the short term (the earliest dating back 17 months) lead us to hope that there will be considerable development of the use of the laser in rhythmological surgery.

Adult↗
PubMed1994

Supraventricular arrhythmia as the cause of sudden death in hypertrophic cardiomyopathy.

Electrophysiological studies with simultaneous echocardiographic control and invasive measurement of intravascular pressures were carried out in a 13-year-old boy with hypertrophic cardiomyopathy who was hospitalized after an episode of aborted sudden death. Ventricular stimulation did not induce ventricular tachycardia, but atrial stimulation induced atrial fibrillation, atrial flutter and non-sustained ventricular tachycardia. Atrial stimulation (S1) at 200 beats.min-1 (10-15 s) also induced significant repolarization abnormalities in the 5-10 post-stimulation beats. Akinesia of the ventricular septum and posterior wall without opening of the mitral valve was documented by echocardiography. A complete anterior systolic motion, not observed under basal conditions, was detected in the first post-stimulation beat. Atrial stimulation at rates over 120 beats.min-1 caused a drop in systolic blood pressure, a rise in pulmonary artery pressure, and a decrease in cardiac output. Despite therapy with propranolol and amiodarone, the patient died suddenly.

Adolescent↗
PubMed1995

Safety and efficacy of intravenous diltiazem in atrial fibrillation or atrial flutter.

This study examines the efficacy of various doses of intravenous diltiazem to control the ventricular response during atrial fibrillation or atrial flutter. Control of the ventricular response of patients with atrial fibrillation and a rapid ventricular response can provide patients with relief of symptoms and improve hemodynamics. Eighty-four consecutive patients with atrial fibrillation or atrial flutter, or both, received an intravenous bolus dose of diltiazem followed by a continuous infusion of diltiazem at 5, 10, and 15 mg/hour. The mean ventricular response and blood pressure were monitored. Overall, 94% of patients (79 of 84) responded to the bolus dose with a > 20% reduction in heart rate from baseline, a conversion to sinus rhythm, or a heart rate < 100 beats/min. Seventy-eight patients received the continuous infusion. After 10 hours of infusion, 47% of patients (confidence interval [CI]: 36%, 59%) had maintained response with the 5 mg/hour infusion, 68% (CI: 57%, 79%) maintained response after the infusion was titrated to 10 mg/hour, and 76% (CI: 66%, 85%) after titration from the 5 and 10 mg/hour infusion to the 15 mg/hour dose. For the 3 diltiazem infusions studied, mean (+/- SD) heart rate was reduced from a baseline value of 144 +/- 14 beats/min to 98 +/- 19, 107 +/- 25, 107 +/- 22, 101 +/- 22, 91 +/- 17, and 88 +/- 18 beats/min at infusion times 0, 1, 2, 4, 8, and 10 hours, respectively. By the end of the infusion, 18% of patients (14 of 78) had conversion to sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

[Modulation of atrioventricular conduction in patients with atrial fibrillation or flutter. Immediate and long-term results].

The modulation of atrioventricular (AV) conduction by radiofrequency catheter ablation of the "slow" AV node pathway reduces the ventricular rate during atrial flutter (AFL) or fibrillation (AF), without affecting AV conduction during sinus rhythm. In this study the acute and long-term effects of AV node modulation in 41 patients with AFL-AF are presented. The arrhythmia was paroxysmal in 34 and chronic in 7 patients, and was responsible in all patients for severe symptoms of heart failure. The procedure was performed during sinus rhythm in 23, AFL in 8, AF in 10 patients, and caused respectively an increase in Wenckebach cycle from 330 +/- 64 to 452 +/- 91 ms (p < 0.001), and a reduction in ventricular rate from 182 +/- 53 to 95 +/- 40 b/min (p < 0.001) and from 170 +/- 40 to 90 +/- 27 b/min (p < 0.001). The arbitrary endpoint of the procedure (Wenckebach cycle > 500 ms during sinus rhythm, maximum heart rate < 100 b/min during AFL-AF) was achieved in 19/41 patients; permanent complete AV block was induced in 6 "non-responder" patients (15%). At a mean follow-up of 15 +/- 7 months (range 1-31) all patients reported a substantial subjective improvement and a better exercise tolerance--as documented by a quantitative questionnaire concerning quality of life--without any recurrence of acute pulmonary edema, syncope or severe hypotension. In 5 patients during paroxysmal AFL-AF, and in 1 patient with chronic AF, a heart rate higher than 120 b/min was documented, and in 3 cases it was associated with severe palpitations. No late AV block occurred. The mean number of hospital-emergency room admissions per patient per year decreased from 3.9 before to 0.2 after the modulation. Considering complete AV block (6 patients, 15%) and clinical failures (6 patients, 15%), the success of the procedure was 70%, and was independent of the rhythm at the time of the procedure; the percentage of AV block was nevertheless higher during AFL-AF (22 vs 9%). Both endpoints of the procedure (Wenckebach cycle > 500 ms; heart rate < 100 b/min) were confirmed to be good predictors of long-term efficacy; on the other hand, a Wenckebach cycle < 430 ms was demonstrated to represent a specific marker of late failure. In conclusion, the study confirms that modulation of AV conduction is feasible in 70% of patients with AFL-AF: in these patients the procedure allows the long-term control of ventricular rate and a substantial improvement in quality of life, avoiding the need for His ablation and pacemaker implantation. "Non-responder" patients can be acutely identified and should be therefore considered condidates for His ablation during the same session.

Adolescent↗
PubMed2005

Severe left ventricular systolic dysfunction increases atrial fibrillation after ablation of atrial flutter.

BACKGROUND: Atrial fibrillation (Afib) that occurs after a successful atrial flutter (AFL) ablation may negate the potential benefits of the ablation. Afib occurs more often when severe left ventricular systolic dysfunction (LVSD) is present. We hypothesized that even after a successful AFL ablation, the incidence of postablation Afib is increased when severe LVSD is present. METHODS: Ninety consecutive patients with LVSD who underwent ablation for AFL at Montefiore Medical Center from August 2001 to January 2005 were classified according to the severity of LVSD. Group 1 (n = 36) consisted of patients with EF < or = 35%, and group 2 (n = 54) consisted of patients with EF 36-55%. There were no statistically significant differences in baseline patient characteristics between the two groups. RESULTS: During a mean follow up of 350 days, Afib occurred in 31% (n = 11; 8 with prior history of AFib) in group 1, and 7.4% (n = 4; all with prior history of Afib) in group 2. Cumulative probability of remaining Afib-free in group 1 versus group 2 was 75% versus 96% at 365 days, and 69% versus 91% at 600 days (P = 0.01). A prior history of Afib did not interact with EF when analyzed with a logistic regression analysis. CONCLUSION: After an AFL ablation, the incidence of Afib is increased, and the probability of remaining free of Afib is decreased, when severe LVSD is present, independent of a prior history of Afib. This finding may have implications for optimal patient selection for AFL ablation, and the use of adjunctive therapies.

Atrial Fibrillation↗
PubMed1997

[Evaluation of biochemical markers of myocardial lesion after radiofrequency ablation. Value of troponin I].

INTRODUCTION AND OBJECTIVES: Radiofrequency catheter ablation is the curative treatment of choice for many cardiac arrhythmias. After radiofrequency ablation there is always a localized endomyocardial necrosis, which is necessary to eliminate the arrhythmia. The volume of the necrosis may be evaluated by the rise of several biochemical markers, classically CK and CK-MB. However, the sensitivity and specificity of these markers are not optimal and are probably less than ideal for this purpose. Cardiac Troponin I (cTnI) is a newly available biochemical marker available, with a high cardiac specificity. We designed this study in order to determine the value of serum levels of several cardiac markers in patients who underwent radiofrequency catheter ablation and to establish the utility of cTnI. METHODS: We analyzed the data from 51 patients who underwent radiofrequency ablation and from 16 control patients. In respect to the ablation target, we included in the study 14 left accessory pathways, 7 right accessory pathways, 12 atrioventricular nodal reentry tachycardia, 5 ventricular tachycardia and 13 atrial flutter or fibrillation. The levels of CK, CK-MB, cTnI, and myoglobin were compared with clinical findings, ST-T wave abnormalities and the presence of arrhythmias after ablation. To evaluate the diagnostic capability for each biochemical marker we used the ROC curves. RESULTS: A pathological value of cTnI was found in 47 out of 51 (92%) patients in the ablation group. CK-MB had a lower sensitivity (63%). The sensitivity for the other biochemical markers ranged from 30% for CK to 67% for Myoglobin. The area under the ROC curve for cTnI was 0.9375, significantly superior to the other biochemical markers (0.86, 0.76, 0.75 for MB, Myoglobin, CK respectively) (p < 0.05). The lowest cTnI released was found in patients after nodal reentry tachycardia ablation and the highest after atrial flutter ablation. cTnI increased above normal values in 4 patients in the control group (patients who underwent an electrophysiological study without catheter ablation). We found a moderate level of correlation between the number of radiofrequency pulses and cardiac cTnI release (r = 0.69; p < 0.0001). The correlation was different in each target, ranging between r = 0.25 (p = NS, 0.43) for atrial flutter and fibrillation to r = 0.99 (p < 0.0001) for ventricular tachycardia. CONCLUSIONS: cTnI had the greatest sensitivity (92%) for detecting minor myocardial damage. Thus, we can conclude that the serum level of cTnI detects the minor myocardial damage produced by radiofrequency ablation.

Adult↗
PubMed1989

Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter.

The effects of esmolol, an ultrashort-acting beta blocker, and verapamil were compared in controlling ventricular response in 45 patients with atrial fibrillation or atrial flutter, in a randomized, parallel, open-label study. Patients with either new onset (less than 48 hours, n = 31) or old onset (greater than 48 hours, n = 14) of atrial fibrillation or flutter with rapid ventricular rate were stratified to receive esmolol (n = 21) or verapamil (n = 24). Drug efficacy was measured by ventricular rate reduction and conversion to sinus rhythm. The heart rate declined with esmolol from 139 to 100 beats/min (p less than 0.001) and with verapamil from 142 to 97 beats/min (p less than 0.001). Fifty percent of esmolol-treated patients with new onset of arrhythmias converted to sinus rhythm, whereas only 12% of those who received verapamil converted (p less than 0.03). Mild hypotension was observed in both treatment groups. Esmolol compares favorably with verapamil with respect to both efficacy and safety in acutely decreasing ventricular response during atrial fibrillation or flutter. Moreover, conversion to sinus rhythm is significantly more likely with esmolol.

Adrenergic beta-Antagonists↗
PubMed1981

Atrial and ventricular vulnerability in a patient with the Wolff-Parkinson-White syndrome.

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter. The atrial and ventricular effective refractory periods were 180 ms and less than 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atrial or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal by-pass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.

Adult↗
PubMed1986

[Electroshock (cardioversion) treatment problems in rhythm disorders].

Some problems associated with the results from the electroshock treatment of 1027 patients with rhythm disorders are discussed, as well as the choice of the necessary quantity of electric energy and the way of preparation of the patients. It was established, that sinus rhythm restoration was attained in 90.1% under planned conditions, and in emergency cases--in 86.9%. The highest percentage of positive results were obtained with atrial fibrillation (95.6), and the lowest--with paroxysmal supraventricular tachycardia (97.7). The results is identical (88%) with ventricular tachycardia and atrial flutter. The duration of the rhythm disorder is of importance for the result, being the best up to the third month after the origination of the disorder, but good results had been obtained with a longer duration. The quantity of energy from 200 to 300 W/s (median 250 W/s) was outlined as optimal. The mean quantity of electric energy used in atrial flutter was 278.8 +/- 51.7, in paroxysmal supraventricular tachycardia--246.3 +/- 57.8 in atrial fibrillation--229.5 +/- 40.7 and in ventricular tachycardia--182.9 +/- 37.5 W/s. The anticoagulant prophylaxis is carried out in the patients with a longer duration of the rhythm disorder, in the patients with heart defects and those with ischemic heart disease (with eventual aneurysm). There was a single pre-treatment with quinidine--0.20 or 0.40.

Aging↗
PubMedDate not supplied

[Antiarrhythmic effects of verapamil].

The effect of verapamil were studied on 50 episodes of supraventricular and ventricular tachycardia in 44 patients. An i.v. dose of 0.10 to 0.15 mg/kg. was used. In 5 cases His bundle electrograms were obtained while maximal dp/dt was determined in 7 others. Sinus rhythm was obtained in 21 (81%) of 26 cases of PSVT. In all cases of rapid atrial fibrillation (n-11), an important decrease in the ventricular response was elicited. Of 7 cases of atrial flutter, verapamil induced sinus rhythm in 3 and a significant decrease in the ventricular rate in 3 others. In 2 out of 6 cases ventricular tachycardia reverted to sinus rhythm. The latency time between the injection and the manifestation of the effect ranged from 2 to 4 minutes. A slight and short-lasting depression of dp/dt was observed in all cases studied. Verapamil produced an increase in the A-H interval in 4 of the 5 cases studied with His bundle recordings. Verapamil was found to be a useful drug to suppress PSVT, to decrease the ventricular response in flutter or atrial fibrillation and to convert some ventricular tachycardias to sinus rhythm. Verapamil should be used with caution in previously digitalized patients and is contraindicated when there is S-A node dysfunction as in the tachycardia-bradycardia syndrome.

Adult↗
PubMed2005

Female patient with proximal myotonic myopathy and ventricular tachycardia.

A 68-year-old woman with known proximal myotonic myopathy was transferred to our hospital for further diagnostic and therapeutic evaluation after successful termination of an episode of sustained ventricular tachycardia. In 2001, the myopathy was diagnosed after symptomatic weakness of the hip flexors. A cardiomyopathy with slight reduction of systolic left ventricular function was found in 2002. Coronary angiography excluded relevant coronary artery disease. The electrophysiologic examination could provoke atrial flutter, but neither a ventricular tachycardia nor a delay in the AV conduction was found. ECG and Holter ECG did not reveal any abnormalities. A reduction of the left ventricular systolic function (EF 45%) with normal size of cardiac chambers was demonstrated by echocardiography. It is known that in the patient group with myotonic dystrophies cardiac involvement manifests itself as cardiomyopathy, conduction disturbance or arrhythmia. However, only a small percentage of all patients with myotonic myopathy actually suffer from cardiac involvement. Among the different types of cardiac involvement, conduction disturbances requiring pacemaker implantation are most frequent. Only some patients develop ventricular tachycardias, and even cases of sudden cardiac death have been described. As a result of the case reports in the literature and the findings in our patient an ICD system was implanted on March 4, 2004.

Aged↗
PubMed1998

Familial atrial standstill with coexistent atrial flutter.

A child with familial atrial standstill and a ventricular pacemaker had syncope due to atrial flutter that was treated by His-bundle ablation. Bradycardia protection alone may be insufficient in patients with atrial standstill.

Atrial Flutter↗
PubMed1984

Beta-blocking drugs for arrhythmias, hypertension, and ischemic heart disease.

Beta-blocking drugs have provided significant improvement in the medical therapy of many types of heart disease. They are more effective in treating young hypertensive patients than elderly hypertensive patients. These drugs reduce the ventricular rate seen in atrial flutter and fibrillation, and they also reduce the frequency of ventricular ectopy. Beta blockers are important adjuncts for control of angina pectoris. When these drugs are given for a period of 1 to 3 years after myocardial infarction they reduce the incidence of reinfarction and the frequency of sudden death as well as reduce the overall mortality rate. Factors that may contribute to the overall decreased mortality include the reduction in the reinfarction rate and an increased threshold for ventricular fibrillation as well as those mechanisms that reduce myocardial oxygen utilization.

Adrenergic beta-Antagonists↗
PubMed1975

[Certain practical problems of recognition and treatment of cardiac rhythm disorders].

Having briefly touched upon the problem of terminology and classification of arrhythmias the authors consider the diagnosis and clinical evaluation of some disorders, including the extrasystole (the significance of the extrasystolic interval), ectopic arrhythmias from the region of the atrio-ventricular junction (with simultaneous consistent or transent disruption of the intraventricular conduction), isolated atrial tachycardia, some variants of auricular fibrillation, flutter paroxysms, paroxysms of ventricular tachycardia, with continued auricular fibrillation in particular, and also the earlier described electrocardiographic phenomenon tentatively interpreted as sinistroatrial fibrillation with dextraatrial tachycardia, as well as major types of disrupted condution. The authors give a brief exposure of their views as to the principles of the treatment. Emphasis is placed on the importance of a comprehensive clinical approach to the diagnostic matters and to the evaluation of arrhythmias, as well as to the fundamental need to define more precisely the pathogenesis of the disturbed rhythm in a concrete patient so as to adopt an effective treatment.

Ajmaline↗
PubMed1995

[Supraventricular tachycardia with wide QRS complexes during Vaughan-Williams class I anti-arrhythmic treatment. Diagnostic and therapeutic implications].

The authors report 8 cases of regular tachycardia with wide QRS complexes during treatment with Vaughan-Williams class 1 antiarrhythmic drugs. These antiarrhythmics, prescribed to prevent atrial fibrillation (3 patients) and atrial flutter (5 patients), were flecainide in 4 cases, propafenone in 2 cases and cibenzoline and hydroquinidine respectively associated with digitoxine and propranolol. These wide complex tachycardias were regular atrial tachycardias with 1/1 conduction to the ventricle. The action of the drug, more pronounced on intra-atrial conduction velocities than on atrioventricular node refractoriness resulted in transformation of flutter at 300 cycles/min with 2/1 conduction and a ventricular rate of 150 cycles/min to atrial flutter at 210 cycles/min with 1/1 ventricular conduction. This acceleration of the ventricular rate was accompanied by widening of the QRS complex. Using the new ventricular tachycardia criteria recently published by Brugada resulted in a diagnostic error in 7 out of the 8 cases. The recording of a wide QRS complex tachycardia in a patient on class 1 antiarrhythmic therapy for an atrial arrhythmia should alert the physician to 1/1 atrial tachycardia despite morphological electrocardiographic criteria of ventricular tachycardia. The 1/1 atrial tachycardia may be poorly tolerated and require emergency treatment. The preventive association of a drug which slows conduction through the atrioventricular node is not always effective.

Adult↗
PubMed1994

Catheter ablation of the atrioventricular node using radiofrequency energy.

BACKGROUND: Catheter ablation of the atrioventricular (AV) junction using stored direct current (DC) energy from a standard DC Cardioverter defibrillator was first reported in 1982. Since then many patients have been treated using this procedure for refractory supraventricular arrhythmias, usually atrial fibrillation and flutter. Undesirable thermal effects such as barotrauma and arcing are largely responsible for complications associated with the use of DC energy. This report details our experience of catheter ablation of the AV junction using radiofrequency (RF) energy in a series of 30 consecutive patients. METHODS: RF ablations were performed using steerable Mansfield (Webster Laboratories) 4 mm tipped electrodes and locally assembled RF energy delivery system. RESULTS: The procedure was successful in 27/30 (90%) patients using RF energy, while three patients required DC energy to achieve successful AV junction ablation. General anaesthesia was required in nine patients, six of whom required this for cardioversion to sinus rhythm so that an adequate His Bundle spike could be recorded and three for DC ablation. Dual chamber permanent pacemakers with automatic mode switching were implanted in four patients who had paroxysmal atrial fibrillation or flutter and the remainder had ventricular rate responsive pacemakers. CONCLUSIONS: In patients with drug refractory paroxysmal atrial fibrillation and flutter and in patients with established atrial fibrillation where control of the ventricular rate is difficult, catheter ablation of the AV junction using RF energy is a safe and effective procedure with a high success rate.

Atrial Fibrillation↗
PubMed1985

Atrial flutter in infancy: diagnosis, clinical features, and treatment.

The clinical features and treatment of atrial flutter in eight infants (four male and four female) less than 2 months of age are presented. Atrial flutter was noted during the first week of life in six of the infants and between 6 and 8 weeks of life in the other two infants. Four of the eight infants had associated structural or functional cardiovascular disease, and in three infants a central venous pressure catheter was present in the atrium at the time atrial flutter was diagnosed. Classic flutter waves were apparent on 12-lead ECGs in only two infants. In six infants, flutter waves were not obvious on standard ECGs, but transesophageal electrogram recordings demonstrated the presence of atrial flutter with second degree atrioventricular block. The atrial cycle length during flutter ranged from 135 to 180 ms (mean 149 ms; mean atrial rate 403 beats per minute); there was a 2:1 ventricular response to atrial flutter. Successful termination of atrial flutter was accomplished using three modes of electrical cardioversion in seven of the eight infants: direct current cardioversion in one, transvenous atrial pacing in one, and transesophageal atrial pacing in five. One asymptomatic infant converted to normal sinus rhythm 24 hours following digoxin administration. One infant had multiple atrial flutter recurrences and required chronic procainamide therapy. In seven of the eight infants, no recurrences have been noted in 6 months to 3 1/2 years of follow-up. These results demonstrate that atrial flutter may be difficult to diagnose in infants with tachycardia unless transesophageal electrogram recording is utilized for evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗