Atrioventricular dissociation.
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Atrial Flutter↗
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Progress toward the development of a safe and effective agent for treating reentrant cardiac arrhythmias: synthesis and evaluation of ibutilide analogues with enhanced metabolic stability and diminished proarrhythmic potential.
A series of ibutilide analogues with fluorine substituents on the heptyl side chain was prepared and evaluated for class III antiarrhythmic activity, metabolic stability, and proarrhythmic potential. It was found that fluorine substituents stabilized the side chain to metabolic oxidation. Many of the compounds also retained the ability to increase the refractoriness of cardiac tissue at both slow and fast pacing rates. The potential for producing polymorphic ventricular tachycardia in the rabbit model was dependent on the chirality of the benzylic carbon. The S-enantiomers generally had less proarrhythmic activity than the corresponding racemates. One compound from this series (45E, trecetilide fumarate) had excellent antiarrhythmic activity and metabolic stability and was devoid of proarrhythmic activity in the rabbit model. It was chosen for further development.
Animals↗
Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: a dose-response study.
OBJECTIVES: Currently available antiarrhythmic drugs have limited efficacy for short-term, rapid termination of atrial fibrillation and atrial flutter. BACKGROUND: Ibutilide fumarate is an investigational class III antiarrhythmic agent that prolongs repolarization by increasing the slow inward sodium current and by blocking the delayed rectifier current. It can be administered intravenously and has a rapid onset of electrophysiologic effects. METHODS: The efficacy and safety of ibutilide were studied in 200 patients with atrial flutter > 3 h in duration or atrial fibrillation 3 h to 90 days in duration. Patients were randomized to receive a single intravenous dose of placebo or an infusion of ibutilide fumarate at 0.005, 0.010, 0.015 or 0.025 mg/kg body weight over 10 min. Conversion was defined as termination of the atrial arrhythmia during or within 60 min after infusion. Forty-one patients received placebo and 159 received ibutilide (0.005 mg/kg [n = 41], 0.010 mg/kg [n = 40], 0.015 mg/kg [n = 38] or 0.025 mg/kg [n = 40]). RESULTS: The arrhythmia terminated in 34% of drug-treated patients. The rates of successful arrhythmia termination were 3% for placebo and 12%, 33%, 45% and 46%, respectively, for 0.005-, 0.010-, 0.015- and 0.025-mg/kg ibutilide. The placebo and 0.005-mg/kg ibutilide groups had lower success rates than all other dose groups (p < 0.05). The mean time to termination of the arrhythmia was 19 min (range 3 to 70) from the start of infusion. Successful arrhythmia termination was not affected by enlarged left atrial diameter, decreased ejection fraction, presence of valvular heart disease or the use of concomitant medications (beta-adrenergic blocking agents, calcium channel blocking agents or digoxin). Arrhythmia termination was not predicted by the magnitude of corrected QT interval prolongation but was associated with a shorter duration of atrial arrhythmia. The most frequent adverse events in ibutilide-treated patients were sustained and nonsustained polymorphic ventricular tachycardia (3.6%). All patients with sustained polymorphic ventricular tachycardia were successfully treated with direct current cardioversion and had no recurrence. The occurrence of proarrhythmia did not correlate with ibutilide plasma concentration. CONCLUSIONS: These data demonstrate that ibutilide is able to rapidly terminate atrial fibrillation and atrial flutter.
Aged↗
Long-term sotalol therapy in patients with arrhythmias.
Sotalol is a pure beta-adrenergic receptor antagonist. The present study was divided into a first and second therapy period. A total of 38 patients with atrial or ventricular arrhythmias were included in the first therapy period. After a drug-free period of approximately two months, 14 of the 38 patients entered the second therapy period and were given oral sotalol. During the two treatment periods, oral sotalol was given in doses ranging from 40 to 480 mg/day for 0.5 to 11 months in the first period and for four to nine months in the second period. Oral sotalol decreased or abolished arrhythmias in 92 per cent of the patients in the first therapy period and in all the patients in the second therapy period. Minor side effects occurred in two patients. Sotalol possesses a unique class III antiarrhythmic action. The electrophysiological profile is different from other beta-adrenergic blocking agents in that sotalol prolongs the duration of the intracellularly recorded action potential. This property may contribute to the antiarrhythmic efficacy demonstrated with sotalol.
Adult↗
The effect of magnesium versus verapamil on supraventricular arrhythmias.
Magnesium has previously been used in the treatment of various arrhythmias, but few randomized and prospective studies are available. In a single-blind study, the efficacy and safety of intravenous magnesium sulfate (bolus doses of 5 + 5 mmol followed by infusion of 0.04 mmol/min) versus verapamil (5 + 5 mg followed by 0.1 mg/min) was evaluated in 57 patients with supraventricular arrhythmias (supraventricular tachycardia, atrial fibrillation, and atrial flutter) of recent onset (less than 1 week). Fifteen (58%) of the patients receiving magnesium (n = 26) converted to sinus rhythm within 4 h, and 16 (62%) within 24 h. Verapamil caused a lower ventricular rate, but only six (19%) of the patients (n = 31) converted to sinus rhythm within 4 h (p < 0.01) and 16 (52%) within 24 h (NS). No side effects were observed during magnesium infusion, whereas six patients receiving verapamil had to be withdrawn from further study medication due to symptomatic side effects (hypotension in three, cardiac failure in three). Magnesium appears to be an effective and safe drug for the treatment of supraventricular arrhythmias. The overall efficacy for conversion to sinus rhythm is at least as effective as with verapamil, and its action is more rapid.
Arrhythmias, Cardiac↗
[Aortic and mitral valve bioprostheses. Normal and pathological M mode echocardiographic aspects].
The M mode echocardiographic recordings of 52 normal mitral bioprostheses (NMB), 7 pathological mitral bioprostheses (PMB), 30 normal aortic bioprostheses (NAB) and 10 pathological aortic bioprostheses (PAB) were reviewed. In normal bioprostheses a significant correlation was observed between the echocardiographic and the "specified" diameters, the diastolic and systolic slopes and the amplitude of anterior motion of the support. In NMB, the end-systolic diameter of the left ventricular outflow tract depended on the "specified" diameter of the bioprosthesis. Paradoxical septal motion was observed in 78 p. 100 of cases. In PMB, the velocity of anterior leaflet opening was significantly increased (p less than 0.001). The end-diastolic internal left ventricular dimension was also increased (p less than 0.01). A significant correlation was found between left ventricular fractional shortening and maximal leaflet separation (p less than 0.05). Normal septal motion was more common (p less than 0.05). In 5 cases of prosthetic valve dysfunction with mitral regurgitation the maximal leaflet separation was greater than normal (p less than 0.001), the diastolic slope of the support was increased (p less than 0.05) and diastolic vibrations of thickened irregular leaflets were observed. Systolo-diastolic vibrations with chaotic leaflet motion were characteristic of cusp tear and/or eversion. Stratified echos behind a support with reduced leaflet excursion was observed in one case of partial thrombosis: a thickened systolic echo with reduced diastolic excursion was observed in a case of degenerative stenosis. The review of 10 PAB showed a reduced amplitude of systolic excursion of the anterior support in cases of aortic regurgitation (p less than 0.05). Systolic vibrations of the cusp were not specific and were observed in normal cases. In severe valvular regurgitation mitral and/or septal diastolic fluttering was observed. Systolic excursion of the cusps was reduced in cases of relative stenosis due to an inappropriately small sized bioprosthesis. Thickening of the diastolic cusp echos was observed in cases of degenerative stenosis. Ventricular dilatation and reduced septal and free wall motion were dysfunction.
Adolescent↗
Does conversion and prevention of atrial fibrillation enhance survival in patients with left ventricular dysfunction? Evidence from the Danish Investigations of Arrhythmia and Mortality ON Dofetilide/(DIAMOND) study.
BACKGROUND: Atrial fibrillation is a common arrhythmia in patients with left ventricular dysfunction associated with increased morbidity and mortality. The present study investigated the potential of dofetilide to restore and maintain sinus rhythm in patients with left ventricular dysfunction, which might reduce mortality and hospitalizations. METHODS AND RESULTS: In the Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) studies, 506 patients were in atrial fibrillation (AF) or atrial flutter (AFl) at baseline. Over the course of study, cardioversion occurred in 148 (59%) dofetilide- and 86 (34%) placebo-treated patients. In these patients, the probability of maintaining sinus rhythm for 1 year was 79% with dofetilide versus 42% with placebo ( P < 0.001). Dofetilide had no effect on all-cause mortality, but restoration and maintenance of sinusrhythm (independent of study treatment) was associated with a significant reduction in mortality (risk ratio [RR], 0.44; 95% CI, 0.30 to 0.64; P < 0.0001). In addition, dofetilide therapy was associated with a significantly lower risk ratio versus placebo for either all-cause (RR, 0.70; 95% CI, 0.56 to 0.89; P < or = 0.005) or congestive heart failure (RR, 0.69; 95% CI, 0.51 to 0.93; P < or = 0.02) rehospitalization. CONCLUSIONS: Dofetilide is safe and increases the probability of obtaining and maintaining sinus rhythm in patients with structural heart disease. The present study suggests that restoration of sinus rhythm--on placebo or dofetilide--is associated with improved survival.
Anti-Arrhythmia Agents↗
Is phosphodiesterase inhibition arrhythmogenic? Electrophysiologic effects in pithed rats and in normoxic and hypoxic rabbit atria of enoximone, a new cardiotonic agent.
The positive inotropic and chronotropic actions of enoximone were confirmed. At concentrations within the clinical range, enoximone prolonged the chronotropic and hypotensive action of isoproterenol in pithed rats. Very high doses of both enoximone and isoproterenol caused ventricular fibrillation in only one of six rats. In isolated rabbit atria, the maximum frequency at which pacing stimuli were followed 1:1 was increased by enoximone, and atrial flutter was consistently induced, then terminated by greatly suprathreshold stimulation. Enoximone significantly shortened action potential duration (APD), but did not exacerbate the APD-shortening induced by hypoxia. Since such hypoxia-induced shortening occurred in the presence of glucose 11 mmol/L and oxygen 20%, it was concluded that it was unlikely to have been caused by the opening of ATP-regulated potassium channels. These animal experiments suggest that enoximone, at concentrations encountered clinically in humans, does not have any electrophysiologic actions that would be likely to increase the probability of arrhythmias.
Animals↗
Use of fast fourier transform analysis of atrial electrograms for rapid characterization of atrial activation-implications for delineating possible mechanisms of atrial tachyarrhythmias.
INTRODUCTION: Different analysis techniques have been developed to help understand and characterize the mechanisms responsible for atrial arrhythmias. We tested the hypothesis that Fast Fourier Transform (FFT) analysis of recorded atrial electrograms (AEGs) will rapidly and accurately identify regular and irregular patterns of atrial activation, and, thereby, may provide evidence suggestive of underlying mechanisms of atrial tachyarrhythmias. METHODS AND RESULTS: During induced atrial tachyarrhythmias in both the canine sterile pericarditis model and canine rapid ventricular pacing-induced congestive heart failure model; 380-404 AEGs were recorded simultaneously from epicardial electrodes on both atria. From AEGs, atrial activation sequences were determined during atrial flutter (AFL), focal atrial tachycardia (AT), and atrial fibrillation (AF). Four-second recording segments of each AEG were subjected to FFT analysis. Frequencies found during FFT analyses in all studies precisely corresponded to the cycle lengths of the AEGs. In AFL and AT, one dominant frequency peak was found throughout both atria. In AF due to multiple unstable reentry circuits, multiple and broad frequency peaks were found in both atria. In AF due to a stable rapid rhythm (driver) in the left atrium with fibrillatory conduction to the rest of the atria, one dominant frequency peak in areas with 1:1 conduction from the driver, and multiple and/or broad frequency peaks in areas with fibrillatory conduction produced by the driver were found. Computation time for all FFT analyses took <5 minutes. CONCLUSION: FFT analysis accurately and rapidly identifies global atrial activation patterns during AFL, AT, and AF, thereby assisting in determining arrhythmia mechanisms.
Animals↗
Reflected reentry, delayed conduction, and electrotonic inhibition in segmentally depressed atrial tissues.
Reflection is a subclass of reentrant cardiac arrhythmias in which reexcitation of the heart occurs as a result of to and fro electrotonically mediated transmission of impulses across a narrow zone of impaired conductivity. Although relatively well characterized in ventricular tissues, the reflection mechanism has not been studied in atrial tissues. In this study we examine the possibility of reflected reentry in segmentally depressed atrial tissues and evaluate conduction characteristics in these preparations. Narrow strips of atrial pectinate muscle or crista terminalis (canine and calf) were placed in a three-chambered bath and the central segment was superfused with an isotonic sucrose solution or an "ischemic" Tyrode's solution. Proximal to distal conduction across the 1.0- to 1.2-mm wide ischemic gap showed step delays as long as 210 ms. Reflected reentry was readily demonstrable when prominent step delays occurred during anterograde conduction of the impulse across the gap. Progressive acceleration of the stimulation rate resulted in progressively greater impairment of anterograde conduction until complete block occurred. The incidence and patterns of reflected reentry were therefore a sensitive function of the stimulation rate. Other features exhibited by these preparations include a slow recovery of excitability following the action potential, postrepolarization refractoriness, and electrotonic inhibition and summation. Our data suggest that the characteristics of conduction and reflection in segmentally depressed atrial tissues are qualitatively similar to those in ventricular tissues. The presence of electrotonic inhibition in atrial may also help to explain the functionally inexcitable zone seen in the vortex of the leading circle model of atrial flutter.
Action Potentials↗
Adenosine-induced atrial pro-arrhythmia in children.
Adenosine has become the preferred acute treatment for common types of supraventricular tachycardia because of its efficacy and safety. There have been a few reports of serious proarrhythmic events associated with its use, including the induction of atrial fibrillation in adult patients. Three instances of adenosine-induced atrial proarrhythmia (two atrial fibrillation and one atrial flutter) have been observed in children with manifest or concealed Wolff-Parkinson-White syndrome at the Hospital for Sick Children, Toronto, Ontario since 1990, which indicates a previously unreported risk of atrial arrhythmia for children as well. Because adenosine may enhance antegrade bypass tract conduction, its use carries a risk of ventricular acceleration, including progression to ventricular fibrillation. Because of such rare and potentially life-threatening adverse effects, appropriate monitoring and precautions are required during the administration of the drug to children and adults.
Adenosine↗
European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias.
Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Efficacy, safety, and determinants of conversion of atrial fibrillation and flutter with oral amiodarone.
Amiodarone is effective for long-term maintenance of sinus rhythm after electrical cardioversion of refractory atrial fibrillation or flutter. To examine its efficacy and safety for pharmacologic conversion of these arrhythmias, we studied 129 patients with refractory atrial fibrillation or flutter who had failed previous intensive conventional antiarrhythmic treatment. In anticipation of electrical cardioversion, patients were loaded with amiodarone, 600 mg/day during a 4-week period. The main outcome measure was pharmacologic conversion during this period. During the loading period, 23 patients (18%) converted to sinus rhythm. When analyzed in a multivariate model, conversion was related to desethylamiodarone plasma level (p = 0.0006), arrhythmia duration (p = 0.04), left atrial area (p = 0.02), and concomitant treatment with verapamil (p = 0.01). During ongoing atrial fibrillation after loading, the ventricular rate decreased from 100 +/- 25 to 87 +/- 27 beats/ min (p <0.001). Amiodarone appeared to be safe and did not have to be discontinued because of intolerable side effects. Thus, amiodarone loading is safe and is still able to convert refractory atrial fibrillation or flutter. Conversion is related to increased desethylamiodarone plasma levels and concomitant treatment with verapamil. Because prolonged loading may increase desethylamiodarone plasma concentrations, this may enhance efficacy and obviate the need for electrical cardioversion.
Aged↗
Transthoracic DC shock may represent a serious hazard in pacemaker dependent patients.
External defibrillation is widely used for the termination of various atrial and ventricular tachyarrhythmias, including pacemaker patients. Our study was intended to evaluate the effects of DC shocks in 36 patients with unipolar pacemakers implanted in the right pectoral region (25 DDD, 10 VVI, 3 AAI). The shocks were delivered with paddles on the anterior surface of the thorax, as far as possible away from the pacemaker. The pacing output was programmed at 0.5 msec and 5 V (25 patients), 4 V (1 patient), and 2.5 V (10 patients). Transient loss of capture occurred in 18 patients (50%). These patients, compared with those without capture failure, received higher peak and cumulative shock energies, respectively, 216 +/- 99 versus 123 +/- 50 joules (P < 0.002) and 352 +/- 62 versus 147 +/- 98 joules (P < 0.004) and had a lower pacemaker pulse amplitude (4.0 +/- 1.2 vs 4.6 +/- 1.0 V, P = 0.11). Failure to capture lasted from 5 seconds to 30 minutes (mean 157 sec). In 15 patients the ventricular stimulation threshold was measured before and serially after cardioversion. A six-fold threshold increase was observed 3 minutes after the shock (P < 0.004) with gradual recovery to nearly baseline values at 24 hours. Transient sensing failure occurred in 7 of the 17 patients in whom it could be evaluated (41%). Furthermore, three cases of shock induced pacemaker malfunctions were observed requiring replacement of the stimulator in two patients. In conclusion, the incidence of loss of capture in pacemaker patients subjected to electrical cardioversion/defibrillation is high.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Combined use of propafenon and lidoflazine in chronic atrial fibrillation and flutter (author's transl)].
Forty-seven patients with chronic atrial fibrillation and (or) flutter in whom the clinical picture and the length of arrhythmia indicated that drug-mediated cardioversion should be tried were treated with a combination of lidoflazine and propafenon. The average daily dosage was 600 mg for propafenon and 180 mg for lidoflazine. Duration of treatment was limited to 8 days. Return to sinus rhythm was achieved in 34 patients. In comparison with monotherapy combined use of the drugs thus led to a clear-cut increase of the conversion rate. Dosage reduction of these differently acting substances decreases the risk of toxic side effects, particularly as both substances have different side effects which in part cancel each other out. It can be assumed that ventricular extrasystoles seen during treatment with lidoflazine as precursor of malignant tachycardia can be suppressed or eliminated by propafenon.
Atrial Fibrillation↗
Etiology of the Austin Flint murmur.
OBJECTIVES: The aim of the study was to determine the mechanism of the Austin Flint murmur. BACKGROUND: More than 100 years after the initial description of the Austin Flint murmur, the etiology of the murmur remains unclear. METHODS: M-mode and two-dimensional echocardiography, conventional and color flow Doppler study, and cine nuclear magnetic resonance (cine NMR) imaging were performed in 24 patients with clinically moderate or severe aortic regurgitation. Mitral valve area was determined by planimetry and pressure half-time measurement. Overlap of the aortic regurgitation and mitral inflow jets was graded 0 (no overlap) to 4 (marked overlap) by Doppler study and cine NMR imaging. The volume of signal loss resulting from turbulent blood flow secondary to the aortic regurgitation jet was determined on cine NMR images, and the extent of contact with the left ventricular endocardium was graded 0 (no contact) to 4 (extensive contact). RESULTS: The presence of an Austin Flint murmur did not correlate with mitral valve area (2.7 +/- 0.8 cm2 with the murmur vs. 2.5 +/- 0.7 cm2 without), overlap of the aortic regurgitation and mitral flow jets (3 +/- 1 vs. 2.3 +/- 1.2), diastolic mitral regurgitation (50% vs. 71%) or fluttering of the anterior mitral valve leaflet (70% vs. 50%). The presence of an Austin Flint murmur correlated best with the volume of signal loss associated with the aortic regurgitation jet on cine NMR imaging (65 +/- 16 ml with the murmur. vs. 38 +/- 11 ml without, p less than 0.001) and the extent of contact of this signal loss with the left ventricular endocardium (2.9 +/- 0.5 vs. 1.5 +/- 0.4, p less than 0.0001). CONCLUSIONS: The Austin Flint murmur is caused by the aortic regurgitation jet abutting the left ventricular endocardium, resulting in the generation of a low-pitched diastolic rumbling.
Aortic Valve Insufficiency↗
Diazepam. A useful hypnotic drug for direct-current cardioversion.
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Adolescent↗