Review of diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia.
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OBJECTIVE: To review the diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia. DESIGN: Retrospective review of published reports: 11 papers about fetal tachyarrhythmia published between 1991 and 2002 were selected for review. MAIN OUTCOME MEASURES: All selected studies were analysed for the type of arrhythmia, degree of atrioventricular block in atrial flutter, occurrence of hydrops fetalis, gestational age at diagnosis, first and second line drug treatment, associated cardiac and extracardiac malformations, and mortality of the fetuses. RESULTS: Atrial flutter accounted for 26.2% of all cases of fetal tachyarrhythmias, and supraventricular tachycardia for 73.2%. Hydrops fetalis was reported in 38.6% and 40.5% of fetuses with atrial flutter and supraventricular tachycardia, respectively (NS). Hydropic fetuses with atrial flutter had higher ventricular rates (median 240 beats/min, range 240-300) than non-hydropic fetuses (220 beats/min, range 200-310) (p = 0.02), whereas the atrial rates were not significantly different (median 450 beats/min, range 370-500). Digoxin treatment resulted in a higher conversion rate in non-hydropic fetuses with fetal tachyarrhythmias than in hydropic fetuses (p < 0.001). The overall mortality of atrial flutter was similar to that of supraventricular tachycardia, at 8.0% v 8.9% (p = 0.7). CONCLUSIONS: The prevalence of hydrops fetalis did not differ in fetal atrial flutter and supraventricular tachycardia with 1:1 conduction. There was no difference between the response rate to digoxin in fetus with atrial flutter or supraventricular tachycardia. Mortality was similar in the two types of tachyarrhythmia. (+info)
Recent advances in the treatment of arrhythmias.
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Advances in endocardial mapping techniques and ablation have greatly increased the indications for catheter-ablation of supraventricular arrhythmias. Rate or rhythm control is a valid treatment option for patients with atrial fibrillation; however, all patients with one or more risk factors should be treated with oral anticoagulants. The early success rate and long-term cure of atrial fibrillation by radiofrequency catheter ablation continues to increase. The number of centers offering this treatment option has increased substantially. Implantable defibrillator-cardioverters are the primary treatment modality for patients with ventricular tachycardia and their role in primary prevention is also being defined. Future advances in arrhythmia management will include improvements in catheter design and energy sources for ablation, and greater monitoring capacity of implantable devices. (+info)
Management of fetal tachyarrhythmia based on superior vena cava/aorta Doppler flow recordings.
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OBJECTIVE: To evaluate a management protocol of fetal supraventricular tachycardia (SVT) based on prior identification of the underlying mechanism. DESIGN AND SETTING: Prospective study in a mother-child tertiary university centre. PATIENTS: During a consecutive 36 month period, 18 fetuses with sustained SVT underwent a superior vena cava/ascending aorta (SVC/AA) Doppler investigation in an attempt to determine the atrioventricular (AV) relation and to treat the arrhythmia according to a pre-established management protocol. MAIN OUTCOME MEASURE: Rate of conversion to sinus rhythm. RESULTS: Seven fetuses had short ventriculoatrial tachycardia, five of these with a 1:1 AV conduction suggesting re-entrant tachycardia. The first choice drug was digoxin and all were converted. One fetus had AV dissociation leading to the diagnosis of junctional ectopic tachycardia, which was resistant to digoxin and sotalol; amiodarone achieved postnatal conversion. One fetus had SVT and first or second AV block; the diagnosis was atrial ectopic tachycardia (AET), which responded to sotalol given as a drug of first choice. Seven fetuses had long ventriculoatrial tachycardia: one with sinus tachycardia (no treatment), one with permanent junctional reciprocating tachycardia (PJRT), and three with AET. The first choice drug was sotalol and all were converted. One AET was classified postnatally as PJRT. Six fetuses had intra-atrial re-entrant tachycardia: five with 2:1 AV conduction and one with variable block. The first choice drug was digoxin. Conversion was achieved in all but one, who died after birth from advanced cardiomyopathy. CONCLUSION: The electrophysiological mechanisms of fetal SVT can be clarified with SVC/AA Doppler. The proposed management protocol has so far yielded a good rate of conversion to sinus rhythm. (+info)
Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist.
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OBJECTIVES: The aim of this study was to evaluate tecadenoson safety and efficacy during conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm. BACKGROUND: Tecadenoson (CVT-510), a novel adenosine receptor (Ado R) agonist, selectively activates the A1 Ado R and prolongs atrioventricular (AV) nodal conduction at doses lower than those required to cause A2 Ado R-mediated coronary and peripheral vasodilation. Unlike adenosine, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without hypotension and bronchoconstriction. METHODS: In this open-label, multicenter, dose escalation study, tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant tachycardia, n = 8) with inducible PSVT sustained for > or =1 min during an electrophysiology study. Seven regimens (0.3 to 15 microg/kg) of up to two identical tecadenoson intravenous bolus doses were administered. RESULTS: After the first or second bolus, PSVT converted to sustained sinus rhythm for > or =5 min in 86.5% (32/37) of the patients, with 91% (29/32) of the conversions occurring after the first bolus (most within 30 s), coincident with anterograde conduction block in the AV node. No effects on sinus cycle length (SCL) or systolic blood pressure were observed. The atrial-His (AH), but not the His-ventricular (HV) interval was prolonged up to 5 min after the final tecadenoson bolus, returning to baseline by 10 min. Tecadenoson was generally well tolerated. CONCLUSIONS: In this study, tecadenoson rapidly terminated sustained PSVT by depressing AV nodal conduction without causing hypotension. After sinus rhythm restoration, there was minimal AH interval prolongation without HV interval or SCL prolongation. (+info)
Dispersion of monophasic action potential duration: demonstrable in humans after premature ventricular extrastimulation but not in steady state.
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Abnormal dispersion of repolarization may contribute to the arrhythmogenic physiologic substrate of ventricular arrhythmia. Geographic dispersion of monophasic action potential duration was determined in steady state (drive cycle lengths 600 and 430 ms) between widely spaced right ventricular endocardial sites (geographic dispersion) in 10 control patients with right ventricular disease and complicating ventricular tachycardia (n = 9), 6 patients with right and left ventricular disease and complicating ventricular tachycardia and 7 patients with ischemic heart disease and complicating ventricular tachycardia. No significant difference in geographic dispersion could be demonstrated among the groups. Difference of monophasic action potential duration at adjacent right ventricular endocardial sites (adjacent dispersion) was determined after ventricular extrastimulation during construction of simultaneous electrical restitution curves in the same patient groups. Maximal adjacent dispersion over the electrical restitution curve was compared between disease and control groups. There was a significant difference in observations of maximal adjacent dispersion in patients with right ventricular disease and complicating ventricular tachycardia (range 5 to 85 ms, median 22.5; 14 pairs of sites; p less than 0.05) and patients with right and left ventricular disease and complicating ventricular tachycardia (range 5 to 50 ms, median 17.5; 14 pairs of sites; p less than 0.05) compared with control patients (range 5 to 20 ms, median 10; 15 pairs of sites). This difference was not evident when patients with ischemic heart disease and complicating ventricular tachycardia (range 5 to 25 ms, median 12.5; 12 pairs of sites) were compared with control patients. Maximal percent monophasic action potential shortening from steady state was significantly greater (p less than 0.001) in both groups with greater adjacent dispersions, and prolongation of activation time at monophasic action potential recording sites after premature extrastimulation tended to be greater in patients with right or right and left ventricular disease and complicating ventricular tachycardia. It is concluded that in disease, exaggeration of monophasic action potential shortening after premature ventricular extrastimulation may contribute to the electrophysiologic arrhythmogenic substrate. (+info)
Left ventricular volume determined echocardiographically by assuming a constant left ventricular epicardial long-axis/short-axis dimension ratio throughout the cardiac cycle.
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OBJECTIVES: The purpose of this study was to develop and test a simplified echocardiographic method to calculate left ventricular volume. BACKGROUND: This method was based on the assumption that the ratio of the left ventricular epicardial long-axis dimension to the epicardial short-axis dimension was constant throughout the cardiac cycle. With use of this constant ratio, the method developed to calculate left ventricular volume at a given point in the cardiac cycle required the left ventricular endocardial long-axis dimension to be measured at only one point in the cardiac cycle. METHODS: Studies were performed in 13 normal dogs, 8 normal puppies, 9 normal pigs, 12 dogs with aortic stenosis, 13 dogs with acute mitral regurgitation, 12 dogs with chronic mitral regurgitation, 7 dogs that had undergone mitral valve replacement and 6 pigs that had had chronic supraventricular tachycardia. Animals with aortic stenosis developed left ventricular pressure overload hypertrophy with a 60% increase in left ventricular mass; chronic mitral regurgitation caused left ventricular volume overload hypertrophy with a 46% increase in left ventricular volume; supraventricular tachycardia caused a dilated cardiomyopathy with a 55% decrease in left ventricular ejection fraction. RESULTS: The left ventricular epicardial long-axis/short-axis dimension ratio remained constant throughout the cardiac cycle in each animal group. End-diastolic and end-systolic volumes calculated with the simplified echocardiographic method correlated closely with angiographically measured volumes; for end-diastolic volume, echocardiographic end-diastolic volume = 1.0 (angiographic end-diastolic volume) -1.8 ml, r = 0.96; for end-systolic volume, echocardiographic end-systolic volume = 0.98 (angiographic end-systolic volume) -0.7 ml, r = 0.95. CONCLUSIONS: Thus the left ventricular epicardial long-axis/short-axis dimension ratio was constant throughout the cardiac cycle in a variety of animal species and age groups and in the presence of cardiac diseases that significantly altered left ventricular geometry and function. The simplified echocardiographic method examined provided an accurate determination of left ventricular volumes. (+info)
Unmasking of a second atrioventricular accessory connection by adenosine in a child with a long RP' reentrant tachycardia.
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A second unidirectional, retrograde accessory atrioventricular pathway was unmasked by adenosine during the intracardiac evaluation of a child with a reentrant long RP' tachycardia. This case is further evidence of the value of adenosine during the evaluation of these types of tachycardias. (+info)
Radiofrequency catheter ablation of incessant, medically resistant supraventricular tachycardia in infants and small children.
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OBJECTIVES: This study retrospectively evaluates initial experience with radiofrequency catheter ablation in a group of seven infants and small children with a history of incessant, medically resistant supraventricular tachycardia. METHODS: Before attempted catheter ablation, all patients had had unsuccessful conventional medical therapy (with digoxin or propranolol, or both) and, in addition, each continued to have daily episodes of supraventricular tachycardia while taking amiodarone or a class IC antiarrhythmic agent alone or in combination. The average patient age was 10 months (range 1 to 27) and the average patient weight was 6 kg (range 3 to 13). Electrophysiologic diagnosis included reentrant supraventricular tachycardia in six patients and atrial ectopic tachycardia in one patient. RESULTS: These seven patients underwent a total of nine catheter ablation procedures. The atrial approach to ablation was employed in eight of the nine procedures. Overall, radiofrequency catheter ablation was totally successful in five of the seven patients, partially successful in one patient and unsuccessful in the remaining patient. The combination of radiofrequency catheter ablation and surgical ablation was successful in controlling tachycardia in all patients; with at least 5 months of follow-up study, no patient has had a recurrence of supraventricular tachycardia or reappearance of a delta wave. CONCLUSIONS: Surgical ablation of arrhythmogenic substrates in the pediatric age group, although rarely indicated, has been found in the past to be safe and effective. Our initial experience with radiofrequency catheter ablation in infants and small children demonstrates that this procedure is a promising nonpharmacologic therapeutic alternative to surgical ablation. (+info)