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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study assessed the long-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branch reentrant ventricular tachycardia. Bundle branch reentrant tachycardia was diagnosed in 16 patients (ejection fraction 31% +/- 15%) who underwent electrophysiology study in our laboratory. All patients had His-Purkinje system conduction delay with mean HV interval of 68 +/- 8 ms. After ablation, right bundle branch block developed in 15 patients. One patient developed complete heart block, which was anticipated. One patient died of heart failure 9 months after ablation. Two patients were successfully bridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients received implantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months after ablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiology study. This patient died suddenly 29 months after ablation. The remaining nine patients were alive and well for a mean follow-up of 19 +/- 10 months. Radiofrequency ablation of the right bundle branch is an effective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellent provided that other types of ventricular tachycardia, when present, are treated as well. This technique may be helpful in management of patients who have unacceptable frequent shocks from their implanted defibrillators and may be helpful in avoiding implantation of such a device completely in others. In some patients with terminal heart failure and incessant ventricular tachycardia, this procedure can function as a bridge to cardiac transplantation.
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PMID:Long-term clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia. 877 Nov 24

We report a case of neonatal lupus erythematosus (NLE) with congenital heart block and severe myocardial failure, which was followed from the 25th week of gestation because of fetal bradycardia. The child was delivered at the 37th week of gestation by elective cesarean section because of echocardiographically documented heart enlargement, pericardial effusion and moderate insufficiency of the mitral and tricuspid valves. In spite of immediate pacing, intubation and supportive treatment, the newborn developed progressive heart failure. Echocardiography showed endocarditis of the mitral valve and diffuse myocarditis. The heart failure resolved under steroid treatment. Our experience supports the early use of steroids in treating myocarditis due to NLE. Intrauterine steroid treatment in the presence of fetal hydrops and congenital heart block is discussed.
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PMID:Neonatal lupus erythematosus with congenital heart block and severe heart failure due to myocarditis and endocardititis of the mitral valve. 879 3

A 7-month-old girl weighing 5.3 kg, presented with atrial septal defect (ASD) and paroximal supraventricular tachycardia (PSVT). The preoperative electrophysiological study could not be performed because of the severe heart failure. On suspicion of a concealed Wolff-Parkinson-White (WPW) syndrome, whose accessory pathways conduct in the retrograde direction only, the operation was performed. The intraoperative epicardial and endocardial mappings revealed the presence of a left-posterior retrograde accessory pathway. This accessory pathway was successfully ablated by a cryoablation using transseptal superior approach. The postoperative course was uneventful without a permanent heart block. We report a successful surgical repair for an infant with concealed WPW syndrome, who revealed severe heart failure because of PSVT and ASD.
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PMID:[Successful repair for concealed Wolff-Parkinson-White syndrome with atrial septal defect in infancy: a case report]. 891 72

We encountered a case of fetal bradycardia (57 bpm) induced by heart block. The continuous intravenous administration of ritodrine to a mother to treat fetal brady-cardia at 28 weeks of gestation successfully increased the fetal ventricular rate by 15 bpm (from 57 to 72 bpm). Pregnancy was continued for 10 weeks, and fetal cardiac failure did not occur. The fetal ventricular rate gradually decreased to 52 bpm after discontinuation of the ritodrine infusion. It is suggested that maternal administration of ritodrine can be considered in a case of life-threatening fetal bradycardia induced by complete heart block.
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PMID:Fetal ventricular rate in case of congenital complete heart block is increased by ritodrine. Case report. 918 44

Complete congenital heart block (CCHB) is the most severe manifestation of neonatal lupus syndrome, associated with a mortality rate of up to 31%. It is caused by irreversible damage to the cardiac conduction system due to the transplacental passage of maternal antibodies to the fetus. Anti-Ro (SSA) and anti-La (SSB) antibodies are usually detected in sera of mothers of children with prenatally diagnosed CCHB and in cardiac tissues of affected newborns. Their pathogeneic role in the development of CCHB has been established in several studies. When CCHB is detected during pregnancy, careful monitoring and delivery are needed before heart failure is developed. Treatment strategies are debatable and may include prophylactic therapy for high-risk pregnant women and a combination of intrauterine plasmapheresis with plasma exchange or with corticosteroids. Pacemaker insertion is required in most infants during the first three months of life. Assays for anti-Ro (SSA) and anti-La (SSB) antibodies should be performed on sera of pregnant women with SLE and newborns with CCHB.
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PMID:Anti-Ro (SSA) and anti-La (SSB) antibodies and complete congenital heart block. 925 27

Ventricular tachycardia (VT) is an uncommon finding in patients with congenitally corrected transposition of the great arteries (CCTGA). Cardiac death in patients with CCTGA has been attributed to complete heart block, systemic ventricular dysfunction, or severe AV valve regurgitation with heart failure. We describe the case of a patient who presented with palpitations and near-syncope that was associated with clinical episodes of VT. Programmed ventricular stimulation revealed easily inducible sustained VT that immediately degenerated to ventricular fibrillation and subsequently required therapy with an implantable cardioverter defibrillator.
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PMID:Ventricular tachycardia: a life-threatening arrhythmia in a patient with congenitally corrected transposition of the great arteries. 960 61

A 21 week fetus was diagnosed with complete heart block. From the first diagnosis until 38 weeks gestation, umbilical venous pulsations occurred during ventricular systole. The ventricular frequency was 49 bpm. The venous pulsations corresponded with the ventricular frequency. At 38 weeks venous pulsations also occurred during ventricular diastole. Umbilical pulsations during diastole were associated with a decrease of ventricular frequency to 28 bpm and fetal hydrops. The venous pulsations during ventricular systole seem to be characteristic of complete heart block. The pulsations during ventricular diastole reflect the fetal heart failure. Doppler ultrasound aids in the diagnosis and surveillance of the fetus with complete heart block.
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PMID:[Doppler ultrasound of the umbilical vein in fetal 3rd degree atrioventricular block]. 974 47

Thyroid storm is a difficult diagnosis in "apathetic" variant of hyperthyroidism. The clinical features may not be evident. Abnormal atrioventricular (AV) conduction, such as complete heart block, in thyrotoxicosis is uncommon. We report a case of a 16-year-old girl presenting with fever, jaundice, heart failure and complete heart block in whom the diagnosis of thyroid storm was initially missed because of the unusual presenting features. Prompt resolution of the conduction abnormality occurred when treatment with carbimazole, intravenous iodide and dexamethasone was instituted.
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PMID:Thyroid storm presenting as jaundice and complete heart block. 991 55

Retrospective studies have suggested that, in patients with sick sinus syndrome, it has been recognized that atrial, dual-chamber, or other so-called physiologic modes of pacing are associated with a lower incidence of atrial fibrillation, stroke, heart failure, and death than is single-chamber ventricular pacing. Retrospective data in patients with atrioventricular block are less robust, but still suggest lower mortality and morbidity with dual-chamber pacing compared with ventricular pacing alone. Overall, the reduction in risk of atrial fibrillation with dual-chamber compared with ventricular pacing has been calculated at 62%, and for death 36%. Retrospective studies are, of course, potentially subject to bias, and there may be a tendency to implant cheaper, simpler pacemakers in older, sicker patients, which could explain the apparent difference in outcome. Prospective studies are, therefore, required; results from 3 such studies, in which pacing mode was randomly allocated, have been recently published. These, in general, support the apparent benefit of dual-chamber pacing in patients with sick sinus syndrome, but give equivocal results in patients with heart block. Other trials are in progress, and their results are awaited. Like all good trials, they will, in addition to providing some answers, generate further questions. They should provide the evidence on which cost-effective pacing policies may be based.
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PMID:Effect of pacing mode on morbidity and mortality: update of clinical pacing trials. 1008 67

Clearly, sudden cardiac death syndrome in heart failure is linked to severely perturbed neurohumoral, hemodynamic, and mechanical systems. Routine antiarrhythmic drug therapy has not proven beneficial and, therefore, there is no justification for using these agents in unselected heart failure patients who are without significant symptomatic ventricular arrhythmia. Aggressive treatment of the failure syndrome seems most important. Because many of the problematic arrhythmias arise from triggering automaticity, which is known to occur in excessive ventricular stretch and wall stress, systemic vascular "unloading" with vasodilators and angiotensin-converting enzyme inhibitors is likely helpful. The most recent American College of Cardiology/American Heart Association Guidelines regarding therapeutic management of heart failure suggest that aggressive pharmacologic treatment of asymptomatic ventricular arrhythmias is best avoided. To be considered strongly for pharmacologic prescription or for implantation of a tachyarrhythmia termination device, a patient should have symptomatic ventricular tachycardia with an episode of syncope or sudden cardiac death syndrome rather than simply having palpitations of asymptomatic, unsustained ventricular tachycardia. Indeed, aggressively treating congestive heart failure with medication often eliminates potentially life-threatening arrhythmias. Appropriate use of vasodilators and, particularly, angiotensin-converting enzyme inhibitors is important. Correction of fluid balance and electrolyte disorders may be helpful to address symptoms and certainly is likely to decrease the potential for morbidity and mortality. On occasion it may be necessary to consider bradyarrhythmia pacemaker insertion or the use of atrioventricular nodal-ablation techniques with subsequent ventricular or atrioventricular pacer insertion. Obviously, sudden cardiac death due to sudden heart block or asystole might be attenuated with this strategy.
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PMID:Sudden cardiac death syndrome and pump dysfunction: the link. 1101 84


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