Surgical treatment of arrhythmias in children

Primary surgical treatment of many tachyarrhythmias in children is now possible. In those with life-threatening arrhythmias not responsive to any form of medical treatment, the choice for surgery is clear. These arrhythmias include atrial fibrillation with the Wolff-Parkinson-White syndrome, PJRT, or atrial ectopic tachycardia with severe congestive cardiomyopathy, incessant ventricular tachycardia in infancy, and recurrent sustained ventricular tachycardia in postoperative congenital heart disease. In the majority of patients, however, surgical treatment remains an option to be weighed carefully against chronic medical treatment. Surgery is now possible with very low mortality for infants and children with Kent bundles, atrial ectopic tachycardia, and the permanent form of junctional reciprocating tachycardia. The mortality, morbidity, and likelihood of eventual resolution of the arrhythmia with each type of management plan should be considered. With possible direct surgical ablation of atrial flutter and newer forms of catheter treatment of arrhythmias, the future looks promising.     

Ventricular arrhythmias: a perspective on management

Antiarrhythmic drugs are associated with a significant incidence of arrhythmogenic effects, as well as other cardiac and extracardiac side effects. Thus, it is important that the decision to treat ventricular arrhythmias be made on the bases of the frequency of the arrhythmia, its qualitative features, and the presence or absence of underlying heart disease. These features influence the risks of sudden arrhythmogenic death.     

Cardiac arrhythmias: the quest for a cure: a historical perspective

During the last 40 years, much progress has been made in our understanding and management of cardiac arrhythmias. A major step in the late 1960s was to combine programmed electrical stimulation of the heart with intracardiac activation recording. This allowed: 1) localization of the site of the block in the atrioventricular conduction system in patients with bradycardia; and 2) identification of the site of origin and the mechanism of supraventricular and ventricular tachycardia. Combining information from intracardiac studies with findings on the 12-lead electrocardiogram (ECG) resulted in much better localization of conduction abnormalities and arrhythmias using the ECG. This new knowledge led to the development of new therapies, such as bradycardia and antitachycardia pacing, and surgery for supraventricular and ventricular tachycardia. A very important development in the treatment of life-threatening arrhythmias was the implantable defibrillator. Growing concern about failure to protect patients at risk for dying suddenly with antiarrhythmic drugs led to a rapid increase in their number. Cure by catheter ablation became possible for patients with different types of arrhythmias. Genetic analysis allowed the identification of different monogenic arrhythmic diseases. Several challenges remain: the epidemic of atrial fibrillation, arrhythmias in heart failure, and sudden death out-of-hospital. One-fifth of all deaths are sudden and unexpected. The important issue is how we are going to prevent these unnecessary deaths from occurring.     

Ventricular arrhythmias in athletes: Role of a comprehensive diagnostic workup

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Ventricular arrhythmias associated with lidoflazine: side-effects observed in a randomized trial

Twenty-four patients received either propranolol, lidoflazine(Clinium), or propranolol/lidoflazine combinations in a studydesigned to evaluate the effect of these drugs in angina pectoris.Five patients developed ventricular tachycardia when receivingeither lidoflazine or lidoflazine and propranolol in combination;one of these patients died. In addition, one patient died suddenlywhile being treated with propranolol alone. Lidoflazine therapywas associated with a significant prolongation of the QT intervalof the electrocardiogram. Lidoflazine either alone or in combinationwith propranolol, appears to induce ventricular tachycardia.     

Ventricular arrhythmias in dilated cardiomyopathy: efficacy of amiodarone

Sixty-five patients with dilated cardiomyopathy were studied by means of 24-hour ECG monitoring. Ventricular arrhythmias were present in 62 (95.4%), of whom 52 (80%) showed a complex form (multiform ventricular extrasystoles, pairs, and ventricular tachycardia). Forty-one patients, presenting with complex ventricular arrhythmias, received antiarrhythmic treatment with amiodarone (600 mg/day in the first week, 400 mg/day in the second week, and 200 to 400 mg/day chronically), and were then controlled with periodic 24-hour ambulatory monitoring. A significant reduction in the number of ventricular extrasystoles was seen in over 70% of patients during a 3-year period. There was also a significant decrease in the incidence of complex ventricular arrhythmias (particularly of ventricular tachycardia). Adverse effects were noted in 23 patients, but only four had to stop treatment. During the follow-up period, 19 patients died: 14 of heart failure, four of sudden death, and one of a noncardiac cause; all patients who died suddenly were not treated with amiodarone (p = 0.022). Complex ventricular arrhythmias are frequent in dilated cardiomyopathy and it is suggested that amiodarone is effective in short- and long-term control of these arrhythmias.     

Ventricular arrhythmias in children: the validity of exercise stress tests for their diagnosis and management

One hundred ninety-six children ranging in age from 4 years to 15 years with premature ventricular contraction (PVC) on a resting electrocardiogram (ECG) underwent exercise tests and 29 of them were found to have significant ventricular arrhythmias. They included 8 patients with 2 PVC's in row, 8 patients with 3-4 PVC's in row, and 13 patients with more than 5 PVC's in row (ventricular tachycardia: VT). These 29 patients were evaluated with exercise tests by two-step exercise ECG (TSE) and by treadmill (TM), and with 24 hour continuous ECG monitoring (Holter monitoring). 141 ECG's, 77 TSE's, 77 TM's and 46 Holter monitoring were obtained in total, and the incidence of the each study revealing findings compatible with the final diagnosis was 3%, 15%, 51% and 26%, respectively. For detection of 2 PVC's in row, the sensitivity of TSE and TM was not different, but for picking up 3-4 PVC's in row and VT, TM was significantly superior to TSE. Among the VT patients, there were a few cases in whom neither TM nor Holter monitoring alone was sufficient to confirm the diagnosis. Children with symptoms suggestive of ventricular arrhythmias should be carefully evaluated with a combination of exercise tests and Holter monitoring.     

A genetic test which can be used to diagnose adult-type hypolactasia in children

Background/ AIMS: Adult-type hypolactasia (primary lactose malabsorption) affects most of world's human population and limits the use of fresh milk due to lactose intolerance. The diagnosis of adult-type hypolactasia has been difficult to establish because of unsatisfactory diagnostic methods. C/T(-13910) single nucleotide polymorphism residing 13910 base pairs from the 5' end of the lactase gene has been shown to be associated with lactase persistence. The aim of the study was to assess the applicability of the C/T(-13910) variant as a diagnostic test for adult-type hypolactasia during childhood. METHODS: Intestinal biopsies were obtained from 329 children and adolescents of African, Finnish, and other White origins aged 0.1-20 years undergoing upper gastrointestinal endoscopy because of abdominal complaints. The biopsies were assayed for lactase, sucrase, and maltase activity and genotyped for the C/T(-13910) variant using polymerase chain reaction minisequencing. RESULTS: The frequency of the C/C(-13910) genotype defining lactase non-persistence was well in agreement in this study with published figures for the prevalences of adult-type hypolactasia in Africans and Whites. The C/C(-13910) genotype was associated with very low lactase activity (<10 U/g protein) in the majority of children tested at 8 years of age and in every child older than 12 years of age giving a specificity of 100% and sensitivity of 93% for the genetic test. The decline of lactase activity was somewhat earlier in African compared with Finnish children with C/C(-13910) genotype (p<0.03). CONCLUSIONS: Genetic test of C/T(-13910) polymorphism can be used as a first stage screening test for adult-type hypolactasia.