Europace Advance Access originally published online on April 27, 2007
Europace 2007 9(8):669-671; doi:10.1093/europace/eum036
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PACING AND LEAD EXTRACTION
Direct intracardiac placement of an automatic implantable cardioverter defibrillator coil lead in a small child
1 4C3 WMC Health Sciences Centre, Division of Pediatric Cardiology, Department of Pediatrics and Stollery Children's Hospital, University of Alberta, Edmonton, Alberta, Canada T6G 2B7; 2 Department of Surgery, University of Alberta, Edmonton, Alberta, Canada; 3 Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
Manuscript submitted 3 January 2007. Accepted after revision 13 February 2007.
* Corresponding author. Tel: +1 780-407-3963; fax: +1 780-407-3954. E-mail address: michalkantoch{at}cha.ab.ca
| Abstract |
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A 3.5-year-old child with hypertrophic obstructive cardiomyopathy and recurrent syncope underwent surgical left-ventricular outflow tract myectomy and implantation of a single-chamber automatic cardioverter defibrillator. A single-coil active fixation lead was introduced via a purse-string suture in the right atrial appendage and the lead tip positioned and fixed in the right-ventricular apex under direct visualization via a small right atriotomy incision. Described configuration may be considered in small children undergoing intracardiac surgery at the time of defibrillator implantation.
Key Words: Child, Automatic implantable cardioverter defibrillator, Hypertrophic cardiomyopathy
| Introduction |
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We present a method of implanting an automatic implantable cardioverter defibrillator (AICD) in a small child who underwent surgical myectomy for hypertrophic obstructive cardiomyopathy (HOCM).
| Clinical summary |
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A term female infant was referred for evaluation of a heart murmur at 8 weeks of age. Echocardiography demonstrated HOCM with a peak systolic gradient of 33 mmHg and systolic anterior motion of the anterior mitral leaflet. At the age of 3.5 years, the child presented with four syncopal spells, and an echocardiogram showed the left-ventricular outflow tract gradient of 70 mmHg despite beta-blockade. Ambulatory Holter monitors showed sinus rhythm and single monomorphic premature ventricular beats. There was no family history of hypertrophic cardiomyopathy, syncope, seizures or sudden unexpected death. A healthy older sister presented with syncopal breath-holding spells as a toddler.
At the time of surgical myectomy and AICD implantation, the child's weight was 10.8 kg and height 89 cm. During cardioplegic arrest and following trans-aortic myectomy, a single-coil active fixation lead (Medtronic 6931, Medtronic Inc., Minneapolis, MN, USA) was introduced via a purse-string suture in the right atrial appendage and the active fixation lead tip positioned in the right-ventricular apex under direct visualization via a small right atriotomy incision. The lead was also secured to the atrial septum just above the limbus of the fossa ovalis with a 5–0 polypropylene suture, leaving a loose loop of excess lead in the right atrium to allow for future growth. The lead was then connected to a Medtronic EnTrust D154VRC device which was placed in a pocket created within the posterior rectus sheath with extension behind the left costal margin (Figure 1).
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Testing of the device showed the ventricular lead R-wave at 15.1 mV, impedance at 637 ohm, and the pacing threshold of 0.8 V at 0.5 ms. It was not possible to induce ventricular fibrillation with 0.5–1.0 J shocks on the T-wave or with 50 Hz alternating current, and the defibrillation threshold (DFT) could not be tested in the operating room. On the following day, ventricular fibrillation was induced with a 0.5 J shock on the T-wave during infusion of dopamine 10 mcg/kg/min and only after an intravenous bolus of 0.02 mg of epinephrine. Sinus rhythm was restored with a single 7 J defibrillation shock by the AICD. The DFT was not tested. The post-operative course was uneventful, and the child was discharged home on the seventh post-operative day.
During 18 months of follow-up, the child presented with frequent single premature ventricular contractions documented with repeat Holter monitors and maximum five beat bursts of polymorphic ventricular tachycardia recorded by the device (CL 220–260 ms). There was no recurrent syncope. Ventricular electrode function remained stable; at the time of routine AICD checks, the R-wave amplitude ranged between 7.2 and 13.1 mV (most recent 12.8 mV), the lead impedance varied between 424 and 512 ohm (most recent 488 ohm), and the pacing threshold was 0.4–0.6 ms at 1 V. The child has been treated with sotalol 5 mg/kg/day.
At 5 years of age (18 months after AICD implantation, weight 13.8 kg), the child underwent programmed ventricular stimulation through the device and under light general anesthesia; no ventricular arrhythmia could be induced. Ventricular fibrillation was induced with a 0.6 J T-wave shock and terminated with a 7 J discharge from the AICD. The DFT was not tested. The device sensed 59 out of 64 ventricular beats at measured CL 120–240 ms (sensitivity set at 1.2 mV).
An echocardiogram recorded 16 months after surgery showed normal right-ventricular function, trivial tricuspid valve regurgitation, and 1.5 m/s blood flow velocity in the left-ventricular outflow tract.
| Discussion |
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Implantation of relatively large devices and coil electrodes in infants and small children requires creative system configurations.1
Recently, two adolescent patients with complex congenital heart defects were reported, in whom right-ventricular active fixation coils were placed through right atriotomy.8
In one patient, one lead was inserted through a small purse-string incision in the right atrial appendage and another defibrillation coil was placed in the pericardium. Both leads were connected to an AICD generator implanted in the left upper quadrant of the abdomen. In the second patient, a transatrial coil lead and an atrial pacing lead were implanted through an incision at the junction between the superior vena cava and the right atrium and connected to a generator implanted in a left pre-pectoral pocket. Apparently, the DFT in both patients was <20 J. The transatrial coil lead function remained stable during 42- and-35 month follow-up.
The decision to implant an AICD in our patient was based on the clinical presentation of syncopal attacks, which was not typical for breath-holding spells and did not permit to rule out their arrhythmic aetiology. Parents requested implantation of an AICD being aware of class II indications and potential complications. We chose the transatrial lead placement for known good long-term performance of intracardiac electrodes in regard to pacing, sensing, and DFTs. Indeed, over 18-month follow-up, the coil lead presented with a stable function in regard to the R-wave amplitude, lead impedance, and the pacing threshold. A small defibrillation vector between the lead in the right ventricle and the AICD generator across the right-ventricular free wall is of concern: still the heart was successfully defibrillated with a 0.5 J/kg biphasic discharge, a year and a half post-implantation. Apparently, configurations consisting of dual-coil transvenous electrodes and pulse generators implanted in the abdominal wall maintain stable chronic DFTs in adult patients.9
A single-coil system in a growing child may require repeat DFT testing, especially in view of reported increasing thresholds in children.10
In conclusion, device configuration described in this report may be considered in small children undergoing intracardiac surgery at the time of AICD implantation. Successful defibrillation at low energy was possible despite close proximity of the right-ventricular single-coil electrode to the defibrillator implanted in the upper abdominal wall. Follow-up DFT testing may be required.
| References |
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