Use of a Permanent Pacemaker Left Ventricle Lead Implant

Review of Literature The ventricular lead for a single or dual permanent pacemaker is routinely positioned in the right ventricular apex (RVA) or right ventricular septum. Maneuvering the lead into the pulmonary artery via the right ventricular outflow tract (RVOT) confirms access to the right ventricle (RV). Gentle retraction of the lead causes it to track through the tricuspid valve and into the RV. With additional effort, the tip of the lead is eventually placed in the proper position in the ventricular apex. Simple observation of the EKG during ventricular pacing can provide confirmation of a properly placed ventricular lead. An article published in 2000 by Nakazato et al. reported that a patient, having received an epicardial lead at the age of 5 and a battery replacement at the age of 11 and 16, was to have another battery replaced at the age of 24. This time the implanted device was planned to be an endocardial system rather than her existing epicardial. The authors state that during the procedure we were unaware that the QRS configuration had not changed from RBBB pattern to left bundle branch block (LBBB) pattern.³ When the patient returned in three months for a routine evaluation, the EKG displayed a RBBB. A chest x-ray image revealed the ventricular lead was positioned in the LV. An article in 2002 indicated a similar situation during an implant procedure at another institution. The operating team did not continuously monitor the ECG pattern of pacing.⁴ After the procedure was completed, the patient was transported to a regular ward. While being observed in the ward, the patient's paced heart rhythm was documented with a RBBB tracing. After documenting the lead's position with a chest x-ray and TEE, the patient was transported back to the lab to reposition the lead and implant it correctly. Ciolli et al. published a medical review article in 2003 that stated only 27 patients² had a device implant with the right ventricular lead inadvertently positioned in the LV. Malposition of a pacemaker lead into the LV might be attributed to several reasons, such as an atrial septal defect, patent foramen ovale or a sinus venous defect in the high right atrium.^{3, 5} Other reasons may be due to a perforation of the interventricular septum, right ventricular apex, or subclavian artery. Paravolidakis et al. reported a case in which the ventricular lead was inadvertently placed through the left subclavian artery, across the aortic valve into the left ventricle.⁶ Complications due to permanent pacing from the LV include transient ischemic attacks, cerebral strokes, and vascular complications⁵ such as thrombosis. Despite thousands of implants, acute complications are relatively rare.¹ There are reports of patients who did not receive anti-coagulation therapy but remained healthy. For instance, Ciolli et al.² reported a patient with a malpositioned left ventricle lead implant who did not receive anti-coagulation therapy for eight years. Fortunately, there were no health problems or complications reported. If a ventricular lead is suspected of being positioned in the LV or coronary sinus (CS), a 12-lead EKG documenting a right bundle branch block^2,5,7,8 during ventricular pacing will be the most common finding. A routine AP chest x-ray and, more importantly, a lateral chest x-ray will further confirm the position of the ventricular lead. A 2-D Echocardiography^2,9 is a very useful tool to document the lead's position. A TEE^4,9,10 is even more helpful by determining the exact location of the lead as well as visualizing any thrombus attached to it. Case Report In December of 2005, a 75-year-old female was admitted to Oklahoma Heart Hospital (OHH) for an elective pulse generator change and lead replacement as indicated. Her medical history included sick sinus syndrome, coronary artery disease and frequent episodes of atrial fibrillation with a rapid ventricular response. Unfortunately, medications were not able to control her rapid ventricular rate. According to her history, she had a dual chamber pacemaker implanted in 2000 that continued to sense, pace and inhibit appropriately. In 2005, during her initial clinical visit, a routine 12-lead EKG tracing demonstrated a RBBB rhythm while being paced. An AP and lateral chest x-ray confirmed that the tip of the ventricular lead was located within the LV and against the lateral wall. On the morning of her procedure, the patient was assessed and prepped by the outpatient nursing staff. After being transported to the EP Lab and assisted onto the procedure table by the EP staff, the patient was attached to supplemental oxygen, a blood pressure cuff, an oxygen saturation finger probe and a five-point EKG for monitoring. A staff EP nurse was assigned to continually monitor the patient's conscious sedation and vital signs during the procedure. The patient's left subclavian area was prepped and draped according to standard sterile procedure. Prior to starting the procedure, preliminary fluoro images were recorded to document the position of the pulse generator and leads. Figures 1 and 2 display the position of the existing pacemaker leads. After a subcutaneous infiltration with 2% lidocaine was completed, a #10 blade scalpel was used to open an area of the tissue. The underlying tissue was carefully cut away to expose the pulse generator. After it was freed from the existing pocket, the surrounding tissue was meticulously dissected away from both leads. When the leads were completely dissected from the tissue and identified, they were disconnected from the pulse generator and tested per standard protocol. The left subclavian vein was accessed with a hollow needle by using the Seldinger technique. A standard pacemaker guidewire was inserted through the needle. After removing the needle, a peel-away sheath was passed over the wire. No attempt was made to remove or revise the position of the left ventricle pacing lead because of the potential risk of complications. The most significant complications that were of concern included damaging the mitral valve apparatus, perforation or thrombus. A new ventricular pacemaker lead was successfully inserted into the RVA and tested to verify a LBBB configuration. After securing the new ventricular lead, a Y-adaptor was connected to both ventricular leads and to the pulse generator in order to pace the ventricles simultaneously. The existing atrial lead was then connected to the pulse generator. Using this configuration, the patient will have the benefit of a poor man's biventricular pacemaker. Figures 3 and 4 display the atrial and both ventricular leads. This adaptation of the ventricular leads for biventricular pacing was perceived to be an acceptable alternative. After returning the pulse generator into the patient's left subclavian pacemaker pocket, the site was closed with suture. After the skin closure was complete, the left subclavian incision site was secured per standard sterile protocol and the patient's left arm was immobilized in an arm sling. The patient tolerated the procedure well, and was awake and alert at the completion of the implant. She was moved to her bed and transported from the EP Lab to an in-house room for an overnight stay. Later in the day while assessing her progress, the importance of appropriate anticoagulation therapy was again discussed with her, as well as the necessity to be closely monitored. No complications were reported or assessed during her stay. The next day she was dismissed from the hospital. Discussion Using the LV for biventricular pacing has previously been reported or suggested. Ciolli et al. reported in their 2003 article that a patent foramen ovale could be considered as a valid route² to implant a left ventricular lead when the attempt to use the CS was unsuccessful. Ciolli et al. called for a study to determine its feasibility and safety.² The report mentioned that a transseptal catheterization technique has been proposed as a possible alternative to implant a left ventricular lead, but the technique requires additional specific competence. Concerns of this technique include the possibility of thrombus on the leads, the question about lead extraction if required in the future, or lead reposition in case of dislodgement. Dr. Stephen Vlay reported in his 2004 article that another alternative route to consider when unable to use the CS for biventricular pacing is the right ventricular outflow tract (RVOT). In his practice, 22 patients over a 20-month period¹¹ receiving this method of pacing improved initially in terms of NYHA functional Class.¹¹ Improvement was evident in the patients' decreased cyanosis and dyspnea and increased exercise tolerance. Dr. Vlay stated that when muscle scarring is a concern, the myocardium in the proximal septum of the RVOT has a blood supply that is usually preserved, allowing the tissue to remain viable. He stated that when the implanted ventricular lead was tested, the tissue provided good sensing and low thresholds. The most recent study concerning biventricular pacing is the Post AV Nodal Ablation Evaluation (PAVE) trial.¹² This trial compared RV-only pacing to biventricular pacing of the RVA and CS after an AV node ablation. In the PAVE study, all devices were implanted on a separate day prior to the AV node ablation. The conclusion of this trial was that patients with atrial fibrillation had a significant improvement with biventricular pacing as compared to RV-only pacing. The improvements were recorded in the ejection fraction and the timed hallway walk test. It was found that patients with impaired systolic function or symptomatic heart failure¹² benefited the most. Conclusion Even though the method of biventricular pacing selected for our OHH patient was not included in the PAVE trial, it is hoped that she will begin to receive an immediate and long-term benefit. She is scheduled to return to our EP Lab in the near future for an AV node ablation, which should ensure biventricular pacing. During subsequent clinical visits, she will be assessed for PAVE trial improvements.