Novel Doppler-guided subxyphoid approach to avoid coronary artery damage during left ventricular epicardial lead placement or ablation.

BACKGROUND: Subxyphoid active left ventricular epicardial (LVE) lead implants or VT ablation are attractive but remain a challenge due to concerns of coronary artery damage. We aimed to see if Doppler-guided positioning could permit safe LVE lead placement without coronary angiography. We evaluated the feasibility of a Doppler flow-guided subxyphoid epicardial screw-in lead fixation in a swine model. METHODS: Acute subxyphoid access to the pericardial space was performed in an anesthetized swine model using a deflectable sheath and a modified needle-derived Doppler flow meter. The audio signal and visual display from the Doppler flow meter were recorded. Coronary angiography was performed to verify the catheter location. A SelectSecure Model 3830 lead (Medtronic) was used to assess pacing in the procedure. RESULTS: In both of two swine, the deflectable catheter was inserted into pericardial space via subxyphoid access. The tip of the deflectable catheter with the Doppler was directed to several locations, from quiet (no nearby coronary artery expected) to typical rhythmic pulsatile sound locations which were maximal when superimposed on a coronary artery. Repeated coronary angiograms confirmed the expected findings. A 3830 active lead was fixed into a quiet location for LVE pacing, and confirmed by angiography as distant from a coronary artery. CONCLUSIONS: Doppler-guided subxyphoid epicardial screw-in lead placement is feasible once the catheter tip is directed and stabilized in a desired LVE location. This obviates the need for repeated (or any) coronary angiography. The Doppler-guided subxyphoid epicardial procedure may also be applicable for epicardial ventricular arrhythmia ablation procedures.

Effect of Steroid Elution on Electrical Performance and Tissue Responses in Quadripolar Left Ventricular Cardiac Vein Leads.

INTRODUCTION: The use of steroid elution (SE) electrode in a cardiac pacing lead is known to suppress myocardial inflammation to lower pacing thresholds (PTs). SE has been widely utilized on the distal electrode of left ventricular cardiac vein (LVCV) leads used in cardiac resynchronization therapy (CRT). However, no paired comparison in effect of SE has been studied in proximal electrodes of quadripolar LVCV leads. METHODS: We evaluated electrical performance and tissue responses of quadripolar LVCV lead electrodes with and without SE in two canine studies with a total of 14 canines. Extended bipolar PT and pacing impedance of the LVCV electrodes to right ventricle coil were collected via an implantable CRT device/programmer or a percutaneous threshold analyzer/pacing analyzer at weeks 0, 1, 2, 4, 6, 8, and 12. Gross and histopathological examinations of the canines were performed at the end of the studies. RESULTS: Our preclinical studies showed that SE had significant effects on the long-term pacing performance of quadripolar LVCV leads. The SE tip and ring electrodes reduced postimplant PT peak and chronic PT, P = 0.038. Histological examination of the perilead tissue capsules at 12 weeks showed a reduced thickness for the location of SE electrodes. CONCLUSION: SE electrodes in quadripolar LVCV leads lower the PTs, and therefore may potentially reduce long-term current drain of CRT systems, thus improving the device longevity. These preclinical data serve as rationale to include SE on proximal electrodes for the Attain Performa LVCV leads and future quadripolar LVCV leads development.

Radiographic predictors of lead conductor fracture.

BACKGROUND: Lead fracture is a limiting factor in high voltage lead durability. Fractures noted with the Medtronic Fidelis leads provide an opportunity to examine factors captured on implant chest x-ray that correlate with risk for lead conductor fracture. We evaluated contributory factors in a large population of fractures. METHODS AND RESULTS: We conducted a retrospective case-control study at 8 Canadian centers that routinely capture anterior posterior and lateral chest x-rays within 2 weeks of implant. Cases were patients that experienced confirmed Medtronic Fidelis 6949 lead fracture based on standard definitions, matched one-to-one to controls for date of implant, sex, and age with normally functioning Fidelis leads from the same center. Select chart data and x-rays were collected for all patients. Radiographic measurements by ≥2 individuals per case/control were blinded to patient status. The data were analyzed using a time to failure multivariable Cox proportional hazards model with stratification for each matched pair. X-ray pairs from 111 fracture patients were compared with 111 controls (age 61.5±12.8 years, 75% male, 221 model 6949 leads). Six parameters included in the statistical analysis were significantly associated with risk of fracture, including slack/tortuosity measures, pulse generator and superior vena cava coil location, and angle of lead exit from the pocket. CONCLUSIONS: Pocket, intravascular and intracardiac lead characteristics on x-ray correlate with risk of lead conductor fracture. These observations may be useful to direct implant technique to optimize lead durability. Validation in larger populations and other lead models may inform the application of these results.

The electrode-tissue interface: the revolutionary role of steroid-elution.

The electrode-tissue interface is that area lying between the cathode of a low-voltage implantable pacemaker or cardioverter-defibrillator (ICD) lead and the endocardium or epi-myocardium of the cardiac chamber being paced. The electrical stimulus that is delivered to this interface is responsible for myocyte depolarization with consequent cardiac contraction. The process by which this occurs is reasonably well understood and any explanation requires a basic understanding of the physics and cellular electrophysiology of pacing. The effective and efficient delivery of electrical energy to the myocardium via the lead is dependent on many factors to be discussed in this review. However, despite numerous evolutionary changes occurring in the cathode's material, design, and surface configuration, it was not until the incorporation of steroid-elution to the electrode-tissue interface that reliable and significantly low stimulation threshold cardiac pacing became possible.

Effect of insulation material in aging pacing leads: comparison of impedance and other electricals: time-dependent pacemaker insulation changes.

BACKGROUND: There has been concern over declining bipolar (BP) impedance (Z) in aging polyurethane (PU) cardiac pacing leads. Subsequently, a prospective study was conducted comparing BP Z, threshold (Th), and R-wave sensing amplitude of 55D PU-insulated (Model 4024, Medtronic, Inc., Minneapolis, MN, USA) and silicone-insulated (Model 5024) leads. METHODS: This study was initiated by The Iowa Heart Center. Patients with Model 4024 (N = 162) or 5024 (N = 120) pacing leads with at least 6 years implant time were enrolled and followed for an additional 5 years. RESULTS: There was a significant drop in the mean BP Z for the Model 4024 population, between enrollment (6 years) and the final endpoint (11 years), which was in contrast to the Model 5024 which did not see a significant drop in its mean BP Z for this same period. The trend difference seen in the means between the two models was statistically significant (P < 0.0001). In addition, a statistically significant relationship was found between dropping BP Z and rising Th (P < 0.0001). The analysis showed that if BP Z dropped below 200 ohms, the probability of having a >3X increase over baseline, in Th at 2.5 V, increases from approximately 3-7% to as high as 30%. CONCLUSIONS: A significant drop in BP Z observed in the PU-insulated Model 4024 lead was not present in the silicone-insulated Model 5024 lead. The statistically significant relationship between dropping BP Z and rising Th helps to understand how to better manage patients with aging leads.

The salty dog: serum sodium and potassium effects on modern pacing electrodes.

BACKGROUND: This study was conducted to characterize the behavior of chronic modern endocardial electrodes with capacitively coupled constant voltage pulse generators in canines. METHODS: Five animals were studied with chronic paired unipolar microporous platinum, and porous steroid-eluting electrodes in the ventricle. Screw-in and passive fixation electrodes were also implanted in the atrium. IV infusions of 500-800 mL of 50 meq KCl in 500 mL Ringer's solution, and 3% NaCl were given over periods of 120 and 80 minutes, respectively, during separate anesthetized monitors. RESULTS: Mean maximum Na+ and K+ achieved was 158 and 8.3 meq/L, respectively. During KCl infusion, ventricular threshold, current, and energy decreased. In the atrium, half the leads went to exit block at approximately 7.0 meq/L K+. Others continued to perform acceptably. The atrial electrogram decreased 70% with no change in the ventricular signal. No change in impedance occurred. During NaCl infusion, no changes in atrial or ventricular threshold occurred while current increased 21%-32%. This resulted in a 40%-55% increase in energy due to a 20% decrease in impedance. The atrial electrogram decreased 32%-36% while the ventricular amplitude decreased 25%. Slew rate decreased 19%-27%. Control studies for effects of heart rate, fluid volume, and anesthesia duration did not cause any changes. CONCLUSION: These data support the conclusion that threshold is a voltage mediated response. Thus, voltage thresholds, not energy, current or pulse duration is the most relevant parameter for safety margin determination. Atrial parameters should be followed during electrolyte imbalances. Correlation in humans is needed.

In vivo biostability of polyether polyurethanes with fluoropolymer and polyethylene oxide surface modifying endgroups; resistance to metal ion oxidation.

Polyether polyurethanes are subject to oxidation catalyzed by, and through direct (redox) reaction with transition metal ions (metal ion oxidation, MIO). The source of the ions is corrosion of metallic parts within an implanted device. A Shore 80A polyether polyurethane was modified with fluoropolymer (E80AF) or polyethylene oxide (E80AP) surface modifying end groups (SME). The SME migrates to the surface to form a covalently bonded monolayer, while maintaining the bulk properties of the polyurethane. In vitro tests in H(2)O(2) solution indicated that both SME's accelerated MIO. Tubing samples containing cobalt mandrels were implanted in the subcutis of rabbits for up to 2 years. In vivo, E80AF significantly slowed the rate of visible degradation, but did not prevent MIO. E80AP had virtually identical visual performance to the unmodified control in vivo. Infrared spectroscopy and molecular weight correlated well with visual appearance. When cracks were seen, polyether soft segment oxidation was occurring. Both E80AP and the control developed severe loss of molecular weight in vivo. The changes were much less severe for E80AF. Thus, contrary to in vitro test results, the PEO SME had no effect at all on MIO resistance, while the fluoropolymer SME produced a significant improvement in biostability.

In vivo biostability of polyether polyurethanes with fluoropolymer surface modifying endgroups: resistance to biologic oxidation and stress cracking.

A series of Shore 80A polyether polyurethanes were synthesized with from 0 to 6% fluoropolymer surface modifying endgroups (SME) to provide the bulk properties of the polyurethane with the surface properties of the fluoropolymer. It was theorized that the fluoropolymer would migrate to the surface, forming a monolayer barrier to the oxidants and crack-driving agents released by macrophages and foreign body giant cells in vivo. In a 12-week biostability screening test, samples strained to 400% elongation appeared to be highly stable. In a longer-term study, the fluoropolymer SME significantly delayed, but did not completely prevent the onset of microcracking and the development of environmental stress cracking in strained samples. Even so, the 4 and 6% SME polymers explanted at 2 years performed significantly better than the control. FTIR analysis did not correlate with SME concentration, but increased hydrogen-bonding index and loss of aliphatic ether (autoxidation) did correlate with the visual appearance and density of microcracks. Significant molecular weight reductions were seen for the SME-free control, but were small (within instrumental error) for the polymers with SME. The use of fluoropolymer as a SME does appear to be warranted as a means to improve polyether polyurethane biostability.

In vivo biostability of shore 55D polyether polyurethanes with and without fluoropolymer surface modifying endgroups.

Polyether polyurethanes are subject to autooxidation and environmental stress cracking (ESC) because of interactions with lysosomal oxygen-free radicals. Oxidation can also be catalyzed by and caused by direct (redox) reaction with transition metal ions (metal ion oxidation, MIO). The source of the ions is corrosion of metallic parts within an implanted device. A previous study on a Shore 80A polyether polyurethane modified with fluoropolymer surface modifying end groups demonstrated improved biostability over unmodified controls. We predicted that this could be extrapolated to the inherently more biostable Shore 55D version (E55DF). While it is difficult to demonstrate significant biodegradation in the harder polymers within a reasonable time frame, we did see excellent biologic autooxidation and ESC resistance for both E55DF and its unmodified Shore 55D (P55D) control. E55DF was slightly, but significantly more resistant to MIO than P55D. This was particularly evident in molecular weight distributions with P55D exhibiting a large decrease in number average molecular weight compared to no change for E55DF. Both were markedly superior to the softer Shore 80A control. It does appear that one can extrapolate accelerated in vivo biostability results with the softer polymers to their harder analogues.

In vivo biostability of polysiloxane polyether polyurethanes: resistance to biologic oxidation and stress cracking.

Polyether polyurethanes are extremely interesting for use in implantable devices. They are, however, susceptible to autoxidative degradation and stress cracking. One approach to improving biostability is to replace some of the polyether with polysiloxane. Shore 80A polyether polyurethanes with 20% (PS-20) and 35% (PS-35) polysiloxane were strained to 400% elongation and implanted in rabbits. Twelve weeks implant showed that both were significantly more biostable than their polysiloxane-free controls. After 18 months implant, PS-20 developed some localized tensile fractures. PS-35 showed no sign of visual damage. Infrared surface analysis does not allow direct evaluation of autoxidation because the Si--O--Si stretch peaks mask the polyether bands. Secondary indicators suggest possible very slight autoxidation of both PS-20 and PS-35 surfaces, but not enough to develop cracks. The polysiloxane-free controls did show substantial infrared evidence of autoxidation. Molecular weights of long-term PS-20 and PS-35 explants were negligibly lower. In comparison, the polysiloxane-free control suffered 35% molecular weight loss. Positive and negative controls performed as expected. PS-20 is recommended for devices that do not sustain high fixed loads. PS-35 is dramatically more biostable than its unmodified polyether analogues and is recommended for use in chronically implantable devices.

In vivo biostability of polysiloxane polyether polyurethanes: resistance to metal ion oxidation.

Polyether polyurethanes are subject to oxidation catalyzed by and through direct (redox) reaction with transition metal ions (cobalt), released by corrosion of metallic parts in an implanted device. Replacing part of the polyether with polysiloxane appears to reduce susceptibility to metal ion oxidation (MIO). In vitro studies indicated that polyurethanes containing 20-35% polysiloxane (PS-20 and PS-35) are about optimum. We implanted tubing samples containing cobalt mandrels in the subcutis of rabbits for periods up to 2 years. After 2 years, only traces of microscopic cracks were seen on half the PS-35 samples, PS-20 significantly delayed MIO, while the polysiloxane-free control was very severely degraded. Infrared spectroscopy established that polyether soft segment oxidation was occurring in PS-20. We could not directly evaluate oxidation in PS-35 because siloxane bands mask the aliphatic ether. Indirect FTIR evidence suggests that there is very slight polyether oxidation that develops early, and then seems to stabilize. The molecular weight of degraded PS-20 decreased. That of microcracked PS-35 decreased negligibly while that of undamaged PS-35 increased slightly after 2-year in vivo. The polysiloxane-free control was profoundly degraded. PS-20 has much improved MIO resistance, while that for PS-35 is highly MIO resistant compared with its polysiloxane-free control.

In vivo biostability of polyether polyurethanes with polyethylene oxide surface-modifying end groups; resistance to biologic oxidation and stress cracking.

Polyethylene oxide (PEO) on polymer surfaces has been reported to reduce cellular adhesion, a very desirable property for cardiac pacing leads. A Shore 80A polyether polyurethane with up to 6% PEO surface-modifying end groups (SME) was evaluated for its chronic in vivo biostability. In a short-term (12 week) screening test, strained samples appeared to develop the same surface oxidation as unmodified polymer, but did not produce visible cracking > or =500x, prompting a longer-term study. By the time the longer-term study was initiated, most of the PEO SME had disappeared from the starting material's surface. After 1 year in vivo, surface oxidation, shallow surface cracking, and environmental stress cracking (ESC) developed on highly strained samples to the point of failure, so that there was no significant difference between the SME polymer and its control (the same polymer without SME). No further change was seen for up to 2 years of implantation. Unstrained PEO SME polymer developed shallow surface cracking, but no ESC up to 2 years of implantation. Thus, PEO SME slightly delayed, but did not stop biodegradation, and under unstrained conditions, has no adverse effect on biostability.