Venous complications of pacemaker/ implantable cardioverter defibrillator (ICD) system implantation rarely cause immediate clinical problems. The challenge starts when patients come for system revision or upgrade. Numerous reports of venous complications such as stenosis, occlusions, and superior vena cava syndrome have been published. We reviewed current knowledge of these complications, management, and their impact on upgrade/revision procedures. One study has suggested that intravenous lead infection promotes local vein stenosis. Another found that the presence of a temporary wire before implantation is associated with an increased risk of stenosis. Although data for ICD leads is based only on three studies-it suggests that the rate of venous complications is very similar to that of pacing systems, and probably data from pacing leads can be extrapolated to ICD leads. Despite 40 years of experience with transcutaneous implanted intravenous pacing systems and dozens of studies, we were unable to identify clear risk factors (confirmed by independent studies) that lead to venous stenosis. Neither the hardware (lead size, number and material) nor the access site choice (cephalic cut down, subclavian or axillary puncture) appears to affect rate of venous complications. A few factors were proposed as predictors of severe venous stenosis/occlusion: presence of multiple pacemaker leads (compared to a single lead), use of hormone therapy, personal history of venous thrombosis, the presence of temporary wire before implantation, previous presence of a pacemaker (ICD as an upgrade) and the use of dual-coil leads. Anticoagulant therapy (for other reasons than pacemaker lead) seemed to have protective antithrombotic effect.

Introduction: Creation of radiofrequency lesions to isolate the pulmonary veins (PV) and ablate atrial fibrillation (AF) has been complicated by stenosis of the PVs. We tested a cryoballoon technology that can create electrical isolation of the PVs, with the hypothesis that cryoenergy will not result in PV stenosis. Methods and Results: Lesions were created in 9 dogs (weight 31–37 kg). Cryoenergy was applied to the PV‐left atrial (LA) interface. Data collected before and after ablation included PV orifice size, arrhythmia inducibility, electrogram activity, and pacing threshold in the PVs. Tissue examination was performed immediately after ablation in 3 dogs and after 3 months (4.8 ± 1.0) in 6 dogs. After ablation there was no localized P wave activity in the ablation zone and no LA‐PV conduction. Before ablation, the pacing threshold was 1.9 ± 1.1 mA in each PV. After ablation, the pacing threshold increased significantly to 7.2 ± 1.8 mA , or capture was not possible. Burst pacing did not induce any sustained arrhythmias. Most dogs had hemoptysis during the first 24 to 48 hours. Acute tissue examination revealed hemorrhagic injury of the atrial‐PV junction that extended into the lung parenchyma. After recovery, the lesions were circumferential and soft with no PV stenosis. Histologic examination revealed fibrous tissue with no PV‐LA interface thickening. Conclusion: This new cryoballoon technology effectively isolates the PVs from LA tissue. No PV stenosis was noted. Acute tissue hemorrhage and hemoptysis are short‐term complications of this procedure. After 3 months of recovery, cryoablated tissue exhibits no collagen or cartilage formation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 281‐286, March 2003)

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In this animal model of AF, LL are not only capable of terminating chronic AF, but also lead to self-termination of AF once the rapid pacing is stopped. Self-termination of AF after induction with rapid pacing was not observed in this AF model in the absence of LL. In the dogs with 6 months of AF, the presence of AF led to increased atrial susceptibility to AF induction by rapid pacing, even with LL and after 6 months of recovery. Incomplete LL allows induction of atrial tachycardia and AF.