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Background: Persistent left superior vena cava (PLSVC) is present in about 0.3–0.5% of the general population and in about 12% of patients with other abnormalities. This congenital anomaly is usually asymptomatic and does not cause any physiological problems. However, it may become a significant problem in multiple clinical situations. Various complications related to PLVSC are encountered in anesthesiological, nephrological, oncological and cardiological procedures. The presence of PLSVC is usually incidentally detected during placement of pacemaker (PM), implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy (CRT) leads. Technical difficulties during lead positioning (especially ventricular leads) are commonly known and often described in the literature. The purpose of the present study was to evaluate the specific methods used for implantation of increasingly complicated pacing systems, finding an optimal strategy in patients with PLSVC, especially with electrotherapy complications. Methods: We performed a single-center retrospective analysis of 11 patients (7 women and 4 men, mean age 60.4 ± 13 years) with PLSVC hospitalized in single Cardiology Department between 2000 and 2012. The clinical characteristic, indications for PM/ICD/CRT implantation, technique of implantation and complications were evaluated. Results: In PLSVC patients, different indications for pacing or resynchronization therapy were represented: sick sinus syndrome (SSS) in 4 patients, 3rd degree atrio-ventricular (AV) block in 4 patients, dilated cardiomyopathy with left bundle branch block in 2 patients, dilated cardiomyopathy and non-sustained ventricular tachycardia episodes in 1 patient. In patients no. 1, 3, 4 and 10 the complications necessitated the change of leads or type of pacing. Transvenous lead extraction was successfully performed in patient no. 1 and 10 with re-implantation of new leads via PLSVC in patient no. 1 and via right superior vena cava in patient no. 10. Patient no. 3 received an additional ventricular lead via PLSVC because of 2nd degree AV block (formerly atrial lead implanted due to SSS). In patient no. 4 with left atrial pacing (lead in coronary sinus), prosthetic mitral valve replacement was combined with epicardial ventricular lead placement. Patients no. 2 and 7 received a CRT device, without technical problems in patient no. 7, whereas in patient no. 2 due to difficulties with left ventricular lead positioning a hybrid approach to epicardial lead pacing was used. In patient no. 8 an ICD was implanted with difficulty in placing defibrillator lead. Patient no. 5 received 2 atrial leads via PLSVC with successful biatrial pacing; patient no. 6 with the necessity of DDD pacing had a (ventricular) lead for left atrial pacing and a typical right ventricular lead. In patients no. 9 and 11 typical DDD pacing was used with contralateral placement of the leads due to anatomical and technical differences. After 12 years of follow-up the survival is 90.9%. Late electrotherapy complications have developed only in patient no. 8 (problems with the defibrillator lead). Conclusions: Patients with PLSVC are a very heterogeneous group with different indications for pacing, therefore individualization of therapy is required. Technical complications connected with pacing of the right heart chambers are commonly known, hence transvenous left atrialor left ventricular lead implantation should be attempted. In case of difficulties in transvenous positioning of the lead, a hybrid or isolated cardiac surgery technique should be considered. Because of the increasing number of electrotherapy complications, these problems are also present in PLSVC patients. Transvenous lead extraction with re-implantation of a pacing system has not been reported yet. For this reason a thorough evaluation of the venous system is required in PLSVC patients before intervention.

We present 24-hour electrocardiography recording with observed DDD pacemaker pacing inhibition. Discussed Holter monitoring fi ndings are puzzling and may result from pacemaker sensing malfunction. However, its aetiology may be diverse. The detailed explanation of underlying mechanisms is provided and literature is reviewed.

Venous stenosis and occlusion (VSO) in the presence of endocardial leads constitute one of the complications of permanent cardiac pacing. At present there are no scientific reports on the influence of sex on the incidence of VSO.The aim of the study was to examine the influence of sex on the incidence of VSO in patients with earlier implanted endocardial leads in a single-center retrospective analysis.The material consists of 284 records of consecutive patients admitted to hospital to undergo electrotherapy procedures. In all patients a contrast venography for ipsilateral venous confluence was performed before the procedure. Patients were divided into two groups according to sex criterion. Groups were compared concerning following parameters: demographic characteristics, cardiac implantable electronic device (CIED) characteristics, comorbidities, CHA2DS2-VASc score, selected risk factors for VSO.Group I consist of 101 females, whereas group II consist of 183 males. Both groups did not differ significantly for age, number of implanted endocardial leads and lead dwell time. In the cohort males were with significantly greater burden of morbidity, reflected by the mean result of CHA2DS2-VASc (P=0.0098). In males there was significantly more often chronic heart failure (P0.0001), chronic obstructive pulmonary disease (P=0.0450) and tobacco use (P=0.0159). Males had more ICD implanted than females (P=0.0270). In the examine cohort 88 patients (31%) had VSO. There was no statistically significant difference in terms of presence of VSO between females and males (P=0.4685). The detailed analysis of the patients with VSO divided according to sex revealed higher morbidity in males.The equality of VSO incidence in groups of males and females along with the predominance of factors protecting against VSO in group of males support the assumption that female gender is a protective factor against the development of VSO, equally as known protective factors in males.

Background Currently, there are no studies in which a CHA 2 DS 2 -VASc score has been used to predict the risk of venous stenosis and occlusion (VSO) in patients after the implantation of a cardiac implantable electronic device (CIED). Methods The material consists of the records of 223 consecutive patients qualified for transvenous lead extraction, generator change and system revisions or upgrades in whom we assessed the utility of a CHA 2 DS 2 -VASc score in the prediction of VSO. The CHA 2 DS 2 -VASc score was calculated retrospectively based on the clinical data. The whole study population was divided into two groups, based on the presence (group I) or absence (group II) of VSO. Using the receiver operating characteristic (ROC) curve, we identified the optimal cut-off point for the CHA 2 DS 2 -VASc score that allowed the prediction of the absence of VSO. Results The venography was performed in 223 consecutive patients aged on average 68.2years (25.7–95.3), 77 females (34.5%). The presence of VSO was detected in 79 (35.4%) patients aged 68.3±14.1years, 30 female (40%) patients—group I. The level of the cut-off point for the CHA 2 DS 2 -VASc score that allowed the prediction of the absence of VSO was 3.0. Conclusion In the whole population the incidence of VSO amounted to 35.4%. The result of the CHA 2 DS 2 -VASc score was a destimulant of VSO occurrence and was characterized by moderate sensitivity (73.4%) and specificity (42.4%) in predicting the absence of VSO. The most significant factor, which prevented VSO development was diabetes.

BACKGROUND Venous stenosis and occlusion in the presence of endocardial leads constitute one of the complications of permanent cardiac pacing either by pacemaker, implantable cardioverter-defibrillator or cardiac resynchronization therapy. OBJECTIVES The aim of this study was to assess the incidence of stenosis and occlusions and determine the risk factors in patients with endocardial leads in a prospective single-center study. MATERIAL AND METHODS Two hundred eighty consecutive patients aged 25-95 years (male 68.8%) were included. A contrast venography examination of the ipsilateral access vein was performed. The whole study population was divided into 2 groups, based on the presence (group I) or absence (group II) of endocardial leads. RESULTS Venous stenosis/occlusion was identified in 51 patients (37.5%) in group I and in 3 patients (3.6%) in group II; p < 0.0001. The lead presence most highly correlated with venous complications (OR = 4.172; p < 0.001). In patients with endocardial leads divided into I A and I B according to venous patency diabetes mellitus was proved in multivariate analysis to be the only protective factor against the development of venous stenosis/occlusion (OR = 0.473; p = 0.010). CONCLUSIONS The presence of endocardial leads is a predisposing factor for venous stenosis/occlusion and increases the risk 4-fold. The venous lesions in the presence of endocardial leads are less frequent among patients with diabetes mellitus.

We report a case of a 73-year-old man, who was scheduled for elective dual chamber pacemaker implantation because of paroxysmal second-degree atrioventricular block. The pacemaker pocket was located in the left infraclavicular fossa. An active fixation ventricular lead was implanted into the right ventricular outflow tract (RVOT) through the left cephalic vein venesection, while another active fixation (Medtronic CapSure 5076MRI) atrial lead was located within the right atrial appendage using left subclavian vein puncture. During the procedure, due to anatomical inconveniences, several attempts at subclavian vein puncture were performed. Difficulties were also encountered during lead introduction through the superior vena cava. At the end of the procedure spontaneous dislocation of the atrial lead occurred. The young doctor repositioned this lead into the free wall of the right atrium (RA). Optimal sensing, pacing, and impedance parameters for both leads were obtained. The day after operation, the patient reported unspecific pain in the upper abdominal region and later strong, intermittent, stabbing pain in the lower chest. These symptoms intensified during inspiration and while lying on left side. The patient negated dyspnoea. On auscultation, normal vesicular breath sounds were heard. Neither pericardial fluid nor signs of RV perforation were found in transthoracic echocardiography (TTE). In the telemetric pacemaker assessment an increased pacing threshold of atrial lead was noticed (from < 0.5 V/0.4 ms during pacemaker implantation to 4.5 V/1 ms in unipolar pacing and 3 V/1 ms in bipolar pacing); no changes in sensing or impedance parameters were found. However, due to the lack of exact assessment of the atrial lead tip positioning, it was impossible to definitively exclude RA perforation (Figure 1 A). The device was reprogrammed to bipolar stimulation, leading to a decrease in reported complaints. Figure 1 A – Echocardiographic study showing parts of the atrial and ventricular lead and no signs of pericardial fluid excess. B – Fluoroscopy after first implantation. C – Fluoroscopy after spontaneous dislocation of atrial lead. D – ... On the next day a lack of atrial lead capture by threshold > 7.5 V/1.5 ms was recorded. Fluoroscopy revealed dislocation of the atrial lead, which was extracted subsequently. New lead was implanted through subclavian vein puncture into the right atrial appendage, obtaining good parameters (Figures 1 B, C). Several hours after reoperation the patient reported resting dyspnoea. Chest radiograph revealed large right-sided pneumothorax (Figure 1 D), which was cured by suction drainage. There are two probable causes of contralateral pneumothorax in the reported case. The first is pleura injury during Seldinger set introduction. Taking into account potential small mediastinal bleeding size, the venous system (especially the extrapericardial part of the superior vena cava) puncture could be done by guidewire (part of the Seldinger set). The second is right atrium, pericardium, and pleura perforation by a primary implanted atrial lead that dislocated or was extracted with subsequent pneumothorax. Because of the lack of fluid excess signs in the pericardial sac (during both physical and radiological examination), the first hypothesis seems more likely. However, contralateral pleural puncture during subclavian vein cannulation cannot be excluded. Treatment by chest tube placement and/or pacing lead reposition or extraction in case of heart perforation seem to provide satisfactory results in most patients with contralateral pneumothorax after pacemaker implantation [1–4]. In some cases a new atrial lead (also epicardial) was implanted and/or atrial or pericardial repair was performed [1, 3].

A 26-year-old patient had a VVI pacemaker implanted at the age of nine due to congenital complete atrio-ventricular block. Unipolar passive-fixation Pacessetter Membrane lead was implanted to the right ventricle apex (Fig. 1A). For the following 17 years, the patient felt well. She underwent an elective device replacement and gave birth naturally. Recently, the patient had transient ischaemic attacks twice with symptoms of syncope accompanied by transient motor aphasia, disorder of vision and right-side hypoesthesia. To give a final neurological diagnosis, magnetic resonance imaging (MRI) of the brain was demanded. Additionally, routine pacemaker follow-up showed an episode of miopotential oversensing. For these two reasons, the patient was qualified for transvenous lead extraction (TLE) with simultaneous implantation of DDD pro-MRI stimulation system. Using a mechanical Cook system, the old ventricular lead was removed and new active-fixation, bipolar Medtronic CapSureFixMRI was initially implanted to the right ventricular outflow tract. However, due to intraoperative dislocation of the lead, it was finally placed in the periapical region of the right ventricle. Atrial lead was implanted to the right atrial appendage. A Medtronic Ensura DR pacemaker was placed in the previous pocket (Fig. 1B). Beginning from the day following the procedure, the patient felt recurring pricking pain in the apical region radiating to the right shoulder. These symptoms aggravated significantly over the following few weeks and were the reason for the patient’s readmission. During the device follow-up, a high pacing threshold was noted (unipolar [UP]: 4.25 V/1 ms; bipolar [BP]: 2.0 V/1 ms). Sudden increase of the threshold value was recorded in the device’s stored data (from 1.3 V/0.4 ms to 2.5 V/0.4 ms in BP configuration). Variation of R wave sensing in BP measurements (from 5 mV to 14.5 mV) synchronised with heart cycle was also detected. Moreover, R wave sensing values were two times higher in BP than in UP measurements. Heart apex perforation by ventricular lead was confirmed in transthoracic echocardiography (TTE) (Fig. 2) and computed tomography (CT) (Fig. 3). Another urgent TLE of the ventricular lead with cardio-surgical back-up was performed. Subclavian vein obstruction revealed in venography before the procedure became a significant difficulty during the TLE procedure (Fig. 4). The perforating lead was removed using a yellow Byrd dilator from Cook Medical. A new lead was implanted to intraventricular septum through regained vessel lumen (Fig. 1C). The whole procedure was uneventful. TTE on the third day after the procedure showed an increased amount of fluid in the pericardial space (from 4 mm to 11 mm), which decreased over the following days. The patient was discharged in good condition. The probable cause of heart perforation was the displacement of lead tip into the channel remaining after removal of the 17-year-old lead.

Background: There is a considerable controversy regarding safety of transvenous lead extraction (TLE) in elderly patients due to their potentially worse general condition, more concomitant diseases, more difficult sedation or analgesia. Moreover, the present experience is not relevant. The aim of the study was the comparison of safety and feasibility of TLE in elderly and middle-aged patients. Methods: We have extracted an ingrown pacemaker (PM)/implantable cardioverter-defibrillator (ICD) leads from 1,060 adult patients (21–70 years) and 192 octogenarians (mean age 83.4 ± 3.1 years) using standard mechanical systems within the last 7 years. We compared effectiveness and complications of the TLE procedures in the two mentioned groups of patients. Results: There were more women in octogenarians referred for TLE (45.3% vs. 36.9%). In addition, more pocket infections (37.0% vs. 24.5%), less non-infective indications for PM (46.9% vs. 57.7%) and ICD systems (7.3% vs. 28.8%) TLE were observed in this group. Leads body dwelling time was similar (76.4 ± 56.8 vs. 83.5 ± 63.0) in both groups. Procedure efficacy (full radiological success 97.4% vs. 94.6%, partial radiological success 2.6% vs. 4.34%), safety measures (major complications 1.6% vs. 1.51%, minor complications 1.0% vs. 1.9%) were similar in both compared groups. Conclusions: Old age does not influence TLE effectiveness. Therefore, TLE can be safely and successfully performed in octogenarians.

Incorrect implantation of a ventricular pacemaker (PM) lead into the left ventricle (LV) is a known problem associated with permanent pacing. The optimal management of such cases identified late has not been clearly established. Generally acceptable management options are: open-chest cardiac surgery using cardio-pulmonary bypass, chronic anticoagulation and antiplatelet-drugs therapy. Rarely, the problem is solved by percutaneous LV lead extraction. We present a case of a patient with DDD pacing and ventricular lead implanted incorrectly into the LV apex region via an atrial septal defect eight years ago. Chronic PM pocket infection developed after replacement of the device. Both leads were extracted percutaneously, and the embolic protection system (Filter-Wire EZ, Boston Scientific) was used to reduce cerebral circulation embolism. The hardest connective tissue adhesions affecting the lead and the anodal ring were found in the LV. Less dense surrounding fibrous tissue around the lead was present at all levels of the venous course of the lead and in the right atrium. Very small fragments of apparently connective tissue remnants were found in cerebral circulation protection filters, and had been removed after the procedure. We conclude that old, permanently implanted LV leads may be extracted percutaneously, especially when there is an increased risk of cardiac surgery, or where the patient’s consent for surgical treatment is lacking. In order to perform the procedure it is recommended to establish a cerebral protection system and intraoperative transoesophageal echocardiography which are mandatory for successful lead removal.

A 65-year-old male patient underwent left-sided placement of implantable cardioverter-defibrillator. At three years after implantation he emerged complaining on left upper limb and left-sided neck edema. Left brachicephalic vein thrombosis due to device leads was recognized. The attending cardiologist referred the patient to university radiology department for venous angioplasty but the patient was admitted to cardiology department. Coronary angiography was performed due to suspicion of ischemic heart disease. However, it showed the presence of foreign body in cardiovascular system - completely intravascular round-tipped guide wire used in Seldinger technique for insertion of the endocardial lead abandoned in left subclavian vein and reaching to superior vena cava. Patient was transferred to third-degree reference lead extraction center. The procedure was performed under general anesthesia in hybrid operating room. Via femoral vein access we introduced Needle's Eye Snare and grasped the guide wire. Then, using polytetrafluoroethylene sheath the tissue adhesions were dissected and the complete guide wire was retrieved.

A man with non-ischemic cardiomyopathy, EF 22%, permanent AF and ICD was admitted for elective device replacement. The need for the optimization of the ventricular rate and avoidance of right ventricular pacing made it necessary to up-grade the existing pacing system using direct His bundle pacing and dual chamber ICD. This enabled the regularization of ventricular rate, avoiding the RV pacing and optimize the beta-blocker dose. The one month follow-up already showed reduction in left ventricle diameter, improvement in ejection fraction, NYHA class decrease to II. The His bundle pacing enabled the optimal treatment of the patient resulting in excellent clinical improvement.