Anna Rydlewska

Heart perforation in patients with permanent cardiac pacing – pilot personal observations

Introduction Heart perforation is a rare complication of pacemaker (PM)/implantable cardioverter-defibrillator (ICD) implantation. Material and methods In our clinic in 2005–2010, 6 patients with heart perforation were hospitalized (3 women, 3 men), mean age 58.6 ±20.8 years (17 to 73 years). The indication to PM/ICD implantation was tachy-brady syndrome in 3 cases, second-degree atrioventricular block, advanced with losses of consciousness, vaso-vagal syndrome type II B with asystole lasting 12 s and recurrent non-sustained ventricular tachycardia in 1 patient. We analyzed patients medical records, X-rays, echocardiography, computed tomography (CT) and procedure protocols. Results The incidence of heart perforation was 0.09%. Symptoms developed 4 to 990 days (mean 186.3 ±394.3) after PM/ICD implantation. The perforation site was found in the right atrial wall in 1 cases and the right ventricular wall in 6 cases. The TTE revealed an accumulation of fluid in the pericardium over 10 mm behind the posterior wall of the left ventricle in all patients. The CT scan confirmed perforation of the heart chambers (atrium and in 6 cases ventricle). In 5 cases the whole device was removed by direct traction or percutaneous lead extraction with pericardiocentesis when necessary (pericardium drainage in 3 cases) while in 1 case cardiac surgery was needed. Conclusions The perforating lead may be removed by direct traction in the operating room with cardiosurgical, anesthesiological and echocardiographical backup. In case of the lead perforation outside the pericardial sac or its atypical location, cardiac surgery is a safer method. The most important diagnostic method remains computed tomography.

Venous Stenosis and Occlusion in the Presence of Endocardial Leads.

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.

Venous stenosis and occlusion in the presence of endocardial leads in patients referred for transvenous lead extraction

Objective The aim of this study was to evaluate the incidence of venous stenosis and occlusion (VSO) in patients referred for transvenous lead extraction (TLE) with regard to the indications for this treatment and to analyse the influence of VSO on efficacy, complications and technical challenges of TLE procedures. Methods The material consists of 133 consecutive TLE procedure records. The contrast venography examination of the ipsilateral access vein was performed prior to the operation. The whole study population was divided into two subgroups, based on the presence (subgroup I) or absence (subgroup II) of VSO. Results Phlebography was performed in 133 patients with age ranging from 25.7 to 86.1 years, 44 female (33.1%). The VSO was confirmed in 48 (36.1%) patients – subgroup I. Most of the patients were referred to TLE due to non-infectious reasons (100 pts—75.2%). The absence of VSO was observed substantially more frequently in patients with diabetes (P = 0.02). Procedural success rate reached 93.3% in subgroup I and 98.8% in subgroup II (P = 0.1). There was no significant difference in the use of advanced tools and alternative access sites. Conclusion The presence of VSO can be expected in one third of patients referred for lead extraction. There is no association between indication for TLE (infected or noninfected lead extraction) and the incidence of VSO. Diabetes proved to have a protective effect on venous patency in the previously mentioned group. VSO does not influence the effectiveness, safety, and the use of additional tools during TLE procedures.

The utility of a CHA2DS2-VASc score in predicting the presence of significant stenosis and occlusion of veins with indwelling endocardial leads.

BACKGROUND Currently, there are no studies in which a CHA2DS2-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 CHA2DS2-VASc score in the prediction of VSO. The CHA2DS2-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 CHA2DS2-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 CHA2DS2-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 CHA2DS2-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.

Effectiveness of atrial versus atrioventricular pacing for sick sinus syndrome during long-term follow-up

BACKGROUND According to the current guidelines, atrioventricular (DDD) pacing is superior to atrial pacing (AAI) in the treatment of sick sinus syndrome (SSS). AIM To compare outcomes of AAI and DDD pacing in patients with SSS during long-term follow-up. METHODS We studied 809 patients, including 86 patients in the AAI group (57 women, mean age 65 ± 15 years) and 723 patients in the DDD group (406 women, mean age 71.5 ± 10 years). Evaluation of outcomes of AAI and DDD pacing in SSS was based on the analysis of medical records of patients who underwent pacemaker implantation. RESULTS Average duration of follow-up was 52 ± 25 months. In the AAI group, 63 of 86 patients remained without intervention. In the DDD group, 661 of 723 patients did not require surgical intervention. Overall, 105 patients died, including 13 in the AAI group and 92 in the DDD group (p = 0.4516). In the AAI group, a high degree atrioventricular block occurred on average after 46.3 ± 8.8 months and its incidence was estimated at 0.85% per year. Atrial fibrillation (AF) developed in 8 patients in the AAI group and 81 patients in the DDD group (p = 0.23). Among aetiological factors of an increased risk of developing AF, only the presence of tachycardia-bradycardia syndrome (hazard ratio [HR] 11.31) and the absence of antiarrhythmic therapy (HR 4.23) significantly increased the risk of AF. Urgent reoperation was needed in 23 patients in the AAI group and 62 patients in the DDD group (p < 0.01). Log-rank test analysis showed a significant effect of the development of AF on the risk of reoperation in this group (p = 0.0420). Lead-related complications were noted in 6 patients in the AAI group and 49 patients in the DDD group (p = 0.94). After 45 months, the risk of reoperation in the AAI group increased significantly due to a need for ventricular lead implantation. CONCLUSIONS 1. Atrial stimulation is safe in SSS but it may be associated with an increased risk of ventricular lead implantation if atrioventricular block or persistent AF with slow ventricular rate develops. 2. DDD and AAI groups did not differ significantly in terms of survival, development of persistent AF, and lead-related complications. 3. Tachycardia-bradycardia syndrome and the lack of antiarrhythmic treatment with beta-blocker and amiodarone increased the risk of persistent AF during long-term follow-up. 4. A higher rate of reoperations in patients with AAI systems, related mainly to development of persistent AF, especially after the fourth year of follow-up, may justify DDD system implantation in SSS.

Relationship between changes in selected thrombotic and inflammatory factors, echocardiographic parameters and the incidence of venous thrombosis after pacemaker implantation based on our own observations.

Introduction Thrombosis (VTh) is a rare dangerous complication of pacemaker implantation (PM). The aim of the study was to determine the dynamics of change in selected thrombotic and inflammatory factors after PM. Material and methods The study involved 81 patients (30 female, mean age: 71.1 years) with PM, divided into two groups. Group A (71 patients) consisted of patients without VTh, whereas group B (10 patients) comprised the patients with VTh. A transthoracic echocardiogram (TTE) and a venous ultrasound (VU) examination were performed. The levels of D-dimers, fibrinogen, tissue factor (TF), factor VII, plasminogen activator inhibitor-1 (PAI-1), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were determined in the venous blood. After PM, the TTE and VU examinations were repeated at 6 and 12 months, and blood analyses were performed within 7 days after PM, and subsequently at 6 and 12 months. Results In 10 patients of group B, symptomatic VTh occurred at a mean time of 13.06 months after PM. Initially, the levels of IL-6, hsCRP, D-dimers, fibrinogen, TF, VII factor and PAI-1 were considerably higher in group B than in group A. In all patients the levels of these factors kept on increasing for up to 7 days after the procedure. In group A they subsequently decreased, whereas in group B they continued to rise. Conclusions Increased levels of inflammatory and thrombotic factors were observed in patients with VTh before and after PM. The factors of highest risk of VTh occurrence were D-dimers, fibrinogen and TF.

Successful anti-tachycardia pacing of a temporary implantable cardioverter-defibrillator used in the treatment of an arrhythmic storm

A 70-year-old woman was admitted to hospital due to recurring symptomatic sustained ventricular tachycardias (VTs). She was diagnosed with ischaemic cardiomyopathy with low ejection fraction (20%). She also had left bundle branch block and chronic heart failure in New York Heart Association class III. Blood electrolyte levels were normal. Coronary angiography showed a preserved effect of previous angioplasty. Clostridium difficile infection was identified. Increasing levels of C-reactive protein and procalcitonin were observed. Despite treatment with metoprolol (100 mg per day) and amiodarone (1200 mg per day), VTs kept recurring; they had morphology of right bundle branch block with right axis deviation and cycle length of 240 ms. Ablation was performed using an anatomical visualisation system (CARTO). Potential map of the left ventricle revealed a large scar region. During left ventricular mapping VTs of the same morphology were induced with programmed ventricular stimulation (PVS). Areas of low conduction were removed. After ablation of late potentials, PVS demonstrated non-induction of VT. No arrhythmias were observed directly after the ablation, but an iatrogenic third-degree atrioventricular block occurred. The patient required temporary stimulation with indications to implantation of a permanent cardiac resynchronisation therapy defibrillator (CRT-D). However, the implantation was contraindicated due to an active infection. Therefore, a temporary external implantable cardioverter-defibrillator (ICD) with dual-coil lead and a conventional ICD was implanted on the opposite side of the planned permanent implantation. The implantation parameters were: R wave — 14 mV, impedance — 537 Ω, threshold — 1.2 V/0.5 ms. Defibrillation threshold test was not performed due to the generally serious condition of the patient. Two detection zones were programmed. The therapy started with anti-tachycardia pacing (ATP) — three attempts of burst: 12 cycles of 88% in the VT zone (141 bpm), followed by cardioversions (CVs), sending shocks between the two lead coils. Ventricular fibrillation zone (214 bpm) therapy consisted only of CVs. The ICD can was placed on the chest wall and attached with adhesives. The patient was scheduled for further infection treatment. After nine days she had recurrent VTs which had similar morphology to those previously observed and were successfully treated by both ATPs and CVs from the temporary ICD (Fig. 1). Further hospitalisation was uneventful. After normalisation of the inflammatory parameters, a permanent CRT-D was implanted. At one and six months of follow-up the patient’s condition improved with no arrhythmias or return of atrioventricular conduction. Treatment of an arrhythmic storm starts with the elimination of a potentially reversible cause, which can be established in about 66% of patients [1]. In this case, no such identifiable cause was found. In such situations treatment with antiarrhythmic medications, sedatives, and invasive methods is required. The OPTIC study showed that prevention of VT recurrence in patients with ICDs is effective with a combination of amiodarone and b-blockers [2]. In our patient, amiodarone with metoprolol did not prevent VT recurrence. The next step in the treatment is ablation, which not only stops electrical storm, but also improves long-term prognosis [3]. In our case VT returned shortly after ablation, probably due to the healing process after the procedure and an active infection. The infection was a reason against immediate implantation of a permanent CRT-D. We decided to use a bridge therapy with an external ICD with classic dual-coil lead, not only to ensure stimulation, but also to shorten the time of necessary treatment application in the case of VT recurrence. The dual-coil lead was implanted because the can was not placed under the skin, but externally. The defibrillation dipole was programmed from coil to coil in order to ensure appropriate defibrillation impedance and prevent skin burning during CV. It proved to be an effective treatment — both ATP and CV were successful. Programming of the VT zone was performed, although it was not line with the guidelines because previous VTs caused immediate decompensation of the patient.

Tricuspid valve regurgitation in the presenceof endocardial leads – an underestimated problem

In about 80% of the population, a small degree of tricuspid insufficiency occurs and therefore is considered almost physiological [1]. Higher mortality has been described among patients with moderate and severe tricuspid regurgitation compared to patients without it, irrespective of the pulmonary pressure value or systolic function of the left and right ventricle [2–4]. A fourfold increase in the risk of substantial tricuspid regurgitation is caused by the presence of the endocardial lead [5]. A chest X-ray examination is used in order to assess the position of the lead in the heart [6]. The influence of endocardial lead position in the chest X-ray on tricuspid valve function and the presence of its insufficiency has not yet been described in the literature.

Heart perforation by pro-MRI right ventricular lead in a 26-year-old woman

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.

Severe tricuspid regurgitation caused by pacemaker lead interference

A 19-year-old patient was admitted to the hospital for routine pacemaker (PM) reimplantation due to battery depletion. A single chamber (VVI) transvenous PM had been implanted when the patient was 11 years old, following previous epicardial stimulation due to congenital atrio-ventricular complete heart block. On admission, the patient was asymptomatic. Electrical parameters of the PM were within normal range. Transthoracic echocardiography (TTE) however revealed severe tricuspid regurgitation (TR) caused by lead interference with the septal platelet of the tricuspid valve (Fig. 1). Chest X-ray showed that the lead was stretched (Fig. 2). Due to significant interference between the lead and the tricuspid valve, the patient was qualified to transvenous lead extraction with simultaneous dual chamber PM implantation (Fig. 3). A new PM with a lead length appropriate to the patient’s dimensions was implanted. In a three-month follow up after the procedure, a significant reduction of TR was observed (Fig. 4). Benign TR is a frequently described phenomenon after PM implantation. However, severe TR is relatively rare. Among possible causes of the regurgitation, several mechanisms have been described: platelet perforation, lead entanglement in valve structures, lead impingement of the platelets, and fibrotic adhesions between platelets and the lead. Possible risk factors are: older age, diastolic heart failure, use of cardioverter-defibrillator leads, and apical stimulation. In the described case, apical PM stimulation led to severe TR. The most probable explanation was tricuspid valve platelet ‘support’ by the lead, which as the patient grew became rectified and began to interfere with the valve. This hypothesis is further supported by the fact that after PM replacement, the regurgitation subsided. Our patient was asymptomatic. Severe regurgitation when diagnosed too late, after tricuspid annulus has extended, may lead to irreversible changes, and lead extraction alone may not resolve the problem. TR when diagnosed and treated early allows cardiosurgical intervention to be avoided along with possible complications, such as heart failure.