Agnieszka Kołodzińska

Abrasions of the outer silicone insulation of endocardial leads in their intracardiac part: a new mechanism of lead-dependent endocarditis.

AIMS The aim of the study was to identify and characterize the morphology of abrasions and to establish the frequency of the phenomena and their association with infective endocarditis (IE). METHODS AND RESULTS A total of 212 endocardial leads removed from 141 consecutive patients-due to IE (32), pocket infection (37), and non-infective indications (72)-were analysed with a stereomicroscope and a scanning electron microscope. The presence of abrasions in the intracardiac part (IP) of the atrial (P < 0.01) and ventricular (P < 0.00002) leads, regardless of its advancement, was strongly associated with IE. There were associations between abrasions in the IP of the ventricular (P < 0.00002) and atrial (P < 0.005) leads and two or more implanted endocardial leads. In atrial leads, there was an association between the presence of any abrasion and passive fixation (P < 0.05), dwell time (P < 0.05), and number of procedures until removal (P < 0.006). The abrasions were classified into three levels of degradation under two subtypes according to the morphology observed with a stereomicroscope. The third level of degradation was the most frequently observed in the IP of the leads. CONCLUSIONS The abrasion of the outer insulation in the IP of silicone leads was significant regardless of the level of degradation and is associated with IE. The abrasions observed in the IP of the leads were similar to those observed in the intravenous and pocket parts, with predomination of the third level of degradation. There was an association between the presence of any abrasion in the IP of the leads and the number of leads, and in the case of atrial leads between abrasions and fixation type, dwell time, and number of procedures until explantation.

Biodegradation of the outer silicone insulation of endocardial leads.

Background—Silicone catheter insulation, larynx prostheses undergo biodegradation. The aims of the study were to verify the conviction that outer silicone lead insulation is biostable and inert in addition to determining the role of macrophages (M) and Staphylococcus aureus (S aureus) strains in the silicone lead insulation degradation. Methods and Results—Leads removed from 8 patients because of infective and noninfective indications were analyzed with stereomicroscope and classified according to Banacha abrasion classification, and additional analysis using scanning electron microscope was performed. The examination revealed excavations of different shape and depth in the abraded areas. Fresh silicone-insulated lead was cut into fragments. The fragments were cultured with RAW 264.7 macrophage cell line for 9 weeks. Additional lead fragments were placed with S aureus strains: ATCC 25923, ATCC 29213, and K9328H. Lead fragments were also cocultured with the bacterial strains and RAW M. In scanning electron microscope analysis, diminution in silicone was observed. All S aureus strains provoked insulation damage after 9 weeks. The lowest level of degradation of insulation concerned ATCC 25923. Silicone lead fragments in cocultures presented a further gone level of silicone biodegradation. Conclusions—S aureus, macrophages separately, and S aureus and macrophages cocultures initiate the biodegradation of silicone insulation. Differences in the level of biodegradation between strains of S aureus were observed, with the most aggressive reaction toward silicone visible in the cocultures. In vivo silicone biodegradation is initiated by tearing among surfaces of the lead insulation, macrophages may be the crucial cells for the process that may be aggravated by pathogen colonization.

Retinoic acid-induced ventricular non-compacted cardiomyopathy in mice

BACKGROUND Precise tissue concentration of retinoic acid (RA) is indispensable for proper interaction of second heart field cells with cardiac neural crest cells and induction of signalling pathways important for normal myocardial growth. AIM Since RA deficiency during embryogenesis induces noncompaction, we hypothesised that excess RA at the stage of heart tube elongation may cause thinning of the myocardial wall which leads to noncompaction. METHODS RA was administered at 70 mg/kg b.w. on 8.5 days post coitus (dpc) to pregnant mice to elicit cardiac malformations in foetuses. We studied noncompaction development in RA-treated mouse offspring. The cardiac noncompaction was evaluated in different stages of heart development as the quotient of the distance between the epicardial surface and trabecular tips(represented by a) and the distance between the epicardial surface and trabecular recesses (represented by b) in RA-treated hearts compared to control non-treated. RESULTS We demonstrated that apart from outflow tract defects such as double outlet right ventricle, transposition of the great arteries and tetralogy of Fallot in foetuses in mouse offspring, noncompaction occurs in about 42% of cases. At the stage of 13 dpc and later in development the ratio a/b was higher in RA-treated hearts exhibiting noncompaction compared to the control hearts. This cardiomyopathy was more evident in the right ventricle than in the left ventricle. CONCLUSIONS Noncompaction caused by RA overdose can be elicited in part of the mouse offspring by administering RA at the stage of cardiac tube elongation.

Toll-like receptor expression and apoptosis morphological patterns in female rat hearts with takotsubo syndrome induced by isoprenaline

Aims: Toll‐like receptors (TLR) and apoptosis were indicated as important factors in heart failure. Our aim was to characterize the morphological pattern of apoptosis, TLR2, TLR4, and TLR6 expression in female rat hearts in the model of takotsubo syndrome (TTS). Main methods: 60 Sprague‐Dawley female rats were treated with a single dose of 150 mg/kg b.wt. of isoprenaline (ISO) or 0.9% NaCl (controls). Hearts were collected 24, 48, 72 h and 7 days post‐ISO injection. 32/60 hearts were used in immunohistopathological studies and 28/60 in real time. Key findings: Apoptosis was observed 24 h post‐ISO in cardiomyocytes, 24, 48, 72 h and 7 days post‐ISO in infiltrating inflammatory cells, 7 days post‐ISO in endothelial cells of vessels. Diffuse TLR4CD68 (CD68, a macrophage marker) and TLR6CD68 positive cells and TLR2, TLR4, TLR6 mononuclear cells were observed in both acute and recovery phase of TTS. In the foci located in the neighborhood of damaged (necrotic/apoptotic) cardiomyocytes in TTS, high (strong) protein expression of TLR2 (TLR2high) was observed: 24, 48, 72 h post‐ISO; TLR4high – 48 and 72 h post‐ISO; TLR6high – 48 h post‐ISO. Whereas in cardiomyocytes of remote myocardium: TLR2high – 72 h post‐ISO; TLR4high – 24 and 72 h post‐ISO; TLR6high – 24 h post‐ISO. TLR2 mRNA was down‐regulated 48 and 72 h post‐ISO whereas TLR4 up‐regulated 7 days post‐ISO. Significance: The expression pattern of apoptosis and TLR differs in the course of TTS in comparison with the control rats. We hypothesize that innate immunity and apoptosis may play a crucial role in TTS pathophysiology.

Microvascular Obstruction Evaluation Using Cardiovascular Magnetic Resonance (CMR) in ST-Elevated Myocardial Infarction (STEMI) Patients

Summary Backround Restoration of blood flow in epicardial coronary artery in patients with acute myocardial infarction can, but does not have to restore efficient blood flow in coronary circulation. The aim of the study was a direct comparison of microvascular obstruction (MVO) detected by rest and stress perfusion imaging and gadolinium enhancement obtained 2 min. (early MVO) and 15 min. (delayed MVO) post contrast. Material/Methods 106 patients with first anterior myocardial infarction were studied. Cardiovascular magnetic resonance (CMR) was performed 5±2 days after primary percutaneous coronary intervention (pPCI). Stress and rest perfusion imaging was performed as well as early and delayed gadolinium enhancement and systolic function assessment. Scoring of segmental function, perfusion defect, MVO and scar transmurality was performed in 16 segment left ventricular model. Results The prevalence of MVO varies significantly between imaging techniques ranging from 48.8% for delayed MVO to 94% with stress perfusion. Median sum of scores was significantly different for each technique: stress perfusion 13 (7; 18), rest perfusion 3 (0.5; 6), early MVO 3 (0; 8), delayed MVO 0 (0; 4); p<0.05. Infarct size, stress and rest perfusion defects were independent predictors of LV EF at discharge from hospital. Conclusions Imaging protocol has a significant impact on MVO results. The study is the first to describe a stress-induced MVO in STEMI patients. Further research is needed to evaluate its impact on a long term prognosis.

Pneumothorax after pacemaker implantation localized contralaterally to the side of implantation - rare, but possible complication.

Case report – An 86-year old patient developed pneumothorax a few hours after pacemaker implantation. Surprisingly, the pneumothorax localized contralaterally to the site of subclavian vein puncture. It was treated with chest tube puncture, under the care of a pneumonologist, resulting in full recovery. Although pneumothorax localized contralaterally to the site of subclavian vein puncture during pacemaker implantation is very rare, it has been reported in the literature.

Transvenous lead removal with a fragment of a papillary muscle - a silent complication.

Tricuspid valve (TV) insufficiency is one of the more important complications in patients with cardiac implantable electronic devices due to the endocardial lead [1]. The frequency of this complication is growing with the increasing number of implanted and removed leads crossing the TV [2] and with trauma upon removal of the old lead that increasingly grows into the heart tissue. However, in some cases, even serious heart damage, tricuspid regurgitation and other symptoms are not observed [3].

A subcutaneous implantable cardioverter-defibrillator (S-ICD) implantation in infection high-risk patient - a case study.

The cardiac device related infective endocarditis (CDRIE) is an important indication for the implantable cardiac device extraction. In patients after recovery from CDRIE, who present indication for implantable cardioverter-defibrilator (ICD) but without necessity for pacing therapy the subcutaneous ICD (S-ICD) seems to be a reasonable alternative. Here we present a patient with CRT-D device transferred to our hospital with the diagnosis of CDRIE and many comorbidities. The patient presented increased inflammatory markers serum level during the entire period of hospitalization, after device explanation and termination of antibiotic therapy. The blood culture tests were negative and transesophageal echocardiography showed no sign of endocarditis, therefore despite inflammatory biomarkers the patient has been implanted with S-ICD.

Transvenous retained lead fragment removal after incomplete extraction assisted by three-dimensional transoesophageal echocardiography

Address for correspondence: Marcin Grabowski, MD, PhD, FESC, 1st Chair and Department of Cardiology, Medical University of Warsaw, ul. Banacha 1a, 02–097 Warszawa, Poland, tel: +48 22 599 19 58, fax: +48 22 599 19 57, e-mail: marcin.grabowski@wum.edu.pl Conflict of interest: none declared Kardiologia Polska Copyright

Lead insulation failure, a serious complication: risk factors and management

“OUTSIDE-IN” ABRASIONS: A NEW PHENOMENA — MORE QUESTIONS THAN ANSWERS We may divide abrasions according to mechanism into “outside-in” and “inside-out” abrasions. The “outside-in” abrasions are well known in the pocket as the result of friction between leads or between the lead and the device, as well as in the venous system, with tearing surfaces among leads, first rib, and clavicle. However, “outside-in” abrasions most frequently appear in the intracardiac part of the lead and are associated with infective endocarditis (IE) [2]. The outer insulation abrasion remains electrically signless unless concomitant inner insulation failure occurs and in the device control both oversensing and undersensing may be observed [3]. The Banacha classification was established to morphologically describe abrasions analysed with an optical microscope, and to facilitate comparison and analysis. The classification distinguishes three levels of silicone in vivo damage: mild, moderate, and severe, all in two subtypes: a and b [2]. A severe abrasion with conductor exposure may be assessed clinically (Fig. 1A) [4]. Insulation abrasion more often concerned patients with sub-pectorally or abdominally implanted devices. Risk factors of intracardiac abrasions are implantation of two or more leads in the heart cavities, and in the case of atrial leads: passive fixation, longer mean dwell time (time from implantation), and three or more procedures proceeding lead extraction [2]. Severe abrasions with conductor exposure were associated with the number of extracted leads, dwell time, location of the lead in the coronary sinus, and excessive lead length in the cardiac chambers [4]. The most important observation was that, irrespective of the abrasion level of degradation in the intracardiac part of the lead, they were associated with IE development [2]. The process of outside-in abrasion may be INTRODUCTION Endocardial leads are the most important parts of cardiovascular implantable electronic device systems. The endocardial lead parts are located in the tissue of the pocket, in the venous system, and finally in the right heart cavities. The three different microenvironments present different impacts on lead body parts, especially the outermost insulation. Lead design also concerns the outer insulation, which has been evaluated since implantation of the first pacemaker. In the current paper we present the different mechanisms of insulation failure of the leads available on the market, and of leads that have been withdrawn from the market but still exist in living patients. The outer lead insulation may dictate the lead reliability. Silicone, polyurethane, fluoropolymers (PTFE, ETFE), and co-polymer silicone-polyurethane (Optim) are materials widely used as insulation of endocardial leads. Insulation breach and abrasions may occur anywhere along the lead. The lead parameters: abnormal sensing amplitudes, abnormal and variant pacing thresholds, and lead impedance abnormalities may be indicators of lead failure. The insulation characteristics of typical damage, lead failure symptoms, and lead management are crucial for patients, theirs doctors, scientists, and manufacturers.