Andrzej Tomaszewski

Lead dependent tricuspid dysfunction: Analysis of the mechanism and management in patients referred for transvenous lead extraction

BACKGROUND Lead-dependent tricuspid dysfunction (LDTD) is one of important complications in patients with cardiac implantable electronic devices. However, this phenomenon is probably underestimated because of an improper interpretation of its clinical symptoms. The aim of this study was to identify LDTD mechanisms and management in patients referred for transvenous lead extraction (TLE) due to lead-dependent complications. METHODS Data of 940 patients undergoing TLE in a single center from 2009 to 2011 were assessed and 24 patients with LDTD were identifi ed. The general indications for TLE, pacing system types and lead dwell time in both study groups were comparatively analyzed. The radiological and clinical effi cacy of TLE procedure was also assessed in both groups with precision estimation of clinical status patients with LDTD (before and after TLE). Additionally, mechanisms, concomitant lead-dependent complications and degree (severity) of LDTD before and after the procedure were evaluated. Telephone follow-up of LDTD patients was performed at the mean time 1.5 years after TLE/replacement procedure. RESULTS The main indications for TLE in both groups were similar (apart from isolated LDTD in 45.83% patients from group I). Patients with LDTD had more complex pacing systems with more leads (2.04 in the LDTD group vs. 1.69 in the control group; p = 0.04). There were more unnecessary loops of lead in LDTD patients than in the control group (41.7% vs. 5.24%; p = 0.001). There were no signifi cant differences in average time from implantation to extraction and the number of preceding procedures. Signifi cant tricuspid regurgitation (TR-grade III-IV) was found in 96% of LDTD patients, whereas stenosis with regurgitation in 4%. The 10% frequency of severe TR (not lead dependent) in the control group patients was observed. The main mechanism of LDTD was abnormal leafl et coaptation caused by: loop of the lead (42%), septal leafl et pulled toward the interventricular septum (37%) or too intensive lead impingement of the leafl ets (21%). LDTD patients were treated with TLE and reimplantation of the lead to the right ventricle (87.5%) or to the cardiac vein (4.2%), or surgery procedure with epicardial lead placement following ineffective TLE (8.3%). The radiological and clinical effi cacy of TLE procedure was very high and comparable between the groups I and II (91.7% vs. 94.2%; p = 0.6 and 100% vs. 98.4%; p = 0.46, respectively). Repeated echocardiography showed reduced severity of tricuspid valve dysfunction in 62.5% of LDTD patients. The follow- -up interview confi rmed clinical improvement in 75% of patients (further improvement after cardiosurgery in 2 patients was observed). CONCLUSIONS LDTD is a diagnostic and therapeutic challenge. The main reason for LDTD was abnormal leafl et coaptation caused by lead loop presence, or propping, or impingement the leafl ets by the lead. Probably, TLE with lead reimplantation is a safe and effective option in LDTD management. An alternative option is TLE with omitted tricuspid valve reimplantation. Cardiac surgery with epicardial lead placement should be reserved for patients with ineffective previous procedures.

Takotsubo syndrome in a patient after renal transplantation

Summary Background Takotsubo syndrome (TTS) is a transient cardiomyopathy of unknown origin, clinically manifesting as acute coronary syndrome (ACS). This syndrome mainly occurs in postmenopausal women and has a temporary relationship with emotional or physical stress. Case Report TTS occurred in 46-year-old female patient on the first day after renal transplantation. The predominant symptoms were connected with ACS, performed with low grade troponin elevation and characteristic shape of left ventricle depicted in echocardiography. Taking into consideration the risk of the development of contrast-induced nephropathy, coronary angiography (CA) was delayed; myocardial perfusion scintigraphy and iodine-123 metaiodobenzylguanidine (123I-mIBG) myocardial uptake were performed to confirm the clinical suspicion. Myocardial perfusion scintigraphy (MPS) performed in rest condition showed normal perfusion but myocardial uptake of 123I-mIBG was impaired. Within 6 months after surgery, full recovery of all biochemical and functional parameters of the left ventricle were observed. At that time CA was done, depicting normal coronary arteries. Conclusions TTS could be diagnosed by the use of non-nephrotoxic tests – 123I-mIBG myocardial scintigraphy, MPS and echocardiography.

QT Interval Prolongation and QRS Voltage Reduction in Patients with Liver Cirrhosis

BACKGROUND Liver cirrhosis is associated with functional abnormalities of the cardiovascular system with co-existing electrocardiographic (ECG) abnormalities. OBJECTIVES The aim was to analyze ECG changes in patients with cirrhosis, to evaluate whether alcoholic etiology of cirrhosis and ascites has an impact on ECG changes. MATERIAL AND METHODS The study involved 81 patients with previously untreated alcoholic cirrhosis (64 patients with ascites, classes B and C according to the Child-Pugh classification; and 17 without ascites, categorized as class A); 41 patients with previously untreated cirrhosis due to chronic hepatitis C (HCV--30 patients with ascites, classes B and C; and 11 without ascites, class A); 42 with alcoholic steatohepatitis and 46 with alcoholic steatosis. The control group consisted of 32 healthy volunteers. Twelve-lead ECG recordings were performed and selected parameters were measured. RESULTS Significantly longer QT and QTc intervals and lower QRS voltage were found in patients with alcoholic and HCV cirrhosis compared to the controls. Significantly lower QRS voltage was found in subjects with ascites than in those without ascites. Removal of ascites significantly increased QRS voltage. CONCLUSIONS In cirrhosis, irrespective of etiology, ECG changes involved prolonged QT and QTc intervals and reduced QRS voltage. Prolonged QT and QTc intervals were not related to the severity of cirrhosis or to the presence of ascites. However, low QRS voltage was associated with the presence of ascites. Removal of ascites reverses low QRS voltage.

Lead-related infective endocarditis: Factors influencing early and long-term survival in patients undergoing transvenous lead extraction

BACKGROUND Lead-related infective endocarditis (LRIE) is a serious infectious disease with uncertain prognosis. OBJECTIVE The purpose of this study was to evaluate the factors that influence survival in patients with LRIE undergoing transvenous lead extraction (TLE). METHODS Clinical data obtained from 500 consecutive patients with LRIE undergoing TLE in the reference center in the years 2006 to 2015 were retrospectively analyzed. We evaluated the effect of demographic, clinical, and procedure-related factors on 30-day and long-term survival (mean 3-year follow-up). RESULTS Analysis of 30-day survival after TLE revealed 19 deaths (3.8%), with long-term mortality (mean 3-year follow-up) of 29.3% (146 deaths). Multivariate analysis showed unfavorable effects of age (hazard ratio [HR] 1.056, 95% confidence interval [CI] 1.030-1.082); decreased left ventricular ejection fraction (HR 0.687, 95% CI 0.545-0.866); renal failure (HR 3.099, 95% CI 1.865-5.150); and presence of vegetation fragments remaining after TLE (HR 1.384, 95% CI 1.089-1.760). Log-rank test and Kaplan-Meier survival curves demonstrated statistically worse prognosis in patients with large vegetations (>2 cm) and with vegetation remnants. Better prognosis was associated with LRIE coexisting with generator pocket infection. CONCLUSION Long-term mortality in LRIE patients is still high. Factors that influence negatively on prognosis include large cardiac vegetations and their remnants after TLE. Such vegetations develop most frequently in patients with decreased left ventricular ejection fraction and renal failure. Probably, early detection of LRIE would tend to limit the formation of large vegetations that invade the adjacent cardiac structures.

Transvenous extraction of an eight-year-old ventricular lead accidentally implanted into the left ventricle

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 patients 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.

Late complications of electrotherapy — a clinical analysis of indications for transvenous removal of endocardial leads: a single centre experience

BACKGROUND Despite advances in electrotherapy, late complications constitute an increasing clinical and therapeutic problem. Transvenous lead extraction (TLE) is becoming a safe and effective approach to the treatment of such complications. AIM To assess indications for TLE and to evaluate safety and efficacy of TLE procedures. METHODS A retrospective clinical analysis of 100 patients with complications of electrotherapy admitted to a tertiary care centre in 2008-2011. RESULTS In 2008-2011, the number of electrotherapy complications increased markedly. The most frequent reason for TLE was lead dysfunction (62% of patients, including 31% with an implanted cardioverter-defibrillator [ICD] and 31% with a pacemaker [PM]). The most common type of lead dysfunction was conductor damage (38% of patients, including 23% with ICD, 15% with PM), followed by late myocardial perforation (14% of patients, including 7% with ICD, 7% with PM), abnormal course of the lead (7% of patients, including 1% with ICD, 6% with PM), and lead insulation failure (3% of patients). Other reasons for TLE were infectious complications (24% of patients, including 15% with PM pocket infection), venous insufficiency (17% of patients, including 10% in whom an indwelling lead was a direct obstacle to switching the pacing mode), and the need to switch the pacing mode (4% of patients). Procedural efficacy was 96% (lead fragments were left in place in 4% of patients). No significant clinical complications were observed in any of the patients in the periprocedural period. CONCLUSIONS Clinical manifestations of electrotherapy complications in the study group varied and included a relatively small number of infectious complications (24%) and a relatively large number of late myocardial perforations (14%). Efficacy and safety of the procedures were very high.

Transvenous removal of endocardial leads with coexisting great vegetation (3.5 cm)--case report.

We discuss a case of transvenous removal of endocardial leads in a patient with initial contraindication for such a procedure due to the size of the vegetation in his right atrium. Simultaneously, the patients progressive general poor condition during the course of infective endocarditis prognosed that cardiosurgical intervention with the use of cardiopulmonary bypass would be unsuccessful. Using an innovative solution, that is placing the Dotters basket in the right ventricular outlet as a protection against massive pulmonary embolism, the leads were removed. An asymptomatic pulmonary embolism caused by defragmented vegetation was revealed after the procedure.

Papillary fibroelastoma as an accidental finding in a multislice computed tomography scan of coronary arteries

Papillary fibroelastomas represent less than 10% of all primary cardiac tumours. They are usually incidental autopsy or surgical findings, or detected during echocardiography or catheterization. The case of a 58-year-old man with typical exertional chest pain hospitalized for an elective multislice computed tomography (MSCT) scan of the coronary arteries is described. The MSCT scan showed a pathological, mobile lesion within the aorta lumen only, not obstructing the ostia of the coronary arteries, and was confirmed by echocardiography. The typical features of the tumour in the MSCT scan and on echocardiography were the basis for the diagnosis of papillary fibroelastomas in the patient. Surgical excision was proposed, but the patient declined.

Extraction of a 17-year-old pacing lead chronically dislocated into the liver vein.

In most cases of lead-dependent infective endocarditis total system removal is the treatment of choice (1-4). The main complications of the extraction procedure include damage to the wall of the heart or major vessels (5,6). We report a case of a 59-year-old man with chronic AF implanted with a ventricular demand (VVI) pacemaker, referred to our center because of symptoms of local pocket infection. Seventeen years earlier the patient was implanted with a ventricular lead, which was found broken on ligature 5 years following implantation. He was then implanted with a new ventricular lead, with the old one left dislocated into liver vein. After the next pacemaker re-implantation 7 months ago, the patient developed symptoms of local pocket infection, and phlebography revealed chronic obstruction of left subclavian and brachiocephalic veins. At admission, transesophageal echocardiography (TEE) revealed vegetation (10x10mm) on the ventricular aspect of the septal tricuspid valve leaflet. After consultation with a cardiosurgeon we decided to perform transvenous lead extraction with full cardiosurgical stand-by. When the pacemaker pocket was opened symptoms of local infection were revealed. Swabs were taken and we then removed the pacemaker and, subsequently, the active ventricular lead with the use of Byrd dilatators. The attempt to liberate the proximal part of the old lead from the liver vein (Fig. 2A, B) with the use of a pigtail catheter introduced via the right jugular vein was unsuccessful. The following attempt was made with the loop of angiographic guide wire (Fig. 2C, D, E). The lead was looped by the guidewire introduced via the pigtail catheter, and the distal part of the guidewire was fixed by a Dotter basket (Fig. 2E, F) Manual traction applied to the guidewire liberated the ingrown part of the lead (Fig. 3A, B) and it progressed into the inferior vena cava (IVC), where it was caught by a Dotter basket (Fig. 3C, D). We subsequently liberated the distal tip of the lead with a 13F sheath (Fig. 3E, F) and removed it along with a small part of ventricular myocardium. There were no complications for the procedure. Considering the pocket infection and sufficient intrinsic rhythm, reimplantation was postponed. Four days after the procedure the patient, in good overall condition, was transferred to a district hospital. Opinions concerning the approach to inactive pacing leads are contradictory. New Heart Rhythm Society (HRS) consensus (4) moves toward this problem; howJV A _1 1_ 10 03 Fig. 1 External pocket view (A), the course of both leads (B); obstruction of left subclavian and brachiocephalic veins (C).

Diagnostic and therapeutic difficulties in a patient with peripartum cardiomyopa-thy with advanced heart failure, complicated by thrombus in both ventricles and pulmonary embolism, with right lower lobe infarction

482 (2 weeks). Due to the symptoms of heart failure in the postpartum period and the suspicion of peripartum cardiomyopathy (PPCM), treatment with bromocriptine was initiated (2.5 mg twice daily over 6 weeks). Because the symptoms of heart failure were still present, we administered levosimendan infusion, after which the patient’s condition significantly improved. Once her renal function stabilized, a chest computed tomogra‐ phy angiography (CTA) was performed, which confirmed thrombi in both ventricles, as well as pulmonary embolism, with right lower lobe in‐ farction (FIGURE 1E–1H). In addition, ultrasound ex‐ amination revealed thrombosis of the right inter‐ nal jugular, subclavian, and common iliac veins. On control TTE, we observed an improvement of the left ventricular EF and a significant reduc‐ tion of mitral and tricuspid valve regurgitation. The size of the thrombi in both ventricles was gradually reduced, until they resolved completely. The patient was hospitalized for 7 weeks and was discharged with an EF of 41%. The treatment recommendation involved rivaroxaban, carvedilol, with low doses of furosemide, spironolactone, and cilazapril. At 7 ‐month follow‐up, a control TTE showed an EF of 55%, with normal systolic pul‐ monary artery pressure. In 2010, the Working Group on PPCM of the European Society of Cardiology defined PPCM as “an idiopathic cardiomyopathy presenting with HF [heart failure] secondary to left ventricular (LV) systolic dysfunction towards the end of preg‐ nancy or in the months following delivery, where A 27 ‐year ‐old woman was admitted to the inten‐ sive cardiac care unit with advanced heart failure and generalized edema. The patient was 2 months after labor by cesarean section. It was her second pregnancy; the first pregnancy was extrauterine 2 years earlier. She did not have any other known risk factors for peripartum cardiomyopathy and pulmonary embolism. Laboratory tests revealed renal and hepatic failure, elevated D ‐dimer lev‐ els (103 457 ng/ml), and significantly increased levels of inflammatory markers. Transthoracic echocardiography (TTE) on admission showed thrombosis in both ventricles, an ejection frac‐ tion (EF) of 23%, a left ventricular end ‐diastolic diameter of 4.5 cm, a right ventricular diame‐ ter of 2.1 cm (body surface area, 1.2 m2), tricus‐ pid annulus plane systolic excursion (TAPSE) of 12 mm, and second to third degree mitral and tricuspid valve regurgitation, with a tricuspid valve regurgitation velocity of 355 cm/s, accom‐ panied by pericardial fluid and pleural effusion (FIGURE 1A–1D). Chest X ‐ray showed pleural effu‐ sion in both cavities with possible inflammatory lesions in the right lower lobe area. Treatment with unfractionated heparin was initiated, followed by administration of low‐ ‐molecular ‐weight heparin, furosemide, dopa‐ mine and dobutamine infusions, and supple‐ mentary oxygen. Alternative treatment options were also considered, including the administra‐ tion of alteplase and thrombectomy, considering the high risk of thrombolysis, multiorgan failure, and the time elapsed from the onset of symptoms CLINICAL IMAGE