Pacemaker Troubleshooting and early complications of pacemaker insertions
The clinical benefit of cardiac pacemakers has been long proven through numerous studies. Millions of pacemakers have been implanted worldwide and, as a result the quality of life for these patients has been drastically improved, not forgetting the reduced morbidity and mortality. The first stimulations through transthoracic electrodes were pioneered by Zoll in the early fifties (Zoll, 1952)), then came percutaneous endocardial pacing in 1959 (Furman & Schwedel. (1959).. A “permanent” pacemaker using epicardial electrodes was first described in 1960 (Chardack, 1960). Pacemakers and implantation techniques have progressed rapidly since the then; Generators are more reliable, more compact, filled with micro-electronic components, can be controlled automatically and remotely and thus providing more options for programmation and monitoring and a longer pacemaker life span (Kusomoto & Goldschlager, 1996; Trohman, et al, 2004). Leads are thinner and more resistant to damage and thus equally longer-lasting.
The latest European guidelines published in 2007 confirmed the classic indications; symptomatic bradyarrhythmias including sinus node dysfunction and atrioventricular or intraventricular conduction disturbances (Vardas et al., 2007). The guidelines also recommended cardiac pacing for specific conditions (vasovagal syncope, hypertrophic cardiomyopathy, heart failure with prolonged QRS duration, etc). Since over 10 years, left ventricular resynchronisation therapy has proved to be beneficial to patients presenting heart failure with complete left bundle block in association with optimal medical treatment; the European guidelines were updated for this indication in 2010 (Dickstein,2010)
The correct implantation of a pacemaker is capital for optimal function. A recent trend shows pacemaker implantation can be performed as successfully in the electrophysiology study environment as in the operating room (Garcia-Bolao & Alegria, 1999). This requires a centre with a qualified team of cardiologists as well as experienced nursing and technical staff. Continued education for the team and follow-up of complications is essential. The cardiologists’ or surgeons’ experience, and the volume of pacemakers implanted in the centre, plays a role in reducing post-implantation complications; thus, guidelines discourage this procedure in centres with a low volume of implantation.
Despite these precautions, some early complications, occurring within the first 6 weeks after implantation, may be observed. Their incidence is probably underestimated (approximately 7%), as is their severity (Kiviniemi et al., 1999; Klug et al., 2003). Less than 5% have to incur reintervention. Per-procedure mortality is extremely rare; only one case was observed in the cohort of 650 patients implanted at Columbia-Presbyterian Medical Centre. The dutch database FLOOWPACE PM has indexed/listed six variables associated with at least one complication prior to hospital discharge; a low body mass index, history of heart failure (one of the principal indications for implantation), a subclavian venous access, an active fixation auricular pacing lead, and double lead implantation. These patients should be considered at risk for complications (van Eck et al., 2007).
2. Clinical cases
Early complications of pacemaker implantation are not uncommon, even in an experienced team of cardiologists or surgeons. Before discharge, careful evaluation of the pacing system is required. Diagnosis of malfunction is not always evident. Most of the patients needed an invasive procedure or medical intervention to prevent further morbidity.
Through practical clinical examples, we aim to elaborate the principal complications of electronic implanted cardiac devices, as well as discuss situations in which the presence of such a device needs to be kept in mind for the work-up of disorders that may or may not seem pacemaker-related.
2.1. Case 1 - Latrogenic pneumothorax resulting from subclavian puncture
A 61 year old man presents to his general practitioner with right thoracic pain and dyspnoea, progressively worsening since three days. He was discharged from cardiology a week before, for implantation of a double chamber pacemaker for sick sinus syndrome with symptomatic atrial fibrillation and bradycardia. Clinical examination revealed good cicatrisation of the implantation site, normal cardiac sounds with no murmur, but abolished respiratory sounds in the right lung. Twelve-lead electrocardiogram (EKG) showed a sinus rhythm with paced ventricular response (typical left bundle block pattern). Chest X-ray confirmed the presence of a complete right pneumothorax (Figure 1). The patient was therefore treated with a chest tube and his recovery was uneventful. The additional hospital stay was three days.
2.2. Case 2 - Skin necrosis, suture line failure, and lead erosion due to a large pocket hematoma
An 80 year old male needed pacing for complete atrioventricular block is re-admitted three months after implantation. Despite daily wound care by a home-based nurse, the suture line at the site of implantation would not cicatrize. Patient history included myocardial infarction for which percutaneous cardiac intervention (PCI) with a bare metal stent was performed, as well as receiving classical medical treatment that included clopidogrel and aspirin on a daily basis. After implantation, a large hematoma formed in the generator pocket. A conservative treatment was initially proposed. On re-admission, the hematoma had almost completely disappeared, but severe skin necrosis was impeding site closure to the extent that the leads were visible with the naked eye. The absence of infection, as proved by numerous negative swab cultures, allowed for the pacemaker generator to be re-implanted under the pectoralis muscle.
2.3. Case 3 - Recurrent syncope due to lead displacement
A 60 year old female patient with no medical history and under no current treatment was admitted for complete atrioventricular block causing shortness of breath and dizziness. Implantation of a double chamber pacemaker was performed with ease. P/R sensings were measured at 3.1 mV and 7.8 mV respectively, and both thresholds for stimulation are 0.5 volt/0.4 msec. The next day, the patient represented with dizziness and faints. Lead displacement was suspected. EKG no longer showed physiological stimulation and chest X-ray confirmed lead displacement (Figure 3). Lead repositioning and active fixation was performed successfully.
|• Failure to OUTPUT: no pacemaker activity. NO SPIKE|
• battery failure or EOL (end of life), battery trauma
lead problems : lead fracture, lead dislodgement, fractured lead insulation, poor lead connection
• oversensing causes (myopotentials, electromagnetic interference, cross-talk phenomenon)
• "cross-talk” phenomenon
• extreme electromagnetic interference
• pseudo-malfonction : hystérésis, normal algorithmes (AV conduction)
|• Failure to CAPTURE: no depolarisation of the cavity. SPIKE without P/QRS complexes|
• normal situation : Functional non-capture—output delivered during refractory period
• inappropriate programming of the pacemaker (too low safe margin)
• lead problems : lead fracture, lead dislodgement, fractured lead insulation, poor lead connection
• myocardial perforation
• elevated pacing threshold :
○ myocardial infarction (necrosis) at the lead tip
○ drugs (eg, flecainide)
○ metabolic abnormalities (eg, acidosis, alkalosis)
|• Oversensing (Oversensing occurs when a pacemaker incorrectly senses cardiac/noncardiac electrical activity and is inhibited from pacing):|
• Myopotentials or muscular activity (particularly the diaphragm or pectoralis muscles)
• cross-talk phenomenon
• electromagnetic interference (eg, Magnetic Resonance Imaging (MRI)
• lead fracture and fractured lead insulation
|• Undersensing (Undersensing occurs when a pacemaker incorrectly misses intrinsic depolarization and paces despite intrinsic activity)|
• Normal device function—misinterpretation : triggered mode, fusion and pseudo-fusion beats, functional undersensing (long refractory periods, blanking period, safety pacing, oversensing)
• poor lead positioning (poor intrinsic signal amplitude), lead dislodgment, lead fibrosis or thrombosis
• magnet application
• battery depletion
• drugs (eg, flecainide, amiodarone)
• metabolic abnormalities (eg, acidosis, alkalosis)
• dyskaliemia (eg, hyperkaliemia)
• ischemia and myocardial infarction
• or electrical shock (transient)
2.4. Case 4 - Minor right ventricular perforation
A 77 year-old patient had a physiological pacemaker implanted for symptomatic sinus bradycardia, with sinus arrest. A few days after the intervention, she presented with continuous chest pain. Upon clinical examination, blood pressure was 130/80 mmHg, heart sounds were regular but a pericardial friction rub was audible. EKG showed a sinus rhythm with ventricular capture. Chest X-ray revealed a ventricular lead projecting further than the apex (Figure 4). Cardiac ultrasounds confirmed myocardial perforation by the lead and a minimal pericardial effusion. We decided to abstain from removing the lead, which would have been to some extent invasive in this elderly patient. Treatment by anti-inflammatory drug was installed and was sufficient for pain relief.
2.5. Case 5 - Skin erosion and exterisation of the generator
An 85 year old female patient is admitted for malaise and confusion. Medical history is positive for asthma treated regularly by corticoids and B2 mimetic aerosols. EKG shows a complete atrioventricular block and, after excluding all reversible causes, a physiological pacemaker is implanted. No complications are noted during her hospital stay. Having regained her autonomy and the confusional episode resolved, the patient returns to her old age home with instructions for routine care for the following weeks. A follow-up is programmed at six weeks and the cardiologist is confronted with a case of skin erosion and exteriorisation of the pacemaker generator (Figure 6). Due to the high risk of infection in this case, the device is removed and a new device is implanted on the contra-lateral side after six weeks of antibiotherapy and with negative hemocultures.
2.6. Case 6 - Ventricular lead malposition and right bundle branch block morphology on EKG
A 55 year old patient with history of hypertension, obesity, diabetes, anterior myocardial infarction and severe left ventricular dysfunction has a defibrillator implanted in primary prevention of sudden death. The follow-up is satisfactory with acceptable sensing, impedance and threshold stimulation values on the device programmer. EKG shoes a sinus rhythm with evident old anterior infarction. Chest X-ray, performed in a recumbent position and under non-optimal condition seems satisfactory and the patient is discharged. Upon follow-up one month later, the parameters of the defibrillator are still satisfactory, but the ventricular stimulation shows atypical right bundle block. Chest X-ray confirms the suspected left ventricular stimulation, via a permeable foramen ovale (Figure 7). Lead replacement is indicated seeing the high risk of thrombo-embolic complications in this young patient.
erroneous left ventricular lead placement in patient with an atrial septal defect
biventricular stimulation or cardiac resynchronisation therapy (CRT) (Figure 8)
epicardial lead placement.
some cases of “normal” right ventricular apical stimulation
2.7. Case 7 - Twiddler syndrome in a psychiatric patient
A 68 year old patient, with a history of chronic obstructive pulmonary disease and psychosis, underwent pacemaker implantation for repeated loss of consciousness due to sinus hypersensitivity. Carotid sinus massage resulted in 10 second pauses. The pacemaker was set in double chamber mode and after satisfactory programmation control (P-R sensing 2.5 mV and 12.5 mV, impedance at 564 ohms and 496 ohms respectively, stimulation thresholds at 0.5 volts/0.4 msec), the patient was discharged to his psychiatric institution. At one month follow-up, the patient has no complaints, though anamnesis is laborious. Check-up of the stimulator shows absence of detection of both P and R waves, and absence of atrioventricular capture despite maximal stimulation. Displaced leads are suspected and confirmed by chest x-ray (Figure 9). The patient later admits to having manipulated the pace generator by repeatedly twisting it around. Correct repositioning and fixation of the leads were conducted.
Risk factors include obesity (adipose tissue being less firm in these patients), female sex, elderly patients, patients known as having stigmata for character disorders (obsessive compulsive tendencies, dementia). Treatment consists of repositioning the leads, and changing them in the event of fracture. Several surgical techniques have been proposed to avoid recurrence; implanting the pacemaker generator under the aponevrosis, active lead fixation (almost always the case with implantable cardioverter-defibrillators), Parsonet's dacron pouches. Patient education, and psychiatric treatment if indicated, should be proposed.
2.8. Case 8 - Early venous thrombosis after defibrillator with resynchronisation (CRT-D) placement
A 73 year old male has a defibrillator with resynchronisation implanted for ischemic cardiomyopathy after an anterior infarction left him with a left ventricular ejection fraction of 25%. He had presented an episode of ventricular tachycardia with syncope. Implantation of the device was by the subclavian route. There were no immediate post-operative complications and good parameters were recorded for all three leads. Three weeks later, the patient complains of discomfort in the left arm, followed by oedema of the whole arm, forearm and hand (Figure 11); ultrasound and vascular tomodensitometry confirmed complete thrombosis of the left subclavian vein, of the axillary vein, leading up until the convergence of the jugular vein. Anticoagulation therapy was commenced and evolution was slow but favourable in the following weeks.
2.9. Case 9 - Unusual tachycardia after implantation of a double-chamber pacemaker
A 75 year old male is admitted for repeated fainting caused by major sinus dysfunction as shown by a 24 hour Holter monitor which revealed pauses of up to 8 seconds and paroxystic atrial fibrillation. Medical history was negative and patient was on no current treatment. EKG at rest showed a sinus rhythm with a frequency of 68 bpm and normal repolarisation. A physiological pacemaker is implanted in the operating room. After the intervention, the patient feels palpitations and an EKG recording shows probable pacemaker-mediated tachycardia (Figure 12). Programmation control shows a P-R sensing of 15.8 mV and 1.2 mV respectively, and threshold values for stimulation both inferior to 0.5 volts for 0.4 msec; a connection error is confirmed during threshold verification. Programming in AAI mode would result in VVI pacing, and programming in VVI mode would result in AAI pacing. Re-intervention allowed the correction of this connection error.
Classical "endless loop" or pacemaker mediated tachycardia is rare with the double chamber generators of today.
it is usually initiated by an extra-systole with a retrograde p wave which is easily detected and sustains the circuit. Pacemaker mediated tachycardia can also be provoked by ventricular extra-systoles, by atrial over-detection (myopotentials, interferences) or underdetection and failure to capture
long post-ventricular atrial refractory period (PVARP), excluding retrograde P wave and retrograde conduction, may prevent pacemaker mediated tachycardia
Runaway Pacemaker is due to a malfunction of the pacemaker generator resulting in life-threatening rapid tachycardia (up to 200 bpm).
the generator may malfunction for various causes, including battery failure or external damage.
the use of a magnet can reduce the rate of the rhythm induced by the defiant pacemaker. Generator replacement is necessary.
Atrioventricular nodal reentrant tachycardia. In this case, the stimulator does not intervene in the circuit.
figure 13 shows the initiation of the common type (slow-fast) of atrioventricular nodal reentrant tachycardia ; this is a typical example where the arrhythmia is triggered by an atrial extrasystole which blocks the rapid pathway of the atrioventricular node and allows flow through the slow pathway and thus initiation of the supraventricular tachycardia circuit
radiofrequency ablation is the treatment of choice.
Other reentrant tachycardia includes
orthodromic circus movement tachycardia using an accessory pathway in the retrograde direction and the AV node in the anterograde direction (concealed or not, in the Wolff-Parkinson-White syndrome)
atrial tachycardia (paroxysmal and nonparoxysmal)
2.10. Case 10 - Recurrent malaise after pacemaker implantation
A man aged 65 with history positive for high blood pressure, diabetes and renal failure actually undergoing haemodialysis receives a pacemaker for complete atrioventricular block with syncope. His treatment includes ramipril, aspirin and insulin. No immediate post-operative complications occur. Just before a haemodialysis session a few days later, the patient complains of feeling faint. An EKG shows evident signs of hyperkaliemia (very wide QRS complexes with tall peaked T waves and obliteration of the ST segment, as well as a long PR interval) and of double chamber stimulation without atrial or ventricular captures (Figure 14). Blood work-up confirms severe hyperkaliemia (potassium 7.8 mEq/L). The atrioventricular underdetection and the absence of capture are caused by the high level of potassium and corrected as soon as kaliemia is normalised by haemodialysis.
2.11. Case 11 - Important dyspnoea and malaise at follow-up
A 68 year old patient was admitted for class III dyspnoea according to the New York Heart Association (NYHA) score and repeated episodes of malaise since implantation of a single chamber pacemaker in another centre. Her personal history is positive for hypertension and sick sinus syndrome with atrial fibrillation associated with a slow ventricular rhythm and pauses of more than 8 seconds, hence the indication for cardiac pacing. Her treatment is comprised of ramipril, amlodipin and an oral anticoagulant, (acenocoumarol). Clinical examination is unremarkable. Blood pressure was 130/80 mmHg. Twelve-lead EKG shows regular ventricular stimulation at 70 beats per minute, and a basal sinus rhythm. Dissociated P waves are seen (Figure 15). Pacemaker syndrome is suspected, and confirmed. The pacemaker was reprogrammed to VVI 30 bpm to avoid deleterious ventricular stimulation in this patient.
/Comments:/ This is not a veritable implantation complication but the erroneous choice of a single chamber pacemaker whereas a physiological (or double chamber) stimulator would have avoided the problem. Pacemaker syndrome is described as a combination of symptoms evoking cardiac failure and hypotension in a patient with a cardiac stimulator (Chalvidan et al., 2000). It is caused by the loss of atrioventricular synchronism leading to a drop in cardiac output, elevated atrial pressure and hypotension. The Mode Selection Trial (MOST) investigators defined pacemaker syndrome as occurring if either one of two different criteria occurred (Link et al., 2004). The first criterion was new or worsened dyspnea, orthopnea, elevated jugular venous pressure, rales, and oedema with ventricular (VA) conduction during ventricular pacing. The second criterion was symptoms of dizziness, weakness, presyncope, or syncope, and a >20 mmHg reduction of systolic blood pressure when the patient had VVIR pacing compared with atrial pacing or sinus rhythm. Its incidence is 7-20% of stimulators in VVI mode with a sinus rhythm. Pacemaker syndrome can also be seen in AAIR mode and in double chamber modes (VDD, DDI, DDD) if the stimulator if programmation is sub-optimal or the stimulation mode is incorrectly selected. Dyspnoea should, besides pacemaker syndrome, evoke:
chronotrope insufficiency, especially during exertion, requiring programmation in rate-responsive mode.
Wenckeback functioning in DDD mode
intermittent dysfunction (sensing and pacing)
2.12. Case 12 - Acute infection of the pocket and the cardiac device
A 45 year old female patient suffering from idiopathic congestive cardiomyopathy with a left ventricular ejection fraction of 35%, class III dyspnoea on the New York Heart Association (NYHA) scale, left bundle branch block morphology, with a QRS duration of 175 msec, on EKG and under optimal medical treatment for over three months receives a pacemaker with left ventricular resynchronisation. Implantation was complicated immediately by left ventricular lead displacement. A Starfix Attain OTW 4194 (Medtronic Inc., Minneapolis, MN, USA) was necessary for stability (The Attain Starfix’s design includes three soft, polyurethane lobes near the lead tip that, when expanded, enable stable lead placement in the target location) (de Meester, 2010). After one month, the implantation site becomes suppurative (Figure 16). Local wound care and 10 day antibiotherapy did not help. Bacteriological studies revealed the presence of pseudomonas aeruginosa. Treatment required complete ablation of the material and prolonged antibiotherapy. Re-implantation on the counter-lateral side in this case was performed two months after the end of the antibiotic course.
Early complications after pacemaker and other cardiac device implantation are not uncommon. Hematoma, skin erosion and pocket infection, as well as lead displacement are the most common of these complications and should be looked for and recognised during routine follow-up, as well as during work-up of any patient presenting a new symptom in the first couple of weeks after implantation. Operator inexperience and implantation in a low-volume centre increases the risk of these complications. Adhesion to good practice and recommended guidelines is indispensable.
Allie D. E. Lirtzman M. D. Wyatt C. H. Vitrella D. A. Walker C. M. 2000Septic paradoxal embolus through a patent ovale after pacemaker implantation. 69 946 8
Barold S. S. Stroobandt R. X. Sinnaeve A. F. 2010 Cardiac Pacemakers and Resynchronization Step by Step: An Illustrated Guide,.
Blommaert D. Mucumbitsi J. De Roy L. 2000Images in cardiology. Ventricular pacing and right bundle branch block morphology: diagnosis and management. Heart. 2000; 83: 666.
Castillo R. Cavusoglu E. 2006 Twiddler’s syndrome: an interesting cause of pacemaker failure 105 119 21
Chalvidan T. . Deharo J. C. . Djiane P. 2000 Les syndromes du pacemaker. 49 224 9
Chardack W. M. Gage A. A. Greatbatch W. 1960A transistorized self-contained, implantable pacemaker for the long-term correction of heart block. Surgery, 48: 643.
Da Costa. A. Lelièvre H. Kirkorian G. et al. 1998Role of the preaxillary flora in pacemaker infections: a prospective study. 97 1791 8
Da Costa. S. S. Scalabrini Neto. A. Costa R. Caldas J. G. Martinelli Fihlo. M. 2002Incidence and risk factors of upper extermity deep vein lseions after permanent transvenous pacemaker implant: a 6-month follow-up prospective study. Pacing Clin Electrophysiol, 25 1301 6
del Rio A. Anguera I. Miro J. M. Mont L. Fowler V. G. Azqueta M. et al. 2003Surgical treatment of pacemaker and defibrillator leads endocarditis. Chest, 121 1451 9.
de Meester A. . Jacques J. M. . Jopart P. . Chaudron J. M. 1996Syncope chez une patiente porteuse d’un stimulateur cardiaque. 115 465 71
de Meester A. 2008Manuel pratique de cardiologie aiguë. 3ème édition. Antoine de Meester éditeur. European Graphics, Strépy-Bracquegnies.
de Meester A. van Ruyssevelt P. Blaimont M. Prioux D. Marcovitch O. 2010Déplacement de la sonde ventriculaire gauche: existe-t-il une possibilité de remédier à ce problème? , 22 295 9
Dickstein K. Vardas P. E. Auricchio A. et al. for the Task Force Members 20102010 focused update of ESC guidelines on device therapy in heart failure. Eur Heart J, 31 2677 87
Ellenbogen K. A. Wood M. A. Shepard R. K. 2002 Delayed complications following pacemaker implantation.Pacing Clin Electrophysiol, 25 1155 8
Essoh E. . Badot D. . Marcovitch O. . de Meester A. 2010Docteur, j’ai le hoquet à l’épaule! Une cause rare de dysfonctionnement d’un défibrillateur implantable. 129 237 40
Furman S. Schwedel J. B. 1959 An intracardiac pacemaker for Stokes-Adams seizures261: 948.
Garcia-Bolao I. Alegria E. 1999 Implantation of 500 consecutive cardiac pacemakers in the electrophysiology laboratory., 54: 339 EOF 43 EOF
Hirschl D. A. Jain V. R. Spindola-Franco H. Gross J. N. Haramati L. B. 2007Prevalence and characterisation of asymptomatic pacemaker and ICD lead perforation on CT. , 30 28 32
Kearney R. Eisen H. J. Wolf J. E. 1994 Nonvalvular infection of the cardiovascular system. 121 219 30
MS Kiviniemi MA Pirnes Eranen H. J. et al. 1999 Complications related to permanent pacemaker therapy., 22: 711 EOF 20 EOF
Klug D. . Marquie C. . Lacroix D. . Kacet S. 2003Complications de la stimulation cardiaque definitive. , 96 546 53
Klug D. Balde M. Pavin D. et al. 2007 Risk factors related to infections of implanted pacemakers and cardioverter-defibrillators: results of a large prospective study. 116 1349 56
Kusomoto F. M. Goldschlager N. 1996Cardiac pacing. , 334 89 97
Le Dolley Y. Thuny F. Bastard E. Riberi A. Tafanelli L. Renard S. et al. 2009Pacemaker Lead Vegetation Trapped in Patent Foramen Ovale. e 223 4
MS Link AS Hellkamp Estes N. A. M. et al. 2004 High incidence of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based pacing in the Mode Selection Trial (MOST)., 43 2066 71
Mahapatra S. Bybee K. A. Bunch T. J. Espinosa R. E. Sinak L. J. Mc Goon M. D. Hayes D. L. 2005 Incidence and predictors of cardiac perforation after permanent pacemaker placement.Heart Rhythm, 2 907 11
Nicholson W. J. . Tuohy K. A. . Tilkemeier P. 2003Twiddler’s syndrome. , 34 1726 7
Oginosawa Y. Abe H. Nakashima Y. 2002 The incidence and risk factors for venous obstruction after implantation of transvenous pacing leads.Pacing Clin Electrophysiol, 25 1605 11
Oupadia P. Ramasswamy K. 1998R-on-T phenomenon” Images in Cardiology 338: 1812 EOF
Res J. C. J. de Priester J. A. AA van Lier van Engelen C. L. J. M. Bronzwaer P. N. A. Tan-H P. Visser M. 2004 Pneumothorax resulting from subclavian puncture: a complication of permanent pacemaker lead implantation 12 101 5
Rozsmus G. Daubert J. P. Huang D. T. Rosero S. Hall B. Françis C. 2005Venous thrombosis and stenosis after implantation of pacemakers and defibrillators. Pacing Clin Electrophysiol, 13 9 19
Sohail M. R. Uslan D. Z. Khan A. H. et al. 2007 Management and outcome of permanent pacemaker and implantable cardioverter-defibrillator infections 49 1851 9
Trohman R. G. Kim M. H. Pinski S. L. 2004 Cardiac pacing: the state of the art. 364 1701 19
van Eck J. W. M. van Hemel N. M. Zuithof P. et al. 2007 Incidence and predictors of in-hospital events after first implantation of pacemakers 9 884 9
BM Van Gelder Bracke F. A. Oto A. Yildirir A. Haas P. C. Seger J. J. et al. 2000 Diagnosis and management of inadvertently placed pacing and ICD leads in the left ventricle: a multicenter experience and review of the literature.Pacing Clin Electrophysiol, 23 877 83
Vardas P. E. Auricchio A. Blanc J. J. et al. 2007for the Task Force Members. Guidelines for cardiac pacing and cardiac resynchronisation therapy. (2007). Europace, 9 959 98
Wiegand U. K. Le Jeune D. Boguschewski F. Bonnemeier H. Eberhardt F. Schunkert H. Bode F. 2004 Pocket hematoma after pacemaker or implantable cardioverter defibrillator surgery: influence of patient morbidity, operation strategy, and perioperative antiplatelet/anticoagulation therapy. 126 1177 86
Zoll P. M. 1952 Resuscitation of the heart in ventricular standstill by external electric stimulation, 247: 768.