Modern Pacemakers - Present and Future

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Complications of Pacemaker Implantation
Michele Schiariti, Mariateresa Cacciola and Paolo Emilio Puddu
University of Rome “La Sapienza” and Ospedali Riuniti, Reggio Calabria,
Italy
1. Introduction
The use of permanent pacemakers (PM) and implantable cardioverter–defibrillators (ICD)
continues to grow worldwide (Birnie et al., 2006; Goldberger & Lampert, 2006) with over 3
million PM and 250000 ICD in use by the end of last century (Chua et al., 2000). The rate of
device implantations is increasing with aging of the general population and expanding
indications. Despite the relative ease of device implantation, the complication risk is still
present and sometimes underestimated. The proposal for this chapter is at addressing the
most common intra-operative and delayed complications with a special eye to the surgical
complications. We will also address electromagnetic interference and psychological
problems.
2. Complications related to the location type
Depending on the location type (venous access, pocket, lead and generator) it is possible to
dissect several different clinical presentations of complications related to PM implantation
which occur, more frequently, in the immediate post-operative course.
2.1 Venous access-related complications
Pneumothorax. This complication occurs uncommonly and is directly related to operator
experience, the difficulty of the subclavian puncture, and is almost eliminated using the
cephalic cut-down technique. However, these traditional comparisons may become obsolete
as the axillary vein cannulation technique (Martin et al., 1996) threatens to eliminate this
controversy. Pneumothorax is often asymptomatic and noted on routine follow-up plain
chest radiograph, but occasionally it requires active medical treatment including intercostal
chest drain and aspiration. Aggarwal et al. (1995, 1996) reported a large series of 1088
consecutive patients; pneumotorax represented an overall rate of 1.9% of subclavian
insertions. There was no significant difference in the pneumothorax rate between dual
chamber (n = 12, 2.1%) and single chamber (n=7, 1.4%). Pneumothorax required active
medical treatment in 8 patients (0 8%); 5 patients had an intercostal chest drain inserted and
3 were treated by aspiration. A further 11 patients (1.0%) developed an insignificant
pneumothorax (< 10% of pulmonary field in chest x-ray film with no symptoms or
progression in subsequent chest radiograph). More recently, Zhan et al. (2008) collected over
67000 patients and presented similar rates. Finally, Pakarinen et al. (2010) also concluded, in
a retrospective 1-year single-centre survey, that short-term implantation-related

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complications of contemporary device therapy are still frequent, and occur much more
frequently when trainees rather than experienced cardiologists are the operators.
Hemothorax. This complication results from trauma to the great vessels rather than the
lung. The risk can be minimized by direct inward and outward passes of the puncture
needle rather than a side-to-side, potentially “lacerating” movement. If an arterial puncture
is performed, recognition, withdrawal, and digital pressure are important. It is important to
remember that the artery needs not be cannulated with the introducer. It is essential to
always check the fluoroscopic path of the guidewire into the inferior vena cava before
introducer insertion. In the Aggarwal et al. (1995) series, the inadvertent arterial puncture
was the most common intra-operative complication which occurred in 27 patients (2.7% of
subclavian insertions): no serious sequelae ensued.
Air embolism. Deep inspiration at the time of central venous access may cause significant
air to be drawn into the venous system due to the physiological negative pressure
developed. It can be prevented through operator care and using introducers with
haemostatic valves. The diagnosis is obvious because it is heralded by a hissing sound as the
air is sucked in and with the fluoroscopic confirmation that follows. Patients are
surprisingly tolerant of this occurrence. Usually no therapy is required, as the air is filtered
and consequently absorbed in the lungs. The real incidence of this occurrence is not clearly
defined in the Literature. However, several cases are reported (Ninio & Hii, 2006; Ostovan &
Aslani, 2007; Turgeman et al., 2004): respiratory distress, hypotension, and arterial oxygen
desaturation were the most frequent consequences, which was related to the size of the
embolus. It is then appropriate to administer 100% oxygen along with inotropic support in
some cases. Aspiration of the embolus from the right heart has also been successfully
reported (Ostovan & Aslani, 2007).
2.2 Pocket-related complications
Hematoma. Pocket hematoma is an acute, relatively common complication after PM or ICD
implantation. It was estimated that 14 to 17% of early reoperations were due to this
complication (Aggarwal et al., 1995; Chauhan et al., 1994). The site of bleeding may be the
pocket or back-bleeding around the lead venous entry site. The use of electro-cautery is
useful to minimize pocket related bleeding. Bleeding from the venous entry site usually
subsides during the procedure but ongoing bleeding is controlled by a firm suture placed
through and around the lead entry/pectoral muscle interface (Pavia & Wilkoff, 2001).
Usually, hematomas are managed conservatively unless expanding in size, tense or painful.
In these occasions, reoperation to evacuate the hematoma and identify and arrest the site of
bleeding is required. Evacuation was required in 1 to 2% of implant cases in a recent series
(Kiviniemi et al., 1999). The risk is increased in anticoagulated patients. The large number of
patients receiving coumarin for atrial fibrillation or valve replacement management of
anticoagulation might be a major determinant of hematoma development. On the other
hand, the complete avoidance of perioperative anticoagulation therapy might promote
thromboembolic events and, in particular, cerebral stroke. Intravenous heparinization has
been shown to be associated with an increased risk of hematoma development (Michaud et
al., 2000) while oral anticoagulation therapy with warfarin did not increase the rate of
pocket hematoma in two small series (al-Khadra, 2003; Goldstein et al., 1998). The increasing
use of low-molecular-weight heparin and more effective inhibition of platelet aggregation

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with ticlopidine/clopidogrel also may affect the susceptibility to intra-operative bleeding
and pocket hematoma. It has been shown that long-term warfarin with an international
normalized ratio of about 2.0 is safe over a 15-year experience (Belott & Reynolds, 2000),
although anticoagulation is in general discontinued for at least the duration of the
procedure. Wiegand et al. (2004) investigated the influence of patient comorbidity,
implantation strategy, operator experience, antiplatelet therapy, and anticoagulation
therapy on hematoma rate on a large series of 3164 devices (2792 pectoral PM and 372 ICD).
Predictors of hematoma occurrence were determined prospectively and were analyzed by
multivariate regression analysis. According to the results of this important investigation
(Wiegand et al., 2004) the following recommendations were given: a) implantation, with the
patient receiving combined ASA and clopidogrel treatment, should be performed only by
very experienced implanters soon after coronary stenting has been performed (i.e. less than
1 month after) in patients who are highly symptomatic or in whom PM or ICD implantation
is vitally indicated; b) in all remaining patients, either therapy with thienopyridine should
be discontinued or implantation should be performed when drug treatment can be safely
stopped; c) perioperative high-dose heparinization should be reserved for patients with
artificial valves (particularly those in the mitral position) and those who have recently
experienced arterial embolism, cardioversion, and deep venous thrombosis or pulmonary
embolism. Continued oral anticoagulation therapy might be a suitable alternative in the
latter patients. All remaining patients who are in need of anticoagulation therapy should
receive low-dose heparinization post-operatively until oral anticoagulation therapy is re-
established.
Erosion and wound dehiscence. It is a sub-acute complication after device implantation
caused by a progressive skin erosion. If the subcutaneous pocket fashioned at the time of
initial implantation is too small for the device, undue tension on the overlying skin may
cause gradual subcutaneous tissue, and possible eventual skin erosion. Care should also be
taken when fashioning the pocket to create the pocket plane on the surface of the muscle. If
the pocket is too superficial, erosion may also occur. In the event of erosion, the associated
potential for infection is high and therefore extraction of the total device-lead system is
usually advised.
Wound pain. Minor wound pain is expected after device implantation, almost always
controlled with simple analgesia. In general, the pre-pectoral site is extremely well-tolerated.
Continuing pain will usually improve or manifest an obvious infection eventually.
However, pain that initially improves then recurs or occurs temporarily remote from the
implant may suggest infection even in the absence of any outward localizing signs, and
consequently may necessitate surgical exploration or even empirical removal and reimplant
at another site. Alternatively, mechanical trauma from the device location adjacent to
anterior chest wall structures may be the culprit. In this situation, device relocation or
pocket revision may be indicated.
Infection. Similar to other prosthetic materials, infections complicate a small proportion of
patients with these devices. Along with the increase in device implantation, the incidence of
device infections has also been increasing, but at a faster rate. (Voight et al., 2006). In the
USA, data from Medicare recipients from 1990 to 1999 showed an increase in the number of
device infections from 0.94 per 1000 recipients to 2.11 per 1000 recipients, an increase of
124%; the estimated rate of infection of endocardial leads being between 1 and 2%, but

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varying from 0.13 to 12.6%. (Cabell et al., 2004; Voight et al., 2006). Grimm et al. (1993)
reported an incidence of ICD system infection ranging from 2 to 8%. The exact reason for a
time-related increase of infections remains unexplained, but it is hypothesized to be due to
increasing co-morbidities in device recipients, improved surveillance and detection of
cardiac device infection, and improving survival of patients with devices (Uslan & Baddour,
2006). The mortality of persistent infection when infected leads are not removed can be as
high as 66% (Rettig et al., 1979). The physical manifestations range from mild systemic
symptoms with no local reaction to fulminant life-threatening sepsis. Early infections (no
more than 60 days from implant) tend to be more clinically evident as opposed to the more
indolent course of late onset infections. These infections can present with only pain at the
implant site. When infection is present, complete device removal with transvenous lead
extraction is followed by antimicrobial therapy with the device reimplanted at a later date.
In the Chua et al. (2000) experience including both PM and ICD leads, the median time for
device reimplantation was 5 days with no subsequent evidence of recurrent or new infection
at a mean follow-up period of 46 weeks. Partial system removal is associated with high
recurrence rate and should be reserved for very selected cases. Once a strong clinical
suspicion for infection is established, the whole system should be considered contaminated.
The time of onset of the infection is extremely variable. Margey et al. (2010) reported a
median duration from device implant or revision to presentation with confirmed cardiac
device infection of 150 days (range 5–2920 days, with an interquartile 25% of 35 days and an
interquartile 75% of 731 days). Fever, chills and malaise were the most common presenting
symptoms. Evidence of generator site inflammation was present in 90%. Frank erosion or
purulent discharge could be identified in 66%. A third of cases met diagnostic criteria for
cardiac device related endocarditis. The majority had non-specific laboratory abnormalities,
including elevation in leukocyte count, anaemia, elevated erythrocyte sedimentation rate, or
C-reactive protein level. Therefore, the clinical diagnosis of device infection is very easy.
Microbiological findings. It is not always possible to define the agent of infection: in a very
recent report (Margey et al., 2010) out of 39 cardiac device infection cases, a causative
organism was identified only in 62%. The most frequent causative organism was methicillin
sensitive Staphyloccoccus aureus (30.8%), followed by coagulase negative Staphylococcus
(20.5%), and Streptococcus species (7.7%). Blood cultures were performed in 84% of the
cardiac device infection group, and were positive in 54% of these cases. Cultures of
generator site tissue and lead tips were performed in those undergoing device extractions
(82%) and were positive in 38 and 18%, respectively. In cases where all 3 swabs were
positive, the same causative organism was identified in each case. Of those patients in
whom blood cultures were negative, all had already received antibiotic therapy by the time
cultures were drawn.
Echocardiographic findings. Cardiac ultrasound does not seem to have an high diagnostic
sensitivity. In the Margey et al. (2010) series 87% of the patients underwent transthoracic
echocardiography during their admission and 36% also underwent transoesophageal
echocardiography. In those in whom echocardiography was performed, vegetations were
identified on the lead in 18%, and involving the heart valves in 5%. The tricuspid valve was
the only valve involved. On the other hand, patients with intracardiac vegetations identified
on transesophageal echocardiogram can safely undergo complete device extraction using
standard percutaneous lead extraction techniques. Permanent devices can safely be
reimplanted provided blood cultures remain sterile. The presence of intracardiac

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vegetations identifies a subset of patients at increased risk for complications and early
mortality from systemic infection despite device extraction and appropriate antimicrobial
therapy (Grammes et al., 2010).
2.3 Lead-related complications
Cardiac perforation. Permanent PM implantation may be complicated by cardiac
perforation, which can lead to longer hospital stays, tamponade, or even death (Aizawa et
al., 2001; Ellenbogen et al., 2002; Garcia-Bolao et al., 2001; Gershon et al. 2000). The incidence
of perforation after permanent PM reportedly is between 0.5% and 2%, but the predictors of
perforation have not been defined (Hill, 1987; Sivakumaran et al., 2002). Lead perforation is
a less-recognized delayed complication of device implantation. Delay in recognition may
prove fatal. Careful evaluation of pacing and sensing thresholds and follow-up
echocardiographic evaluation is mandatory to remain vigilant for this potentially fatal
complication. The clinical manifestations of significant perforations are variable and include
chest pain, dyspnoea, and hypotension. These signs, in conjunction with a new pericardial
effusion immediately following permanent PM implantation, suggest PM-related cardiac
perforation. Predictors of post implantation pericardial effusion, which serves as a marker of
perforation, include concomitant use of trans-venous PM, steroid use within 7 days, and
older age. Perforation of the right ventricle as a late complication of device implantation is
rare and requires a high suspicion for prompt recognition and intervention. Routine chest
radiography may not be diagnostic, and further testing such as CT scan and
echocardiography are essential, combined with PM interrogation, for evaluation of high
thresholds. A higher clinical suspicion should be maintained in the elderly, in whom
perforation occurs more frequently (Mahapatra et al., 2005). In addition, consideration
should be given in the elderly to implant the lead in sites other than the right ventricular
apex, such as the right ventricular septum or outflow tract, in an attempt to minimize the
risk of this complication later during the follow-up. Acute perforation of the right atrium or
right ventricle has been reported in up to 1% of patients (Chauhan et al., 2005).
Malposition. There have been several reports of inadvertently lead malposition during PM
implantation. Some of those are related to cardiac structural abnormalities. In patients with
an atrial septal defect lead could be erroneously implanted in the left ventricle. The presence
of a right bundle branch block configuration during ventricular pacing should induce the
suspect of a malposition that can be confirmed by a lateral chest x-ray or by ultrasound. The
malposition could be discovered years after the implantation and pacing (Vanhercke et al.,
2008). There are not recommendations about the removal of lead if there are not concomitant
complications such thrombus, embolism or the posterior mitral leaflet perforation causing
an acute mitral incompetence (Seki et al., 2009; Van Gelder et al., 2000). In any case, if timely
removal of a malpositioned lead in the left ventricle, through a patent foramen ovale or
atrial septal defect is not performed, life-long anticoagulation with warfarin should be
recommended. Cases are reported too of a malpositioned lead, which had inadvertently
been inserted into the left subclavian artery and passed through the aortic valve into the left
ventricular apex (Reising et al., 2007), despite the finding of an apparently elevated
“venous” pressure at the time of insertion. The error was not detected despite the anterior–
posterior chest radiography (no lateral view), electrocardiograms, and a computed
tomography scan of the chest with contrast during which the lead was said to be in the right
ventricle. Careful analysis of post-procedure electrocardiograms and lateral chest x-ray film

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images can minimize the chance that such an error will go undetected There is no consensus
as to how to proceed in cases such as this because few are reported in the Literature, which
may also be related to publication bias. Recently, it was suggested that transcatheter lead
removal should not be performed because of an inability to detect the presence of thrombi
on the lead wires (Van Gelder et al., 2000). To our knowledge, the risk of trauma to the valve
leaflets has not yet clarified. However, cases of endocarditis have been reported, including
one with a large aortic valve vegetation (Schulze et al., 2005).
Lead dislodgement. Lead dislodgement is a clinically relevant and possibly dangerous
occurrence. It typically occurs either early (within the first 6 weeks of implantation) or late
(beyond the first 6 weeks of implantation), occasionally very late dislodgments were also
described (Tokano et al., 2004). Early dislodgements are more common then late
dislodgements. Atrial lead dislodgment occurs more commonly than ventricular
dislodgements in the early period (Chauhan et al., 2005). The incidence of early
dislodgement of a ventricular lead in a DDD PM was 0.5 to 2.5% (Aggarwal et al., 1995;
Fortescue et al., 2004). Lead dislodgment occurs less commonly as a consequence of
advancements in pacing lead placement and lead design. After dislodgement, the lead
usually remains intracardiac but cases are described where leads were completely pulled
out (Von Bergen et al., 2006), as in the lead dislodgement secondary to a “ratchet-like”
mechanism through the sewing sleeve. Fluoroscopy is occasionally needed to identify the
location of the lead tip. However, some mechanisms of PM lead dislodgement involve
retraction of the lead toward the generator. This includes Twiddler’s syndrome, which
refers to lead dislodgement due to conscious or unconscious manipulation of the pulse
generator causing it to rotate around its long axis (Abrams & Peart, 1995; Bracke et al., 2005;
Chauhan et al., 1994; Higgins et al., 1998; Newland & Janz, 1994; Solti et al., 1989). Typically,
placement beneath the pectoral muscle and suturing the generator to the underlying fascia
is thought to preclude the patient from manipulating the device. Additionally, “Reel
syndrome” (Carnero-Varo et al., 1999; Vural et al., 2004) has been described, which entails
the generator rotating around its transverse axis “reeling” in the lead. In certain adult
populations, such as in patients with a history of significant weight loss, the "Sagging Heart
syndrome" may represent a previously unrecognized cause of acute lead dislodgment (Iskos
et al., 1999). It is a rare form of lead dislodgment that may occur due to an unexpected and
marked postural descent of the heart after permanent PM implantation. Iskos et al. (1999)
described this, in 2 patients, which was related to a history of morbid obesity followed by
weight loss of over 40 kilograms. Lead replacement with active fixation leads was required
in both cases.
2.4 Generator-related complications
Set screw loose. Set screw could be a cause of complication: although PM infections that
were apparently localized at set screw site were reported (Henrikson & Brinker, 2006), the
most important complications are related to the loose of set screw and of electrical contact.
Inappropriate mode switching in a dual chamber PM due to oversensing of a high
frequency signal from a conductor/ring discontinuity (loose set screw) was reported by
Kuruvilla et al. (2002). A retrospective review of complications with connectors and lead-to-
header interfaces was performed (Tyers et al., 1992) years following 649 pacing procedures
between 1980 and 1990. There were 88 lead revisions (13.6%), 81 device replacements or
modifications (12.5%), and 480 new implants (74%) using devices of 5 manufacturers. Two

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basic connector types were studied, one utilizing a set screw and the other using a side-lock
compression fitting. The set screw makes electrical contact and mechanically secures the
lead connector pin with a set screw insulated by a self-sealing grommet or an integral or
separate set screw cover. The side-lock makes electrical contact with an automatic spring
mechanism while the plastic lead terminal is secured in the connector block of the
pacemaker by a Delrin side-lock compression fitting. The follow-up during at most 12 years
of 459 set screw connector devices gave 14 complications (3.1%) whereas 82 side-lock
connector devices were followed for up to 5 years with 1 complication (1.2%). The set screw
and side-lock connectors were reliable over the period of follow-up. Although the
complication rate appeared lower with the side-lock, follow-up was shorter and the number
of implants smaller. With the leads used in this study (Tyers et al., 1992), the side-lock
proved to be a desirable feature due to simplicity, speed, safety, and ease of use. One
limitation is the requirement for a precise IS-1 connector terminal diameter.
3. Complications unrelated to the location site
There are a series of complications after PM or ICD implantation, more frequently occurring
late after insertion, which do not recognize a clear-cut relation with the location site and
rather present as a more generalized syndrome.
3.1 Superior vena cava syndrome
Superior vena cava syndrome (SVCS) is characterized by gradual, insidious
compression/obstruction of the superior vena cava. Although the syndrome can be life-
threatening, its presentation is often associated with a gradual increase in symptomatology.
For this reason, diagnosis is often delayed until significant compression of the superior vena
cava has occurred. Initially, there are few symptoms, however, over time, symptoms of
superior vena cava compression/obstruction gradually develop. As the compression
becomes more severe, the patient may develop shortness of breath and swelling of the arms
and face. SVCS is chiefly associated with malignancy. Currently, more than 90% of patients
with SVCS have an associated malignancy as the cause. Of the nonmalignant causes of
SVCS, thrombosis from central venous instrumentation (catheter, PM, guidewire) is an
increasingly common event, especially as these procedures become more common. PM-
induced SVCS is a rare complication of permanent PM insertion, with an estimated
prevalence ranging from 1:40000 to 1:250, and usually occurring more than 1 month after
implantation (Bolad et al., 2005; Gilard et al., 2002; Spittel & Hayes, 1992). The obstruction is
internal and composed of thrombus, fibrosis, or a combination of the two, typically
involving the pacing wires within the superior vena cava (Spittel & Hayes, 1992). Although
the mortality associated with benign causes of SVCS is low, those patients who become
symptomatic are often debilitated by it, necessitating intervention. Various therapies have
been used to treat PM-related SVCS. The various treatment modalities used to relieve SVCS
symptoms may be summarized under the following categories: a) anticoagulation (heparin,
warfarin, acenocoumarol, phenprocoumon, dicumarol); b) thrombolysis, either systemic or
catheter-directed (tissue plasminogen activator, urokinase, alteplase, or streptokinase); c)
surgical, intervention on superior vena cava using a spiral saphenous vein conduit, or
reconstruction using a pericardial patch, or a thrombectomy; d) balloon venoplasty alone;
and e) stenting of the lesions (usually preceded by venoplasty) using wallstents, SMART

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stents, Palmaz stents, or Z stents. There is no current consensus about their relative efficacy
and merits. Riley et al. (2010) recently reviewed and summarized all of the reported cases of
this complication that were treated in order to aid clinical decision making and spur future
research in this area. It was recognized from the outset of this venture that any attempt at a
pooled analysis of results could be significantly hampered by the small number of cases in
each treatment group and publication bias, particularly the underreporting of treatment
failures and of SVCS recurrences after initially successful interventions. The poor efficacy of
anticoagulation and thrombolysis is not surprising given that histological studies in cases of
lead-induced SVCS have shown that only a minority of cases are due to thrombosis without
concomitant fibrosis; these types of lesions usually present relatively soon after device
implantation. The majority are due to fibrotic narrowing and superimposed thrombosis,
particularly if symptoms develop after more than a year (Gilard et al., 2002); among patients
reported in this survey, the median interval between implantation and onset of SVCS
symptoms was 48 months. Therefore, residual superior vena cava stenosis after successful
thrombolytic therapy is likely a factor in re-thrombosis and short symptom-free periods
(Leonelli et al., 2000). The disappointing results of venoplasty alone may also reflect high
rates of restenosis. For example, patency rates as low as 30% have been reported at 1-year
following balloon dilations of benign axillary and subclavian vein stenoses (Bolad et al.,
2005; Frances et al., 1995; Gilard et al., 2002; Spittel & Hayes, 1992). The short-term results of
surgery and stenting are more encouraging but the paucity of data on long-term efficacy
and outcomes is a matter of concern. Even though surgical reconstruction has been practiced
for over three decades, adequate follow-up data were only available for 17 patients over a
median period of 16 months. Given that surgical reconstruction is a highly invasive and
expensive undertaking, it is not surprising that percutaneous intervention employing
venoplasty plus stenting has become the most commonly reported treatment for SVCS.
3.2 Pericarditis
The first reported case of pericarditis following permanent PM implantation was published
in 1975 (Kaye et al., 1975). Pericarditis should be distinguished from acute or delayed lead
perforation in which a migration of the electrode tip is observable. In pericarditis there are
no changes in the tip position at x-ray examination and no changes in pacing or sensing
thresholds (Ellenbogen et al., 2002). To date only a few cases of pericarditis related to PM
implantation have been published (Ellenbogen et al., 2002; Kaye et al., 1975; Kono et al.,
2008; Levy et al., 2004; Snow et al., 1987; Vinit et al., 2007;). Clinical manifestation of
pericarditis resembled the classic post-pericardiotomy syndrome with pleuritic chest pain,
dispnoea, and the presence of pericardial and pleurical effusion, raised erythrocyte
sedimentation rate without polyarthopathy. Usually, effusion does not require pericardio-
centesis because of the small size of effusion that responds to non steroid drugs or to
steroids. Large effusion volumes could requires pericardiocentesis when tamponade is
present. In the Greene et al. (1994) and Levy et al. (2004) series a higher incidence of
pericarditis was found when active fixation leads were used overall for atrial stimulation.
Several reported cases were related with an atrial active-fixation lead (Schiariti et al., 2009;
Sivakumaran et al., 2002). Generally, pericarditis after permanent PM implantation has a
benign and self-limited course. However, replacement of an active-fixation lead with a
passive one has also been reported in order to prevent recurrence of pericarditis (Schiariti et
al., 2009).

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3.3 Undersensing
Loss of ventricular sensing could be caused by dislodgment or mechanical damage to the
lead connected to the system, as perforation of the insulating sheath. Sometimes
undersensing could be resolved after repositioning the lead, restoring its integrity with
silicone adhesive as described by Costeas & Schoenfeld (1991), or reprogramming the
device. In the past the ability to attach an unprotected unipolar lead to a bipolar connector,
shared by the Voluntary (VS-1) and International (IS-1) designs, invited the possibility of
injury to the insulating sheath by accidental tightening of the proximal screw. Sensing in PM
and ICD is crucial to normal device behaviour. Since both devices treat different
arrhythmias, the technical approach to signal detection is also completely different. A PM
has a fixed threshold of sensing, above which events are sensed and therapy of the device
withheld. On the other hand, the defibrillator has a variable threshold of sensing to detect
tachyarrhythmias, with sometimes very small and changing electrogram amplitudes. Van
Casteren et al. (2009) described undersensing of ventricular fibrillation due to interference
between a PM and defibrillator in the same patient. The R-on-T phenomenon is a well-
known entity that predisposes to dangerous arrhythmias. Typically, a premature ventricular
complex occurring at the critical time during the T wave of the preceding beat precipitates
ventricular tachycardia and fibrillation. This phenomenon can occur not only in
asynchronous ventricular PM, but also in synchronous PM, if loss of sensing of the intrinsic
rhythm becomes evident (Chemello et al., 2010).
3.4 Oversensing
Oversensing is a phenomenon potentially leading to ICD malfunctioning by interfering with
intracardiac signals and usually is related to myopotentials, T-waves, electrical spikes of an
additionally implanted PM or other technical devices i.e. microwaves, stimulation therapy
in physiotherapy, and electric coagulation (Lin et al., 2004; Schulte et al., 2001; Secemsky et
al., 1982; Weretka et al., 2003). The ICD system often misinterprets these cardiac/non-
cardiac potentials as a malignant arrhythmia and delivers inappropriate shock therapy,
which in many patients is an extremely uncomfortable event and greatly affects quality of
life. In some cases, inappropriate therapy delivery is described as potentially life-threatening
(Kiviniemi et al., 1999), especially when the shock falls in the vulnerable phase of QRS
complex, triggering ventricular tachycardia or ventricular fibrillation (VF). Rauwolf et al.
(2007) evaluated in a large cohort of 518 ICD patients the incidence and various types of
ventricular oversensing (VO), the occurrence of inappropriate shock deliveries as well as the
frequency of complications requiring invasive procedures to solve VO during a long-term
follow-up. The most frequent oversensing mechanism was observed as T-wave oversensing
in 10 patients, 8 (1.5%) patients were noticed with VO due to myopotentials; 5 patients
suffered from VO due to electrode failure and consecutive noise sensing with inadequate
therapy delivery. Double-counting was recorded in 4 patients, leading to 8 inadequate
shocks in 2 patients and short episodes without therapy delivery; 3 patients experienced VO
according to electromagnetic field interference with the ICD device by inducing an
alternating current in the sensing electrode or to alternating current. In 1 patient, microwave
energy was applied for pain relief at the skin close to the ICD pocket. The signals from
electromagnetic field transmitter were detected from the atrial and ventricular channel of
the ICD, misinterpreted as VF inducing an inappropriate shock delivery. The second patient
had VO while swimming through an electrically opening pool door. In another case, the

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inadequate shock was due to an alternating current application during physiotherapy
session using electric stimulation of the skin. There were 6 patients who had an ICD and an
additionally implanted PM. There were different reasons for these double device
implantations: a) first ICD generation with large volume were implanted abdominally; b)
first ICD generation were only available as single-chamber devices; c) pre-existing
biventricular pacemaker for CHF therapy; and d) insurance requirements (Geiger et al.,
1997; Shivkumar et al., 2000).
3.5 Crosstalk
The oversensing of an atrial pacing pulse in the ventricular channel, has been described
primarily in patients with unipolar PM and high atrial outputs (Helguera & Pinski, 2005).
Although their high operating ventricular sensitivity could make ICD prone to cross-talk
inhibition, this complication has been very uncommon. Crosstalk is one of the serious
complications occurring with dual-chamber PM and ICD and it is defined as the
inappropriate detection of a spontaneous or PM-generated event in one channel by the other
channel, which can cause the inhibition of the second channel’s output. There are two
functions designed to prevent the crosstalk inhibition. One is the ventricular blanking
period that coincides with the atrial stimulus. This prevents the detection of the atrial spike
or activation that could cause the inhibition of the ventricular channel output. An additional
backup system is the ventricular-safety-pace, which prevents asystole if crosstalk occurs due
to atrial far-field activity sensed after the blanking period of the ventricular electrode.
3.6 Pacemaker syndrome
The PM syndrome consists of the cardiovascular signs and symptoms of heart failure and
hypotension induced by the loss of both A-V and V-V synchrony that is associated with
right ventricular apical pacing. It was first described by Mitsui et al. (1969) and occurs with
single o dual chamber pacing mode. The clinical adverse effect are most severe when intact
ventriculo-atrial conduction is present. Atrial contraction can coincide with ventricular
systole against closed atrioventricular valve. This situation may lead to raised mean
pressures in both atria, to atrial dilatation and retrograde blood flow into vena cava and
pulmonary veins and contributes to decreased cardiac output. Nishimura et al. (1982)
showed a great decrease in blood pressure more than 20 mmHg is suggestive of PM
syndrome. When ventricular function is normal, estimates of atrial contribution to cardiac
output vary from 15-20%. In elderly patients, in hypertensive cardiomyopathy, hypertrophic
cardiomyopathy, and restrictive cardiomyopathy, the atrial kick contributes as much as
50%. The reduction in cardiac output associated with non physiologic pacing and loss of
atrioventricular synchrony triggers changes in vascular tone. The autonomic nervous system
enhances sympathetic activity modulated by arterial baroceptors which are triggered by low
blood pressure (Alicandri et al., 1978; Ellenbogen et al., 1990; Pehrsson et al., 1988). The
increase in left atrial, pulmonary and left ventricular filling pressures result in inhibitory
reflexes mediated by vagal nerve and in increased production of atrial natriuretic peptide, a
potent arterial and venous vasodilator (Theodorakis et al., 1992). The opposing reflexes may
cause an inadequate vasoconstrictor response and decrease vascular tone. The dual chamber
pacing does not ensure that pacemaker syndrome will not develop (Travill & Sutton, 1992).
When the leads stimulate the myocardium to depolarize, paced depolarization of both atria
and ventricles occurs cell to cell fashion rather than via usual conduction pathways. This

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depolarization is slower and less efficient and can result in dyssyncrony of atria and
ventricles and of the right and left sides of the heart. It is necessary to program an
appropriate atrioventricular delay between 120 and 200 ms. Too much short a delay reduces
filling of the ventricles in diastole and of the atria during systole; too much a long one may
produce asynchrony. In presence of atrio-ventricular block a rapid atrial pacing (AAI or
AAIR) prevents the regular atrial filling and reduce cardiac output. Many patients cannot
tolerate the rapid pacing associated with activity mode (Ellenbogen et al., 1997; Ellenbogen
et al., 2007). An inappropriate mode switching of DDDR pacing in response to interference
noise or dying battery, then rhythm change, can also cause PM syndrome. The retrograde
depolarization of the atria which occurs with dual- o single–chamber devices can cause
endless-loop tachycardia or PM-mediated tachycardia (Pioger et al., 2007).
The majority of symptoms of PM syndrome are likely attributable to the reduction in cardiac
output that is associated with right ventricular pacing. It induces a contraction similar to
that caused by left bundle branch block, asynchronous ventricular contraction leading to
altered diastolic filling time, increase in mitral regurgitation and reduction in left ventricular
ejection fraction (Lamas & Ellenbogen, 2004). The cardiac output is greater during AAI
pacing than with dual-pacing DDD. Wigger (1925) showed that ventricular pacing results in
reduced ventricular-pump function in mammals. Ventricular desyncronization imposed by
pacing results in chronic left ventricular remodeling, including asymmetric hypertrophy
and dilatation. Ventricular pacing increases atrial pressure and size, as well as to favor the
development of electrophysiological proprieties that could facilitate the development of
atrial fibrillation. In patients with an ICD, dual-chamber pacing paradoxically led to
increased risks of heart failure, hospitalization and death by a factor of 1.6 by inducing
ventricular pacing (Wilkoff et al., 2002). Bordachar et al. (2004) showed an increase in
cardiac output from 2.2 l/min at baseline to 3.8 l/min with institution of biventricular
pacing in patients with heart failure.
Symptoms of PM syndrome are nonspecific and diagnosis depends heavily on correlation
between onset of symptoms and onset of pacing or change in pacing mode. The PM
interrogation plays a crucial role in determining PM mode contribution to symtoms:
dyspnoea on exertion, paroxysmal nocturnal dyspnoea, orthopnoea, hypotension, pre-
syncope and syncope (Furman, 1994). Physical examination can often reveal elevated neck
veins, rales, and pedal oedema. Syncope is uncommon and usually associated with systolic
blood pressure declines of greater than 20 mmHg. The other symptoms attributed to PM
syndrome include easy fatigability, malaise, headache, and sensation of fullness and
pulsations in the head and neck. A diagnosis can be confirmed by placing a magnet over the
PM, converting the system to VOO mode at predetermined rate to induce ventriculo-atrial
conduction and symptoms (upright) (Ross & Kenny, 2000). ECG, Holter monitor or event
recorder may reveal a prolonged PR interval, ventriculo-atrial conduction, or atrio-
ventricular dissociation. Echocardiogram may show decreased cardiac output with
ventricular pacing versus conduct sinus activity or atrio-ventricular synchronous pacing.
Symptoms usually resolve after reprogramming PM parameters, such atrio-ventricular
delay, postventricular atrial refractory period, sensing level, and pacing threshold voltage or
using hysteresis to help maintain atrio-ventricular synchrony in patients with VVI PM and
intact sinus node function or addition of an atrial lead.
The incidence of PM syndrome in various studies ranges from 25% (Travill & Sutton, 1992)
to 83% (Heldman et al., 1990), depending to large degree on diagnostic criteria and to the

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therapy used for diagnosis. When surgical revision is required to upgrade a patient from
VVIR pacing, the incidence has been low, 2.7% in the Canadian trial of Physiolgic Pacing
(Connolly et al., 2000). In the PASE (Lamas et al., 1998) and MOST (Lamas et al., 2002)
studies in which devices could be easily upgraded to DDDR mode by simple
reprogramming, the incidence of PM syndrome was higher. The PM syndrome may also be
underestimated or it may be subclinic. The symptoms often have been ascribed to the aging
process, to the worsening of heart failure or to coronary artery disease. Memory deficit in
elderly patients complicate reporting of symptoms. Therefore, up to 75% of patients who
have felt generally well for many years with single-chamber PM have noted improvement in
their quality of life after upgrading to dual–chamber PM at the time of a pulse-generator
change (Sulke et al., 1992).
Atrio-ventricular dyssynchrony is associated with atrial fibrillation and, therefore,
thromboembolic complications, and also heart failure. The investigators have assumed the
same complications for PM syndrome. The results of completed randomized clinical trials of
PM mode selection have been somewhat conflicting. Andersen et al., (1994) compared AAI
with VVI pacing in 225 patients with sinus node dysfunction and demonstrated persistent
reduction in primary endpoints of atrial fibrillation, thromboembolic events, chronic atrial
fibrillation , and all cause mortality in AAI paced group. In the PASE study 407 patients in
sinus rhythm and bradycardia were randomized to VVIR or DDDR. There was a 26%
crossover rate due to the development of PM syndrome but no difference in quality of life,
death, stroke, first hospitalization for heart failure, development of atrial fibrillation were
observed. Also larger trials, the Canadian Trail of Physiologic Pacing and MOST performed
to randomizing 2568 and 2020 patients to atrial-based or ventricular pacing failed to show
differences in the endpoints, stroke or death. Only the incidence of atrial fibrillation was
lower with dual-chamber pacing. In subsequent analyses of MOST data the percentage of
ventricular pacing correlated with risk of congestive failure. This percentage was greater in
DDR versus VVIR mode (90% versus 58%). The ventricular dyssyncrony induced by pacing
even when atrio-ventricular synchrony is preserved increases the risk of PM syndrome,
heart failure hospitalization and atrial fibrillation. The benefit derived from atrio-ventricular
sequential pacing is likely counterbalanced by detrimental effects of frequent and
unnecessary right ventricular pacing. These observations have led to renewed interest in
single-chamber atrial pacing (Pioger et al., 2007) for sinus node dysfuncition and the
development of new dual-chamber PM algorithms designed to minimize right ventricular
pacing (Sweeney et al., 2007a) and additional research will determine if different forms of
ventricular pacing, such as biventricular or ventricular-septal pacing, will improve outcome
in patients who require ventricular stimulation.
3.7 ICD-specific complications
After the first clinical implantation (Mirowski et al., 1980), numerous primary and
secondary prevention trials resulted in rapid expansion of indication for use of ICD. In the
successive 15 years, the annual ICD insertion has increased by 20-fold (Maisel et al., 2006).
Consequently, the number of implanted ICD system and the number of patients with longer
follow-up has continuously increased. Despite advances in system design and
manufacturing to answer to any different clinical situation, device malfunctions and
software glitches will continue to occur. The increasing complexity in ICD hardware with
significant proportion of biventricular resynchronization devices may result in higher

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complications rates. The surgical complications, infection or erosion, hematoma,
pneumothorax, are similar in type and frequency to those seen with routine PM
implantation (DiMarco, 2003). The other generator–related complications are defined as
early generator depletion (less than 4 years after implantation), recalls, power reset and lead
connector problems (an average of 1.4% per patient-year) (Ezekowitz et al., 2007). The lead
is a life-line whose purpose is to convey critical information about heart’s rhythm to the ICD
generator and, in turn, to deliver life-sustaining therapy when needed. The long-term
reliability of the leads is the main problem. ICD leads are significantly more complex than
PM leads and must allow high voltage energy delivery for defibrillation when necessary
and, may be inherently more susceptible to failure. The mechanical stress can cause fracture
in a lead or failure in insulation by chronic excessive pressure on the body of the lead by the
ligature used for fixation (Dorwarth et al., 2003) or the subclavian crush syndrome
(Antonelli et al., 1998) or the higher activity patients or the multiple leads or the anatomic
reasons in females. The insulation degradation by breakdown of polyurethane polymers
due, in most cases, to metal ion oxidation like in the Medtronic models 6936 and 6966. This
lead failure can produce oversensing following appropriate shocks (Ellelbogen et al., 2003).
It is likely that this problem remains clinically silent until a high-voltage shock is delivered.
Detection of a ring-to-coil impedance drop and a high short interval counter may be a useful
indicator of middle insulation breach. The newer lead models have multi-lumen design with
steroid elution: each conductor is individually insulated by silicon rubber, which should
prevent the lead injury. Silicone leads also seem to be prone to insulation failure (Mewis et
al., 1997). More than half of lead defects (56%) results from insulation failure (Kleemann et
al., 2007). The lead defect depends mainly on follow-up time after implantation. The lead
survival rates at 5 and 8 years are 85% and 60%, respectively (Kleemann et al., 2007). The
annual lead failure rate, defined as lead-related problem requiring surgical revision, reaches
2.5% in 5 years (Eckstein et al., 2008) and 20% in 10 years old leads (Kleemann et al., 2007).
The great variation observed in ICD lead survival is due to variety of factors including
variable study definitions of lead malfunction, variable performance of models and patient
characteristics and implantation techniques (Maisel & Kramer, 2008). The lead dislocation
and exit block tend to occur early, while the other problems are more evenly distributed
over time (Duray et al., 2009). The left ventricular lead dislocation reaches rate varied
between 0%, 4.7% and 7.5% for increased complexity to implant procedure in the coronary
sinus (Duray et al., 2009). The dislocation can be observed on x-ray combined with
significant changes in sensing/pacing performance. The exit block is a failure to capture at
reasonable device output without change in impedance and lead position. The lead fracture
results in changes in impedance (more than 2000 Ohm), in changes in sensing/pacing
performance (intermittent o permanent) and is confirmed by fluoroscopy. The oversensing
is sensing of artifacts (chaotic, far field, T-wave, myopotential, noise from contact with
another lead) without significant change in lead impedance o position, similar to what seen
with PM. The other recorded problems are: unstable impedance measurements, R-wave
reduction and loss of capture (Eckstein et al., 2008).
The tools available to detect impending ICD lead failure are limited. At implantation, all
ICD systems are tested including determination of sensing, lead and shock impedances,
pacing thresholds, and defibrillation thresholds after repetitive induction of ventricular
fibrillation. Follow-up, every 3-6 months or early as needed, consisted of interrogation and
retrieval of all stored data since last visit, as well determination of sensing, impedance

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measurements, and pacing thresholds. The need for increased surveillance of patients with
older leads should include test for oversensing during provocative maneuvers and
measurement of high voltage coil and pace/sense impedances and defibrillation
underthreshold testing. A big help could have come from wireless home monitoring of
device than can immediately detect any abnormality thus reducing the risk for patients
(Corrado et al., 2009). Anyway electrical testing, x-ray, fluoroscopy, or direct visualization
may be used to detect lead abnormalities but are imprecise.
ICD dysfunction may result in failure to deliver therapy for ventricular tachycardia and thus
result in syncope or sudden death. Pooled data of randomized clinical trials that involve
around 3500 patients indicate an ICD-unresponsive sudden-death rate of nearly 5%
(Anderson, 2005). Primary ventricular arrhythmia detection is based on the tachycardia
detection rate which is usually programmed with a safety margin of 20 beats/min below the
clinical arrhythmia. But there is high (30%) slow ventricular tachycardia incidence (less than
150 beats/min) in ICD recipients without prior history of slow ventricular tachycardia
(Sadoul et al., 2005). The patients could exhibit symptoms such as syncope, palpitations, and
congestive heart failure, leading to hospital admission and sometimes death. A low
detection rate may lead to inappropriate therapy during supraventricular tachycardia. Most
ICD can be programmed to enhance the discrimination between supraventricular and
ventricular arrhythmias by additional criteria such sudden onset, stability, ventricular
electrogram morphology or vector timing and correlation, and relationship between the
atrium and ventricle. For terminating monomorphic tachycardias, antitachycardia pacing is
standard technique and is painless for patient. But is not always effective and can accelerate
ventricular tachycardia or, if applied during a supraventricular rhythm, induce a ventricular
arrthymia and following shock. Trappe et al (1995) reported an acceleration rate of only 3%
in selected patients with recurrent inducible ventricular tachycardia that had been
successfully terminated during predischarge test. Inappropriate delivery of ICD therapy,
triggered by artefacts due to lead dysfunction, extraneous noise interference, or rapid atrial
rates, mainly during atrial fibrillation or sinus tachycardia, remains a major clinical
challenge.
Clinical trial experience has revealed that up to 25% of patients receive inappropriate shocks
(Germano et al., 2006). ICD shocks reduce the physical functioning and mental well-being
and increase anxiety of patients while obligating strict driving restrictions. The risk of death
with inappropriate shocks in SCD-HeFT was increased by a factor of 2, while for an
appropriate shock the risk was increased by a factor of more than 5. The arrhythmia much
likely signaling a meaningful change in patient’s clinical status, including a worsening of
heart failure and myocardial ischemia with abnormalities in the levels of electrolytes. An
examination of randomized trials for primary and secondary prevention has shown that the
number of appropriate shocks exceed the sudden death and overall mortality rate in the
control group (Germano et al., 2006). Many episodes may have been nonsustianed nonfatal
events. Therefore, there are appropriate shocks and necessary shocks. Alternatively the ICD
proarrhytmic effect may be considered (Tung et al., 2008). The pacing–associated short-long
sequences were found at the onset of 21% to 35% of all episodes of ventricular tachycardia
and fibrillation (Sweeney et al., 2007b). Device malfunction or local lead effect with
mechanical irritation and late fibrosis may be potential mechanism for ventricular
arrhythmias. The reversal activation wavefronts from epicardial resynchronization increases
dispersion of refractoriness with demonstrated improvement of ventricular arrhythmias and

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sudden death after implantation (Basu et al., 2007). Nevertheless, ICD is clinically proven to
improve survival in selected patients at risk for sudden cardiac death, but monitoring of this
device remains critical to inform physicians and patients about device performance and to
identify underperforming products as early as possible. The last highly publicized recall of
Sprint Fidelis (Medtronic Inc., Minneapolis, Minnesota) lead was issued October 2007 (Food
and drug Administration, 2007). The higher rates of lead fracture (2.3% to 6.7% at 30
months) led to more media-provoked mass hysteria as about 268000 patients were at risk in
the world. The lead failure produced inappropriate shocks and ICD storm due to sensing of
electrical noise: 5 deaths were reported in initial advisory (Catanchin et al., 2008). To
overcame the problems of lead insertion and of lead failure an entirely subcutaneous
implantable cardioverter-defibrillator was designed and tested. A report of the initial
evaluation was recently published (Bardy et al., 2010).
Any effort to development ICD technology should be mainly directed to reliability of the
system and to patient safety. Electrical storm is defined as a state of cardiac electrical
instability manifested by several episodes of ventricular tachyarrythmias over a short period
of time, there or more appropriate ventricular detection in 24 hours, usually requiring
antitachycardia pacing or the delivery of multiple electrical shocks. It occurs in
approximately 25% of ICD patients within 3 years, with typically 5-55 individual ventricular
tachyarrythmias within one storm (Israel & Barold, 2007). The majority of episodes are
ventricular tachycardias. Electrical storm consists of monomorphic ventricular tachycardia
by reentry but ventricular fibrillation indicating acute ischemia is rare. The aetiology of
electric storm is not clearly understood. The factors contributing to storm onset are:
worsening of cardiac function, electrolyte disturbance, autonomic imbalance, drug
proarrhythmia, a context with other illness, psychological stress, excess ethanol
consumption and cardiac resynchronization therapy (Kantharia et al., 2006). In 35% of the
patients storms represent their first event. The majority of storms occurred during winter
(Greene et al., 2000). The immediate mortality is low, but the re-admission to hospital are
frequent (50-80%). The prognosis is relatively good with an overall survival at 2 years of
95% and at 6 years of 77.5%. These patients could be treated with amiodarone i.v., and with
reprogramming high rate pacing. The key intervention is reduction of elevated sympathetic
tone by beta blockers and frequently benzodiazepines. Substrate mapping and radio
frequency ablation may be useful in treatment and prevention.
3.8 Removal of devices
The value of extraction of infected or hazardous epicardial and endocardial PM or ICD leads
is well established (Rusanow & Spotnitz, 2010) by open or percutaneous techniques
including all lead types and indications. PM and ICD infections generally respond to
antibiotics, complete hardware removal, and a hardware free interval. However, these
principles cannot always be invoked, and the risk of complications is likely to increase when
hardware cannot be completely removed or when a hardware-free interval is unsafe or
inadvisable. Percutaneous lead extraction is superior to open extraction in terms of safety
and comfort, but epicardial extraction techniques remain critically important in selected
patients. Lead extraction is performed in the operating room under general anesthesia, with
pump standby. Temporary transvenous pacing wires are placed when indicated despite
presence of vegetations until a permanent system can safely be implanted.

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Recommendations for extraction of chronically implanted transvenous pacing and
defibrillator lead were published by Love et al. (2000). The percutaneous techniques should
be attempted first in all patients except those presenting with large vegetations, atrial
thrombus, epicardial leads, or ICD patches. After endocardial leads are dissected free at
their venous entry site, anchoring collars are removed. A gentle traction is applied and if
failed, a locking stylet could be inserted into the lead, and traction should be again
attempted. If this too failed, telescoping sheaths could be advanced over the lead,
maintaining countertraction with the locking stylet. Techniques described by Byrd et al.
(1985; 1990) and electrosurgical dissection by means of an equipment manufactured by
Cook Medical Inc (Bloomington, IN) or Excimer laser (Spectranetics Corp., Colorado
Springs, CL) are used to extract heavily fibrotic leads. More recently, a new extraction tool,
the Evolution mechanical dilator sheath (Cook Medical, Bloomington, IN), was introduced.
It uses a rotational mechanism with a stainless-steel bladed tip to overcome fibrosis and cut
adherences. Its rotational mechanism allows the sheath to advance down the lead body
while cutting fibrotic attachments. The outer sheath covers the cutting edge when cutting
activity is not desired so that venous walls are protected from damage. In addition, a shorter
Evolution dilator sheath (Shortie) has been designed with a sharper and tougher blade to
facilitate venous access in cases with extensive calcification under the clavicle. Initial
experience with the Evolution mechanical dilator sheath for lead extraction has been
reported recently (Hussein et al., 2010). Extensive surgical debridement of the pocket is
performed using electrocautery and blunt dissection. Timing of device reimplantation is
based primarily on sterility of blood cultures, but also on resolution of vegetations.
Reimplantation is usually performed on the contralateral side. In select cases, an ipsilateral
lateral sub-pectoral location may be used depending on the extent of pocket infection.
Persistent inability to extract the lead prompted conversion to an open technique, when
indicated. The commonest open technique after failed endocardial extraction was
pursestring or snare-controlled right atriotomy through a median sternotomy (Byrd et al.,
1990). Median sternotomy with cardiopulmonary bypass are used in the presence of atrial
or superior vena cava thrombi, or large vegetations on the leads or on the tricuspid valve.
Epicardial leads and patches were removed through a median sternotomy or left, right, or
subxiphoid thoracotomy. The surgical approach is based on lead and patch location
according to the the North American Society of Pacing and Electrophysiology Guidelines
(Love et al., 2000).
4. Electromagnetic interference (EMI)
Electrical devices generate electromagnetic fields that may interfere with PM and ICD. The
incidence of that interference is still controversial and only partially explored because the
plenty of new electronic devices that are continuously introduced. These facts forced
physicians to adopt very restrictive rules for use of electronic devices by patients who had
cardiac implantable devices, on the other hand industries paid more attention to project safe
devices. Nowadays third-generation mobile phones, Universal Mobile Telecommunication
System (UMTS), were recently introduced in Europe. The safety of these devices with regard
to their interference with implanted devices was studied among 100 patients by Ismail et al.
(2010) who concluded that third-generation mobile phones are safe for patients with
permanent PM regardless of atrial and ventricular sensitivity settings. This is due to the
high-frequency band for this system (1800-2200 MHz) and the low power output between

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0.01 W and 0.25 W. Also media players cause telemetry interference with PM, but it is not
known whether they cause direct interference with them. Thaker et al. (2009) studied the
interaction between PM and 3 different media players. PM interference was categorized as
type I, II, or III. Types I and II interferences described telemetry interference and type III
interference was defined as any direct interference with PM function or programmed
parameters. It was concluded that media players cause telemetry interference with PM, but
they do not directly interfere with PM function. Recently Lee et al. (2009) published the
evidence that interferences could be generated by magnetic field of portable headphones.
PM or ICD function was assessed in 100 patients during exposure to 8 different models of
portable headphones to determine the incidence of clinically relevant magnetic interference.
The magnetic field strength of the headphones was also measured in vitro. They concluded
that clinically relevant magnetic interference from portable headphones occurred in 30 (30%)
of 100 patients and more commonly affected ICD than PM patients (21/55, 38.2% versus
9/45, 20.0%; P = .048). All patients affected by magnetic interference experienced a magnet
response, characterized by asynchronous pacing in PM patients and by inhibition of
tachyarrhythmia detection in ICD patients. In all but one of the 30 cases of magnetic
interference, removal of the headphones from the patient's chest immediately restored
normal device function. Headphones with a measured magnetic field strength more or
equal to 10 Gauss at 2 cm were much more likely to cause magnetic interference than were
those with lower magnetic field strength (30/100 patients versus 0/100 patients; p <0.0001).
Magnetic interference was not observed when headphones were placed more than 3 cm
apart from the skin surface. It was concluded that clinically significant magnetic interference
can occur when portable headphones are placed in close proximity to implanted PM and
ICD. Patients with such a device should be advised to keep portable headphones at least 3
cm distant from their device.
5. Psychological problems
All studies concerning the quality of life in patients instrumented with PM or ICD are
limited by the inability to mask therapy. The recorded effects can reflect the beliefs and
expectations of patients. The patients may perceive the device as an electronic security or as
a source of physical and emotional discomfort. Introducing a foreign body into the heart
may cause a change in body image, cause problems in psychosocial adaptation and
contribute to development of affective disorders. There are differences in intrusiveness of
the two devices: ICD shocks are often painful and are delivered at unpredictable times,
while pacing is unlikely felt by the patients. The interval between follow-up visit is closer for
ICD patients who are encouraged to contact the clinic when they experience some problems
and they can feel more dependent. Over 70% of the PM recipients are at least 70 years old
(Ross & Kenny, 2000). It is difficult to examine the quality of life in the elderly because of
age–related cardiovascular and cerebrovascular physiological changes, including reduced
cardiac output, blunted autonomic compensatory responses and altered cerebral
autoregulation. The aging and the development of the other conditions may overwhelm the
moderate improvements in cardiovascular functional class and minimize the long-term
effect on general quality of life. Depression and anxiety are more common in patients with
permanent PM than in the general population. In one trial the quality of life was found to be
similar to that of patients who require long-term hemodialysis (Lamas et al., 2002). Aydemir
et al. (1997) reported that 19.1% of PM patients warranted a psychiatric diagnosis, and 10.7%

Modern Pacemakers - Present and Future
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were clinically depressed. Pycha et al. (1990) identified depression of moderate severity in
35% of ICD patients, Heller et al. (1998) in 20-58%. In other studies the prevalence of
affective disturbance is relatively low (Duru et al., 2001). There are important
methodological differences that may account for divergent results: some studies have used
short-term design and have measured quality of life with non standard instruments. In
PASE study, in which the primary end-point was quality of life, no overall benefit from
dual-chamber pacing as compared with single-chamber ventricular pacing was found
(Lamas et al., 1998). Only patients with sinus-node dysfunction did appear to benefit from
dual-chamber pacing, but those with PM implanted because of heart block did not. In
individual patient the quality of life appeared to improve after upgrading to dual-chamber
(Sulke et al., 1992), while it was lower at time of PM syndrome than at time of implantation.
PM implantation improved health-related quality of life. The mode select was associated
with much smaller, but significant, improvements in several domains, particularly physical
function (Fleischmann et al., 2006). Atrioventricular synchronous pacing has a beneficial
effect on most domains of quality of life in patients with hypertrophic obstructive
cardiomyopathy refractory to drug treatment (Gadler et al., 1999). In a large primary-
prevention population with moderately symptomatic heart failure ICD therapy was not
associated with adverse quality effects during 30 months of follow-up (Mark et al., 2008).
The occurrence of ICD shocks was associated with increased psychological distress in both
patients and their families. The quality of life of patients in the month after a shock was
significantly decreased in perceived general health, physical and emotional functioning,
social functioning, and self-rated health. This result did not persist however, because the
shock experience remembers the patients have a device with a life preserving function. They
report limitations in their activities and admit anxiety about battery depletion and technical
problems. The most distressing aspects of receiving a shock are the lack of warning,
multiple shocks, nervousness, fear of sudden death, dizziness, weakness and chest soreness.
Educational interventions and support group might incorporate knowledge about the
effects of devices, to facilitate anticipatory guidance and preparation of patient and family
members for ICD shocks.
6. Conclusion
Strict adherence to the widely accepted guidelines and recommendations, awareness of
potential complications, and a meticulous approach to the implant and post implant
techniques and follow-up may certainly reduce the incidence of complications after
implantation of PM and ICD, more than often life-saving devices. To be aware of PM and
ICD complications is an essential first step for good clinical practice in this area.
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