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Transcript
360 Cardiology
Pacemaker syndrome
Pacemaker therapy has become an important therapeutic option for patients with heart
rhythm conditions worldwide. Te number of elderly patients needing pacemakers is on
the increase due to an ageing population worldwide. Pacemaker syndrome consists of
the cardiovascular signs and symptoms of heart failure and hypotension induced by right
ventricular (RV) pacing.
Dr Satnam Singh Research Registrar, University of Aberdeen, Level 3, Polwarth building, Aberdeen
email [email protected]
Pacemaker syndrome is a term
proposed in 1979 by Erbel and
refers to symptoms and signs in
the pacemaker patient caused by
inadequate timing of atrial and
ventricular contractions.1 It was first
described in 1969 by Mitsui et al2 as
an iatrogenic disease characterised
by the disappearance of symptoms
with restoration of atrioventricular
synchrony (AV synchrony).
It means if atria and ventricles
contract at appropriate timings (as
close to physiological), pacemaker
syndrome can be prevented.
It has been postulated that
the greater the AV dyssynchrony,
the greater the incidence of this
syndrome. VVI pacing (Single
Chamber Ventricular Pacemaker)
is the commonest pacemaker
mode, but as it is a single chamber
pacing (Table 1), it can create AV
dyssynchrony.3,4
The lack of normal
atrioventricular synchrony may
result in decreased cardiac output.
In most cases this syndrome can
be cured by dual chamber pacing,
which relieves almost all the
symptoms. This is because dual
chamber pacing is more close to
normal physiology than single
chamber pacing. However, there
are several reports of pacemaker
GM | Midlife and Beyond | July 2011
syndrome occurring in dual
chamber modes.5,6 It can even
occur with AAI pacing with long
PR intervals.
Incidence
Te overall incidence of pacemaker
syndrome is very difficult to
estimate but is about 20% in a
landmark trial called the Mode
Selection Trial (MOST).7 It occurs
with equal frequency in both sexes
and can occur at any age.8 In this
trial 2010 patients were randomly
assigned to VVIR (Ventricular Rate
Modulated Pacing) versus DDDR
(Dual Chamber Rate Adaptive
Pacemaker) pacing modes. This
trial was a single blinded study
enrolling around 2000 patients
with sick sinus syndrome.
All patients were implanted
dual chamber pacemakers
programmed to VVIR or DDDR
before implantation. Pacemaker
syndrome was a secondary
endpoint studied. Severe
pacemaker syndrome developed
in nearly 20% of VVIR-paced
patients and improved with
reprogramming to the dualchamber pacing mode.
Clinical presentation
Symptoms of pacemaker
syndrome are non-specific and
Key points
•
•
•
•
Pacemaker syndrome refers to symptoms and signs in the
pacemaker patient caused by inadequate timing of atrial and
ventricular contractions.
Te lack of normal atrioventricular synchrony may result in
decreased cardiac output.
Te strongest predictor of pacemaker syndrome appears to be
a high percentage of ventricular paced beats according to the
MOST trial.
Quality of life improved significantly afer patients were
upgraded to dual chamber pacing.
www.gerimed.co.uk
may be confused with the ageing process. Moreover
elderly patients report less symptoms due to
memory deficits or other reasons. Tere has been a
considerable overlap among the signs and symptoms
of pacemaker syndrome and physiological ageing
symptoms. Nevertheless commonly patients present
with the nonspecific symptoms ranging from
fatigability to syncope and these occur during the
time the ventricles are being stimulated by the pulse
generator. Postulated mechanisms include loss of AV
synchrony, vasodepressor reflexes, and retrograde
atrial activation.
The strongest predictor of pacemaker
syndrome appears to be a high percentage
of ventricular paced beats according to the
MOST trial.
Diagnosis
Te diagnosis of pacemaker syndrome is based on the
clinical features listed in table 2 especially in a patient
with a VVIR pacemaker and the disappearance of
all or most of the symptoms with upgrading of the
pacemaker to a dual chamber one.
Plasma ANP levels have also been used a marker
of non-physiological pacing in the PASE trial and
elevated levels (>90pgml) can be helpful in the
diagnosis. On upgrading the pacemaker to DDDR,
there should be a prompt decline in ANP levels and
prompt resolution of symptoms.9–12
Pacemaker syndrome is more likely if the systolic
blood pressure drops more than 20mmHg during
ventricular pacing (VVIR).13 Despite attempts
to identify clinical variables and biochemical
markers that predict the development of pacemaker
syndrome, multiple studies have failed to identify
any consistency.
Management
In the past two decades, a vast majority of
cardiologists have modified their practice by
shifing away from VVI/VVIR pacing. Patients with
pacemaker syndrome after VVIR pacing can be
managed by upgrading to a DDDR system. Rarely, a
patient with a dual chamber pacemaker may present
with similar symptoms of pacemaker syndrome,5,6
which needs pacing clinic follow up for ensuring
www.gerimed.co.uk
Cardiology 363
Table 1: Types of pacemaker
Table 2: Clinical features of pacemaker syndrome
VVI pacing: Tis is by far
the most common type of
pacemaker mode. It senses
spontaneous ventricular
impulses and paces the
ventricles only when needed.
Dual chamber pacing: Tis
is said to happen when both
the atria and the ventricles
are paced with one lead in the
atria and the other lead in the
ventricle.
AAI pacing: Tis is a
pacemaker similar to the VVI
except that it senses and paces
the atria, thereby maintaining
the sequence of atrial and
ventricular contraction.
Neurological: Dizziness, near syncope, and confusion
Heart failure: Dyspnoea, orthopnoea, paroxysmal nocturnal
dyspnoea, and peripheral oedema
Hypotension: Seizure, mental status change, diaphoresis, and signs
of orthostasis and shock
Low cardiac output: Fatigue, weakness, dyspnoea on exertion,
lethargy, and lightheadedness
Hemodynamic: Pulsation in the neck and abdomen, choking
sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds,
and headache
Heart rate related: Palpitations associated with arrhythmias.
that the atrial lead is working and
by avoiding atrial non-tracking
modes (DDI or DVI). Avoiding
atrial non-pacing modes, reducing
the lower pacing rate to encourage
conduction of underlying rhythm,
use of hysterisis (delaying pacing
to maximize benefit to patient),
and withdrawal of any rate limiting
medications affecting sinus node
are all helpful.
Conclusion
The MOST trial showed no
baseline demographic, clinical
or pacemaker implant variables
predictive of pacemaker syndrome.
A high percentage of paced beats
during follow up was the only
independent predictor. Patients
noticed significant deterioration
in their quality of life with the
syndrome and it improved
significantly afer being upgraded
to dual-chamber pacing. Because
www.gerimed.co.uk
patients who will develop
pacemaker syndrome cannot be
accurately identified at the time of
implantation, it may be advisable
to treat all patients with atrialbased pacemakers. VVI pacing
should be used only in patients
with chronic or persistent atrial
fibrillation with good chronotropic
response to exercise, or with
transient bradycardic arrhythmias.
Conflict of interest: none
References
1. ErbelR.Pacemakersyndrome.Am J
Cardiol 1979;44:771–2
2. MitsuiT,HoriM,SumaK,etal.The
“pacemaking syndrome” [abstract].
In: Jacobs JE, eds. Proceedings
of the eighth annual international
conferenceonmedicalandbiological
engineering. Chicago: Association
for the Advancement of Medical
Instrumentation1969;29:3
3. Witte J, Bondke H, Muller S.
The pacemaker syndrome: a
haemodynamic complication of
ventricularpacing.Cor Vasa1988;30:
393–99
4. TorresaniJ,EbagostiA,Allard-Latour
G.PacemakersyndromewithDDD
pacing.PACE1984;7:1148–51
5. Vardas PE, Travill CM, Williams
TDM, et al. Effect of dual chamber
pacing on raised plasma atrial
natriureticpeptideconcentrationsin
completeatrioventricularblock.BMJ
1988;296:94
6. Stangl K, Weil J, Seitz K, et al.
Influence of AV synchrony on the
plasma levels of atrial natriuretic
peptide(ANP)inpatientswithtotal
AVblock.PACE1988;11:1176–81
7. LamasGA,OravEJ,StamblerBS,et
al.Qualityoflifeandclinicaloutcomes
in elderly patients treated with
ventricular pacing as compared to
withdualchamberpacing.Pacemaker
SelectionintheElderlyInvestigators.
N Eng J Med1998;338:1097–1104
8. Lamas GA, Lee K, Sweeney M, et
al.Themodeselectiontrial(MOST)
in sinus node dysfunction: design,
rationale,andbaselinecharacteristics
ofthefirst1000patients.Am Heart J
2000;140(4):541–51
9. NollB,KrappeJ,GokeB,MaischB.
Influenceofpacingmodeandrateon
peripheral levels of atrial natriuretic
peptide (ANP). PACE 1989; 12:
1763–68
10. Travill CM, Williams TDM, Vardas
P, et al. Hypotension in pacemaker
syndromeisassociatedwithmarked
atrial natriuretic peptide (ANP)
release[abstract].PACE1989;12:93
11. LiebertHP,O’DonoghueS,Tullner
WF, et al. Pacemaker syndrome in
activityresponsiveVVIRpacing.Am J
Cardiol1989;64:124–26
12. Cunningham TM. Pacemaker
syndrome due to retrograde
conductioninaDDIpacemaker.Am
Heart J1988;115:478–89
13. AusubelK,FurmanS.Thepacemaker
syndrome.Ann Intern Med1985;103:
420–29
July2011| Midlife and Beyond | GM