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Pacemaker Syndrome

  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Nov 24, 2014
 

Background

Although pacemakers provide relief from life-threatening arrhythmias and can improve quality of life significantly, they also can function in a nonphysiologic manner, which is accompanied by nontrivial morbidity. Ventricular pacing has been noted to sacrifice the atrial contribution to ventricular output; in some instances, atrial contraction occurs against closed atrioventricular (AV) valves, producing reverse blood flow and nonphysiologic pressure waves.

McWilliam described a reduction in blood pressure in response to electrical stimulation of a cat's ventricle in 1889.[1] Since the first pacemaker was implanted in 1958, investigators have reported decreased cardiac output in humans as a response to ventricular pacing (see the Cardiac Output calculator). In response to decreased cardiac output, the majority of patients demonstrate aortic and carotid baroreceptor reflex activity, which increases total peripheral resistance (TPR) to maintain constant blood pressure. In some patients, TPR does not increase in response to decreased cardiac output, which results in decreased blood pressure.[2, 3, 4] The combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of TPR response, and nonphysiologic pressure waves contributes to symptoms collectively known as pacemaker syndrome.

The definition of pacemaker syndrome has evolved and been the subject of discussion since 1969, when Mitsui and colleagues first reported a constellation of symptoms they thought to be rate-related in patients with ventricular pacemakers.[5, 6] Successive definitions have sought to include data from later investigations into the pathophysiology of the symptoms produced. Furman redefined pacemaker syndrome in a 1994 editorial in which he included the following elements[7] :

  • Loss of AV synchrony
  • Retrograde ventriculoatrial (VA) conduction
  • Absence of rate response to physiologic need

Ellenbogen and colleagues focused on clinical utility and proposed that "pacemaker syndrome represents the clinical consequences of AV dyssynchrony or suboptimal AV synchrony, regardless of the pacing mode."[8]

Recently, most authors have recognized that pacemaker syndrome, which initially was described in patients with ventricular pacemakers, is related to nonphysiologic timing of atrial and ventricular contractions, which may occur in a variety of pacing modes. Some have proposed renaming the syndrome "AV dyssynchrony syndrome," which more specifically reflects the mechanism responsible for symptom production.

AV dyssynchrony may occur outside the setting of pacemakers, however, as noted by Furman, who described the following nonpacing conditions[7] :

  • Extremely prolonged first-degree AV block
  • Nodal rhythm more rapid than the atrial rate, as might occur in children with sinus node dysfunction after congenital defect repair

Such examples have been termed "pseudopacemaker syndrome," in an effort to reserve the term pacemaker syndrome only for cases involving pacemakers. Other examples of pseudopacemaker syndrome have been described, including hypertrophic cardiomyopathy with complete AV block.[9]

The working definition of pacemaker syndrome currently includes the following:

  • A constellation of specific symptoms occurs.
  • Symptoms occur in the setting of a pacemaker, temporary or permanent.
  • Symptoms result from loss of physiologic timing of atrial and ventricular contractions.

The last condition may be unnecessary, and it helps blur the distinction between definition of syndrome and elucidation of cause. It also excludes at least one mechanism known to contribute to production of the constellation of symptoms, specifically, ventricular activation pattern.

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Pathophysiology

Loss of physiologic timing of atrial and ventricular contractions, or AV dyssynchrony, leads to multiple mechanisms of symptom production. Several large trials have focused on pacing mode in the setting of sinus node dysfunction as a mechanism of symptom production.[10, 11, 12, 13] Physiologic pacing is associated with fewer symptoms in the setting of complete heart block.[14, 15] An altered ventricular activation pattern contributes to decreased cardiac output and, consequently, to symptom production. See the Cardiac Output calculator.

Loss of atrial kick

Estimates of atrial contribution to cardiac output vary from 15-25% in healthy hearts at rest. However, in cases of decreased ventricular compliance, atrial kick may contribute as much as 50% to cardiac output. Causes of decreased ventricular compliance include diseases such as hypertensive cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathies, and it also occurs in some elderly patients. Inappropriate pacing in these patients can result in loss of atrial kick and can significantly reduce cardiac output.

Cannon a waves

Atrial contraction against a closed AV valve can cause pulsation in the neck and abdomen, headache, cough, and jaw pain.

Increased atrial pressure

Ventricular pacing is associated with elevated right and left atrial pressures, as well as elevated pulmonary venous[16] and pulmonary arterial pressures, which can lead to symptomatic pulmonary and hepatic congestion.

Increased production of atrial natriuretic peptide

Ventricular pacing leads to decreased cardiac output, with resultant increase in left atrial pressure and left ventricular filling pressure. These pressure increases result in increased production of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).[17, 18] ANP and BNP are potent arterial and venous vasodilators that can override carotid and aortic baroreceptor reflexes attempting to compensate for decreased blood pressure. Patients with pacemaker syndrome exhibit increased plasma levels of ANP, and patients with cannon a waves have higher plasma levels of ANP than those without cannon a waves.

VA conduction

A major cause of AV dyssynchrony is VA conduction. Retrograde conduction leads to delayed, nonphysiologic timing of atrial contraction in relation to ventricular contraction. Nishimura and colleagues showed that patients with intact VA conduction have a greater decrease in blood pressure in response to ventricular pacing than patients with AV dissociation.[19] As is discussed in Causes, many conditions other than VA conduction promote AV dyssynchrony.

Ventricular activation pattern

The nonphysiologic depolarization pattern produced by pacemakers may be responsible for lower cardiac output with ventricular paced rhythms. Placement of pacemaker leads in the apex of the right ventricle results in initiation of ventricular depolarization in the right ventricular apex, causing an altered pattern of ventricular depolarization and contraction. In a small sample of patients, Rosenqvist and colleagues demonstrated a 10% greater cardiac output during atrial inhibited (AAI) pacing, with physiologic ventricular depolarization, compared with AV sequential, or dual-mode, dual-pacing, dual-sensing (DDD) pacing, with retrograde ventricular depolarization initiated in the right ventricular apex.[20]

The importance of ventricular activation pattern has been more recently highlighted with the advent of biventricular pacing. Bordachar and colleagues 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.[21]

A study by Mollazadeh et al, however, suggested that with regard to non-DDD pacing, the biventricular and left ventricular modes provide no significantly greater benefit for systolic blood pressure than does right ventricular pacing; the report also indicated that DDD-biventricular pacing does provide such benefits. The study involved 40 patients with a biventricular pacing device, with patients switched between different pacing modes. The investigators found that the mean systolic blood pressure did not differ between ventricular-only pacing modes but that it was significantly higher in patients undergoing DDD biventricular pacing. The study also determined that palpitations and dyspnea occurred in 22.5% of patients when they were switched from DDD-biventricular mode to right or left ventricular-only pacing and in 12.5% of patients when switched from DDD-biventricular mode to non-DDD – biventricular pacing.[22]

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Epidemiology

Frequency

United States

Several factors complicate efforts to study the incidence of pacemaker syndrome. Symptoms of pacemaker syndrome are nonspecific, occur in settings other than cardiac pacing, and often have been ascribed to the aging process. In addition, memory deficits in elderly patients complicate reporting of symptoms.

Ausubel and Furman estimated the incidence of pacemaker syndrome to range from 7% (symptoms severe enough to warrant pacemaker revision) to 20% (mild to moderately severe symptoms).[23]

The overall incidence of pacemaker syndrome, as prospectively defined in the Mode Selection Trial (MOST), was 18%, with an incidence of 16% at 1 year after pacemaker implantation.[24]

Heldman and colleagues suggested the possibility of a subclinical pacemaker syndrome by comparing dual-chamber pacing to ventricular pacing in the same patients. While their study was small and subject to bias and methodological shortfalls, they nonetheless detected a recognizable syndrome in 83% of patients paced in the ventricular inhibited (VVI) mode, with 65% of patients having moderately severe to severe symptoms.[25]

In a small study, Sulke and associates found that up to 75% of patients who were satisfied with VVI pacing nonetheless benefited from upgrade to DDD mode pacing, which suggests the existence of a subclinical pacemaker syndrome.[26]

Pacemaker syndrome occurs with equal frequency in both sexes, and it can occur at any age.

Mortality/Morbidity

The prognosis is excellent with correction of pacing mode.

No direct data are available regarding morbidity and mortality rates associated with pacemaker syndrome.

Investigators have estimated frequency and severity of pacemaker syndrome sequelae by examining patients with AV dyssynchrony and assuming similar statistics; for the purpose of establishing incidence statistics, patients with pacemaker syndrome may be considered a subset of patients with AV dyssynchrony. Estimates of frequency and severity of pacemaker syndrome sequelae largely come from studies examining morbidity and mortality rates associated with different pacing modalities in the sick sinus syndrome.[10] VVI pacing creates AV dyssynchrony, which is used as a surrogate for the pacemaker syndrome; VVI statistics are compared to either AAI or DDD statistics, which are presumed to represent physiologic pacing.

AV dyssynchrony is associated with atrial fibrillation and, therefore, thromboembolic complications, and also is associated with chronic heart failure. By extension, investigators have assumed the same complications for pacemaker syndrome. Following is a discussion of the incidence of these complications, as revealed by studies investigating different pacing modalities, mostly in the setting of sick sinus syndrome, a frequent indication for pacemaker implantation.

Complications

Complications of AV dyssynchrony include atrial fibrillation, thromboembolic events, and heart failure.

Pacemaker syndrome also can be complicated by syncope or near syncope. Individuals may develop a subjectively worse quality of life with ventricular pacing than they had prior to pacemaker implantation, or they may endure a persistently degraded quality of life, as suggested by Sulke's study of subclinical pacemaker syndrome.

Complications of treatment may include the same complications of pacemaker implantation if reimplantation, additional lead placement, or explantation is involved. These complications include infection (4%), pneumothorax (1%), cardiac perforation and tamponade, bleeding, and pain.

Atrial fibrillation

In patients with sick sinus syndrome, VVI pacing leads to a higher rate of atrial fibrillation than does physiologic (ie, AAI or DDD) pacing. Estimates of chronic atrial fibrillation incidence are summarized in the table. The data presented in the following table reveal an annual incidence of chronic atrial fibrillation of 5-13% for VVI versus 0.7-1.7% for AAI pacing. Studies with combined data for AAI and DDD pacing show an annual incidence of 0-4.5%.

Table. Incidence of Atrial Fibrillation in Patients with Pacemakers (Open Table in a new window)

Study Patients



(number)



Total Incidence



(%)



Follow-up



(years)



Annual Incidence



(%)



    VVI AAI DDD   VVI AAI DDD
Frielingsdorf[27] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[28] 1061 22 3.9   AAI: 2.75



VVI: 3.25



6.77 1.42  
Hesselson[29] 8827 14-57 0-23   AAI: 1-8



VVI: 3-8



Cannot be determined
Hesselson[29] 950 38 7   7 5.43 1.00  
Santini[30] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[31] 75 41 2* AAI: 3.25



VVI: 5.17



7.9 0.62*
Rosenqvist[32] 168 47 6.7   4 11.8 1.68  
*Combined AAI and DDD

 

Thromboembolic events

The relative risk for thromboembolic events parallels the risk for development of chronic atrial fibrillation. In patients with sinus node disease, thromboembolic events occur more frequently in patients who are paced in the ventricular mode than in patients with atrial pacing. Data from studies by Sutton and Kenny[28] , Sasaki and colleagues[31] , and Andersen and colleagues[33] have revealed an annual incidence of thromboembolic events of 4-8% for VVI and 0.6-2% for AAI pacing.

Heart failure

Fewer studies have analyzed incidence and severity of heart failure as a sequela of AV dyssynchrony than have analyzed occurrences of atrial fibrillation and thromboembolic events. Rosenqvist and colleagues showed the incidence of new heart failure to be 9% with VVI versus 4% with AAI pacing.[32] Andersen et al showed significantly less severe heart failure by NYHA (New York Heart Association) class with AAI pacing than with VVI pacing.[33] Sasaki and associates found a trend toward increased incidence of heart failure with VVI pacing than with AAI or DDD pacing.[31]

Mortality

Mortality rates for various pacing modalities in sick sinus syndrome have been well studied, and most studies show that VVI pacing is associated with a higher annual mortality rate than AAI or DDD pacing. Rosenqvist and colleagues[32] and Santini and colleagues[30] studied mortality rates in sick sinus syndrome, comparing VVI with AAI pacing. They obtained data remarkably similar in annual incidence to that provided in the survey of 11 studies by Frielingsdorf and colleagues[27] . Pooling data from the 3 studies yields an annual all-cause mortality rate of 5.9-7.5% for VVI and 2.2-3.2% for AAI pacing.

Sasaki et al found similar rates of 6.8% with VVI pacing and 3.8% for combined AAI and DDD pacing modalities in sick sinus syndrome.[31] Hesselson et al found higher mortality rates, 14% for VVI and 9% for DDD pacing, but still demonstrated that VVI pacing is associated with a higher mortality rate than is DDD pacing.[29]

In one of the few prospective randomized trials, Andersen and colleagues reported an annual mortality rate of 9.4% for VVI and 6.2% for AAI pacing, but this difference lost statistical significance in the multivariate analysis.[33] Zanini et al found that pacing mode had a greater effect on mortality than did the indication for pacing, sinus node dysfunction versus atrioventricular block.[34]

Other studies of note include that of Alpert and associates, which demonstrated no significant difference in mortality rates between VVI and combined DDD and dual-mode, ventricular inhibited (DVI) pacing modalities in patients without preexistent heart failure.[35] In patients with preexistent heart failure, the difference in annual mortality rates—8.6% for VVI and 5.0% for combined DDD and DVI pacing—reached significance. In their survey of 6 relevant studies, Sutton and Kenny found no survival advantage in patients with sick sinus syndrome of VVI pacing over no pacing.[28] These studies perhaps demonstrate the significant disadvantage of any ventricular stimulation in the setting of sinus node dysfunction.

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Contributor Information and Disclosures
Author

Daniel M Beyerbach, MD, PhD Medical Director, Cardiac Rhythm Program, The Christ Hospital; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University

Daniel M Beyerbach, MD, PhD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher Cadman, MD Decatur Memorial Hospital Heart and Lung Institute

Christopher Cadman, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

References
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Pronounced PR interval prolongation. The effect of this PR interval prolongation on AV dyssynchrony is demonstrated in this ECG image.
AV dyssynchrony resulting from severe PR interval prolongation in the setting of sinus rhythm. In this ECG, the PR interval is prolonged to the point that the P wave occurs coincident with the peak of the T wave. Compare to the prior image of the same patient with a slower sinus rate.
Accelerated idioventricular rhythm with retrogradely conducted P waves. This ECG demonstrates a mechanism of AV dyssynchrony that might lead to pseudopacemaker syndrome.
Junctional rhythm with retrogradely conducted P waves. If symptoms of pacemaker syndrome develop, increasing the lower rate limit for pacing may help to restore AV synchrony.
Retrogradely conducted P waves are visible directly following each ventricular-paced complex.
This is an ECG tracing of a patient with continuous atrioventricular synchronous (DDD) pacing prior to development of symptoms. Atrial stimulation (open arrows) is followed by visible P waves. Wide QRS complexes follow ventricular stimulation (solid arrows).
This is an ECG tracing of a patient with atrioventricular (AV) dissociation and resultant pacemaker syndrome. Native atrial depolarizations (arrows) move progressively closer to pacemaker-stimulated ventricular depolarizations. Ventricular pacemaker stimuli (arrowheads) are greater in amplitude than those visible in the previous image, consistent with mode reversion from AV synchronous (DDD) to ventricular inhibited (VVI), which includes a switch from bipolar pacing (low amplitude) to unipolar pacing (higher amplitude).
Table. Incidence of Atrial Fibrillation in Patients with Pacemakers
Study Patients



(number)



Total Incidence



(%)



Follow-up



(years)



Annual Incidence



(%)



    VVI AAI DDD   VVI AAI DDD
Frielingsdorf[27] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[28] 1061 22 3.9   AAI: 2.75



VVI: 3.25



6.77 1.42  
Hesselson[29] 8827 14-57 0-23   AAI: 1-8



VVI: 3-8



Cannot be determined
Hesselson[29] 950 38 7   7 5.43 1.00  
Santini[30] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[31] 75 41 2* AAI: 3.25



VVI: 5.17



7.9 0.62*
Rosenqvist[32] 168 47 6.7   4 11.8 1.68  
*Combined AAI and DDD
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