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* From the Cardiology Service, Walter Reed Army Medical Center, Washington, DC.
Correspondence to: MAJ Thor T. Markwood, MC, USA, Cardiology Service, Walter Reed Army Medical Center, 6900 Georgia Ave NW, Building 2, Room 4A-44, Washington, DC 20307-5001; e-mail: thor.Markwood{at}na.amedd.army.mil
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Abstract |
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Key Words: artificial pacemaker • bradycardia • heart rate • sick sinus syndrome
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Introduction |
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Case Report |
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His examination demonstrated a resting HR of 69 beats/min and a BP of 117/71 mm Hg. The findings of the rest of his examination were normal. An ECG demonstrated normal sinus rhythm at a rate of 62 beats/min, normal axis, and no evident conduction abnormality or changes consistent with ischemic heart disease. The results of all laboratory examinations, which included CBC count, measurement of BUN, creatinine, and electrolyte levels, liver function tests, thyroid function tests, Lyme and Chagas antibody tests, were normal. A transthoracic echocardiogram demonstrated normal biventricular function and valvular function. No ventricular aneurysms were seen, and the estimated pulmonary arterial pressure was 15 to 20 mm Hg. Selective coronary angiography demonstrated normal epicardial anatomy with no evident atherosclerotic plaque.
Despite maximal effort, he only achieved a maximal HR of 100 beats/min on his initial maximal stress testing (Table 1 ). The patient received a diagnosis of sinus node CI. After atrial pacing demonstrated an AV node Wenckebach threshold of 155 beats/min, the patient underwent single-chamber atrial pacemaker implantation. At the 6-week follow-up for final programming, the patient noted only minimal improvement in symptoms. The results of repeat maximal exercise testing, shown in Table 1 , demonstrated an inadequate rate response to exertion. The pacemaker rate response slope was increased to allow a higher HR for any level of activity. A week later, the patient had normal functional capacity with adequate rate response function, as demonstrated by the follow-up maximal stress test results that are shown in Table 1 . The patient reported a marked improvement in exercise tolerance.
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Discussion |
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Noting that submaximal exercise HRs increase in a linear manner with oxygen consumption, Wilkoff and Firstenberg9
described a metabolic-chronotropic relation. The normal predicted HR at any stage of exercise is given by the following formula:
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where MET is the metabolic equivalent (or oxygen consumption [in milliliters/kilogram/minute]/3.5), METSstage is the MET at a particular stage, METSpeak is the peak functional capacity during the test, HRstage is the HR at a particular stage, and HRrest is the HR at rest.
They confirmed this concept with a cohort of 537 healthy subjects who underwent maximal exercise testing using either a standard Bruce protocol or a chronotropic assessment exercise protocol. The metabolic chronotropic relation was consistent regardless of age, peak functional capacity, resting HR, and exercise protocol. Using this concept, chronotropic competence is defined as the response to exertion that provides a metabolic-chronotropic relation slope of between 0.8 and 1.3 (95% confidence interval).
Katritsis and Camm1 propose a standard definition for CI based on anatomic and physiologic differentiation. They defined CI as the inability of the HR to achieve at least 80% (an arbitrary percentage) of the predicted value according to the Astrand formula (220 - age) at peak exercise. Sinus node CI is the inability of the sinus node to achieve 80% of the predicted HR. Sinus node CI is further subcategorized as specific (due to the sinus node dysfunction) or functional (due to arrhythmias interfering with sinus node activity). Junctional (or ventricular) CI is the inability of the AV node to achieve 80% of the predicted HR in patients with atrial fibrillation or AV block.
Recent studies suggest that the simple definition of CI as an inability to achieve a maximum HR of > 85% predicts a clinically meaningful patient population.4 10 11 However, optimal pacemaker programming may require a more sensitive determination of inadequate chronotropic response. In this population, the chronotropic index of Wilkoff and Firstenberg9 may better define an appropriate chronotropic response.
The exact mechanism for CI has not been clearly defined, although factors responsible for CI include sinus node dysfunction, ischemic heart disease, autonomic dysfunction, and left ventricular dysfunction.2 Sinus node dysfunction is a well-described cause for CI and has been reviewed.12 Inappropriate chronotropic responsiveness is also seen in > 50% of patients with chronic atrial fibrillation,6 in up to 24% of patients with congestive heart failure,13 14 and after cardiac transplantation.15
The evaluation of symptoms suggestive of CI, such as fatigue or dyspnea, include the determination of CI by exercise testing and searching for the etiology of CI through medical history, physical examination, laboratory testing, and imaging studies. The evaluation should be directed by the differential diagnosis of CI.
The treatment of CI should begin with a determination of the severity of symptoms and an evaluation for possible reversible causes such as medication side effect, hypothyroidism, or ischemic heart disease. Successful treatment of the underlying etiology may preclude the need for further therapy.
Theophylline is a consideration for temporary treatment if suspected reversible or temporary CI, in extremes of age, or in others in whom permanent pacemaker insertion is not desirable. The THEOPACE study16 confirmed that theophylline could improve some symptoms of sinus node dysfunction compared to placebo. In the study, 107 patients were randomized in three arms to a control arm, to a theophylline therapy arm, or to a dual-chamber rate-responsive pacemaker insertion arm. In a 48-month follow-up, both treatment arms demonstrated a lower risk of overt heart failure, but only pacing lowered the risk of syncope.
Rate-responsive pacing is the treatment of choice for irreversible symptomatic CI. The possibilities for pacemaker selection include single-chamber pacing in the atrium or the ventricle, or dual-chamber pacing. Concerns regarding the development of chronic atrial fibrillation or AV nodal disease have limited the use of single-chamber atrial modes in sinus node dysfunction in favor of dual-chamber pacing. However, clinical and diagnostic procedures can predict a group of patients with CI who are at low risk for the development of atrial fibrillation or the progression to AV block. One group of investigators found the risk for development of chronic atrial fibrillation is < 1.5% per year in patients with sinus node dysfunction who are < 70 years old with no history of paroxysmal atrial fibrillation before implantation.17 Valvular heart disease also was noted to be an independent risk marker for the development of atrial fibrillation.18 Rosenqvist and Obel19 reviewed 28 other series of sick sinus syndrome and found a < 1% annual incidence of significant AV conduction defect (defined as second-degree or third-degree block) in patients < 70 years old without evident intraventricular conduction delay. Gillis20 outlined contraindications to single-chamber atrial pacing to include documented AV block, intraventricular conduction delay on ECG, age > 70, Wenckebach block during pacing of < 120 beats/min, bundle of His to a ventricular conduction interval of > 75 ms, or infrahisian block with atrial pacing. Therefore, single-chamber atrial pacing is appropriate in selected CI patients.
Furthermore, it is likely that single-chamber atrial pacing is superior to ventricular pacing. The frequency of progression to atrial fibrillation, and the number of thromboembolic events and potential episodes of heart failure are decreased with atrial pacing compared with ventricular pacing.21 22 23 The results of retrospective analyses and randomized trials21 23 24 suggest improved mortality with atrial pacing as well. A recent prospective randomized trial25 confirmed decreased progression to atrial fibrillation and heart failure with dual-chamber pacing compared to ventricular pacing. The Mode Selection Trial in Sinus-Node Dysfunction evaluated 2,010 patients with sick sinus syndrome (21% with concomitant AV conduction defect) who were prospectively randomized to dual-chamber vs ventricular pacing.25 After a mean follow-up period of 33 months, no difference in the primary end point of death or nonfatal stroke was demonstrated, but dual-chamber pacing led to a 21% decrease in the risk of atrial fibrillation with an improvement in heart failure score and small improvement in quality-of-life score.
CI necessitates the addition of rate responsiveness to the pacemaker. Although the benefit of rate-responsive pacing has been questioned by some investigators,26 several studies2 27 have demonstrated that rate responsiveness is the most important contributor to an increase in cardiac output and exercise tolerance, and that the benefit applies across pacing modes. As none of the current sensors can mimic the sinus node completely, postimplant follow-up, including exercise testing, is important for the programming of optimal rate response settings in each patient.
Multiple studies demonstrate a poor prognosis in patients with CI (Table 2 ). Ellestad and Wan3 reported a subgroup analysis of 85 patients who had CI along with a normal ST-segment response with maximal treadmill testing. They had a similar risk of angina, MI, or death as those with an ischemic ST-segment response. Later studies evaluating approximately 3,800 patients undergoing treadmill stress testing also demonstrated an increased risk of death or major adverse cardiac events in patients with CI.28 29 Wiens et al30 noted that CI was a specific marker for obstructive coronary artery disease, as defined by > 70% stenosis on coronary angiography. Lauer et al10 reviewed a subset of 1,575 patients from the Framingham study, and found greater cardiovascular morbidity and mortality in the subgroup with CI even after adjusting for traditional cardiovascular risk factors. Further work by Lauer and coworkers4 11 31 demonstrated that CI independently predicts mortality even after adjusting for the severity of perfusion defects by thallium, the amount of ischemia by stress echo, or coronary artery disease severity by angiography. The mechanism by which CI is associated with increased mortality is unclear but may be related to abnormalities in autonomic regulation.
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In conclusion, CI is defined as an inadequate HR response to stress. The management of patients with CI requires searching for an underlying etiology and determining the presence and severity of the underlying symptoms. As demonstrated in the presented case, rate-responsive permanent pacemaker implantation is an effective therapy and should be considered for the treatment of symptomatic patients whose conditions do not have a reversible cause. The selection of single-chamber vs dual-chamber pacing should be individualized. The prognosis of CI is variable and dependent on underlying etiology.
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Footnotes |
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The opinions or assertions herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the Army or the Department of Defense.
Received for publication June 17, 2003. Accepted for publication June 19, 2003.
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This article has been cited by other articles:
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  C. Melzer, J. Witte, R. Reibis, H.J. Bondke, W. Combs, K. Stangl, G. Baumann, and H. Theres Predictors of chronotropic incompetence in the pacemaker patient population. Europace, January 1, 2006; 8(1): 70 - 75. [Abstract] [Full Text] [PDF]
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