(Circulation. 1996;93:1520-1526.)
© 1996 American Heart Association, Inc.
Articles |
Impaired Heart Rate Response to Graded Exercise
Prognostic Implications of Chronotropic Incompetence in the Framingham Heart Study
From the Department of Cardiology, Cleveland Clinic Foundation, Cleveland, Ohio (M.S.L.); the Department of Cardiology, the New York Hospital-Cornell Medical Center, New York, NY (P.M.O.); the Department of Preventive Medicine and Epidemiology, Boston (Mass) University School of Medicine (M.G.L.); and the Framingham Heart Study, National Heart, Lung, and Blood Institute, Framingham, Mass (M.G.L., J.C.E., D.L.).
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Abstract |
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Background Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample.
Methods and Results In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking ß-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise ("chronotropic response index"). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P<.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors.
Conclusions An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.
Key Words: mortality • heart rate • exercise testing • coronary heart disease
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Introduction |
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Recently, there has been increasing interest in the role of autonomic nervous system regulation in heart disease. Heart rate (or RR cycle) variability, one marker of autonomic activity, has been found to be an important marker of risk both among survivors of myocardial infarction1 and among healthy adults in the Framingham Heart Study.2 Therefore, we were interested in studying an easily obtained measure that reflects autonomic regulation, namely, the heart rate response to a standard, graded exercise test.3 4 We hypothesized that just as reduced heart rate variability is associated with an adverse outcome,1 2 so would an attenuated heart rate response to exercise be predictive of risk.
In patients with known coronary heart disease an attenuated exercise heart rate response, sometimes referred to as chronotropic incompetence,5 has been associated with an adverse prognosis.5 6 7 8 Although a blunted heart rate response to exercise has been shown to be a predictor of subsequent coronary heart disease events in asymptomatic individuals, this finding was not clearly independent of concurrent ischemic ST-segment changes, age, physical fitness, and standard coronary heart disease risk factors.9
The purpose of this study was to determine the relation between exercise heart rate response and prognosis in asymptomatic subjects from the Framingham Heart Study. End points of interest included all-cause mortality and coronary heart disease events.
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Methods |
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Study Sample
The Framingham Heart Study was initiated in 1948 as an epidemiological study of cardiovascular disease precursors. In the early 1970s, offspring and spouses of offspring of the original study cohort were enrolled in the Framingham Offspring Study. Study design and selection criteria for the original and offspring cohorts have been described in detail elsewhere.10 11 12 Members of the Offspring Study have undergone follow-up examinations 8, 12, and 16 years after the initial examination. At the time of the second Framingham Offspring Study examination, subjects underwent a physician-obtained medical history, physical examination, ECG, exercise treadmill test according to the Bruce protocol,13 and fasting blood tests including glucose and lipid profiles. Informed consent was obtained from all subjects.
To be eligible for this study, subjects had to undergo exercise treadmill testing. Exclusion criteria included prevalent coronary heart disease, technical problems with the treadmill, an inability to reach stage 2 in a standard Bruce protocol (to eliminate confounding effects of very early heart rate responses due to anxiety and also to reduce possible effects of occult angina presenting as very poor exercise tolerance), and use of ß-blockers at the time of the treadmill test. Heart rate blunting calcium blockers like verapamil and diltiazem were not yet in widespread use. This analysis was restricted to men because there were only 20 deaths in the women studied.
Clinical Data
At baseline examination, which occurred between 1979 and 1983,
all subjects had height and weight measured. Obesity was assessed using
body mass index (weight in kilograms divided by height in meters
squared, kg/m2). Systolic blood pressure was
obtained by a physician using a mercury column sphygmomanometer: two
readings were averaged. Baseline hypertension was defined as a
systolic blood pressure of 140 mm Hg or more, a
diastolic blood pressure of 90 mm Hg or more, or use of
antihypertensive medication.14 Diabetes was defined as use
of insulin or oral hypoglycemic agents or a fasting blood glucose of at
least 140 mg/dL (7.77 mmol/L) at the index examination. Usual levels of
physical activity were assessed by a questionnaire in which subjects
were asked how many hours per day were spent engaging in sleep,
sedentary activity, and slight, moderate, and heavy physical activity.
Based on the answers to these questions a physical activity index was
calculated.15
Subjects were followed for a mean of 7.7 years for all-cause mortality and incident coronary heart disease events. The coronary heart disease end points included incident angina pectoris, coronary insufficiency (unstable angina with documented ischemic ST-segment changes), myocardial infarction, sudden and nonsudden coronary heart disease deaths, and coronary revascularization (coronary artery bypass grafting or percutaneous transluminal coronary angioplasty). All available medical records, ECGs, and laboratory data were reviewed by a committee of three physicians to assign cardiovascular disease diagnoses. This committee had no knowledge of the subjects' exercise responses. The criteria for cardiovascular disease diagnoses have been described in detail elsewhere.16
Exercise Testing
All subjects underwent standard treadmill exercise testing on
the same day as the baseline examination according to the Bruce
protocol.13 Exercise was stopped when subjects achieved a
target heart rate (in beats per minute) defined as 85% of the age- and
sex-predicted maximum heart rate,17 which in men were
age 16 to 20 years, maximum heart rate 179; age 21 to 24 years, 177;
age 25 to 29 years, 175; age 30 to 34 years, 173; age 35 to 39 years,
172; age 40 to 44 years, 170; age 45 to 49 years, 168; age 50 to 54
years, 166; age 55 to 59 years, 164; age 60 to 64 years, 162; and age
65 to 69, 158. Other reasons for stopping exercise included participant
request, limiting chest discomfort, dyspnea, fatigue, leg discomfort,
hypotension, an excessive increase in systolic blood pressure
(peak systolic pressure 
250 mm Hg), 2 mm ST-segment
depression, or significant ventricular ectopy (including
frequent ventricular beats and nonsustained
ventricular tachycardia). Heart rate and blood
pressure were measured at rest, during each stage of exercise, at peak
exercise and during recovery. An ST-segment response was considered
ischemic if there was at least 1 mm (0.1 mV) of additional
(versus the resting ECG) horizontal or downsloping ST-segment
depression measured 80 msec after the J-point. Exercise capacity in
metabolic equivalents (METs) was estimated based on a
previously published nomogram relating to the Bruce
protocol18 : stage 2, 7.1 METs; stage 3, 9.9 METs; stage 4,
13.5 METs; and stage 5, 16.5 METs. Subjects were not credited with
achieving any given stage of exercise unless they reached the point
when blood pressure was measured, namely, 1.5 to 2.0 minutes into that
stage.
Statistical Analyses
Assessment of heart rate response. The exercise heart
rate response was assessed in three ways: (1) ability or failure to
achieve the target heart rate, (2) actual increase in heart rate from
rest to peak exercise (in beats per minute), and (3) the ratio of heart
rate to metabolic reserve used by stage 2 of exercise. All
subjects by definition had to achieve stage 2; thus using measurements
at this stage of exercise enables inclusion of all
subjects.19 This last measure of chronotropic competence
is based on the notion that a valid measure of heart rate response must
take into account age, resting heart rate, and exercise
capacity19 ; it is not merely a marker of treadmill time.
Percent metabolic reserve (MR) used by any stage of
exercise can be defined as
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In an analogous fashion, the percent heart rate reserve (HRR) used by any stage of exercise is
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In a healthy subject, the ratio of heart rate to metabolic reserve used by any stage of exercise (heretofore referred to as the chronotropic response index) is roughly 1, a reflection of the association between heart rate response and metabolic work during exercise.19 A low ratio implies chronotropic incompetence, which can be distinguished from effects of age, resting heart rate, and physical fitness on the heart rate response to exercise.19 This ratio should be accurate despite the submaximal nature of the exercise test because of the linear relationship between heart rate and metabolic work during exercise.19
To confirm that the chronotropic response index is relatively independent of age, resting heart rate, and physical fitness, Pearson correlation coefficients (along with standard errors of the estimate) were calculated relating chronotropic response index and heart rate increase with exercise to age, resting heart rate, and exercise capacity in METs.
Description of baseline and exercise characteristics.
Subjects were grouped according to ability to achieve target heart rate
and group-specific values of baseline and exercise characteristics
were determined. In separate analyses, subjects were split
according to tertiles of the chronotropic response index, with the
lowest tertile representing the greatest degree of
chronotropic incompetence. The tertile partition values were 0.15 to
0.95 for the lowest tertile, 0.95 to 1.13 for the middle tertile, and
1.13 to 1.77 for the highest tertile. Subjects were not divided into
quartiles because this would have left too few events per quartile for
meaningful descriptions. ANOVA and 
2 tests were
used to compare means and proportions among groups.
Outcome analyses. The end points of this study were all-cause mortality and incident coronary heart disease; none of the subjects had coronary heart disease at baseline. For descriptive purposes, Kaplan-Meier cumulative incidence plots of all-cause mortality and incident coronary heart disease were constructed according to ability to achieve target heart rate and according to tertiles of the chronotropic response index.
The Cox proportional hazards model20 was used to quantify the associations between exercise heart rate responses and these end points. For analyses of mortality, Cox models were adjusted for age, ST-segment response, valvular disease, pulmonary disease, body mass index, smoking status, hypertension, hypertension treatment, diabetes, physical activity index, and the ratio of total to HDL cholesterol. Because valvular disease and pulmonary disease were uncommon, they were combined for modeling purposes. Models of coronary heart disease incidence were adjusted for age, ST-segment response, body mass index, smoking status, hypertension, hypertension treatment, diabetes, and the ratio of total to HDL cholesterol.
In supplementary analyses, the sample was restricted to subjects who remained free of events during the 2 years of follow-up to reduce any potential bias caused by subclinical conditions at the time of exercise testing.
To investigate the possibility of a J-shaped curve (in
which subjects with an excessive heart rate response in early exercise
might be at increased risk) further analyses were restricted to
those with a chronotropic response index of at least one. Subjects with
a chronotropic response index of 1.3 were considered to have a high
chronotropic response. Their risks for all-cause mortality and
incident coronary heart disease were compared with subjects
whose chronotropic response indexes were between 1.0 and 1.3 using Cox
regression analyses.
Proportional hazards analyses were performed using PROC PHREG of the SAS statistical packages21 on a Sun Sparcstation 2.
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Results |
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Baseline Characteristics
The baseline characteristics of eligible subjects are summarized in Tables 1
and 2. None of the subjects
had atrial fibrillation or congestive heart failure at baseline and
none was taking digitalis. Of the 1575 men, 327 (21%) failed to
achieve 85% of the age-predicted maximum heart rate. Compared with
subjects who achieved their target heart rate, those who failed to do
so were older, had higher mean values for body mass index, resting
blood pressures, and total to HDL cholesterol ratio, and
were more likely to smoke cigarettes, have clinical hypertension, and
pulmonary disease (Table 1). The most commonly used
antihypertensive drugs included thiazide diuretics (n=96),
-methyldopa (n=27), loop diuretics (n=3), spironolactone
(n=3), and miscellaneous other agents including -blockers and
direct vasodilators (n=54).
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When subjects were divided according to tertiles of chronotropic
response index, there were no marked differences in age, blood
pressure, body mass index, resting heart rate, and the ratio of total
to HDL cholesterol; smoking was somewhat more prevalent
among those in the lowest tertile of chronotropic response index (Table 2
). The physical activity index was unrelated to chronotropic response
(Tables 1 and 2).
The exercise characteristics of subjects are summarized in Tables 3 and 4. Reasons for stopping exercise
included dyspnea (n=83), leg discomfort (n=75), marked ischemic
ST-segment response (n=24), excessive increase in systolic
blood pressure (n=8), participant request (n=7), complex
ventricular ectopy (n=4). One subject stopped because of
chest discomfort. As expected, the chronotropic response index was
about 1.0 in subjects who reached their target heart rate but was lower
(0.86±0.22, P<.0001) in those who did not achieve the
target heart rate. Subjects who failed to achieve target heart rate
were more likely to exhibit an ischemic ST-segment response
(18% versus 13%, P=.054); they also had a lower exercise
capacity (Table 3). When divided according to tertiles of chronotropic
response index, there were no marked differences in abnormal ST-segment
response; exercise capacity was slightly higher among subjects in the
highest tertile of chronotropic response index (Table 4).
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Heart Rate Measures and Age, Resting Heart Rate, and Exercise
Capacity
The increase in heart rate with exercise was weakly correlated
with age (r=-.41, SEE=0.023), resting heart rate
(-.62, SEE=0.020), and exercise capacity in METs
(r=.52, SEE=0.022). In contrast, the chronotropic response
index was uncorrelated with age (r=.005, SEE=0.025), resting
heart rate (r=-.01, SEE=0.025), and it was only weakly
correlated with exercise capacity in METs (r=.21,
SEE=0.024). The physical activity index was not correlated with the
chronotropic response index (r=-.003). The
chronotropic response index represents an exercise heart rate
response variable that is uncorrelated or minimally correlated with
age or level of physical fitness.
Prognostic Implications of Exercise Heart Rate
Response
During a mean of 7.7 years of follow-up there were 55 deaths:
14 from coronary heart disease, 27 from cancer, 2 from other
cardiovascular causes, and 12 from miscellaneous
causes. There were 95 incident coronary heart disease events
including 45 myocardial infarctions, 44 cases of angina pectoris or
coronary insufficiency, and 6 sudden cardiac deaths. No cases
of coronary revascularization occurred as
incident coronary heart disease events.
An inability to achieve target heart rate and a lower chronotropic
response index were related to a higher incidence of all-cause
mortality (Figs 1 and 2) and
coronary heart disease events (Figs 3 and 4).
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All-Cause Mortality
Of the 327 men who failed to reach the target heart rate, 21 (6%)
died; however, of the 1248 who achieved their target heart rate only 34
(3%) died. There were 23 deaths (4%) among those in the lowest
tertile of chronotropic response index, 16 (3%) deaths in the middle
tertile, and 16 (3%) in the highest tertile. In unadjusted
analyses, failure to achieve target heart rate was associated
with an increased risk of death, but after adjusting for several
covariates it was no longer predictive of death risk. The increase in
heart rate was inversely related to mortality risk after adjusting for
the same covariates (P=.04). Similarly, an impaired early
heart rate response through stage 2 of exercise, as assessed by the
chronotropic response index was predictive of mortality
(P<.05). See Table 5.
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Coronary Heart Disease Events
Of the 327 men who failed to reach their target heart rate, 44
(14%) experienced a coronary event (25 had myocardial
infarctions, 15 developed angina pectoris, and 4 had sudden cardiac
death as the initial presentation of coronary heart
disease); of the 1248 men who reached their target heart rate, only 51
(4%) experienced a coronary event. There were 44 (8%)
coronary heart disease events among those in the lowest tertile
of chronotropic response index, 35 (7%) in the middle tertile, and 16
(3%) in the highest tertile. Failure to achieve target heart rate was
associated with an increased risk of incident coronary heart
disease when studied alone. After adjusting for age, ST-segment
response, body mass index, smoking, hypertension, hypertension
treatment, diabetes, physical activity index, and the ratio of total to
HDL cholesterol, failure to achieve target heart rate
remained predictive of coronary heart disease events (adjusted
hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74;
P=.02). The increase in heart rate was inversely predictive
of incident coronary heart disease after adjusting for the same
covariates (P=.0003). Similarly, the chronotropic response
index was inversely predictive of incident coronary heart
disease (P=.001). See Table 5.
Late Events
In analyses restricted to subjects who had at least 2
years of event-free follow-up, similar associations of heart
rate response with late incident coronary heart disease events
were noted, with no material difference from the prior results (Table 6
is provided for reviewers). None of the heart rate
variables was independently predictive of late all-cause
mortality.
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Impact of an Excessive Heart Rate Response in Early
Exercise
It might be postulated that subjects with high chronotropic
responses (chronotropic response index 1.3) are at increased risk for
an adverse outcome. There were 891 subjects with a chronotropic index
of at least 1; during follow-up there were 26 deaths and 44
incident coronary heart disease events. Compared with subjects
with a chronotropic index between 1.0 and 1.3, those with an index
exceeding 1.3 had a similar all-cause mortality rate (hazard ratio,
1.34; 95% confidence interval, 0.54 to 3.35; P>.5) and
comparable risk of coronary heart disease events (hazard ratio,
0.88; 95% confidence interval, 0.39 to 1.99; P>.7).
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Discussion |
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In this group of 1575 men derived from a population-based sample, an impaired heart rate response on standard exercise testing was related to the risk of an adverse outcome after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors including diabetes, smoking, hypertension, antihypertensive therapy, and the ratio of total to HDL cholesterol. An impaired heart rate response was associated with higher total mortality and with increased risk of coronary heart disease. In addition, a blunted heart rate response was associated with late incident coronary heart disease events (events occurring at least 2 years after the treadmill test).
The heart rate response to exercise is related to a complex interplay among many factors including age, sex, physical conditioning, sympathetic drive, baroreceptor reflexes, and venous return, as has been reviewed elsewhere.7 Several studies have demonstrated an association between failure to achieve a predicted heart rate and coronary artery disease prognosis.5 6 7 8 9 Only one of those was population-based9 ; in that study, failure to attain 90% of the age-predicted maximum heart rate was predictive of coronary heart disease risk. That study, however, did not rigorously adjust for ST-segment changes and traditional coronary risk factors in multivariable models. Another study of employed men found sustained slow heart rates may be predictive of a higher risk of cardiac death.22 In that study there were no noted exclusions for ß-blocker use or preexisting coronary heart disease.
The mechanism by which an impaired exercise heart rate response may be associated with increased risk of coronary heart disease is unclear. An attenuation of sympathetic drive has been demonstrated for patients with established heart failure23 ; perhaps a similar attenuation may occur in very early subclinical manifestations of cardiovascular disease. Another possible explanation is that an impaired exercise heart rate response may well represent an early manifestation of cardiac ischemia.5
The association of an impaired exercise heart rate response and increased mortality and coronary risk may be analogous to the association of reduced heart rate variability (or RR cycle variability) with adverse outcome.1 2 A recent report from the Framingham Heart Study2 found that time-domain and frequency-domain variables derived from a 2-hour Holter monitor recording predicted mortality risk in conjunction with standard cardiovascular risk factors. In contrast to these measures of heart rate variability, the exercise heart rate response may represent an easily and routinely obtained measure that is associated with autonomic regulation.
The increased risk associated with an impaired heart rate response may
reflect decreased physical fitness, which has been shown to be
predictive of cardiac risk.24 Since the exercise tests
obtained in this study were submaximal, our ability to accurately
assess the impact of physical fitness is limited. To separate effects
of physical fitness from heart rate response, analyses were
performed looking only at heart rate response during early exercise
(through stage 2 of a Bruce protocol). In models of mortality and
coronary heart disease risk, the chronotropic response index
was predictive of risk. Of note, the chronotropic response index was
only weakly (r=.21) associated with exercise capacity (and
therefore was not merely a marker of treadmill duration or physical
fitness) and was unassociated with age or resting heart rate. Among
subjects in the highest tertile of chronotropic response index exercise
capacity was slightly higher (13.5 versus 12.7), an association that
was statistically significant given the large sample size but not
particularly marked. In contrast, failure to achieve target heart rate
was strongly associated with age (P<.0001), resting heart
rate (P=.02), and physical fitness (P<.001)
(Tables 1 and 3). Increase in heart rate with exercise was also
correlated with age, resting heart rate, and physical fitness. Thus, of
the three measures of heart rate response we considered, the
chronotropic response index comes closest to a pure measure of
chronotropic competence. Also, baseline physical activity, in the form
of a physical activity index,15 was also considered and
was found to be unassociated with chronotropic response. It did not
influence the association between chronotropic incompetence and adverse
outcome.
Inability to achieve target heart rate was associated with a higher likelihood of an ischemic ST-segment response, a lower exercise capacity, and an adverse coronary heart disease risk factor profile. As such, these true confounders of the association of heart rate response to exercise with risk for death and coronary heart disease needed to be considered. Stratification was impractical with several confounders,25 so multivariable proportional hazards models were adopted. We assumed that the primary variables have certain mathematical relations to the risks of death and of developing coronary disease, and also that those relations are not modified by confounders. Although the data were too sparse to check these assumptions fully, we found that the results from unadjusted and adjusted models were consistent with our expectations: the effect estimated for each primary variable was attenuated somewhat upon adjustment for confounders.
There are other potential limitations of this study. The study sample was all male and overwhelmingly white, so the results may not apply to females and nonwhites. Despite the increased risks associated with attenuated exercise heart rate responses, most of the deaths and coronary heart disease events occurred in individuals who did achieve their target heart rate and who were in the top two tertiles of chronotropic response index. Exercise capacity in METs was estimated, not directly measured using gas exchange techniques. We were unable to document the accuracy of the estimated exercise capacity or metabolic reserve, which was used for calculating chronotropic index because metabolic testing was not used at Framingham during the testing period. Thus, the chronotropic index is a calculated, rather than a directly measured value. The use of the Bruce protocol, with its incremental stages, may result in an overestimation of exercise capacity.26 The major stopping point for our exercise test was achievement of a target heart rate, based on 85% of the age-predicted maximum, which has a fairly high standard deviation7 and which, therefore, may not be ideally applicable for individual subjects. The use of a submaximal test, instead of a symptom-limited test, may be a potential limitation, since many individuals could have achieved higher heart rates than they did. By truncating heart rate increase with exercise in this way, the differences were diminished between heart rate increases in those who failed, compared with those who reached their target heart rate. This, if anything, would attenuate the association between heart rate response and outcome; there would be a bias toward no effect.
Despite these limitations, heart rate response to exercise was associated with an increased risk for death and coronary heart disease even after considering ST-segment response to exercise, baseline physical activity, and traditional coronary disease risk factors. Furthermore, we have demonstrated that the chronotropic response index, a measure of exercise heart rate response that is relatively independent of age, resting heart rate, and physical fitness, is a strong predictor of outcome.
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Footnotes |
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Reprint requests to Dr Lauer, Department of Cardiology, Cleveland Clinic Foundation, Desk F-15, 9500 Euclid Ave, Cleveland, OH 44195.
Received September 27, 1995; revision received January 16, 1996; accepted January 22, 1996.
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 M. Unverdorben, A. van der Bijl, L. Potgieter, C. Venter, S. Munjal, Qiwei Liang, B. Meyer, and H.-J. Rothig Effects of Different Levels of Cigarette Smoke Exposure on Prognostic Heart Rate and Rate--Pressure-Product Parameters Journal of Cardiovascular Pharmacology and Therapeutics, September 1, 2008; 13(3): 175 - 182. [Abstract] [PDF]
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F Gomez-Gallego, C Santiago, M Moran, M Perez, J L Mate-Munoz, M F. del Valle, J C Rubio, I Garcia-Consuegra, C Foster, I A L Andreu, et al. The I allele of the ACE gene is associated with improved exercise capacity in women with McArdle disease Br. J. Sports Med., February 1, 2008; 42(2): 134 - 140. [Abstract] [Full Text] [PDF]
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E. Ingelsson, M. G. Larson, R. S. Vasan, C. J. O'Donnell, X. Yin, J. N. Hirschhorn, C. Newton-Cheh, J. A. Drake, S. L. Musone, N. L. Heard-Costa, et al. Heritability, Linkage, and Genetic Associations of Exercise Treadmill Test Responses Circulation, June 12, 2007; 115(23): 2917 - 2924. [Abstract] [Full Text] [PDF]
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N. J. Leeper, F. E. Dewey, E. A. Ashley, M. Sandri, S. Y. Tan, D. Hadley, J. Myers, and V. Froelicher Prognostic Value of Heart Rate Increase at Onset of Exercise Testing Circulation, January 30, 2007; 115(4): 468 - 474. [Abstract] [Full Text] [PDF]
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P. Kligfield and M. S. Lauer Exercise Electrocardiogram Testing: Beyond the ST Segment Circulation, November 7, 2006; 114(19): 2070 - 2082. [Full Text] [PDF]
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H C Routledge and J N Townend Why does the heart rate response to exercise predict adverse cardiac events? Heart, May 1, 2006; 92(5): 577 - 578. [Abstract] [Full Text] [PDF]
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S. Y. Jae, B. Fernhall, K. S. Heffernan, M. Kang, M.-K. Lee, Y.-H. Choi, and W. H. Park Chronotropic response to exercise testing is associated with carotid atherosclerosis in healthy middle-aged men Eur. Heart J., April 2, 2006; 27(8): 954 - 959. [Abstract] [Full Text] [PDF]
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K K A Witte, J G F Cleland, and A L Clark Chronic heart failure, chronotropic incompetence, and the effects of {beta} blockade Heart, April 1, 2006; 92(4): 481 - 486. [Abstract] [Full Text] [PDF]
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K. P. Savonen, T. A. Lakka, J. A. Laukkanen, P. M. Halonen, T. H. Rauramaa, J. T. Salonen, and R. Rauramaa Heart rate response during exercise test and cardiovascular mortality in middle-aged men Eur. Heart J., March 1, 2006; 27(5): 582 - 588. [Abstract] [Full Text] [PDF]
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H.-F. Tse, C.-W. Siu, K. L.F. Lee, K. Fan, H.-W. Chan, M.-O. Tang, V. Tsang, S. W.L. Lee, and C.-P. Lau The Incremental Benefit of Rate-Adaptive Pacing on Exercise Performance During Cardiac Resynchronization Therapy J. Am. Coll. Cardiol., December 20, 2005; 46(12): 2292 - 2297. [Abstract] [Full Text] [PDF]
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M. Lauer, E. S. Froelicher, M. Williams, and P. Kligfield Exercise Testing in Asymptomatic Adults: A Statement for Professionals From the American Heart Association Council on Clinical Cardiology, Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention Circulation, August 2, 2005; 112(5): 771 - 776. [Abstract] [Full Text] [PDF]
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M P Frenneaux Autonomic changes in patients with heart failure and in post-myocardial infarction patients Heart, November 1, 2004; 90(11): 1248 - 1255. [Abstract] [Full Text] [PDF]
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G. J. Balady, M. G. Larson, R. S. Vasan, E. P. Leip, C. J. O'Donnell, and D. Levy Usefulness of Exercise Testing in the Prediction of Coronary Disease Risk Among Asymptomatic Persons as a Function of the Framingham Risk Score Circulation, October 5, 2004; 110(14): 1920 - 1925. [Abstract] [Full Text] [PDF]
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 M. K. Aktas, V. Ozduran, C. E. Pothier, R. Lang, and M. S. Lauer Global Risk Scores and Exercise Testing for Predicting All-Cause Mortality in a Preventive Medicine Program JAMA, September 22, 2004; 292(12): 1462 - 1468. [Abstract] [Full Text] [PDF]
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B. Azarbal, S. W. Hayes, H. C. Lewin, R. Hachamovitch, I. Cohen, and D. S. Berman The incremental prognostic value of percentage of heart rate reserve achieved over myocardial perfusion single-photon emission computed tomography in the prediction of cardiac death and all-cause mortality: Superiority over 85% of maximal age-predicted heart rate J. Am. Coll. Cardiol., July 21, 2004; 44(2): 423 - 430. [Abstract] [Full Text] [PDF]
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M. S. Lauer Chronotropic incompetence: Ready for prime time J. Am. Coll. Cardiol., July 21, 2004; 44(2): 431 - 432. [Full Text] [PDF]
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G. Erikssen, J. Bodegard, J. V. Bjornholt, K. Liestol, D. S. Thelle, and J. Erikssen Exercise testing of healthy men in a new perspective: from diagnosis to prognosis Eur. Heart J., June 1, 2004; 25(11): 978 - 986. [Abstract] [Full Text] [PDF]
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 R. B. McCully, V. L. Roger, S. R. Ommen, D. W. Mahoney, K. N. Burger, W. K. Freeman, and P. A. Pellikka Outcomes of Patients With Reduced Exercise Capacity at Time of Exercise Echocardiography Mayo Clin. Proc., June 1, 2004; 79(6): 750 - 757. [Abstract] [PDF]
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P. J. Gentlesk, T. T. Markwood, and J. E. Atwood Chronotropic Incompetence in a Young Adult: Case Report and Literature Review Chest, January 1, 2004; 125(1): 297 - 301. [Abstract] [Full Text] [PDF]
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A. Elhendy, D. W. Mahoney, B. K. Khandheria, K. Burger, and P. A. Pellikka Prognostic significance of impairment of heart rate response to exercise: Impact of left ventricular function and myocardial ischemia J. Am. Coll. Cardiol., September 3, 2003; 42(5): 823 - 830. [Abstract] [Full Text] [PDF]
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A. P. Morise and F. Jalisi Evaluation of pretest and exercise test scores to assess all-cause mortality in unselected patients presenting for exercise testing with symptoms of suspected coronary artery disease J. Am. Coll. Cardiol., September 3, 2003; 42(5): 842 - 850. [Abstract] [Full Text] [PDF]
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Committee Members, R. J. Gibbons, G. J. Balady, J. Timothy Bricker, B. R. Chaitman, G. F. Fletcher, V. F. Froelicher, D. B. Mark, B. D. McCallister, A. N. Mooss, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: A report of the American college of cardiology/American heart association task force on practice guidelines (committee to update the 1997 exercise testing guidelines) J. Am. Coll. Cardiol., October 16, 2002; 40(8): 1531 - 1540. [Full Text] [PDF]
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R. J. Gibbons, G. J. Balady, J. Timothy Bricker, B. R. Chaitman, G. F. Fletcher, V. F. Froelicher, D. B. Mark, B. D. McCallister, A. N. Mooss, M. G. O'Reilly, et al. ACC/AHA 2002 Guideline Update for Exercise Testing: Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines) Circulation, October 1, 2002; 106(14): 1883 - 1892. [Full Text] [PDF]
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 T. Wakabayashi, T. Nakata, A. Hashimoto, S. Yuda, K. Tsuchihashi, M. I. Travin, and K. Shimamoto Assessment of Underlying Etiology and Cardiac Sympathetic Innervation to Identify Patients at High Risk of Cardiac Death J. Nucl. Med., December 1, 2001; 42(12): 1757 - 1767. [Abstract] [Full Text] [PDF]
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L. A. Diaz, R. C. Brunken, E. H. Blackstone, C. E. Snader, and M. S. Lauer Independent contribution of myocardial perfusion defects to exercise capacity and heart rate recovery for prediction of all-cause mortality in patients with known or suspected coronary heart disease J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1558 - 1564. [Abstract] [Full Text] [PDF]
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E. O. Nishime, C. R. Cole, E. H. Blackstone, F. J. Pashkow, and M. S. Lauer Heart Rate Recovery and Treadmill Exercise Score as Predictors of Mortality in Patients Referred for Exercise ECG JAMA, September 20, 2000; 284(11): 1392 - 1398. [Abstract] [Full Text] [PDF]
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A. P. Morise Are the American College of Cardiology/American Heart Association Guidelines for Exercise Testing for Suspected Coronary Artery Disease Correct? Chest, August 1, 2000; 118(2): 535 - 541. [Abstract] [Full Text] [PDF]
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C. R. Cole, J. M. Foody, E. H. Blackstone, and M. S. Lauer Heart Rate Recovery after Submaximal Exercise Testing as a Predictor of Mortality in a Cardiovascularly Healthy Cohort Ann Intern Med, April 4, 2000; 132(7): 552 - 555. [Abstract] [Full Text] [PDF]
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S. Gammenthaler, P. Palatini, X. Jouven, P. Ducimetiere, M. S. Lauer, and C. R. Cole Recovery of Heart Rate after Exercise N. Engl. J. Med., March 2, 2000; 342(9): 662 - 663. [Full Text]
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M. Robbins, G. Francis, F. J. Pashkow, C. E. Snader, K. Hoercher, J. B. Young, and M. S. Lauer Ventilatory and Heart Rate Responses to Exercise : Better Predictors of Heart Failure Mortality Than Peak Oxygen Consumption Circulation, December 14, 1999; 100(24): 2411 - 2417. [Abstract] [Full Text] [PDF]
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C. R. Cole, E. H. Blackstone, F. J. Pashkow, C. E. Snader, and M. S. Lauer Heart-Rate Recovery Immediately after Exercise as a Predictor of Mortality N. Engl. J. Med., October 28, 1999; 341(18): 1351 - 1357. [Abstract] [Full Text] [PDF]
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R.L. Popp Stress echocardiography results in context Eur. Heart J., October 2, 1999; 20(20): 1450 - 1451. [PDF]
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U K H Wiegand, F Bode, R Schneider, A Brandes, H Haase, H A Katus, and J Potratz Development of sinus node disease in patients with AV block: implications for single lead VDD pacing Heart, June 1, 1999; 81(6): 580 - 585. [Abstract] [Full Text]
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A Elhendy, R T van Domburg, J J Bax, P R Nierop, M L Geleijnse, M M Ibrahim, and J R T C Roelandt The functional significance of chronotropic incompetence during dobutamine stress test Heart, April 1, 1999; 81(4): 398 - 403. [Abstract] [Full Text]
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A. Cohen-Solal, Y. Esanu, D. Logeart, F. Pessione, C. Dubois, G. Dreyfus, R. Gourgon, and P. Merlet Cardiac metaiodobenzylguanidine uptake in patients with moderate chronic heart failure: relationship with peak oxygen uptake and prognosis J. Am. Coll. Cardiol., March 1, 1999; 33(3): 759 - 766. [Abstract] [Full Text] [PDF]
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M. S. Lauer, G. S. Francis, P. M. Okin, F. J. Pashkow, C. E. Snader, and T. H. Marwick Impaired Chronotropic Response to Exercise Stress Testing as a Predictor of Mortality JAMA, February 10, 1999; 281(6): 524 - 529. [Abstract] [Full Text] [PDF]
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M. S. Lauer, R. Mehta, F. J. Pashkow, P. M. Okin, K. Lee, and T. H. Marwick Association of chronotropic incompetence with echocardiographic ischemia and prognosis J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1280 - 1286. [Abstract] [Full Text] [PDF]
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D. Roach, A. Sheldon, W. Wilson, and R. Sheldon Temporally localized contributions to measures of large-scale heart rate variability Am J Physiol Heart Circ Physiol, May 1, 1998; 274(5): H1465 - H1471. [Abstract] [Full Text] [PDF]
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A Cohen-Solal, P Barnier, F Pessione, P Seknadji, D Logeart, T Laperche, and R Gourgon Comparison of the long term prognostic value of peak exercise oxygen pulse and peak oxygen uptake in patients with chronic heart failure Heart, December 1, 1997; 78(6): 572 - 576. [Abstract] [Full Text] [PDF]
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P. M. Okin, M. S. Lauer, and P. Kligfield Chronotropic Response to Exercise: Improved Performance of ST-Segment Depression Criteria After Adjustment for Heart Rate Reserve Circulation, December 15, 1996; 94(12): 3226 - 3231. [Abstract] [Full Text]
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M. H. Ellestad Chronotropic Incompetence : The Implications of Heart Rate Response to Exercise (Compensatory Parasympathetic Hyperactivity?) Circulation, April 15, 1996; 93(8): 1485 - 1487. [Full Text]
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A. Fowler-Brown, M. Pignone, M. Pletcher, J. A. Tice, S. F. Sutton, and K. N. Lohr Exercise Tolerance Testing To Screen for Coronary Heart Disease: A Systematic Review for the Technical Support for the U.S. Preventive Services Task Force Ann Intern Med, April 6, 2004; 140(7): W-9 - W-24. [Abstract] [Full Text] [PDF]
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