Background The increase in heart rate that accompanies exerciseis due in part to a reduction in vagal tone. Recovery of theheart rate immediately after exercise is a function of vagalreactivation. Because a generalized decrease in vagal activityis known to be a risk factor for death, we hypothesized thata delayed fall in the heart rate after exercise might be animportant prognostic marker.
Methods For six years we followed 2428 consecutive adults (mean[±SD] age, 57±12 years; 63 percent men) withouta history of heart failure or coronary revascularization andwithout pacemakers. The patients were undergoing symptom-limitedexercise testing and single-photon-emission computed tomographywith thallium scintigraphy for diagnostic purposes. The valuefor the recovery of heart rate was defined as the decrease inthe heart rate from peak exercise to one minute after the cessationof exercise. An abnormal value for the recovery of heart ratewas defined as a reduction of 12 beats per minute or less fromthe heart rate at peak exercise.
Results There were 213 deaths from all causes. A total of 639patients (26 percent) had abnormal values for heart-rate recovery.In univariate analyses, a low value for the recovery of heartrate was strongly predictive of death (relative risk, 4.0; 95percent confidence interval, 3.0 to 5.2; P<0.001). Afteradjustments were made for age, sex, the use or nonuse of medications,the presence or absence of myocardial perfusion defects on thalliumscintigraphy, standard cardiac risk factors, the resting heartrate, the change in heart rate during exercise, and workloadachieved, a low value for heart-rate recovery remained predictiveof death (adjusted relative risk, 2.0; 95 percent confidenceinterval, 1.5 to 2.7; P<0.001).
Conclusions A delayed decrease in the heart rate during thefirst minute after graded exercise, which may be a reflectionof decreased vagal activity, is a powerful predictor of overallmortality, independent of workload, the presence or absenceof myocardial perfusion defects, and changes in heart rate duringexercise.
Although attention has been given to the prognostic implicationsof changes in heart rate during exercise,1,2,3 the prognosticvalue of the rate of decline in heart rate after the cessationof exercise has not been well characterized. The rise in heartrate during exercise is considered to be due to the combinationof parasympathetic withdrawal and sympathetic activation.4 Thefall in heart rate immediately after exercise is consideredto be a function of the reactivation of the parasympatheticnervous system.5 Because increased vagal activity has been associatedwith a reduction in the risk of death,6 we hypothesized thatthe rate of recovery of the heart rate immediately after exercisemay be an important prognostic marker.
The purpose of this study was to examine the usefulness of theheart-rate recovery after exercise as a long-term prognosticmarker in a population of consecutive patients referred forexercise testing with single-photon-emission computed tomographyand thallium scintigraphy at a single center. We specificallyfocused on overall mortality as an unbiased, objective end point.7
Methods
Patient Population
The study cohort was made up of consecutive adult patients whowere referred to the Cleveland Clinic Foundation for a firstsymptom-limited exercise test and single-photon-emission computedtomography with thallium scintigraphy between September 1990and December 1993.8,9 We included patients who were candidatesfor initial angiography.10 Patients were excluded if they hada history of coronary angiography, previous cardiac surgery,an implanted pacemaker, congestive heart failure or use of digoxin,congenital or valvular heart disease, the preexcitation syndrome,or left bundle-branch block (because of the potential for falsepositive findings of myocardial perfusion defects on thalliumscintigraphy during exercise in patients with these factors).Patients were also excluded if a valid Social Security numberwas not included in their registration or if data on the recoveryof heart rate were not available. All patients gave informedconsent before testing; the protocol was approved by the institutionalreview board of the Cleveland Clinic Foundation.
Clinical Data
Before the patients were tested, a review of each patient'schart and a structured interview were conducted to gather dataon symptoms, medications, coronary risk factors, previous cardiacevents, and other diagnoses.9 Hypertension was defined as asystolic blood pressure of 140 mm Hg at rest, a diastolic bloodpressure of 90 mm Hg at rest, or treatment with antihypertensivemedication.11 Diagnoses of diabetes mellitus and chronic lungdisease were determined on the basis of chart review, interviewswith the patients, and use of medication by the patients. Ahistory of coronary disease was considered present when therewere documented hospitalizations for myocardial infarction orunstable angina. The presence of a lipid disorder was definedby the use of lipid-lowering medication at the time of testing.Cardioactive medications were classified as beta-blockers, nondihydropyridinecalcium-channel blockers (e.g., diltiazem and verapamil), orvasodilators (e.g., nifedipine, alpha-adrenergic blockers, andangiotensin-converting–enzyme inhibitors).
Exercise Testing
Exercise testing of most of the patients was conducted accordingto the standard and modified Bruce protocols.12 Whether cardioactivemedications were used on the day of the test was left to thediscretion of the referring physician. So that workload couldbe more accurately estimated, the patients were not allowedto lean on the handrails. Midway through each stage of exercise,at peak exercise, and one minute after the cessation of exercise,data on symptoms, heart rate and rhythm, blood pressure (asmeasured by indirect arm-cuff sphygmomanometry), and estimatedworkload (as determined on the basis of standard tables)12 inmetabolic equivalents (MET; 1 MET equals 3.5 ml of oxygen uptakeper kilogram of body weight per minute) were collected and enteredinto a computer data base. The patients were encouraged to reachsymptom-limited maximal exercise; the achievement of the targetheart rate (based on age) alone was not a sufficient reasonfor the termination of testing. Chronotropic response duringexercise was defined as the percentage of the heart-rate reserve(the difference between the maximal achievable heart rate [220beats per minute minus age in years] and the resting heart rate)used at peak exercise. A failure to use 80 percent of the heart-ratereserve was considered to be evidence of an impaired chronotropicresponse.13 This measure is an independent predictor of mortality.8
Recovery of Heart Rate
After achieving peak workload, all the patients spent at leasttwo minutes in a cool-down period during treadmill testing ata speed of 2.4 km (1.5 mi) per hour and a grade of 2.5 percent.This period was considered the recovery period. The value forthe recovery of heart rate was defined as the reduction in theheart rate from the rate at peak exercise to the rate one minuteafter the cessation of exercise.
We determined an abnormal value for the recovery of heart rateby finding the maximal value for the log-rank chi-square teststatistic for all possible cutoff points between the 10th and90th percentiles for the study cohort.14 A secondary abnormalvalue was based on the value for the 10th percentile for thestudy cohort.
Thallium Scintigraphy
The scintigraphic methods used in our laboratory between 1990and 1993 have been described in detail elsewhere.15 We determineda modified summed score on the thallium stress test for eachpatient by dividing the number of segments of the left ventriclewith either fixed or reversible perfusion defects during thalliumscintigraphy by the total number of segments. We have previouslyreported on the associations between such defects and mortality.8,9,16
End Points
The mean follow-up time was six years. The primary end pointwas death from all causes, identified through a search of theSocial Security death index by Epidemiology Resources (Newton,Mass.). This index has previously been validated and is slightlyless sensitive but more current and specific than the NationalDeath Index.17
Statistical Analysis
For descriptive purposes, the patients were divided into twogroups on the basis of the value for the recovery of heart rate.Continuous variables are presented as means ±SD. Differencesbetween groups were compared with the use of Student's t-test,Wilcoxon's rank-sum test, and the chi-square test, as appropriate.
The value for heart-rate recovery was related to mortality fromall causes by univariable and multivariable Cox regression analyses.18We performed stratified analyses of prespecified subgroups definedaccording to age, sex, history of coronary disease, the chronotropicresponse during exercise, the presence or absence of perfusiondefects on thallium scintigraphy, and the use or nonuse of medications.Logarithmic and quadratic transformations and potential interactionswere assessed for improvement of fit. To assess further theassociation of heart-rate recovery with mortality, the populationwas divided according to quintiles of values for recovery, withrelative risks and confidence intervals calculated on the basisof comparisons with the highest quintile. The Cox proportional-hazardsassumption was confirmed by inspection of log [–log (survivalfunction)] curves.
To assess the association between heart-rate recovery and exercisecapacity, the study cohort was divided into sex-specific decilesof exercise capacity, measured in MET. Differences in the proportionof patients with an abnormal value for heart-rate recovery (12beats per minute) were compared with use of the chi-square testfor trend.19 Logistic-regression analysis was used to assessthe effects of exercise capacity and medications on heart-raterecovery after adjustment for age, sex, and the presence orabsence of perfusion defects on thallium scintigraphy.20 Allanalyses were performed with the SAS statistical package (version6.12, SAS Institute, Cary, N.C.).
Results
Characteristics of the Patients at Base Line and during Exercise
There were 2428 patients who met all inclusion criteria. Themedian value for heart-rate recovery was 17 beats per minute,with a range from the 25th to the 75th percentile of 12 to 23beats per minute. A cutoff value of 12 beats per minute wasfound to maximize the log-rank test statistic. An abnormal valuefor heart-rate recovery was found in 639 patients (26 percent).
The base-line characteristics of the patients according to whethertheir heart-rate recovery was normal or abnormal are summarizedin Table 1. As compared with the patients with a normal valuefor heart-rate recovery, those with an abnormal value (12 beatsper minute) were older, had higher resting heart rates, weremore likely to have hypertension or diabetes, were more likelyto smoke, and were more likely to have Q waves on the electrocardiogramor a history of coronary artery disease. They were also morelikely to take nondihydropyridine calcium-channel blockers orvasodilators. There were no marked differences between the groupsin the use of beta-blockers.
Table 1. Base-Line Characteristics of the Patients According to the Value for the Recovery of Heart Rate after Exercise.
During exercise, the patients with an abnormal value for heart-raterecovery, as compared with those with a normal value, had lowerincreases in heart rate from base line (an increase of 61±21beats per minute vs. an increase of 81±20 beats per minute,P<0.001) and were more likely to have an impaired chronotropicresponse during exercise (45 percent vs. 23 percent of patients,P<0.001). They were also more likely to have perfusion defectson thallium scintigraphy (23 percent vs. 19 percent, P=0.01).There were no differences between the groups in the percentageof patients with abnormal ST-segment response (19 percent vs.21 percent, P=0.2) or angina during treadmill testing (15 percentvs. 14 percent, P=0.6).
Heart-Rate Recovery and Mortality
During six years of follow-up, there were 213 deaths from allcauses (9 percent). An abnormal value for heart-rate recoverywas strongly predictive of death (mortality at six years, 19percent vs. 5 percent; relative risk, 4.0; 95 percent confidenceinterval, 3.0 to 5.2; P<0.001). Of the 213 patients who died,120 (56 percent) had an abnormally low value for heart-raterecovery.
As a predictor of death, an abnormally low value for heart-raterecovery had a sensitivity of 56 percent, a specificity of 77percent, a positive predictive value of 19 percent, and a negativepredictive value of 95 percent. When the value for the 10thpercentile (a decrease of eight beats per minute) was used asa cutoff, the sensitivity was 33 percent, the specificity 90percent, the positive predictive value 24 percent, and the negativepredictive value 90 percent; the relative risk was 4.1 (95 percentconfidence interval, 3.0 to 5.4; P<0.001).
Analyses stratified according to age, sex, history of coronarydisease, the chronotropic response during exercise, the presenceor absence of perfusion defects on thallium scintigraphy, andthe use or nonuse of medications are presented in Table 2. Alow value for heart-rate recovery was predictive of death inall subgroups, although the association was weaker among thepatients with an impaired chronotropic response during exerciseand those taking vasodilators or nondihydropyridine calcium-channelblockers.
Table 2. Associations between a Low Value for the Recovery of Heart Rate and Mortality in Prespecified Subgroups.
A low value for heart-rate recovery was predictive of deathwhen considered as a continuous variable, especially after logarithmictransformation; a decrease in exercise capacity, the presenceof perfusion defects on thallium scintigraphy, and an impairedchronotropic response during exercise were also predictive ofdeath (Table 3). Figure 1 shows the relative risk of death accordingto the quintile of heart-rate recovery; once this value droppedbelow 10 to 15 beats per minute there was a marked increasein the risk of death. Values above 15 to 20 beats per minute,however, were not associated with further improvements in prognosis.
Figure 1. Estimates of the Relative Risk of Death within Six Years According to Heart-Rate Recovery One Minute after Cessation of Exercise.
Circles represent the relative risk of death for each of the quintiles as compared with the quintile with the greatest reduction (5th). Dashed lines represent the 95 percent confidence interval. The abbreviation bpm denotes beats per minute.
Multivariable Cox Regression Analyses
After adjustments were made for age; sex; resting heart rate;heart-rate increase during exercise; exercise capacity; thepresence or absence of hypertension, smoking, chronic lung disease,diabetes, Q waves on the electrocardiogram, a history of coronaryartery disease, right bundle-branch block, and angina duringtreadmill testing; the use or nonuse of beta-blockers, nondihydropyridinecalcium-channel blockers, lipid-lowering therapy, and vasodilatormedications; and perfusion defects on thallium scintigraphy,a low value for heart-rate recovery emerged as the strongestpredictor of death (adjusted relative risk, 2.0; 95 percentconfidence interval, 1.5 to 2.7; P<0.001). Other independentpredictors included decreased exercise capacity (P<0.001),male sex (P<0.001), increased age (P<0.001), the presenceof perfusion defects on thallium scintigraphy (P=0.006), anda smaller increase in heart rate during exercise (P=0.006).
If an impaired chronotropic response during exercise was substitutedin the regression model for the change in the heart rate duringexercise, a low value for heart-rate recovery remained independentlypredictive of death (adjusted relative risk, 2.0; 95 percentconfidence interval, 1.8 to 2.7; P<0.001), whereas an impairedchronotropic response during exercise was not as strongly predictive(adjusted relative risk, 1.7; 95 percent confidence interval,1.2 to 2.3; P=0.002). Similar results were obtained when thevalue for heart-rate recovery was considered as a continuousvariable. When the value for the 10th percentile (eight beatsper minute) was used as the cutoff for an abnormal value forheart-rate recovery, it emerged as an independent predictorof mortality (adjusted relative risk, 1.7; 95 percent confidenceinterval, 1.3 to 2.4; P<0.001).
Effects of Revascularization
During the first three months after exercise stress testing,79 patients (3 percent) underwent coronary-artery bypass graftingand 41 (2 percent) underwent percutaneous revascularization.The inclusion of any revascularization procedure — orof coronary-artery bypass surgery only — in supplementarymultivariable Cox regression analyses had no effect on the associationsbetween the value for heart-rate recovery and mortality fromall causes.
Determinants of Heart-Rate Recovery
There was a strong association between decreasing exercise capacityand an abnormal value for heart-rate recovery in both men andwomen (Figure 2). Among the patients with a normal result onthallium scintigraphy, exercise capacity was lower in the presenceof an abnormal value for heart-rate recovery (men, 7.9 MET vs.9.8 MET in patients with a normal value; women, 6.0 MET vs.7.4 MET; P<0.001 for both comparisons). In a logistic-regressionanalysis in which adjustments were made for age, sex, and thepresence or absence of perfusion defects on thallium scintigraphy,independent predictors of an abnormal value for heart-rate recoveryincluded a decrease in exercise capacity (adjusted odds ratiofor a decrease of 2.5 MET, 2.4; 95 percent confidence interval,2.1 to 2.8; P<0.001) and the use of vasodilators (adjustedodds ratio, 1.3; 95 percent confidence interval, 1.1 to 1.6;P=0.01). There were no independent associations between theuse of beta-blockers or calcium-channel blockers and an abnormalvalue for heart-rate recovery.
Figure 2. Association between Sex-Specific Deciles of Physical Fitness and Abnormal Values for the Recovery of Heart Rate One Minute after the Cessation of Peak Exercise.
A value of 12 beats per minute for the recovery of heart rate was considered abnormal. Increasing levels of physical fitness were strongly correlated with decreasing rates of abnormal values for the recovery of heart rate among men and women (for men: chi-square for trend=207, P<0.001; for women: chi-square for trend=97, P<0.001).
Recovery of Systolic Blood Pressure
The median reduction in systolic blood pressure during the firstminute of recovery was 8 mm Hg (25th and 75th percentiles, 0and 20 mm Hg). There was no association between the recoveryof systolic blood pressure and mortality (relative risk of deathassociated with a fall of 5 mm Hg in systolic blood pressure,1.01; 95 percent confidence interval, 0.97 to 1.05; P=0.70).
Discussion
Among the patients undergoing exercise testing and single-photon-emissioncomputed tomography with thallium scintigraphy, all of whomwere candidates for initial coronary angiography, the failureof the heart rate to fall rapidly during early recovery afterexercise was associated with increased overall mortality, evenafter adjustments were made for standard cardiovascular riskfactors, changes in the heart rate during exercise, the useor nonuse of medications, exercise capacity, and the presenceor absence of myocardial perfusion defects. Whether measuredas a categorical or a continuous variable, a low value for heart-raterecovery was among the strongest predictors of death. Althoughonly 26 percent of the population we studied had an abnormallydelayed decrease in the heart rate, the majority of the patientswho died (56 percent) had an abnormally low value. This is insharp contrast with most risk factors, which, although theyidentify high-risk groups, predict only a minority of deaths.
A low value for heart-rate recovery was predictive of deathin a number of important subgroups, including the elderly, women,patients with a normal chronotropic response during exercise,and those taking beta-blockers. It is noteworthy that the patientswho had both a normal chronotropic response during exerciseand a normal heart-rate recovery had a six-year mortality rateof only 3 percent, or 0.5 percent per year. The associationbetween heart-rate recovery and mortality was weaker among thepatients taking nondihydropyridine calcium-channel blockersand vasodilators; it is possible that these medications mayhave blunted heart-rate recovery by causing a marked fall inblood pressure after exercise.
The mechanisms by which impaired heart-rate recovery confersan increased risk of death, even among patients without heartfailure or myocardial perfusion defects, are not clear. Imaiet al. examined the physiologic characteristics of heart-raterecovery after exercise in healthy adults, athletes, and patientswith chronic heart failure.5 They demonstrated that, in allthree groups, vagal reactivation was the principal determinantof the decrease in heart rate during the first 30 seconds ofrecovery and that this mechanism was independent of age andthe intensity of exercise. Heart-rate recovery was rapid inathletes but was blunted in patients with heart failure andwas completely abolished by the administration of atropine.In our study, we also found a marked inverse association betweenheart-rate recovery and exercise capacity. Because increasedvagal activity has been associated with a reduction in the riskof death,6 we hypothesized that the heart rate after exercisemay be an important predictor of mortality.
The Autonomic Tone and Reflexes after Myocardial Infarctionstudy21 was a large, prospective, multicenter study in whichpatients who had had myocardial infarctions were stratifiedaccording to markers of autonomic control. Both markers used— variability in heart rate and baroreflex sensitivity— proved to be strong predictors of outcome. Our studyextends these findings in two important ways. First, we demonstratedthe prognostic importance of an autonomic marker in a broaderpopulation. Second, the value for the recovery of heart rateis a simple marker that is easily calculated on the basis ofdata already contained in a standard exercise test and doesnot require 24-hour Holter monitoring or specialized baroreflex-sensitivitytesting.
Because this study was performed at a single tertiary care center,it is possible that there were biases with respect to patientreferral and population sampling. The thallium scintigraphictechniques in this study were those in use during the early1990s, and the techniques of today may yield better prognosticresults. Two important predictors of prognosis, dilatation ofthe left ventricular cavity and increased lung uptake of thalliumwith exercise,22 could not be included in the analysis becauseof the very small number of patients in this low-risk cohortwho had these findings.
Formal measures of left ventricular function, an important predictorof mortality, were not available. To decrease the effect ofimpaired cardiac function, we purposely excluded patients witha history of heart failure, revascularization, or use of digoxin.In addition, consideration of the total number of abnormal segmentson thallium scintigraphy may also have partly accounted forthe effects of left ventricular dysfunction.
A reduction in the heart rate of 12 beats per minute after thecessation of exercise was used as the definition of a low valuefor the recovery of the heart rate. This cutoff was determinedby calculating the maximal value for the log-rank chi-squaretest statistic for all possible cutoff points between the 10thand 90th percentiles. One disadvantage of this method is thatit overstates the association as compared with what would beseen in an independent data set. Therefore, it is essentialthat these findings be confirmed in other populations. If the10th percentile (indicating a decrease in the heart rate ofeight beats per minute) is used as the cutoff, the specificityand positive predictive value of this method for mortality areimproved. However, the improvement comes at the expense of ahigher mortality rate (2 percent per year vs. 1 percent peryear) in the group with what is defined as a normal value forheart-rate recovery; this mortality rate may be unacceptablyhigh for some clinicians.
A low value for heart-rate recovery after exercise testing,which has been previously shown to be a marker of decreasedvagal activity, is a powerful and independent predictor of therisk of death. This marker is simple to calculate from datathat are already contained in the results of standard exercisetests and may be valuable for the assessment of risk in routineclinical practice.
Source Information
From the Departments of Cardiology (C.R.C., F.J.P., C.E.S., M.S.L.), Cardiothoracic Surgery (E.H.B.), and Epidemiology and Biostatistics (E.H.B.) and the George M. and Linda H. Kaufman Center for Heart Failure (M.S.L.), Cleveland Clinic Foundation, Cleveland.
Address reprint requests to Dr. Lauer at the Section of Heart Failure and Cardiac Transplantation Medicine, Department of Cardiology, Desk F25, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, or at lauerm{at}ccf.org.
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Exercise Capacity and Mortality
Palatini P., Ko D. T., Hebert P. R., Krumholz H. M., Perlo D. H., Myers J., Froelicher V., Balady G. J.
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347:288-290, Jul 25, 2002.
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140 mm Hg at rest, a diastolic blood pressure of 
12 beats per minute) were compared with use of the chi-square test for trend.19 Logistic-regression analysis was used to assess the effects of exercise capacity and medications on heart-rate recovery after adjustment for age, sex, and the presence or absence of perfusion defects on thallium scintigraphy.20 All analyses were performed with the SAS statistical package (version 6.12, SAS Institute, Cary, N.C.). 
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