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PREVENTIVE CARDIOLOGY
SUMMER 2005
167
REVIEW PAPER • CME
Heart Rate Recovery After Exercise and
Endothelial Function—Two Important
Factors to Predict Cardiovascular Events
Po-Hsun Huang, MD;1 Hsin-Bang Leu, MD;1 Jaw-Wen Chen, MD;1,2 Shing-Jong Lin, MD, PhD1,2,3
An attenuated heart rate recovery immediately
after exercise, thought to be a marker of reduced
parasympathetic activity, has been demonstrated
to be an independent predictor of all-cause
mortality in several large-scale studies; however,
the mechanisms by which impaired heart rate
recovery confers an increased risk of death are
not clear. From clinical observation, vagal reactivation was thought to be the major determinant
of the decrease in heart rate during the first 30
seconds of recovery, independent of age and
the intensity of exercise; however, patients with
attenuated heart rate recovery were also shown
to have lower exercise workload, shorter exercise
duration, lower numbers achieving 90% target
heart rate, and even impaired endothelial function. This review focuses on the roles of heart
rate recovery and endothelial function in predicting future mortality and their interaction. (Prev
Cardiol. 2005;8:167–170) ©2005 Le Jacq Ltd.
O
ver the past few years, several large clinical
studies have clearly demonstrated the potential value of heart-rate recovery (HRR) immediately after exercise as a simple and valuable tool for
predicting clinical events and mortality.1–5
During 6 years of follow-up, Cole et al.1 showed, in
a large-scale study of 2428 subjects (mean [±SD] age,
57±12 years; 63% men) without a history of heart
From the Division of Cardiology, Department of Internal
Medicine, Taipei Veterans General Hospital, Taipei,
Taiwan;1 the Cardiovascular Research Center,2 and the
Institute of Clinical Medicine,3 National Yang-Ming
University, Taipei, Taiwan
Address for correspondence:
Shing-Jong Lin, MD, PhD, Division of Cardiology,
Taipei Veterans General Hospital, No. 201, Sec. 2,
Shih-Pai Road, Taipei, Taiwan
E-mail: sjlin@vghtpe.gov.tw
Manuscript received July 7, 2004;
revised December 22, 2004;
accepted January 7, 2005
www.lejacq.com
ID: 3847
failure or coronary revasculization, that a low value of
HRR was a strong predictor of death in a number of
important subgroups, including the elderly, women,
patients with normal chronotropic response during
exercise, and even those taking β blockers. In another
large cohort study of 9454 subjects (mean [±SD] age,
53±11 years; 78% men) referred for exercise electrocardiography, HRR was shown to provide prognostic
information additional to the established treadmill
exercise score.2 After adjusting for age, sex, exercise
capacity, left ventricular systolic function, presence or
absence of myocardial ischemia, and other confounders, an abnormal HRR remained predictive of death
(adjusted hazard ratio, 2.09; 95% confidence interval, 1.49–2.82; p<0.001).4 Patients who had both a
normal chronotropic response during exercise and a
normal HRR had a 6-year mortality rate of only 3%,
or 0.5% per year.1 In the Framingham Heart Study,5
which included a younger population (mean age, 43
years), very rapid HRR immediately after exercise
was shown to be associated with lower risk of coronary heart disease and cardiovascular disease, but not
related to all-cause mortality. To date, most of the
clinical trials seem to support the prognostic value of
HRR after exercise to predict future mortality and
cardiac events (Table).
A reduction in the heart rate of 12 or fewer beats in
the first minute after the cessation of exercise was used
as the definition of a low value for HRR in several of
the large-scale studies.1,2,4 This value was determined
by calculating the maximal value for the log-rank
chi-square test statistic between the 10th and 90th
percentiles. In fact, there is no agreed-upon cutoff
value for abnormal HRR in the literature. Some studies have used ≤12 bpm, and others have adopted ≤18
bpm.1,2,4,5 If 12 bpm is used as the cutoff value, the
specificity and positive predictive rate for prediction
of mortality and cardiovascular events are improved.
When HRR decreased less than 12 beats in the first
minute after exercise, risk of mortality increased markedly. The studies varied in types of exercise protocol,
and several studies included a 2-minute cool-down
period.1,2,4 This period was considered a recovery
period. However, the impact of these features—with
Preventive Cardiology (ISSN 1520-037X) is published quarterly (Feb., April, June, Sept.) by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by Le jacq Ltd. All rights reserved. No part of this
publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing
from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes,
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168
SUMMER 2005
PREVENTIVE CARDIOLOGY
Table. Previously Published Prognostic Studies of Abnormal Heart-Rate Recovery7
Enrolled (N)
Mean age (yr)
Mean followup (yr)
Men (%)
Asymptomatic
(%)
History of
PCI (%)
History of
CABG (%)
Protocol
Cool-down
exercise
Heart-rate
recovery
“low” limit
(bpm)
Main finding
Comments
COLE ET AL.1
2428
57
6
NISHIME
ET AL.2
9454
53
5.2
DIAZ ET AL.3
5234
44
12
WATANABE
ET AL.4
7163
60
6.7
MORSHEDI-MEIBODI
ET AL.5
5438
57
3
SHETLER
ET AL.6
2193
59
6.8
63
NA
78
75
61
100
75
NA
63
NA
100
0
0
NA
0
17
13
0
0
8
0
24
14
0
Bruce
symptomlimited
Bruce
symptomlimited
Bruce
symptomlimited
Variable
Ramp
Yes
Yes
Bruce
85% agepredicted
heart rate
No
Yes
No (left decubitus
position)
No (supine)
≤12 in 1 min
≤12 in 1 min
≤42 in 2 min
≤12 in 1 min
≤18 in 1 min
≤22 in 2 min
HRR is a
powerful
predictor
of overall
mortality
HRR and
treadmill
exercise
score were
independent
predictors of
mortality
Abnormal
HRR
predicts
death
even after
submaximal
exercise
HRR is an
independent
predictor of death
even in the absence
of a cool-down
period
HRR at 1 or
2 min was
validated as
a prognostic
measurement
No effect of
β-blocker
use
Not predictive
of death
among
patients
taking β
blockers
β blockers
excluded
Enhanced risk
stratification
of exercise
nuclear
imaging
when HRR
and exercise
capacity are
considered
No
No prognostic effect
of ischemia
No effect of
β-blocker
use, no
prognostic
effect of
ischemia
NA=not available; PCI=percutaneous coronary intervention; CABG=coronary artery bypass graft surgery; HRR=heart rate recovery
or without a cool-down period—on the prognostic
value of HRR after exercise remains uncertain.
AUTONOMIC CONTROL OF HRR
The exact mechanisms by which attenuated HRR
is associated with an increased risk of death are not
yet understood. Previous studies had shown that the
autonomic system plays a central role in regulating
cardiovascular function in both healthy and diseased
populations. Augmented reflex sympathetic activity
to the heart can precipitate cardiac arrhythmia, but
activation of parasympathetic reflexes may contribute
to cardiac electrical stability. Patients with congestive
heart failure have an activated sympathetic nervous
system to compensate for the reduction in cardiac output, and plasma norepinephrine provides a sensitive
index of the activity of the sympathetic nervous system
and is highly predictive of subsequent mortality.8–11
It is known that beat-to-beat fluctuations in the
heart rate are under autonomic control, and thus
heart-rate variability (HRV) can provide insight
into parasympathetic and sympathetic influences
on the sinus node. HRV can be measured in
the time and/or frequency domain during shortterm (10 minute) and long-term (24 hour) Holter
recordings. A high degree of HRV is found in
compensated hearts with good function, whereas
HRV can be decreased with severe coronary artery
Preventive Cardiology (ISSN 1520-037X) is published quarterly (Feb., April, June, Sept.) by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by Le jacq Ltd. All rights reserved. No part of this
publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing
from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes,
please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.
SUMMER 2005
disease, congestive heart failure, aging, and diabetic
neuropathy.12 In the Framingham Heart Study,
Tsuji et al.13 showed that the estimation of HRV by
ambulatory monitoring offers prognostic information beyond that provided by the evaluation of traditional cardiovascular disease risk factors. Another
method used to evaluate autonomic function is
baroreflex sensitivity. The underlying concept is
to study the reflex heart-rate response to physiologic activation or inhibition of the baroreceptors secondary to drug-induced changes in arterial
pressure. Overall, baroreflex sensitivity decreases
whenever the autonomic balance shifts toward
sympathetic activation and increases whenever the
autonomic balance shifts toward parasympathetic
dominance. La Rovere et al.14 showed that markers
of HRV and baroreflex sensitivity were both strong
predictors of outcome in patients with myocardial
infarctions. These clinical data clearly demonstrated the relationship of enhanced sympathetic activity and mortality. Numerous methods are available
to assess sympathetic activity, but techniques for
evaluating parasympathetic activity and its clinical
implications are more limited.
It has been suggested that the link between
HRR and mortality may be related to vagal tone
and physical fitness. Based on studies of normal
individuals with and without autonomic blockade,
Savin et al.15 initially postulated that “sympathetic
withdrawal contributes more to HRR soon after
peak exercise, with parasympathetic activation
playing a greater role later in recovery at lower
heart rates.” Their data, however, also showed a
slower HRR after parasympathetic blockade (atropine) infusion than without it, suggesting an important role for parasympathetic reactivation in early
HRR. Crouse et al.16 found initial heart-rate kinetics post-exercise to be unaffected by β blockade.
These findings imply that sympathetic activity withdrawal does not contribute significantly to initial
HRR after exercise termination. Thereafter, Imai
et al.17 examined the physiologic characteristics of
HRR after exercise in healthy adults, athletes, and
patients with chronic heart failure. They found that
beat-to-beat heart-rate decay for the first 30 seconds and the first 120 seconds were markedly prolonged by atropine administration in normal volunteers, indicating that both time constants are mainly
regulated by vagal reactivation. Moreover, beat-tobeat heart-rate decay for the first 30 seconds was
almost independent of the exercise intensity and
sympathetic blockade, whereas the change at 120
seconds was affected by sympathetic nerve activity and exercise work load. These results clearly
indicated that beat-to-beat heart-rate decay for the
first 30 seconds is mediated primarily by vagal reactivation, independent of sympathetic withdrawal.
Vagally mediated HRR after exercise was accelerated in well-trained athletes, but blunted in patients
with chronic heart failure.17 Pierpont et al.18 tested
PREVENTIVE CARDIOLOGY
169
the time constant obtained by fitting post-exercise
HRR to a first-order exponential decay curve as an
index of parasympathetic activity, and proved again
that HRR immediately post-exercise was a useful
index of parasympathetic activity.
ENDOTHELIAL FUNCTION
AND INTERACTION WITH
AUTONOMIC FUNCTION
The endothelium is a complex endocrine and
paracrine organ that affects vascular tone, smooth
muscle cell proliferation, platelet aggregation,
monocyte and leukocyte adhesion, and thrombosis.
Endothelial function plays a key role in determining the clinical manifestations of established atherosclerotic lesions and cardiovascular events.19
All major risk factors for atherosclerosis, such as
hyperlipidemia, diabetes, hypertension, and smoking, are associated with impaired endothelial function. Clinically, endothelial function is most often
assessed as a vasodilator response to pharmacologic
or mechanical stimulation. Coronary endothelial vasodilator dysfunction has been shown to be
related to long-term atherosclerotic disease progression and cardiovascular event rates.20 Impaired
flow-mediated vasodilation (FMD) in the brachial
artery has been proved to be closely correlated
with endothelial dysfunction in coronary artery disease, suggesting that endothelium-dependent vasodilation impairment is a generalized atherosclerotic
process.21,22 Several reports have presented data on
the interaction between the sympathetic nervous
system and endothelial function. Hijmering et al.23
tested the hypothesis that increased sympathetic
outflow may interfere with endothelium-dependent
FMD. Pathophysiologically relevant sympathetic
stimulation was achieved by baroreceptor unloading, using a lower-body negative-pressure box. The
investigators demonstrated that increased sympathetic activation could markedly suppress endothelium-dependent FMD in healthy adults. They mentioned a specific inhibitory effect of sympathetic
activation on shear-mediated NO release.
Research with animal models has also demonstrated that chronic sympathetic arousal was
associated with endothelial injury, which could
be prevented by β-adrenergic blocking agents.24,25
Pettersson et al.25 tested the hypothesis that sympathetic activation might lead to an increase in
endothelial injury. They used chloralose anesthesia
to induce sympathetic activation in normal rabbits,
and found an approximate five-fold increase in the
number of injured endothelial cells in unbranched
and circumostial areas of the rabbits’ thoracic aortae.
This injury was greatly inhibited by pretreatment
with metoprolol, indicating that sympathetic activation-induced endothelial injury was mediated by β1
adrenergic receptors. Hemodynamic mechanisms—
including endothelium cell injury due to intermittent
or long-term increased shear stress and alteration of
Preventive Cardiology (ISSN 1520-037X) is published quarterly (Feb., April, June, Sept.) by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by Le jacq Ltd. All rights reserved. No part of this
publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing
from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes,
please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.
170
PREVENTIVE CARDIOLOGY
flow pattern with impact mainly in the large arteries—may account for the typical target organ damage observed in hypertension and is involved in the
development of atherosclerotic lesions.26,27
Few reports have explored the relationship
between decreased vagal activity and endothelial
function—especially in patients with attenuated
HRR after graded exercise. Recently, we reported28
clinical data showing a significant relation between
the extent of HRR and endothelial function. Sixtysix patients with suspected coronary artery disease
were enrolled, and a noninvasive method of brachial ultrasound was used to measure endotheliumdependent FMD and endothelium-independent
nitroglycerin-mediated vasodilation. In the study,
patients with attenuated HRR were shown to
have significantly lower exercise workload, lower
numbers achieving 90% target heart rate, shorter
exercise duration, and even lower endotheliumdependent FMD. After multivariate analysis, HRR
remained an independent predictor of endothelial
dysfunction after adjustment for age, sex, smoking
history, exercise habits, hypertension, diabetes mellitus, medications, and lipid profiles. These findings
suggested that autonomic function plays a key role
in the process of atherosclerosis, and may partly
explain why subjects with abnormal HRR have
more cardiovascular events or increased mortality.
CONCLUSIONS
It is now widely recognized that both HRR and
endothelial function are independent predictors
of the risk of death and have usefulness in clinical
application. Although the underlying mechanisms
of the reduced endothelial function are multifactorial, more and more data have shown the critical
role of autonomic dysfunction in the pathogenesis
of atherosclerosis. Future research is needed to
determine how to manage patients with abnormal
HRR and make clear the true mechanism and role
of the autonomic system in modulating the shear
stress-mediated pathway.
REFERENCES
1 Cole CR, Blackstone EH, Pashkow FJ, et al. Heart-rate
recovery immediately after exercise as a predictor of mortality. N Engl J Med. 1999;341:1351–1357.
2 Nishime EO, Cole CR, Blackstone EH, et al. Heart rate
recovery and treadmill exercise score as predictors of
mortality in patients referred for exercise ECG. JAMA.
2000;284:1392–1398.
3 Diaz LA, Brunken RC, Blackstone EH, et al. 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. 2001;37:1558–1564.
4 Watanabe J, Thamilarasan M, Blackstone EH, et al. Heart rate
recovery immediately after treadmill exercise and left ventricular systolic function as predictors of mortality: the case of
stress echocardiography. Circulation. 2001;104:1911–1916.
5 Morshedi-Meibodi AM, Larson MG, Levy D, et al. Heart
rate recovery after treadmill exercise testing and risk of cardiovascular disease events (The Framingham Heart Study).
Am J Cardiol. 2002;90:848–852.
SUMMER 2005
6 Shetler K, Marcus R, Froelicher VF, et al. Heart rate recovery: validation and methodologic issues. J Am Coll Cardiol.
2001;38:1980–1987.
7 Gibbons RJ. Abnormal heart-rate recovery after exercise.
Lancet. 2002;359:1536–1537.
8 Cohn JN, Levine TB, Olivari MT, et al. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med. 1984;311:819–823.
9 Robertson D, Johnson GA, Robertson RM, et al.
Comparative assessment of stimuli that release neuronal
and adrenomedullary catecholamines in man. Circulation.
1979;59:637–643.
10 Lake CR, Ziegler MG, Kopin IJ. Use of plasma norepinephrine for evaluation of sympathetic neural function in man.
Life Sci. 1976;18:1315–1326.
11 Kopin IJ, Lake CR, Ziegler MG. Plasma levels of norepinephrine. Ann Intern Med. 1978;88:671–680.
12 Kleiger RE, Miller JP, Bigger JT, et al. Decreased heart rate
variability and its association with increased mortality after
acute myocardial infraction. Am J Cardiol. 1987;59:256–262.
13 Tsuji H, Venditti FJ, Manders ES, et al. Reduced heart rate
variability and mortality risk in an elderly cohort. The
Framingham Heart Study. Circulation. 1994;90:878–883.
14 La Rovere MT, Bigger JT Jr, Marcus FI, et al. Baroreflex
sensitivity and heart-rate variability in prediction of total
cardiac mortality after myocardial infarction. Lancet.
1998;351:478–484.
15 Savin WM, Davidson DM, Haskell WL. Autonomic contribution to heart rate recovery from exercise in humans. J
Appl Physiol. 1982;53:1572–1575.
16 Crouse SF, Sterling J, Tolson H, et al. The effect of betaadrenergic blockade on heart rate recovery from exercise. J
Cardiopulm Rehabil. 1989;9:202–206.
17 Imai K, Sato H, Hori M, et al. Vagally mediated heart rate
recovery after exercise is accelerated in athletes but blunted
in patients with chronic heart failure. J Am Coll Cardiol.
1994;24:1529–1535.
18 Pierpont GL, Stolpman DR, Gornick CC. Heart rate recovery post-exercise as an index of parasympahtetic activity. J
Auton Nerv Syst. 2000;80:169–174.
19 Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of
coronary artery disease and the acute coronary syndrome.
N Engl J Med. 1992;326:310–318.
20 Schachinger V, Britten MB, Zeiher AM. Prognostic impact
of coronary vasodilator dysfunction on adverse longterm outcome of coronary heart disease. Circulation.
2000;101:1899–1906.
21 Anderson TJ, Uehata A, Gerhard MD, et al. Close relation
of endothelial function in the human coronary and peripheral circulation. J Am Coll Cardiol. 1995;26:1235–1241.
22 Celermajer DS, Sorensen KE, Bull C, et al. Endotheliumdependent dilation in the systemic arteries of asymptomatic
subjects related to coronary risk factors and their interaction. J Am Coll Cardiol. 1994;24:1468–1474.
23 Hijmering ML, Stroes ES, Olijhoek J, et al. Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation. J Am Coll Cardiol. 2002;39:683–688.
24 Ablad B, Bjorkman JA, Gustaffson D, et al. The role of
sympathetic activation in atherosclerosis: effects of betablockade. Am Heart J. 1988;116:322–327.
25 Pettersson K, Bejne B, Bjork H, et al. Experimental sympathetic activation causes endothelial injury in the rabbit
thoracic aorta via beta 1-adrenoceptor activation. Circ Res.
1990;67:1027–1034.
26 Kaplan JR, Manuck SB. Antiatherogenic effects of beta-adrenergic blocking agents: theoretical, experimental, and epidemiologic considerations. Am Heart J. 1994;128:1316–1328.
27 Pauletto P, Scannapieco G, Pessina AC. Sympathetic drive
and vascular damage in hypertension and atherosclerosis.
Hypertension. 1991;17(4 suppl):III75–81.
28 Huang PH, Leu HB, Chen JW, et al. Usefulness of attenuated heart rate recovery immediately after exercise to predict
endothelial dysfunction in patients with suspected coronary
artery disease. Am J Cardiol. 2004;93:10–13.
Preventive Cardiology (ISSN 1520-037X) is published quarterly (Feb., April, June, Sept.) by Le Jacq Ltd., Three Parklands Drive, Darien, CT 06820-3652. Copyright ©2005 by Le jacq Ltd. All rights reserved. No part of this
publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing
from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes,
please contact Sarah Howell at showell@lejacq.com or 203.656.1711 x106.
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171
CME QUESTIONS AND ANSWERS
Insert your answers on the response page
1. Which of the following is true regarding postexercise heart rate recovery (HRR)?
A. All studies of HRR show that it predicts allcause mortality
B. HRR has been found to be a prognostic factor
in women
C. HRR predicts mortality in patients taking
β-blocking drugs during exercise testing
D. None of the above
3. Which of the following statements is/are true?
A. Diabetes is the only cardiac risk factor not
associated with impaired endothelial function
B. Endothelium-dependent vasodilation of the
brachial artery correlates poorly with coronary
artery endothelium-dependent vasodilation
C. Recent evidence suggests a correlation between
low HRR and impaired endothelial function
D. B and C
2. All of the following statements are true except:
A. In current studies, HRR values between <12
and <18 bpm have been variously considered abnormal
B. Elevated plasma norepinephrine predicts
increased mortality in patients with heart
failure
C. High heart rate variability is an indicator of
cardiac electrical instability
D. Heart rate variability decreases with aging
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