Hypertension. 1999;33:622-625
(Hypertension. 1999;33:622-625.)
© 1999 American Heart Association, Inc.
Need for a Revision of the Normal Limits of Resting Heart Rate
Paolo Palatini, MD
From the Department of Clinical and Experimental Medicine, University of
Padova, Padova, Italy.
Correspondence to Professor Paolo Palatini, MD, Dipartimento di Medicina Clinica E Sperimentale, University of Padova, via Giustiniani, 2, 35128 Padova, Italy. E-mail palatini{at}ux1.unipd.it
Key Words: heart rate, resting commentary risk factors
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Introduction
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The current definition of sinus
tachycardia is a heart rate
>100 beats per minute
(bpm).
1 This limit was set arbitrarily
when heart rate was
not yet regarded as a risk factor for cardiovascular
disease,
probably with the main purpose of distinguishing between a
disease
state (fever, thyrotoxicosis, anemia, congestive heart failure,
etc)
and a normal condition.
 |
Tachycardia as a Cardiovascular Risk
Factor
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In recent years, interest has been aroused by the awareness
that
fast heart rate is a potent precursor of hypertension,
atherosclerosis,
and their sequelae.
2 3 4 5 6 7 8 9 10
In addition, many leading
epidemiological studies have shown that
tachycardia is associated
with an increased risk of death
from cardiovascular and
noncardiovascular
causes. This relationship has been
found in general populations,
3 4 5 6 7 in elderly
individuals,
9 and in hypertensive cohorts.
10
In all of these studies, the heart rate value above that in
which a
significant increase in risk was observed was below
the 100 bpm
threshold (Table 1
). Only in the study by
Levy et
al
3 was tachycardia defined as a heart
rate >99 bpm, but
in that study the cutoff between normal and high
heart rate
was chosen arbitrarily, and the highest heart rate value
measured
during the examination was taken to define the subject's
heart
rate. In all the other studies, the threshold level between
normal
and fast heart rate was between 79 and 90 bpm.
View this table:
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Table 1. Heart Rate Values Above Which a Significant Increase in Risk
Was Found: Data From 9 Epidemiological Studies
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The normalcy limits of a clinical variable can be established
according to different criteria. For many parameters, such
as most biochemical indexes, the 95% confidence interval is calculated
to identify the upper normal limit of the variable. This
statistical approach does not appear suitable for those clinical
variables in which the relationship with the level of risk is a
continuous one. A typical example is observed with blood pressure, in
which the upper normal limits were set arbitrarily.11
Blood pressure was considered abnormal by the World Health Organization
when it was greater than the level at which the increase in risk became
considerable. This level roughly corresponded to the highest quintile
of the blood pressure distribution in the populations of the
industrialized countries.12 In most of the studies
reported in the Table, subjects were considered to have
tachycardia if they were in the highest quintile of the
heart rate distribution, and an increase in the risk of
coronary events and/or cardiovascular and total
mortality was found in the subjects of the top quintile. In the
Framingham study, for example, a 6-fold increase in the relative risk
of sudden death was seen in the subjects of the top heart rate quintile
in comparison with those of the bottom quintile.6 In the
Framingham study, a linear relationship was found between heart rate
and mortality,6 although in other studies, a J-shaped
relation5 or a sigmoidal relation9 was
observed. However, in all studies, the excess in risk was present
chiefly in the subjects of the highest heart rate quantile.
 |
Is There a Level of Heart Rate That Separates Two Populations With
Normal and High Heart Rate?
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Some years ago, Spodick et al
13 attempted to redefine
the normal
limits of heart rate on the basis of the results obtained in
a
population of subjects aged 50 to 80 years. By the addition
of 2 SD
to the mean heart rate value, Spodick et al found upper
normal limits
of 93 bpm for resting heart rate in the men and
of 95 bpm in the women,
which are above those found to be associated
with an increased risk of
mortality by most investigators.
4 5 6 7 8 9 10 Moreover, the
Spodick approach implies the existence
of a normal distribution for
heart rate in the general population.
Recent results obtained in our
laboratory indicate that this
is not the case. In fact, in the Belgian,
the HARVEST, and the
Tecumseh populations we found that the
heart rate distribution
was significantly skewed among men and women
from Tecumseh.
14 Similar results were obtained in a recent
analysis of the Mirano
population,
15 in which both
men and women showed a skewed distribution
of resting heart rate
(unpublished observations). Mixture analysis
showed that in all
these populations, the distribution of heart
rate was explained by the
mixture of 2 homogeneous subpopulations,
a larger one with
"normal" heart rate and a smaller one with
"high" heart rate.
Mixture analysis is a statistical test used
in the biological
sciences to investigate whether a mixture
of normal distributions
better explains the variation of a trait
than a single distribution
when overlap exists between the subpopulations.
16 This is
an entirely objective way to establish a cutoff level
between normal
and abnormal values, which avoids the necessity
for establishing
arbitrary threshold levels. With the use of
this method in the above
mentioned populations, we identified
cutoffs varying from 80 to 85 bpm
for resting heart rate measured
by the physician in the
clinic.
14 The percentage of subjects
with a high heart
rate ranged from 12.3% to 29.8% in the various
male and female
populations. These results show that 2 subpopulations
with normal and
high heart rate can be separated within a general
population and that
the threshold level between the 2 subpopulations
is around 80 to 85
bpm.
 |
Effect of Treatment in Subjects With Tachycardia
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If tachycardia is a strong risk factor for
cardiovascular disease,
antihypertensive drugs that
also decrease heart rate should
be more beneficial in hypertensive
subjects with fast heart
rate. However, no clinical trial has been
implemented as yet
with the specific purpose of studying the effects of
cardiac
slowing on morbidity and mortality in hypertension. The only
available
data on the effect of heart rate reduction in humans stem
from
retrospective analyses of subjects with myocardial
infarction
or congestive heart failure. These results suggest that
ß-blockers
are effective in reducing mortality only in subjects with
a
high baseline heart rate.
17 Carvedilol, for example, has
been
reported to cause a marked reduction in mortality in subjects
with
congestive heart failure,
18 but the benefit was clear
only
in patients with a heart rate >82 bpm. An association
between the
reduction in heart rate and mortality has been shown
also with
amiodarone, which improved survival in patients with
congestive
heart failure, but only in subjects with heart rate
>89
bpm.
19 According to some investigators, the upper normal
limit
of a clinical variable should be defined as the level at
which
the benefits of treatment outweigh the risks or, in other words,
as
a treatment threshold.
20 The data obtained in subjects
with
myocardial infarction or congestive heart failure suggest that
for
heart rate this level should be set in the range of 80 to
89
bpm.
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Bradycardia
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Sinus bradycardia is said to exist in the adult when the sinus
node
discharges at a rate <60 bpm.
1 Sinus bradycardia may
occur
as a consequence of a disease such as increased intracranial
pressure,
myxedema, hypothermia, and vasovagal syncope. In
epidemiological
studies in general populations or hypertensive cohorts,
no increased
risk of mortality was generally found for the lower
extreme
of heart rate. Only in the Chicago Heart Association Study were
low
heart rates (<60 bpm) related to an increase in sudden
death.
5 However, in that study, subjects with
bradyarrhythmias at ECG
were not excluded, and, thus, the
excess in mortality could
be explained by subjects with bradycardia
having important bradyarrhythmias.
In the elderly subjects of
the CASTEL study in which all individuals
with bradyarrhythmias
at standard ECG had been excluded, we
found a better prognosis in the
subjects with heart rate lower
than 64 bpm and as low as 50 bpm than in
those with heart rates
between 64 and 80 bpm.
9 This
suggests that there is not an
increase in risk of mortality for the
lower extreme of heart
rate, provided the subject has been checked for
possible sinoatrial
dysfunction. Unlike tachycardia, sinus
bradycardia does not
appear to be a distinct clinical entity. With
mixture analysis,
we could not identify a subpopulation of
subjects with bradycardia
at the lower extreme of the heart rate
distribution in any of
the populations examined.
14
 |
Looking for a New Definition of Tachycardia
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Although there are no objective data that allow us to establish
new
normal limits for resting heart rate, it seems clear that the
traditional
100 bpm value is not appropriate to define the threshold
below
that in which heart rate can be considered safe. The
epidemiological
studies listed in the Table
> clearly demonstrate
that the association
between heart rate and the
cardiovascular risk occurs for levels
well below the
100 bpm value. Also, the results of the intervention
trials in
postmyocardial infarction patients or in subjects
with congestive
heart failure suggest that the limit of normality
of heart rate should
be set below 100 bpm. On the basis of the
data from the literature and
the results obtained with mixture
analysis in our laboratory,
we suggest a new consensus: for
men, it appears reasonable to set the
upper normal value of
heart rate at 85 bpm. Because of the higher heart
rate commonly
seen in women (3 to 7 bpm greater),
2
a slightly higher threshold
should be adopted for them. Conversely, a
lower limit should
be set in the elderly. Heart rate has been reported
to decline
slowly with age, with an average decrease of 1 bpm every 8
years.
2 The cutoff between normal and high heart rate
found in our
laboratory in elderly men (80 bpm)
9 was
slightly lower than
that found in younger adults by most investigators
(Table
).
Hypertensive individuals,
11 myocardial
infarction patients,
21 and subjects with congestive heart
failure
18 19 usually have
higher values of heart rate than
healthy controls. However,
this does not mean that the level of risk
related to heart rate
is shifted toward higher values in these
patients. A recent
report in subjects with acute myocardial infarction
showed that
the risk of death sharply increases for heart rate values
>80
bpm.
21 Another well recognized factor that affects
heart rate
is physical training.
22 Tachycardia
may be a marker for decreased
physical fitness, which in turn may
increase risk of cardiovascular
death. However, high
heart rate turned out to be a predictor
of
cardiovascular mortality also in the studies that
controlled
for energy expenditure.
7 Thus, physical
activity can be regarded
as a useful and
physiological method for decreasing heart rate,
and
its well known cardioprotective action could be at least
partially
because of its effect on heart rate. The increase
in heart rate
variability caused by endurance training
22 could
also
contribute to the beneficial effects conferred by regular
exercise. An
inverse correlation has been reported between heart
rate variability
and mortality from myocardial infarction and
other
cardiovascular causes.
23 Thus, not only
the mean heart
rate value but also its variability seems to be related
to cardiovascular
morbidity and mortality.
The above mentioned heart rate limits can be of help for better
defining the cardiovascular risk profile of a given
individual, but we are still unable to say whether a reduction of heart
rate below those levels could confer any benefit in terms of life
expectancy, especially in hypertensive patients. As for the opposite
extreme of the heart rate range, the data from the literature do not
allow the identification of any clinically meaningful limit. In fact,
no increased risk of mortality was generally found for the lowest
values of sinus heart rate. With the above mentioned approach, Spodick
et al13 identified the level of 50 bpm as the lowest
normal limit of heart rate, but there is no indication from the
literature that a heart rate below that limit is really hazardous in
the absence of sinoatrial dysfunction. It is obvious that a low heart
rate, particularly in unfit elderly subjects, may need further
evaluation for sinoatrial node dysfunction or other diseases.
 |
Conclusions
|
|---|
Heart rate has been neglected for a long time as a clinical
parameter,
and it is time that this variable receives
the consideration
it deserves in clinical practice. Although official
upper normal
limits for resting heart rate are not yet available, the
data
of the literature are sound and indicate that these limits should
be
set well below 100 bpm, the threshold currently used to define
tachycardia,
to probably around 85 bpm. Heart rate can
become a useful tool
in clinical practice and research in the future
provided the
criteria for measurement are strictly standardized by the
scientific
societies. We suggest that criteria similar to those adopted
for
blood pressure assessment be used with heart rate. The clinician
must
consider all of the circumstances that may produce variations
in
heart rate and attempt to control or avoid them before taking
the
measurement. At least 2 readings taken over a 30-second
period should
be averaged. In addition, heart rate should be
checked by the use of
repeated visits before a final diagnosis
is made, because a
"white-coat tachycardia" can occur in some
patients in
the presence of healthcare professionals. We have
recently demonstrated
that the day-to-day variability of clinic
heart rate is 40% greater
than that for heart rate recorded
over 24 hours.
24 If
heart rate is measured by 24-hour recording
or with automatic
devices, lower values should be expected.
14 The evolution
of our understanding of the relationship between
heart rate and
mortality will dictate that different levels
of heart rate are taken,
which depends on the method of measurement,
as the upper limit of the
normal heart rate is reached.
Received October 5, 1998;
first decision October 28, 1998;
accepted November 24, 1998.
 |
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