Need for a Revision of the Normal Limits of Resting Heart Rate

Paolo Palatini

Hypertension. 1999;33:622-625
doi: 10.1161/01.HYP.33.2.622
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1999 American Heart Association, Inc. All rights reserved.
Print ISSN: 0194-911X. Online ISSN: 1524-4563

The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://hyper.ahajournals.org/content/33/2/622

Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published
in Hypertension can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial
Office. Once the online version of the published article for which permission is being requested is located,
click Request Permissions in the middle column of the Web page under Services. Further information about
this process is available in the Permissions and Rights Question and Answer document.

Reprints: Information about reprints can be found online at:

http://www.lww.com/reprints

Subscriptions: Information about subscribing to Hypertension is online at:

http://hyper.ahajournals.org//subscriptions/

Downloaded from http://hyper.ahajournals.org/ by guest on August 2, 2014

 Commentary
Need for a Revision of the Normal Limits of
Resting Heart Rate
Paolo Palatini, MD
T he 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
In recent years, interest has been aroused by the awareness
that fast heart rate is a potent precursor of hypertension,
atherosclerosis, and their sequelae.210 In addition, many
leading epidemiological studies have shown that tachycardia
is associated with an increased risk of death from cardiovas-
cular and noncardiovascular causes. This relationship has
been found in general populations,37 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 al3 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 subjects heart rate. In all the other studies,
the threshold level between normal and fast heart rate was
between 79 and 90 bpm.
The normalcy limits of a clinical variable can be estab-
lished 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
Received October 5, 1998; first decision October 28, 1998; revision accepted November 24, 1998.
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@ux1.unipd.it
(Hypertension. 1999;33:622-625.)
1999 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org
622
Downloaded from http://hyper.ahajournals.org/ by guest on August 2, 2014
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 Fra-
mingham 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?
Some years ago, Spodick et al13 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 10 Moreover, the Spodick approach im-
plies 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 sub-
populations, 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
 Palatini February 1999 623

Heart Rate Values Above Which a Significant Increase in Risk Was Found: Data From 9 Epidemiological Studies
HR Cutoff, bpm HR Method Used
Measurement: for Cutoff
Author (Study) Men Women Type (No.) Identification Study Outcome
Levy et al (US Army officers)
3 99 zzz Pulse (1) Arbitrary 5-y cardiovascular mortality in subjects with
HR.99 bpm far in excess compared with
subjects with HR#99 bpm
Medalie et al4 (Israeli government employees)* 90 zzz Not specified Highest tertile Age-adjusted rate/1000 of MI over 5 y: 61 in
top tertile and 40 in bottom tertile (P defined
as significant)
Dyer et al5 (Chicago-People Gas Co)* 79 zzz From ECG Highest quintile Age-adjusted 15-y all-cause mortality rate in
the HR quintiles: x2520.1, P#0.001
Dyer et al5 (Chicago-Heart Association)* 86 zzz From ECG Highest quintile Age-adjusted 5-y all-cause mortality rate in
the HR quintiles: x2520.4, P#0.001
Dyer et al5 (Chicago-Western Electric)* 89 zzz Pulse (1) Highest quintile Age-adjusted 17-y all-cause mortality rate in
the HR quintiles: x2521.05, P#0.001
Kannel et al6 (Framingham) 87 87 From ECG Highest quintile Age-adjusted 26-y sudden death mortality rate
in top HR quintile vs others: P,0.001
Gillum et al7 (NHANES) 84 84 Pulse (1) Arbitrary Odds ratios for risk-adjusted 10-y all-cause
mortality for HR.84 bpm: black men, 1.71
(1.142.56); white men, 1.81 (1.262.60);
black women, 1.95 (1.163.27); white women,
NS. Reference are subjects with HR,74 bpm.
Palatini et al9 (CASTEL) 80 84 Pulse (3) Highest quintile Odds ratios for risk-adjusted 12-y
cardiovascular mortality for HR.80 bpm: men,
1.38 (0.942.03), P50.005; women, NS.
Reference are subjects with HR from 64 to 80
bpm.
Gilman et al10 (Framingham) 84 84 From ECG Arbitrary Odds ratios for risk-adjusted 36-y all-cause
mortality for each 40-bpm increment in HR.
Men, 1.98 (1.522.59); women, 1.87
(1.372.56)
HR indicates heart rate; y, years; MI, myocardial infarction; NHANES, National Health and Nutrition Examination Survey; and CASTEL, CArdiovascular STudy in the
ELderly.
*Male population; elderly subjects; hypertensive cohort; data adjusted for age, smoking, blood pressure, cholesterol, and other confounders.

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
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 b-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
Downloaded from http://hyper.ahajournals.org/ by guest on August 2, 2014
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.
Bradycardia
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
624 Heart Rate Normal Limits
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 progno-
sis 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
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 post
myocardial 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 failure18,19
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 training22 could also contrib-
ute to the beneficial effects conferred by regular exercise. An
inverse correlation has been reported between heart rate
Downloaded from http://hyper.ahajournals.org/ by guest on August 2, 2014
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 cardiovas-
cular 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 eval-
uation 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 offi-
cial 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 measure-
ment 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 profes-
sionals. 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.
References
1. Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald
E, ed. Heart Disease. Philadelphia, Pa: WB Saunders Co; 1997:640 704.
2. Palatini P, Julius S. Heart rate and the cardiovascular risk. J Hypertens.
1997;15:317. Review.
3. Levy RL, White PD, Stroud WD, Hillman CC. Transient tachycardia:
prognostic significance alone and in association with transient hyper-
tension. JAMA. 1945;129:585588.

4. Medalie JH, Kahn HA, Neufeld HN, Riss E, Goldbourt U. Five-year
myocardial infarction incidence-II: association of single variables to age
and birthplace. J Chronic Dis. 1973;26:329 349.
5. Dyer AR, Persky V, Stamler J, Paul O, Shekelle RB, Berkson DM,
Lepper M, Schoenberger JA, Lindberg HA. Heart rate as a prognostic
factor for coronary heart disease and mortality: findings in three Chicago
epidemiologic studies. Am J Epidemiol. 1980;112:736 749.
6. Kannel WB, Wilson P, Blair SN. Epidemiologic assessment of the role of
physical activity and fitness in development of cardiovascular disease. Am
Heart J. 1985;109:876 885.
7. Gillum RF, Makuc DM, Feldman JJ. Pulse rate, coronary heart disease,
and death: the NHANES I epidemiologic follow-up study. Am Heart J.
1991;121:172177.
8. Selby JV, Friedman GD, Quesenberry CP Jr. Precursors of essential
hypertension: pulmonary function, heart rate, uric acid, serum cholesterol,
and other serum chemistries. Am J Epidemiol. 1990;131:10171027.
9. Palatini P, Casiglia E, Julius S, Pessina AC. Heart rate: a risk factor for
cardiovascular mortality in elderly men. Arch Intern Med. In press.
10. Gillman MW, Kannel WB, Belanger A, DAgostino RB. Influence of
heart rate on mortality among persons with hypertension: The Fra-
mingham Study. Am Heart J. 1993;125:1148 1154.
11. Julius S, Hansson L. General clinical aspects of hypertension. In: Genest
J, Kuchel O, Hamet P, Cantin M, eds. Hypertension. New York, NY.:
McGraw-Hill Book Co; 1983:679 682.
12. James GD, Baker PT. Human population biology and blood pressure:
evolutionary and ecological considerations and interpretations of popu-
lation studies. In: Laragh J, Brenner BM, eds. Hypertension. New York,
NY: Raven Press; 1995:115126.
13. Spodick DH, Raju P, Bishop RL, Rifkin RD. Operational definition of
normal sinus heart rate. Am J Cardiol. 1992;69:12451246.
14. Palatini P, Casiglia E, Pauletto P, Staessen J, Kaciroti N, Julius S.
Relationship of tachycardia with high blood pressure and metabolic
abnormalities: a study with mixture analysis in three populations. Hyper-
tension. 1997;30:12671273.
Downloaded from http://hyper.ahajournals.org/ by guest on August 2, 2014
Palatini February 1999 625
15. Casiglia E, dEste D, Ginocchio G, Colangeli G, Onesto C, Tramontin P,
Ambrosio GB, Pessina AC. Lack of influence of menopause on blood
pressure and cardiovascular risk profile: a 16-year longitudinal study
concerning a cohort of 568 women. J Hypertens. 1996;14:729 736.
16. Schork NJ, Weder AB, Schork MA, Bassett DR, Julius S. Disease
entities, mixed multi-normal distributions, and the role of the hyperkinetic
state in the pathogenesis of hypertension. Stat Med. 1990;9:301314.
17. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic
drug therapy in acute myocardial infarction: an overview of results from
randomized controlled trials. JAMA. 1993;270:1589 1595.
18. Packer M, Bristow MR, Cohn JN, Colucci WS, Fowler MB, Gilbert EM,
Shusterman NH. The effect of carvedilol on morbidity and mortality in
patients with chronic heart failure. N Engl J Med. 1996;334:1349 1355.
19. Nul DR, Doval HC, Grancelli HO, Varini SD, Soifer S, Perrone SV,
Prieto N, Scapin O. Heart rate is a marker of amiodarone mortality
reduction in severe heart failure. J Am Coll Cardiol. 1997;29:1199 1205.
20. Pickering TG. Modern definitions and clinical expressions of hyper-
tension. In: Laragh JH, Brenner BM, eds. Hypertension. New York, NY:
Raven Press; 1995:1721.
21. Zuanetti G, Mantini L, Hernandez-Bernal F, Barlera S, di Gregorio D,
Latini R, Maggioni AP. Relevance of heart rate as a prognostic factor in
patients with acute myocardial infarction: insights from the GISSI-2
study. Eur Heart J. 1998;19(Suppl F):F19 F26.
22. Somers V, Conway J, Johnston J, Sleight P. Effects of endurance training
on baroreflex sensitivity and blood pressure in borderline hypertension.
Lancet. 1991;337:13631368.
23. Malik M, Camm AJ. Heart rate variability. Armonk, NY: Futura Pub-
lishing Co, Inc; 1995.
24. Palatini P. Office versus ambulatory heart rate in the prediction of the
cardiovascular risk. Blood Press Monit. 1998;3:173180.
KEY WORDS: heart rate, resting n commentary n risk factors