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1103
JACC Vol. 31, No. 5
April 1998:1103–9
CARDIOVASCULAR PHYSIOLOGY
Influence of Body Height on Pulsatile Arterial Hemodynamic Data
HAROLD SMULYAN, MD, FACC, SYLVAIN J. MARCHAIS, MD,* BRUNO PANNIER, MD,†
ALAIN P. GUERIN, MD,* MICHEL E. SAFAR, MD,† GÉRARD M. LONDON, MD*
Syracuse, New York and Fleury-Mérogis and Paris, France
Objectives. This study sought to present evidence that short
stature is a hemodynamic liability, which could explain in part the
inverse relation between body height and cardiovascular risk.
Background. Other explanations for the association of short
stature with increased cardiovascular risk include advancing age,
reduced pulmonary function, genetic factors, poor childhood
nutrition and small-caliber coronary arteries. This study adds
another factor—the physiologic effects of reduced body height on
the arterial tree, which increase left ventricular work and jeopardize myocardial perfusion.
Methods. Four hundred two subjects were studied: 149 with
end-stage renal disease and 253 with normal renal function.
Measurements included blood pressure, body height, cardiac cycle
length, carotid to femoral artery pulse wave velocity, carotid
artery pulse waves (by applanation tonometry) and the arrival
time of reflected waves. Calculations included the carotid augmen-
tation index, carotid artery compliance and the diastolic to
systolic pressure–time ratio (an index of myocardial supply and
demand).
Results. On linear and stepwise multiple regression, body
height correlated with all variables except mean blood pressure.
Conclusions. The early systolic arrival of reflected waves in
short people in this group acts to stiffen the aorta and increase the
pulsatile effort of the left ventricle, even at the same mean blood
pressures. Short stature also induces a faster heart rate, which
increases cardiac minute work and shorten diastole. Stiffening
lowers the aortic diastolic pressure and, coupled with a shortened
diastole, could adversely influence myocardial supply. Although
indirect, this evidence supports a physiologic hypothesis for the
body height– cardiovascular risk association.
(J Am Coll Cardiol 1998;31:1103–9)
©1998 by the American College of Cardiology
A relation between body height and the risk of cardiovascular
disease, specifically coronary heart disease (CHD), was reported as early as 1951 by Gertler et al. (1), and has been
repeatedly observed in the last 15 years (2–15). The observation has been reported from many countries including England
and Wales (6,7,14), Norway (16), Finland (17), Sweden (5,10)
and the United States (2,4,8,11–13,15), and persists even after
adjustment for known CHD risk factors. Gender has not been
an issue, because the phenomenon occurs in both women and
men, although not always in the same study (8,12,15). Disclaimers have arisen, not about the presence of the observation, but rather about its explanation.
Aging (16) and abnormal lung function (13,18,19) have
been proposed as factors that influence the statistical association between short stature and CHD. However, when these
factors are accounted for within the statistical models, the
association persists, albeit weaker (8,11,14,16). The role of
environmental factors, such as poor socioeconomic conditions
and low birth weight, have been frequently reported in the
United Kingdom (6,7,9,20,21), but have not been confirmed in
the United States, where the relation has been found in women
of all levels of education (8) and in the relatively homogeneous
populations of nurses and physicians (11,15). Explanations
based on the pathophysiologic mechanisms of cardiovascular
diseases may be more direct and therefore more persuasive as
explanations for the relation between CHD and short stature.
Although there are no known direct genetic links connecting
body height to CHD, short stature and a predisposition for
CHD are both known to “run in families” (10,13). This could
be explained in part by an analysis of the Coronary Artery
Surgery Study (CASS) registry data, which showed that among
patients who underwent coronary artery bypass graft surgery,
the coronary arteries were smaller and the operative mortality
higher in short people (4). Similar conclusions were reached in
patients undergoing percutaneous transluminal coronary angioplasty (22).
In the published data, there is information to suggest a
physiologic explanation for this phenomenon. Comparative
physiologists have observed a consistent relation between body
length, arterial path length and heart rate in animals (23,24).
Although well described among species, this relation is not
documented within the same species. If true in humans, short
stature and arterial length would shorten the cardiac cycle
length and increase ventricular minute work. Furthermore, a
From the Department of Medicine, State University of New York Health
Science Center, Syracuse, New York; *Clinic Manhes, Fleury-Mérogis, France;
and †Department of Internal Medicine, Broussais Hospital and Inserm U337,
Paris, France. Financial support for this study was provided by Groupe d’Etude
Physiopathologie Insuffisance Renale, Fleury Mérogis and by Laboratoires
Synthelabo, Meudon-La-Foret, France.
Manuscript received July 23, 1997; revised manuscript received January 7,
1998, accepted January 13, 1998.
Address for correspondence: Dr. Harold Smulyan, Department of Medicine,
State University of New York Health Science Center, 750 East Adams Street,
Syracuse, New York 13210. E-mail: [email protected].
©1998 by the American College of Cardiology
Published by Elsevier Science Inc.
0735-1097/98/$19.00
PII S0735-1097(98)00056-4
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Abbreviations and Acronyms
CCA
5 common carotid artery
CHD
5 coronary heart disease
DBP
5 diastolic blood pressure
DPTI/SPTI 5 diastolic/systolic pressure–time index
ESRD
5 end-stage renal disease
MBP
5 mean blood pressure
PP
5 pulse pressure
PWV
5 pulse wave velocity
SBP
5 systolic blood pressure
Dtp
5 travel time of reflected wave
short arterial tree brings arterial pulse wave reflection sites
closer to the heart. Reflected pressure waves then return to the
aorta in systole, rather than diastole, and amplify the primary
wave. This would increase the pulsatile work of the left
ventricle and make the ventricle potentially more vulnerable to
any form of heart disease, especially CHD.
The association between cardiovascular risk and short
stature has been supported in patients with end-stage renal
disease (ESRD) studied in our laboratory (25–27). In this
group, a strong inverse correlation has been observed between
body height and arterial wave reflections (25–27). Because
patients with ESRD are known to have stiff arterial trees (28)
and reduced body height as a consequence of kidney disease,
our working hypothesis is that this pattern may be a representation of the same physiologic mechanism present in comparative physiologic studies and also suggested by the preliminary
study of a small group of 85 normotensive and hypertensive
subjects (27). Thus, the purpose of the present study was to
correlate body height with several measures of pulsatile arterial hemodynamic data in a large group of normal and hypertensive subjects, with and without the presence of ESRD.
Establishing these correlations should allow us to add
ventricular-vascular mismatch as a physiologic mechanism to
the other factors already presented as explanations for the
body height– cardiovascular risk phenomenon.
Methods
Subjects. Measurements were made in 402 subjects: 149
with ESRD on dialysis and 253 with normal renal function.
Those with normal renal function were asymptomatic hospital
employees with no known disease or patients with minor,
noncirculatory disturbances who were matched in terms of age
and gender with the ESRD group. Because patients with
ESRD may have normal or elevated blood pressures, 60
patients with uncomplicated essential hypertension were included in the normal renal function group so that the blood
pressure of both groups would also be matched. In all hypertensive patients, with or without ESRD, all beta-blocking drugs
and calcium channel antagonists were discontinued 4 weeks
before the study to avoid any confounding effects these drugs
might have on heart rate relations. Measurements in patients
JACC Vol. 31, No. 5
April 1998:1103–9
Figure 1. Contour of the carotid pressure waveform recorded at the
speed of 100 mm/s in a hypertensive patient. PP 5 pulse pressure; Ppk
5 mid to late systolic peak; P1 5 early inflection point; Dtp 5 travel
time of the reflected wave.
with ESRD were made just before their mid-week dialysis
(25–27). The augmentation index was measured in 333 subjects: 195 with ESRD and 138 with normal renal function.
Measurements of carotid artery compliance were carried out in
155 subjects: 102 with ESRD and 53 with normal renal
function. All subjects in both groups were also evaluated for
height, heart period and brachial artery pressures. Patients
with known CHD, valvular heart disease, cerebral vascular
disease, peripheral vascular disease, congestive heart failure or
diabetes mellitus were excluded from both study groups. The
studies were approved by the institution’s Review Committee,
and each subject gave written informed consent.
Blood pressure and cardiac cycle length. Brachial artery
pressures were measured with a cuff and mercury sphygmomanometer after 15 min of recumbency. Systolic blood pressure
(SBP) and diastolic blood pressure (DBP) were recorded at
the first and fifth Korotkoff phases. The average RR interval
during three respiratory cycles on the body surface electrocardiogram (ECG) was calculated for the heart period.
Common carotid artery (CCA) pressure and waveform.
The CCA waveform was recorded noninvasively with a penciltype probe incorporating a high fidelity strain gauge transducer
(SPT-301, Millar Instruments) on a Gould 8188 recorder
(Gould Electronique, Ballainvilliers, France) at a paper speed
of 100 mm/s. A detailed description of this system has been
published previously (29 –31). The tonometer is internally
calibrated using a Millar preamplifier (TCB-500).
SBP and pulse pressure (PP) may increase from the central
to peripheral arteries, while the reductions in diastolic or mean
blood pressure (MBP) from the ascending aorta to the radial
artery does not exceed 2 to 3 mm Hg (32–34). Therefore, the
CCA pressure wave was calibrated assuming that brachial and
carotid artery DBPs and MBPs were equal. MBP on the CCA
pressure wave was identified from the area of the CCA
pressure wave in the corresponding heart period, and set equal
to brachial MBP. CCA pressure amplitude (PP) was then
computed from the brachial artery DBP and the position of
MBP on the CCA pressure wave (29 –31,35,36).
The CCA pressure wave was analyzed according to Murgo
et al. (37) (Fig. 1). The height of the late systolic peak (Ppk)
above the inflection point (Pi) is DP, where DP 5 Ppk 2 Pi. The
DP to PP ratio defines the augmentation index, which represents the effect of arterial wave reflections on blood pressure in
the central arteries. The Dtp represents the travel time of the
pulse wave to peripheral reflecting sites and back. The intraob-
JACC Vol. 31, No. 5
April 1998:1103–9
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BODY HEIGHT AND ARTERIAL HEMODYNAMIC DATA
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Table 1. Baseline Data
Age (yr)
Weight (kg)
Height (cm)
Gender ratio (M/F)
Systolic BP (mm Hg)
Diastolic BP (mm Hg)
Heart period (ms)
Aortic PWV (cm/s)
Dtp (ms)
Augmentation index (%)
21
2
27
CCA compliance (kPa zm z10 )
DPTI/SPTI
Normal Renal Function
(n 5 195)
ESRD
(n 5 138)
p Value
48.9 6 20 (17 to 98)
68.8 6 13 (33 to 122)
168.5 6 11 (138 to 197)
1.40
141 6 25 (103 to 236)
83 6 14 (53 to 120)
918 6 149 (570 to 1,326)
907 6 223 (540 to 1,720)
133 6 30 (60 to 210)
7.9 6 16.4 (229.7 to 144.1)
52.9 6 16.9 (13 to 87)
61 6 13 (39 to 98)
163 6 19 (138 to 198)
1.43
149 6 31 (86 to 231)
82 6 15 (51 to 129)
859 6 133 (600 to 1,283)
1,117 6 337 (561 to 2,294)
107 6 23 (60 to 164)
23.6 6 15 (224 to 155)
NS
, 0.001
, 0.025
NS
NS
NS
, 0.01
, 0.001
, 0.001
, 0.001
(n 5 53)
(n 5 102)
5.5 6 2.3 (2 to 12)
1.78 6 0.28 (1.14 to 2.41)
4.8 6 2.2 (1.35 to 12.4)
1.49 6 0.32 (0.85 to 2.39)
, 0.05
, 0.001
Data are presented as mean value 6 SD (range). BP 5 blood pressure; CCA 5 common carotid artery; DPTI 5
diastolic pressure–time index; ESRD 5 end-stage renal disease; F 5 female; M 5 male; PWV 5 pulse wave velocity;
SPTI 5 systolic pressure–time index; Dtp 5 time from onset of carotid pulse to inflection point.
server correlation for repeated measurements of carotid contour was excellent (r 5 0.97 for augmentation index, with a
variability of 3.7 6 0.7%). Interobserver reproducibility concerning the augmentation index was also high (r 5 0.96, with
an interobserver difference of 4.0 6 1.0%).
CCA diameters. CCA diameters and wall motion were
measured by a high resolution B-mode (7.5-MHz transducer)
echo tracking system (Wall-Track system), allowing assessment
of arterial wall displacement during the cardiac cycle. A
complete detailed description of this system has been published previously (36). The radiofrequency signal over six
cardiac cycles is digitized and stored in a large-memory computer. Two sample volumes, selected under cursor control, are
positioned on the anterior and posterior walls. The vessel walls
are continuously tracked by sample volumes according to
phase, and the displacement of the arterial walls is obtained by
auto correlation processing of the Doppler signal. The accuracy of the system is 630 mm for CCA diastolic diameter (Dd)
and ,1 mm for the stroke change in CCA diameter (Ds 2 Dd,
where Ds is the systolic diameter). The repeatability coefficient
of the measurements was 60.273 mm for CCA diameter and
60.025 mm for Ds 2 Dd. Diameters were measured on the
right CCA, 2 cm below the bifurcation. CCA lumen crosssectional area (LCSA) was calculated as LCSA 5 p (CAA
diameter)2/4. A localized echo structure encroaching into the
vessel lumen was considered to be a plaque if the CCA
intima-media thickness was .50% thicker than neighboring
sites (29). Measurements of CCA diameter were always performed in plaque-free arterial segments.
CCA compliance. CCA compliance was determined from
changes in CCA diameter between systole and diastole and the
simultaneously measured CCA PP (DP) according to the
following formula: CCA compliance 5 (p Dd[Ds 2 Dd]/2) DP
(m2zkPa21z1027). The repeatability coefficient of the measurement was 0.52 m2zkPa21z1027.
Diastolic/systolic pressure–time index (DPTI/SPTI). This
index is calculated as the ratio of the area under the diastolic
to the area under the systolic portion of the carotid tonometer
tracing, with zero as baseline (38 – 40). These areas, measured
by computer, were averaged for 10 beats. Reproducibility has
been previously reported (25–27,40).
Carotid-femoral artery pulse wave velocity (PWV).
Carotid-femoral artery PWV was determined using the footto-foot method (30,41). Transcutaneous Doppler flow velocity
recordings were carried out simultaneously at the base of the
neck over the CCA and the femoral artery in the groin with an
8-MHz Doppler unit (SEGA M842, Société d’Electronique
Générale et Appliquée, Paris, France) and a Gould 8188
recorder. The time delay (t) was measured between the feet of
the flow waves recorded at these points. The distance (D)
traveled by the pulse wave was measured over the body surface
as the distance between the two recording sites minus that
from the suprasternal notch to the carotid artery recording site.
PWV was calculated as PWV 5 D/t. The reproducibility of the
measurement for aortic PWV, expressed as the percent mean
(6SD) value, was 5.3 6 3.6% (25–28). The distance between
the suprasternal notch and the femoral artery recording site
was also used as an approximation of aortic length.
Statistics. Data are presented as mean values 6 SD. The
Student t test was used to compare patients with ESRD with
those with normal renal function. Simple linear regression
analysis correlated body height with other variables individually. Stepwise multiple regression analysis assessed the percent
variation in individual measurements explained by body height
and other interrelated factors.
Results
Table 1 compares the mean values of the group with ESRD
with those of the group without renal disease. As described in
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Table 2. Linear Correlations With Body Height as Dependent Variable
Independent Variable
No. of Pts
r Value
p Value
333
333
157
0.52
0.42
0.33
, 0.001
, 0.001
, 0.003
157
402
402
402
0.31
0.30
0.23
0.08
, 0.001
, 0.001
, 0.001
NS
0.47
0.33
, 0.001
, 0.02
0.25
0.21
, 0.005
, 0.05
Entire Group
Dtp (ms)
Augmentation index (%)
DPTI/SPTI
CCA compliance
(kPa21zm2z1027)
Heart period (ms)
Age (years)
Mean BP (mm Hg)
Normal Renal Function
Augmentation index (%)
DPTI/SPTI
195
53
End-Stage Renal Disease
Augmentation index (%)
DPTI/SPTI
138
102
Pts 5 patients; other abbreviations as in Table 1.
the Methods section, the two groups are matched for age,
gender and blood pressure, but differ significantly in all other
measurements, including heart period.
Correlations were calculated for body height against all
other variables for the overall group and for the subgroups
separately (Table 2). For the overall group, there was no
relation between body height and MBP (r 5 0.08), but
significant correlations were found between body height and
Dtp (r 5 0.52, p , 0.001), cardiac cycle length (r 5 0.30, p ,
0.001), CCA compliance (r 5 0.31, p , 0.002) and age (r 5
0.23, p , 0.001). Scatterplots for the relation between body
height and Dtp and body height and heart period are shown in
Figure 2. Although these correlations are highly significant,
linear regression analysis alone fails to consider the interrelation among the variables. Therefore, stepwise multiple regression analysis was carried out to determine how much of the
variation in each of these measurements was due to body
height and other factors (Table 3). For example, when PWV
and body height are considered as independent variables of
Dtp, body height explains 27% of the variation in Dtp, whereas
the two together explain 71%. This finding is probably explained by the interrelation between PWV and body height.
Nonetheless, body height has a significant influence on the
time elapsed between the onset of the pulse and the detected
arrival of the reflected wave. With regard to the augmentation
index and its partial coefficients, body height explained only a
small part of the variance, whereas the total of height, age,
PWV and brachial artery SBP accounted for 61% of the
variance (Table 3). Fifty eight percent of the variations in
DPTI/SPTI were accounted for by height, age, SBP and heart
period. Body height explained 11% of the variability, but the
largest contributor was heart period. This was probably due to
shortening of the diastolic more than the systolic interval by
faster heart rates, as well as the correlation of body height with
diastolic interval (r 5 0.40, p , 0.001).
Figure 2. Linear regression of body height to travel time of reflected
wave (top panel) and heart period (bottom panel).
Similarly, CCA compliance was 9.0% explained by body
height, whereas the addition of age and SBP accounted for a
total of 46% of the variation. When the variations in heart
period were similarly analyzed, body height explained 9% of
the variations, whereas the addition of PWV explained 7%
more, for a total of 16%. Although the percent variations
explained by body height are small, all are highly significant.
For easy review, these data are shown in Table 3.
Table 3. Stepwise Multiple Regression
Dependent Variable
Dtp (ms)
Augmentation index (%)
DPTI/SPTI
CCA compliance (kPa21zm2z1027)
Heart period (ms)
Independent
Variable
Sequential r2
Value
PWV (m/s)
Body height (cm)
Age (yr)
Body height (cm)
PWV (m/s)
BA SBP (mm Hg)
Body height (cm)
Age (yr)
BA SBP (mm Hg)
Heart period (ms)
Body height (cm)
Age (yr)
BA SBP (mm Hg)
Body height (cm)
PWV (m/s)
0.27
0.71
0.35
0.43
0.53
0.61
0.11
0.21
0.31
0.58
0.09
0.31
0.46
0.09
0.16
BA 5 brachial artery; SBP 5 systolic blood pressure; other abbreviations as
in Table 1.
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SMULYAN ET AL.
BODY HEIGHT AND ARTERIAL HEMODYNAMIC DATA
A number of relations with body height were significantly
different in the groups with and without renal disease (Table
2). The correlation coefficient for body height and augmentation index for the entire group was 0.42 (p , 0.001), but for the
ESRD group, it was 0.25 (p 5 0.004) and for the nonrenal
disease group 0.47 (p , 0.001). The slopes of these regression
lines were significantly different (p , 0.01). Similarly, the body
height to DPTI/SPTI correlation for the overall group was
0.33, but it was 0.21 (p 5 0.036) for the ESRD group and 0.33
(p 5 0.016) for the nonrenal group.
The distance between the suprasternal notch and the
femoral artery recording site offered an estimate of aortic
length. This aortic length measurement correlated strongly
with body height (r 5 0.93, p 5 0.001). However, aortic length
correlations with augmentation index, Dtp, heart rate and
DPTI/SPTI were only equal to or less than those observed
using body height. Therefore, aortic length values were not
analyzed further.
produces arterial tortuosity, increasing path length, but aging
also stiffens the aorta and increases PWV, which returns the
reflected wave to the aorta in systole. In short people even with
normal wave velocities, the reflected waves return to the aorta
earlier in systole, mimicking the effects of aging and requiring
more pulsatile effort from the left ventricle. The importance of
reflected waves in short people can be inferred from the strong
relation of arrival times of the reflected waves (Dtp) and of the
augmentation index to body height (r 5 0.52 and 0.42,
respectively). Interestingly, the increase in left ventricular
pulsatile work imposed by these reflected waves can occur
when MBP and systemic vascular resistance are both normal.
Body height and heart rate. Body height is a physiologic
variable in another way. Comparative physiologists have observed a consistent relation between body length and heart rate
in animals of different sizes (23). Because the wave velocities
are similar in most animals, the heart rate– body length relation has been explained by the biologic need to have the
reflected waves return to the aorta in diastole rather than in
systole, to minimize the cardiac work of pulsations. An alternative explanation has been provided by Westerhof (24), who
argued that the heart rate in animals of various sizes best
relates to the rate of diastolic decay (time constant) of the
arterial pulse. This is so because small arterial trees have small
capacitances and require accordingly small stroke volumes to
maintain the equivalent arterial pressures found in the animal
kingdom. Cardiac cycle length must therefore be short to
provide brief diastolic periods and prevent diastolic pressures
from falling too low to maintain coronary perfusion. Fast heart
rates in short animals meet these needs. Although the body
length– heart rate relation is well described among different
species, it has been only rarely applied in the same species (46).
The principle also holds in humans in the present series,
where, despite multiple factors influencing heart rate in both
groups, body height showed an r value of 0.32 when correlated
with heart rate. Even when age and PWV were included in
multiple stepwise regression analysis, body height remained a
small but significant determinant of heart rate. An increased
heart rate alone is another way in which reduced body height
increases cardiac work.
Mechanism of increased cardiovascular risk. The combination of augmented systolic waves, which increase ventricular
systolic work, and faster heart rates, which shorten diastole,
operates to increase the need and decrease the opportunity for
myocardial perfusion. This scenario has been well summarized
by the DPTI/SPTI index (38,39,43,47). Although this index
does not provide a complete description of myocardial vulnerability (39), it does offer a means of approximating ventricular
requirements and the potential for receiving it (in the absence
of coronary obstruction) in a single value. In the present study,
body height correlated significantly with this index, reflecting
again the relations among stature, systolic pressure augmentation and heart rate.
Carotid compliance, as expected, also correlated with body
height in both groups, indicating increased stiffness in people
of short stature. The correlation coefficient was lower than that
Discussion
The major findings of this study are that short stature is
associated with faster heart rates, shortened return times for
reflected waves and increased augmentation of the primary
systolic pulse, but is independent of MBP. These positive
factors each operate to increase the stroke and minute work of
the left ventricle, while reducing the diastolic time and pressure available for coronary filling. Although indirect, this
evidence supports a physiologic explanation for the increased
risk of cardiovascular disease in short people.
Body height and reflected waves. In this study, carotid
pulse waves were used as a substitute for aortic pulses, a
substitution that has been validated previously (42). Using
carotid artery pulses as a surrogate (42), reflected waves to the
aorta can be detected and semiquantified by use of the
tonometric technique. These waves, initially described and
classified by Murgo et al. (37), are easily identified and their
arrival timed (Dtp) from the onset of the primary pulse. The
absolute magnitude of reflected waves cannot be measured,
but the augmentation index offers a means of estimating their
relative amplitude. Clinical credence has been lent to the
augmentation index because it has been previously found to
relate to left ventricular mass (25). This is probably due to an
increase in left ventricular pulsatile work, a longer left ventricular ejection time and the need for the left ventricle to respond
to an inappropriately timed late systolic increase in pressure
(43)—all of which are liabilities in patients with CHD.
Arterial wave reflection sites are numerous and diffuse, but
have been approximately localized, for the lower part of the
body, to a region extending from the renal arteries to the aortic
bifurcation (37,44). Because people of short stature necessarily
have correspondingly short arterial trees, their reflecting sites
are closer to the heart. The effect of reduced path length has
also been demonstrated in young children (45) whose low body
height and short arterial tree cause their aortic pulses to
resemble those of the elderly. In contrast, aging in adults
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April 1998:1103–9
observed with other variables, owing to the concomitant influence of age and SBP as shown by stepwise multiple regression
analysis.
The correlations among body height and the circulatory
variables already described showed no differences between
women and men. This finding implies that the relations are
physiologic and not gender induced. If true, the intrinsic
shorter stature of women should make them, other factors
being equal, more vulnerable to CHD than men. This was
found to be the case for women and their risk of myocardial
infarction in the Framingham study (12).
The findings not only apply to men and women, but also to
normal subjects, hypertensive patients and patients with
ESRD. Although the correlations cannot be strictly applied to
other patient groups, the principles which underlie the findings
are likely to apply widely.
Conclusions. These data show body height to be a determinant of the timing and magnitude of reflected arterial
pulses. These reflections alter the shape of the aortic pulse,
which increases left ventricular pulsatile work and left ventricular mass and alters the myocardial need and the potential
supply relations. The risks imposed by these changes are even
greater in patients with ESRD, who have an increased predisposition for CHD when compared with subjects with normal
renal function. The influence of body height on the risks of
CHD, due to reflected waves, are exerted in many ways: by
increasing heart rate, by stiffening the aorta in late systole and
by reducing aortic diastolic pressure and duration. The correlations between body height and the many variables which
relate to ventricular vulnerability are small but significant. This
is not surprising, because these factors are interrelated, as
illustrated by the stepwise multiple regression calculations.
Accounting for these interrelations demonstrates how body
height operates as a risk factor. Multiple regression analysis
weakens the correlations between body height alone and
individual variables, but does not eliminate them. This suggests
that body height itself survives as a risk factor for CHD,
perhaps not a powerful one, but a risk factor nonetheless.
9. Yarnell JWG, Limb ES, Layzell JM, Baker IA. Height: a risk marker for
ischaemic heart disease: prospective results from the Caerphilly and Speedwell heart disease studies. Eur Heart J 1992;13:1602–5.
10. Allebeck P, Bergh C. Height, body mass index and mortality: do social
factors explain the association? Public Health 1992;106:375– 82.
11. Hebert PR, Rich-Edwards JW, Manson JE, et al. Height and incidence of
cardiovascular disease in male physicians. Circulation 1993;88(Pt. 1):1437–
43.
12. Kannam JP, Levy D, Larson M, Wilson PWF. Short stature and risk for
mortality and cardiovascular events: the Framingham Heart Study. Circulation 1994;90:2241–7.
13. Cook NR, Hebert PR, Satterfield S, Taylor JO, Buring JE, Hennekens CH.
Height, lung function, and mortality from cardiovascular disease among the
elderly. Am J Epidemiol 1994;139:1066 –76.
14. Leon DA, Smith GD, Shipley M, Strachan D. Adult height and mortality in
London: early life, socioeconomic confounding, or shrinkage? J Epidemiol
Community Health 1995;49:5–9.
15. Rich-Edwards JW, Manson JE, Stampfer MJ, et al. Height and the risk of
cardiovascular disease in women. Am J Epidemiol 1995;142:909 –17.
16. Waaler HT. Height, weight and mortality: the Norwegian experience. Acta
Med Scand 1984;Suppl 679:1–56.
17. Notkola V, Punsar S, Karvonen MJ, Haapakoski J. Socio-economic conditions in childhood and mortality and morbidity caused by coronary heart
disease in adulthood in rural Finland. Soc Sci Med 1985;21:517–23.
18. Strachan DP. Ventilatory function, height, and mortality among lifelong
non-smokers. J Epidemiol Community Health 1992;46:66 –70.
19. Walker M, Shaper AG, Phillips AN, Cook DG. Short stature, lung function
and risk of a heart attack. Int J Epidemiol 1989;18:602– 6.
20. Barker DJP, Osmond C. Infant mortality, childhood nutrition, and ischaemic
heart disease in England and Wales. Lancet 1986;1:1077– 81.
21. Martyn CN, Barker DJP, Jespersen S, Greenwald S, Osmond C, Berry C.
Growth in utero, adult blood pressure, and arterial compliance. Br Heart J
1995;73:116 –21.
22. Weintraub WS, Wenger NK, Kosinski AS, et al. Percutaneous transluminal
angioplasty in women compared with men. J Am Coll Cardiol 1994;24:81–90.
23. O’Rourke M. Arterial Function in Health and Disease. Edinburgh:
Churchill-Livingstone, 1982;170 – 82.
24. Westerhof N. Heart period is related to the time constant of the arterial
system and not to minimum of impedance modulus. In: Hosoda S, Yaginuma
T, Sugawara M, Taylor MG, Caro CG, editors. Recent Progress in Cardiovascular Mechanisms. Newark (NJ): K. Harwood Academic Publishers,
1994:115–28.
25. London G, Guerin A, Pannier B, Marchais S, Benetos A, Safar M. Increased
systolic pressure in chronic uremia: role of arterial wave reflections. Hypertension 1992;20:10 –9.
26. Marchais SJ, Guerin AP, Pannier BM, Levy BI, Safar ME, London GM.
Wave reflections and cardiac hypertrophy in chronic uremia: influence of
body size. Hypertension 1993;22:876 – 83.
27. London GM, Guerin AP, Pannier BM, Marchais SJ, Metivier F. Body height
as a determinant of carotid pulse contour in humans. J Hypertens 1992;10
Suppl 6:S93–5.
28. London GM, Marchais SJ, Safar ME, et al. Aortic and large artery
compliance in end-stage renal failure. Kidney Int 1990;37:137– 42.
29. Roman MJ, Saba PS, Pini R, et al. Parallel cardiac and vascular adaptation
in hypertension. Circulation 1992;86:1909 –18.
30. London GM, Pannier B, Guerin AP, Marchais SJ, Safar ME, Cuche JL.
Cardiac hypertrophy, aortic compliance, peripheral resistance, and wave
reflection in end-stage renal disease: comparative effects of ACE inhibition
and calcium channel blockade. Circulation 1994;90:2786 –96.
31. Kelly R, Daley J, Avolio A, O’Rourke M. Arterial dilation and reduced wave
reflection: beneficial effects of Dilevalol in hypertension. Hypertension
1989;14:14 –21.
32. O’Rourke MF. Arterial Function in Health and Disease. Edinburgh:
Churchill-Livingstone, 1982:94 –132, 185–243.
33. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 3rd ed. London: Lea & Febiger,
1990:216 –50.
34. Kroeker EJ, Wood EH. Comparison of simultaneously recorded central and
peripheral arterial pressure pulses during rest, exercise and tilted position in
man. Circ Res 1955;3:623–32.
35. Armentano R, Megnien JL, Simon A, Bellenfant F, Barra J, Levenson J.
References
1. Gertler MM, Garn SM, White PD. Young candidates for coronary heart
disease. JAMA 1951;147:621–5.
2. Vlietstra RE, Frye RL, Kronmal RA, Sim DA, Tristani FE, Killip T. Risk
factors and angiographic coronary artery disease: a report from the Coronary
Artery Surgery Study (CASS). Circulation 1980;62:254 – 61.
3. Marmot MG, Shipley MJ, Rose G. Inequalities in death-specific explanations of a general pattern? Lancet 1984;1:1003– 6.
4. Fisher LD, Kennedy JW, Davis KB, et al. Association of sex, physical size,
and operative mortality after coronary artery bypass in the Coronary Artery
Surgery Study (CASS). J Thorac Cardiovasc Surg 1982;84:334 – 41.
5. Peck A, Vagero DH. Adult body height, self perceived health and mortality
in the Swedish population. J Epidemiol Community Health 1989;43:380 – 4.
6. Smith GD, Shipley MJ, Rose G. Magnitude and causes of socioeconomic
differentials in mortality: further evidence from the Whitehall study.
J Epidemiol Community Health 1990;44:265–70.
7. Barker DJP, Osmond C, Golding J. Height and mortality in the counties of
England and Wales. Ann Hum Biol 1990;17:1– 6.
8. Palmer JR, Rosenberg L, Shapiro S. Stature and the risk of myocardial
infarction in women. Am J Epidemiol 1990;132:27–32.
JACC Vol. 31, No. 5
April 1998:1103–9
36.
37.
38.
39.
41.
Effects of hypertension on viscoelasticity of carotid and femoral arteries in
humans. Hypertension 1995;26:48 –54.
Benetos A, Laurent S, Hoeks AP, Boutouyrie PH, Safar ME. Arterial
alterations with aging and high blood pressure: a noninvasive study of carotid
and femoral arteries. Arterioscler Thromb 1993;13:90 –7.
Murgo JP, Westerhof N, Giolma JP, Altobelli SA. Aortic input impedance in
normal man: relationship to pressure wave forms. Circulation 1980;62:105–
16.
Buckberg GD, Towers B, Paglia DE, Mulder DG, Maloney JV. Subendocardial ischemia after cardiopulmonary bypass. J Thorac Cardiovasc Surg
1972;64:669 – 84.
Hoffman JIE, Buckberg GD. The myocardial supply: demand ratio—a
critical review. Am J Cardiol 1978;41:327–32.
Avolio AP, Chen SG, Wang RP, Zhang CL, Li MF, O’Rourke MF. Effects
of aging on changing arterial compliance and left ventricular load in a
northern Chinese urban community. Circulation 1983;68:50 – 8.
SMULYAN ET AL.
BODY HEIGHT AND ARTERIAL HEMODYNAMIC DATA
1109
42. Kelly R, Karamanoglu M, Gibbs MB, Avolio A, O’Rourke M. Noninvasive
carotid pressure wave registration as an indicator of ascending aortic
pressure. J Vasc Med Biol 1989;1:241–7.
43. Weber KT, Janicki JS. Instantaneous force-velocity-length relations in
isolated dog heart. Am J Physiol 1977;232:H241–9.
44. Latham RD, Westerhof N, Sipkema P, Rubal BJ, Reuderink P, Murgo JP.
Regional wave travel and reflections along the human aorta: a study with six
simultaneous micromanometric pressures. Circulation 1985;72:1257– 69.
45. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. New York: Arnold/Oxford
University Press, 1998:371–2.
46. Bonaa KH, Arnesen E. Association between heart rate and atherogenic
blood lipid fractions in a population: the Tromso study. Circulation 1992;
86:394 – 405.
47. Barnard RJ, MacAlpin R, Kattus AA, Buckberg GD. Ischemic response to
sudden strenuous exercise in healthy men. Circulation 1973;48:936 – 42.